Visit our website for additional outstanding products E LSEVI ER SCI ENCE
www.elsevierhealth.com
A System of Orthopaedic Medicine
We dedicate this book to our long-suffering wives and children and thank them for their patience, understanding and support.
For Chllrchill Livingstone: Editorial Director, Health Professions: Mary Law Project Development Manager: Dinah Thorn Project Manager: Derek Robertson Designer: Judith Wright
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
/�\ �� :u
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
U�
of drug.,
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 advi<>ed to confinn that the information, e'ipecial1y with regard to drug u:,age, complies with the latest legislation and standards of practice.
Tho
_. policy kS to use piper manutlCtured from 1U1l1inlble lorHl'
Printed
In
China by RDc.. Lroup Umitl'
I
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).
REFERENCES 1 . Bon.ica H, Albe Fessard D. Advances in Pain Research and Therapy. Raven Press, New York, 1976. 2. Elton D, Stuart GV, Burrows GD. Self-esteem and chronic pain.
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!
hyaluronan chain
pro
O""'
���il�
Figure 3.1 The complex shape of proteoglycans. Polysaccharide molecules (GAGs) bound to a central protein core: proteoglycans are in turn bound to a long central chain of hyaluronan to form a proteoglycan aggregate. This arrangement is typical of cartilage. In other types of connective tissue hyaluronan chains may be absent. Redrawn from Walker PS4 with permission .
because of the negative charges, remains stable; removal of the load immediately remodels the origi nal position of the fibres (Fig. 3.2). The ability to resist compressive forces is best illustrated by the proteo glycans of articular cartilage. aggregate of proteoglycans
collagen fibre Impression of the interaction between proteoglycan aggregates and collagen fibres in cartilage. The negatively charged GAGs in proteoglycans influence the arrangement of the positively charged collagen fibres. In load conditions collagen is moved but because of these charges constantly steered and stabilized.
Figure 3.2
Fibrous elements The fibrous elements are collagen and elastin - both insoluble macromolecular proteins. Collagen is the main structural protein of the body with an organization and type that varies from tissue to tissue. Collagen fibres are commonest in ordinary connective tissue such as fascia, ligament and tendon. The fibrillar forms have great tensile strength but are relatively inelastic and inextensi ble. By contrast elastin can be extended to 150% of its original length before it ruptures. Elastin fibres return a tissue to its relaxed state after stretch or other consider able deformation. They lose elasticity with age when they tend to calcify. Box 3.1 outlines the components of collagen. The basic molecule of collagen is procollagen, synthe sized in the fibroblast, illustrated in Figure 3.3, boxes 1-4. It is formed of three polypeptide chains (a-chains). Each chain is characterized by repeating sequences of three amino acids - glycine, proline and lysine joined together in a triple helix. The helical molecules are secreted into the extracellular space where they slowly polymerize and crosslink (Fig. 3.4). They overlap each other by a quarter of their length, lie parallel in rows and are collected into large insoluble fibrils. The fibrils unite to form fibres, finally making up a bundle. An aggregate of bundles
CHAPTER 3 - CO N N E CTIVE TISS U E 3 5
Box 3.1 Components of connective tissue Cells • fibroblasts ....... fibrous connective tissue • chondrocytes ....... cartilage • osteoblasts and osteocytes ....... bone Extracellular matric • fibres: collagen ....... framework of the ECM elastin--.. extensible element of ECM • proteoglycans: hydrators. stabilizers and space fillers of ECM • glycoproteins: stabilizers and linkers of ECM • fluid
makes up a whole structure such as a ligament or a tendon. The individual bundles are in coils which increases their structural stability and resilience and permits a small physiological deformation before placing the tissue under stress and in consequence permits a more supple transfer of tractive power in the structure itself and at points of insertion (Fig. 3.5). The process of collagen synthesis is stimulated by some hormones (thyroxine, growth hormone and testosterone) although corticosteroids reduce activity.
1
Amino acids
Figure 3 . 4 Crosslinking a n d interspaces between head a n d tall o f neighbouring tropocollagen molecules. They overlap each other by a quarter of their length. Molecules in the same parallel row are separated from each other by small interspaces.
Connective tissue collagen can be classified into different types of which at least 14 are now genetically characterized and the others are being investigated. In the context of this book the most important are: •
•
2 Assembly 01
Type I: the most abundant of all collagen. Strong thick fibres packed together in high density. It predominates in bone, tendon, ligament, joint capsule and the annulus fibrosus of the intervertebral disc. Type II: thin fibres found in articular cartilage and the nucleus pulposus of the intervertebral disc. They
3 Hydroxylalion of proline and lysine in
polypeptide chain
including glycine.
polypeptide chain
proline and lysine
4 Assembly of Ihree hydroxylated polypeptide chains into one procollagen molecule
synthesis of mucopolysaccharides in Goigi apparatus and addition to protein
Ground substance ..------J�
8 Aggregation of
7
Aggregation of
Passage of
5 Addtion of
tropocollagen to
procollagen to
carbohydrate
form collagen fibres
form collagen fibrils
extracellular space
mOiety
and bundle of fibres
==
Figure 3.3
6
collagen fibrils to
Diagram showing the successive steps in collagen synthesis by fibroblasts.
36 SECTION ONE - G ENERAL PRINCI PLES
to the stress they experience. Collagen bundles in liga ments and tendons are very strong and rupture usually takes place at the bony attachments rather than by tearing within their substance. The tensile strength of col lagen has been estimated at 50-125 N / mm2, depending on the specimen tested.6 Other studies have reported loads on human collagen with failure of 40 kg with the anterior cruciate ligament and 91 kg for the plantar fascia.5,7 It is the regular arrangement of intermolecular bonds or crosslinks between adjacent molecules that gives collagen its high tensile strength.
Irregular types The irregular types consist of collagen and elastin inter lacing in all directions. It is loose, extensible and elastic and found between muscles, blood vessels and nerves. It binds partly together although allowing a considerable amount of movement to take place. In the sheaths of muscles and nerves and the adventitia of large blood vessels, the tissue is more dense with a high proportion of collagen fibres to protect these structures against considerable mechanical stress. The dura mater is also an example of an irregular connective tissue sleeve.
(b) Figure 3.5 (a) Unloaded collagen fibres in a human knee ligament. (b) Physiological deformation after stress. From Kennedy et a/5 with permission.
•
particularly function in association with a high level of hyaluronan and sulphated proteoglycans to provide a hydrated and pressure-resistant core. Type III: essentially present in the initial stages of wound healing and scar tissue formation. It secures early mechanical strength of the newly synthesized matrix. These relatively thin, weak fibres are replaced by the strong type I fibres as healing proceeds.
In relation to the degree of orientation of fibrous tissue elements, ordinary connective tissues can also be classified into regular and irregu lar types (Fig. 3.6).
Regular types Highly fibrous tissues such as ligaments, tendons, fascia and aponeuroses are predominantly collagenous and show a dense and regular orientation of the fibres with respect to each other. The direction of the fibres is related
Vascularization Connective tissue is poorly supplied with blood vessels. In dense fibrous tissues these usually run parallel to and between the longitudinal bundles with communicating branches across these. Lymphatic vessels are more numerous, especially in loose connective tissues such as the dermis. They are also abundant in tendons and tendon sheaths. Innervation Dense connective tissues, for example, ligaments, tendons and fascia, have a rich supply of afferent nerve endings. The various sensory receptors transmit informa tion to the central nervous system about changes in length and tension which allows constant monitoring of the position and movement of a joint as well as of injurious conditions that threaten these structures. Structural and physiological studies8,9 have shown the presence of at least four types of receptor. Three of these have encapsulated endings but the fourth consists of free unencapsulated endings. •
•
Type 1 (Ruffini endings) are present in the superficial layers of a fibrous joint capsule. They respond to stretch and pressure within the capsule and are slow adapting with a low threshold. They signal joint position and movement. Type 2 are particularly located in the deep layers of the fibrous capsule. They respond to rapid
CHAPTER 3 - CONN ECTIVE TISS U E 37
•
•
movement, pressure change and vibration but adapt quickly. They have a low threshold and are inactive when the joint is at rest. Type 3 are found in ligaments. They transmit informa tion on ligamentous tension so as to prevent exces sive stress. Their threshold is relatively high and they adapt slowly. They are not active at rest. Type 4 are free unencapsulated nociceptor terminals which ramify within the fibrous capsule, around adja cent fat pads and blood vessels. They are thought to sense excessive joint movements and also to signal pain. They have a high threshold and are slow adapt ing. Synovial membrane is relatively insensitive to pain because of the absence of these nerve endings.
All these receptors influence muscle tone via spinal reflex arcs which are formed by the same nerves that supply the muscles which act on the joint. Parts of the joint capsule supplied by a given nerve correspond with the antagonist muscles. Tension on this part of the capsule produces reflex contraction of these muscles to prevent further overstretching of the capsule. In conse quence all receptors have an important function in sta bilization and protection of the joint. After rupture of a capsule, ligament perception is considerably disturbed because of the disruption of the transmission of afferent information. For example in a sprained ankle there is loss of control of locomotion. Even months after repair of ligamentous and capsular tissues has taken place, perception may still be distorted.
STRUCTURES CONTAINING CONNECTIVE TISSUE
Joint capsules and ligaments (Fig. 3.7) In synovial articulations the bones are linked by a fibrous capsule of parallel and interlacing connective tissue fibres - a cuff that encloses the joint cavity. With some exceptions, each end is attached in a continuous line around the artic ular ends of the bones concerned. Within this the capsule is lined by synovial membrane. Localized thickenings in the capsule form the ligaments of the joint - tough and unyielding collagen fibres that generally lie parallel to each other. Some joints also have ligaments that are extra- or intracapsular in position. Capsuloligamentous structures attach to the bone in two different ways: • •
Figure 3.6
Connective tissue: A, regular (Aa, ligament; Ab, tendon); S, irregular.
Superficial fibres attach to the periosteum. Deeply situated fibres penetrate the bone, change into fibrocartilage and mineralized fibrocartilage and fuse with bone collagensJO (Fig. 3.8). This arrangement helps to transmit tensile forces onto a broad area at the junction of ligaments or tendons with bone; the chance of failure under excessive load is thus reduced.
38 SECTION ONE - G ENERAL PRINCIPLES
Synovial membrane --+�.......,.
........:; .. -----1 ; t:ot-t- Articular cartilage
Figure 3.7
Example of a synovial joint.
Ligaments restrict the freedom of movements at joints in an indirect way and must be seen, with some excep tions, as local reinforcements of the joint capsule at points of special stress. In ligaments, collagen comprises about 70-80% of the dry weight in contrast to elastin which is only 3-5%. The proteoglycan content is also low. Tissue collagen in these structures is responsible for their resist ance to deformation and individual collagen fibres deform only slightly (6-8%). Other parts of the capsule are thin, pliant and somewhat elastic to allow flexibility during normal movement. The mechanical response of a ligament to a load can be represented on a load-deformation curve (Fig. 3.9). In the first part of such a curve (its foot) the ground substance is almost completely responsible for absorbing the stress and displaces the fibres in the direction of the stress. When the load is increased, ligamentous tissue responds slowly and maximum resistance to distraction is only possible if there is enough time for realignment of the col lagen bundle. The linear part of the curve shows the slow elastic stretching of the collagen. During this stage, recov ery of the original shape of the tissue occurs when the deforming load is removed. This slow rate of deforma tion is known as 'creep deformation'. Even in this linear part of the curve, breaking of intermolecular crosslinks begins. For this reason it is assumed that, in physiological circumstances, the load on ligaments is kept within that shown in the foot of the curve, where collagen is not yet under undue strain and the role of ground substance is
Figure 3.8 Attachment of ligament to bone. Deeply situated fibres change into fibrocartilage and mineralized fibrocartilage before penetrating the bone and fuse with bone collagen. From Ham10 with permission.
maximal.ll The composition and the amount of gel ground substance are therefore important in load bearing. On reaching the yield point, a non-elastic or plastic deformation occurs and the ligament progres sively ruptures. Some investigators have found that in bone-ligament-bone preparations separation occurs at the point of insertion.12 In normal circumstances, mechanical stress i nduces early firing of mechanoreceptors in capsuloligamentous
o
Deformation (in
%)
-7%
Diagram showing the mechanical response of the anterior cruciate ligament of the knee to a load. 1. Foot of the curve, the ground substance alone almost completely absorbs the stress. 2. Linear part of the curve, slow elastic stretching of the collagen which is known as 'creep deformation'. 3. Yield point. A non-elastic or plastic deformation occurs. 4 and 5. The ligament progressively ruptures. Redrawn from FrankeP2 with permission.
Figure 3.9
C HAPTER 3 - CON N E CTIVE TISSUE 39
tissues. This causes a well-balanced reflex action of all musculotendinous units acting across the joint to avoid inert tissue becoming overloaded and damaged. If this muscular defence fails, strain falls on the ligament which is w1able to stabilize the joint and so ruptures.
Synovial membrane and fluid The synovial membrane lines the non-articular parts of synovial joints such as the fibrous capsule and the intra-articular ligaments and tendons within the margins of articular cartilage. The internal surface of the membrane has a few small synovial villi which increase in size and number with age. It also has flexible folds, fringes and fat pads. These accommodate to movement so as to occupy potential spaces and may promote the distribution of synovial fluid over the joint surfaces. Structurally the membrane consists of a cellular intima one to four cells deep that rests upon a loose connective tissue subintima and contains the vascular and lymphatic network which has an important function in the supply and removal of fluid. On ultrastructural examination, two cell types (A and B) are apparent. These are closely involved not only with the production of synovial fluid1 3 but also in the absorption and removal of debris from the joint cavity. The A cells especially have marked phago cytic potential.14 Some synovial cells can also stimulate the immune response by presenting antigens to lympho cytes if a foreign material threatens the joint cavity.15 Synovial fluid is a clear, viscid (glairy) substance formed as a dialysate but it does contain some protein. It occurs not only in synovial joints but also in bursae and tendon sheaths. Secretion and absorption are functions of the cells of the intima and of the vascular and lymphatic plexus in the subintima. The synovial initima cells also secrete hyaluronan molecules into the fluid and much evidence has accumulated to show that the viscoelastic and plastic properties of the fluid are largely determined by its hyaluronan content. Chains of hyaluronan bind proteins; these complexes are negatively charged and in turn bind water. The biophysical process is similar to that of the proteoglycans in the matrix of connective tissue and a thick viscous liquid which resembles egg white is formed. Its viscosity varies widely according to circum stances. With a low rate of shear, water is driven out of the hyaluronan-protein complexes and the fluid becomes highly viscous; increase in shear lowers viscosity and the fluid tends to behave more like water. In contrast to vis cosity, elasticity increases with higher rates of shear. Both viscosity and elasticity decrease with increasing pH and temperature.16 Cartilage Articular cartilage is essentially a specialized type of connective tissue.
Composition. Although the same three tissue elements - cells, ground substance and fibres - are present, their properties differ from ordinary connective tissue and determine its biochemical and biomechanical behaviour.
The composition of proteoglycans in the ground sub
In the superficial layer, chrondroitin sulphate is a prominent constituent in the GAGs but the deeper layers contain more and more keratan sulphate. A high concentration of chrondroitin sulphate stimulates the condensation of thin collagen fibres to form a dense network at the surface but keratan sulphate enhances syntheSiS of thick, easily movable fibres in the deeper layers. This adapted synthesis influences the local architecture and strength and resist ance to compressing and shearing forces. stance changes with increasing deptb.
Cartilage cells or chondrocytes occupy small spaces in the
They are involved in the production and turn over both of type II collagen and ground substance, processes stimulated by variation in load. Chondrocytes change with increasing depth from the surfacel,17 (Fig. 3.10). In the superficial stratum (zone 1), cells are small, flattened and disposed parallel to the surface. They are surrounded by fine tangentially arranged collagen fibres. A thin superficial layer of this zone has been shown to be cell-free. Cell metabolism in this part is low, which is consistent with the absence of wear and tear in normal healthy tissue. The cells of the intermediate stratum (zone 2) are larger and more
matrix.
Zone 1 Zone 2
Zone 3
'tide mark' Zone 4
Subchondral bone
Figure 3.10 Zones in articular cartilage. Zone 1, cells, small and flattened, disposed parallel to the surface; zone 2, cells become larger and more rounded; zone 3, cells are largest and arranged in columns, perpendicular to the surface; zone 4, mineralized cartilage. The border between mineralized and non mineralized cartilage is called the 'tide mark'.
40
S ECTION O N E - G ENERAL PRI N C I PLES
rounded and those in the radiate stratum (zone 3) are la rge, rounded and arranged in columns perpendicular to the surface. In these deeper zones, cells are screened from the coarse fibres by a coat of pericellular matrix bordered by a network of fine collagen fibres. In this way, cells are protected against the stresses generated by load conditions. The collagen fibres vary in structure and position with
In the superficial or tangential stratum, a dense network of fine fibrils is arranged tangential to the articular surface to resist tensile forces that result from compression on certain points of the articulating surface during normal activities. Analysis has also shown the existence of certain 'tension trajectories' in accordance with the more or less fixed patterns of tensile forces that take place during movements. These preferential directions have been elab orated during growth as a result of forces acting on the joint. Near the border of the joint, the fibrils blend with the periosteum and joint capsule. In the intermediate stratum, collagen fibres are coarser and more spread out to pursue an oblique course that forms a three-dimensional network. In non load conditions the fibres are orientated at random but when load is applied they are immediately stretched in a direction perpendicular to that of the applied force (Fig. 3.11b). When the load is removed the fibres return to their original oblique position. This behaviour partly explains the resilience and elasticity of cartilagenous tissue. increasing depth from the surface (Fig. 3.11a).
(a)
(c) • \
I �
(a) Arrangement of collagen fibres in articular cartilage. (b) and (c) Functioning of collagen fibres in articular cartilage. (b) non-load condition, (c) during load they are stretched in a direction perpendicular to the direction of force.
Figure 3.11
In the radiate stratum, collagen fibres are arranged radially and correspond with the fibrous architecture of the subchondral and osseous lamina. The result is a series of arcades which extend from the deepest zone towards the surface. Characteristics of cartilage. These include low metabolic and turnover rates, rigidity, high tensile strength, and resistance to compressing and shearing forces while some resilience and elasticity is retained. The proportion of collagen in matrix increases with age. On the basis of variations in the matrix and the number of fibres present, cartilage in the locomotor system is divided into two types: hyaline and fibroelastic. Most cartilage is hyaline: exceptions are the surfaces of the sternoclavicular and acromioclavicular joints and of the temporomandibular joints, all of which are of dense fibrous tissue. Although the light microscope appearance of hyaline cartilage is translucent, electron microscopy shows a system of fine fibrils and fibres. The water content is up to 80%. Strength, resistance and elas ticity are the results of the proteoglycans in the ground substance together with the specific properties of the collagen fibres. Negatively charged proteoglycans bind a large number of water molecules and causes the cartilage to swell. Swelling is limited, however, by the increasing tension of the collagen fibre networks in the superficial and deep layers which are closely intercon nected. The result is an elastic buffer that, together with the elasticity of the periarticular structures, dissipates the effect of acute compressive forces. It also provides the articular mechanism with some degree of flexibility, particularly at the extremes of range. If the load is applied over a very short time, cartilage deforms in an 'elastic' way almost without disturbance of its water content. However, if compression is maintained for hours, water is displaced to surrounding regions that are under less or no compression and the compressed cartilage undergoes 'plastic' deformation. In engineer ing terms, this slow predictable rate of deformation is known as 'creep' and is greatest wi thin the first hour of compression. When the deforming load is removed, recovery of the original shape of the tissue occurs at a rate that is specific for each form of cartilage. Water transport during dynamic load conditions prob ably also has significance in the transport of nutrients and metabolites to and from the chondrocytes. Articular cartilage lacks a nerve supply and is also completely avascular. Nutrition is derived from three sources: synovial fluid, vessels of the synovial mem brane and vessels in the underlying marrow cavity which penetrate the deepest part of the cartilage over a short distance. This last source is available only during growth because, after growth is completed, the matrix at the deepest part of the cartilage becomes impregnated
CHAPTER 3 - CONN ECTIVE TISSUE 41
vJith hydroxyapatite crystals which form a zone of calcified cartilage impenetrable by blood or lymph vessels (Fig. 3.10, zone 4). Articular discs and menisci consist of fibroelastic carti lage and are predominantly fibrous. They separate certain articular surfaces that have a low degree of con gruity (e.g. the knee and the radiocarpal joint). Their functional roles are to improve the fit between joint surfaces, distribute weight over a larger surface, absorb impacts and spread lubricant. With age articular cartilage becomes firmer but also thinner and more brittle. The number of cells decreases. In normal healthy joints these changes are extremely slow. Erosion particularly occurs when joints become dehydrated or when synovial fluid viscosity perma nently alters. Replacement of an eroded surface by prolif eration of deeper layers has not been demonstrated. Deposits of calcification and surface ruptures are signs of degeneration. Except in young children regeneration cannot be expected. However, there is evidence that a defect can be filled with newly synthesized collagen.
Synovial bursae In situations where skin, tendons, muscles or ligaments move in relation to other structures under conditions that involve fluctuating pressure, synovial bursae are formed to reduce friction. They can be compared with flattened sacs of synovial membrane which create discontinuity between tissues and provide complete freedom of movement over a short distance. A capillary film of synovial fluid on their internal surfaces acts as a lubricant. Depending on their position they are classified as subcutaneous, subtendinous, submuscular or subfascial bursae. Sometimes they communicate with the joint cavity with which their synovial membranes are continuous. Nerves Peripheral nerves also possess supporting connective tissue. Within the nerve trunk the efferent and afferent axons are grouped together in a number of fasciculi (Fig. 3.12). The bundled axons in the fasciculi lie roughly parallel, surrounded by loose delicate collagen fibres running longitudinally along them. Both struc tures show a wavy appearance which disappears when gentle traction is applied. Each fasciculus is surrounded by a fibrous perineurium, a regular structure of flattened laminae of fibroblasts alternating with fine collagen, running in various direc tions. These fibroblasts are connected together and form a diffusion barrier against noxious chemical products, bacteria and viruses. In this way, the enclosed axons are to some extent isolated from the external environment. Inside this perineural tube a protein-poor liquid flows
centrifugally. This axoplasma is cerebrospinal fluid, which is re-assimilated into the blood circulation at the end of the peripheral nerve. In this respect, the spinal canal and the endoneural spaces are continuous. The epineurium encases the nerve trunk as a collagen coat with little regular organization. Connective tissue surrounding nerves serves as an important mechanical protection to maintain the conductile properties of the nerve .IS During movement, nerves are potentially exposed to tensile forces that can be avoided by mobil ity in relation to surrounding structures. Here, the wavy form of both axons and surrounding collagen fibres is an important consideration: this 'waviness' of the axons is paramount, allowing them to remain relaxed even when the collagen fibres are stretched. Thus, within the normal range of movement, the axons will be protected by the tensile force of the collagen component. When there is a severe sprain or fracture perhaps with disloca tion, the range of plastic deformation of collagen can be exceeded and ultimately rupture of collagen fibres and neurotmesis results. The tolerance of nerves to tension is much greater than it is to compression. However, the mobility of nerves allows them to move laterally, so avoiding a compressive force. When space is inadequate for such movement or the nerve is firmly anchored - which is the case in cervi cal nerve roots - the epineurium may absorb a certain amount of pressure but sooner or later the blood supply within the nerve is affected by increasing compression. Further compression may result in interference with the conductile properties of the nerve. In such circumstances, the Schwann cells and subsequently the myelinated sheath are damaged. Although the axons remain intact, action potentials become blocked, leading to loss of sensory and motor function (see Ch. 2). nerve trunk
fasciculus with bundled axons surrounded by endoneurium
axon
Figure 3.12 Connective tissue in peripheral nerves: epineurium, a collagen coat that encases the nerve trunk; perineurium, fine collagen and laminae of fibroblasts that surround each fasciculus; endoneurium, loose delicate collagen that surround axons in the fasciculi.
42
SECTION O N E - G E N ERAL PRI NCI PLES
Muscles Muscular tissue consists of specialized cells or myofibrils embedded in a network of fine connective tissue that transmits the pull of the muscle cells during contraction to the adjacent parts of the skeleton. For this purpose, connections exist between the muscle cells and the finest collagen fibres of the connective tissue network. The muscle cell or myofibril consists of sarcomeres or myofilaments - the basic contractile units of a muscle arranged in parallel (Fig. 3.13). In each sarcomere two types of filament are distinguishable, chemically charac terized as actin and myosin. The actin filaments are each attached at one end to the inner side of the cell mem brane forming the so-called Z-line. At the other end they are free and interdigitate with the central myosin filaments. During muscle contraction, the actin filaments slide in relation to the myosin towards the centre of the sarcomere which brings the attachments at the Z-lines closer together with shortening of the whole contractile unit. Exercises increase the number of myofibrils (hyper trophy). During periods of immobilization cell volume decreases (atrophy). Groups of sarcomeres are arranged in parallel to form muscle fibres. These in turn are arranged in bundles or fasciculi of various sizes within the muscle. The network of the fine collagen fibrils within a fascicu lus is known as the endomysium and fills the spaces between muscle fibres. In this way, each muscle fibre is surrounded by a thin sheet of connective tissue that pro vides the pathway for the capillaries, which lie mainly par allel with the muscle fibres and facilitate the exchange of metabolites between muscle fibres and the capillary bed. The perimysium is the stronger connective tissue that surrounds each fasciculus. It consists of parallel bundles of collagen that are partly arranged in a circular manner around the muscle fibres as well. These bundles are in close connection with the collagen of the endomysium. Finally, the whole muscle is surrounded by the stout epimysium, which is continuous with the septa of the outer perimysium and blends with the connective tissue that forms the tendon, fascia or aponeurosis. At the myotendinal junctions the connective tissue of the endo-, peri- and epimysium becomes very fibrous and thickens, whereas the muscle fibres taper or flatten and show terminal expansions. The connection is so strong that rupture hardly ever occurs at the tendon or at the insertion of the tendon into bone and seldom at the myotendinal junction. Nerve supply to muscles. Skeletal muscles are supplied by one or more nerves. Each may contain both motor and sensory fibres. The motor fibres comprise a-efferents, which supply extrafusal muscle fibres, 'Y-efferents, which
fasciculus
myofilaments
Diagram showing the various levels of organization within a skeletal muscle, from whole muscle through fasciculi, fibres, myofibrils, myofilaments, down to molecular dimensions. The myofilaments are the basic contractile units of a muscle. Groups of myofilaments are arranged in parallel to form muscle fibres. These, in turn, are arranged in bundles or fasciculi. A network of connective tissue transmits the pull of the muscle cells during contraction via a tendon to the adjacent parts of the skeleton.
Figure 3.13
CHAPTER 3
-
CONNECTIVE TISSUE 43
run to the muscle spindles, and autonomic efferents, which supply the smooth muscles of the vascular wall. A single ex motor neurone umervates each muscle fibre unit, which may contain from 1 to 2000 fibres. This functional unit is a motor unit. Sensory fibres are distributed among the muscle spindles and nociceptors.
Tendons These structures are largely composed of collagen fibres with a low amount of proteoglycans. On a dry weight basis, collagen represents 60-80% of the total weight of tendon.19 Tendons, which consist of fascicles of collagen fibres nmning parallel and partly interweavu1g, are highly resist ant to extension (Fig. 3.14). Although elastin is absent and their collagen is difficult to stretch, tendons are neverthe less slightly stretchable. The wavy form of the fibres, together with the interweaving pattern of the fascicles, results in a slight elongation at the moment of muscle con traction which damps any abrupt pull on the insertion. At the surface, the epitendineum or tendon sheath consists of irregularly arranged condensed collagen as well as elastin fibres. It is continuous with the loosely arranged connective tissue that permeates the tendon between its fascicles and provides a route of ingress and egress for vessels and nerves. At the insertion, the colla gen bundles of the tendon permeate into bone. It has been shown2o,21 that the insertion of the connective tissue of ligaments into bone involves a transition from non mineralized through mineralized fibrocartilage to bone. In young growing tendons, fibril diameter and tensile strength can be increased by exercise. In adults, however, the effect is minimal although regularly applied tension is necessary to maintain structural integrity. Immobilization has demonstrated loss of tensile strength (see below, p. 46). The nerve supply to tendons appears to be entirely afferent. Vascularization of tendons is low - the reason they appear white. Small arterioles ramify U1 the inter-
Phalanx distalis
Figure 3.14 Fascicles of collagen fibres forming a tendon. Redrawn from Warwick and Williams1 with permission.
fascicular intervals and are accompanied by veins and lymphatic vessels. Passage of vessels through the teno osseous junction seems not to occur. Where tendons pass under ligamen ts or through osteofibrous tunnels, synovial sheaths are formed which separate the tendon completely from its surroundings. These synovial sheaths have two concentric layers, sepa rated by a thin film of synovial fluid and form a closed double-walled cylinder (Fig. 3.15). The fluid acts as a lubricant and ensures easy mobility of the tendon. The internal (visceral) layer is attached to the tendon and the external (parietal) layer to neighbouring structures such as periosteum and retinaculum.
TRAUMA TO SOFT CONNECTIVE TISSUE
INTRODUCTION Soft tissue injury involves damage to the structural elements of connective tissue with ruphlre of arterioles and venules. A general inflammatory reaction follows (Table 3.1), one role of which is defensive in that it prompts the subject to restrict activities while recovery takes place.
_ -:� Phalanx proximalis _ :.--=.,.",.,
L----Vagina synovial is --------' '------Tendon --------'
Figure 3.15 Synovial sheath of the deep flexor tendon of a finger.
44 SECTION ONE - G ENERAL PRI NCIPLES
Table 3.1 Stages of repair after mechanical damage to soft connective tissue
Stage
Reaction Inflammation: clearance of debris and preparation for repair Vasoconstriction (5-10 min) followed by vasodilatation and increased capillary permeability leading to: Exudation Liquid component Fibrinogen Cellular component Granulation: formation of scar tissue Vascular infiltration Fibroblast proliferation
III
(48 h to 6 weeks)
Remodelling (starts at the third week and may continue for 1-3 years): Devascularization Maturation Remodelling
Regardless of the site of injury and the degree of damage, healing comprises three main phases: inflamma tion, proliferation (granulation) and remodelling. These events do not occur separately but form a continuum of cell, matrix and vascular changes that begin with the release of inflammatory mediators and end with the remodelling of the repaired tissue. Connective tissue regenerates largely as a consequence of the action of inflammatory cells, vascular and lymphatic endothelial cells and of fibroblasts.22,23
INFLAMMATION The first reaction is vasoconstriction of small local arteri oles that lasts about 5-10 minutes and is followed by active vasodilatation and increased blood flow for 1-3 days. In major injuries with damage to blood vessels, blood escapes to form a haematoma that temporarily fills the injured site. Within the haematoma, fibrin accumu lates and platelets bind to collagen fibrils to form a clot that provides the framework for invasion of vascular cells and fibroblasts.24 The vascular changes and further inflammatory reactions are initiated by chemical media tors released from destroyed tissue cells.25,26 Mast cells release heparin (anticoagulant) and histamine (vascular dilator). Plasma cells produce bradykinins and sub stance P (pain and vasodilatation). Platelets produce serotonin, prostaglandins and growth factors that stimulate migration, proliferation and differentiation of cells.27,28 In addition, mediators cause migration of leukocytes into the injured area and swelling of the endothelial cells that line vascular channels. The endothelial cells pull away from their attachment to each other to leave sizeable gaps between cells that increase
the permeability of vessels and so allow plasma, cells and proteins to escape. As a result, the presence of these proteins enhances the flow by osmosis of more plasma into the injured extracellular space. The whole process is the exudative phase. The liquid part of the plasma exudate dilutes potentially noxious substances and products of cell destruction and helps in their elimination by the supply of globulins and enzymes. Another important substance is fibrinogen which forms an extensive network of fibrin into which fibro blasts can migrate along with other reparative cells. The cellular parts of the exudate are: Neutrophil granulocytes responsible for phagocytosis and proteolysis of the products of cell destruction. • Lymphocytes which increase permeability and help to activate the phagocytosis of damaged cells. • Macrophages whose role is probably to engulf and digest protein and to supply amino acids to the fibroblast; macrophages remain present throughout the entire inflammatory phase to assist in the phagocytosis of tissue debris and are also key cells in repair. The well-known clinical signs of inflammation are: swelling, warmth, pain , tenderness and fu n ctional loss a defensive reaction of the body that prompts the subject to restrict activities while recovery takes place. •
-
REPAIR It is worthwhile to mention that only the synovial cap sules of the joints, skeletal muscle and bone are, to some degree, capable of regeneration . All other connective tissues heal by repair with the formation of collagen and thus scar tissue. Once the exudative phase has cleared debris by dilu tion and phagocytosis, fibroblasts and capillaries migrate along the fibrin network. The process of vascular infiltra tion, fibroblast proliferation and the deposition of colla gen usually begins within 48 hours of injury overlapping with the end of the exudative phase and the later remod elling phase. Repair is begun and directed by the release from macrophages of chemotactic agents which attract · fibroblasts and endothelial cells, secrete growth factors which stimulate these cells to proliferate and produce lactic acid which enhances the syntheSiS of collagen by fibroblasts. High levels of corticosteroids prevent the migration of macrophages. During their proliferation, fibroblasts develop into cells termed myofibroblasts that generate a traction-like activity on the matrix required for the reduction of any gap in the healing area.29 Capillaries, at the edge of the injured area, send forward buds which then turn and meet each other to
CHAPTER 3 - CON N ECTIVE TISS U E 45
form new capillary loops capable of maintaining a cir culation that ensures oxygen and nutritional supply in the relatively hypoxic region where the healing tissues meet and, at the same time, enables the removal of metabolic waste products. These new capillaries are fragile and stay within the support of newly synthe sized collagen which has already been deposited ahead of the formation of the capillary loops. The highly vas cular mass produced gives the surface of the tissue its granular appearance and hence its name - granulation tissue. By the fourth or fifth day after injury the amount of collagen is significant and there is a progressive but gradually slower increase up to 6 weeks after injury. Corticosteroids decrease the number of fibroblasts and result in a diminished formation of collagen fibres and possibly a weaker fibrous scar. Normally the initial arrangement of collagen fibres is at random but after 6 weeks tensile strength continues to increase because of orientation of fibres along the lines of stress in the injured tissue (remodelling).
REMODELLING Around the end of the third week maturation begins - the process of reshaping and strengthening the scar tissue by removing, reorganizing and replacing cells and matrix. A better structural orientation and increase in tensile strength result.3o •
•
First, vascularization decreases and many of the new vessels atrophy and disappear as the blood supply becomes appropriately adjusted to the needs of the scar tissue. Second, the amount, form and strength of scar colla gen changes: the immature and weak tissue with a random orientation of fibres in three planes is remod elled into linearly arranged bundles of connective tissue. The process is the result of a number of factors, including turnover of collagen, fibre linkage and increased intermolecular bonding.
It is now generally recognized that internal and exter nal mechanical stress applied to the repair tissue is the main stimulus for remodelling. Tension by gentle move ments in ftmctional directions reorientates the collagen and breaks any weak or unnecessary crosslinks that may have formed. Mechanical stress thus has its greatest influence on remodelling at this time. Non-functional collagen is cleared away by phagocytosis.31-35 Remodelling may continue for years although more slowly as time passes. The tensile strength of replaced or repaired collagen in ligaments reaches 50% of normal by 6-25 months after injury and 100% only after 1-3 years.36 The strength of a scar formed in an injured
muscle increases faster because of its superior vascular supply.25
SELF-P ERP ETUATING INFLAMMATION The linear sequence of events described above - an inflammatory reaction followed by repair and remodel ling - is typical for acute wounds, either accidental or surgical. Orthopaedic medicine, however, also deals with chronic repetitive strains and tissue disruptions, overuse phenomena and excessive tension on devitalized tissues. Here the reaction of the tissues involved is often not linear; the inflammation may be prolonged and the for mation of scar tissue excessive and inappropriate. Rest usually initiates adhesion formation in and around the healing breach. Oedema raises tissue tension and causes pain, so impeding functional movements that are extremely important in the early stage of regen eration. Without proper movement there is no balance between formation and lysis of the regenerating ele ments of the involved tissue. Proper alignment of colla gen does not result and the final form of the scar tissue tends to remain ill-organized. Any small stress applied to an inappropriate tissue is sufficient to disrupt newly formed fibres in the healing breach. This in turn starts another inflammatory response and a vicious circle of chronic repetitive disruptions of inferior quality connec tive tissue will result. If such a state of chronic inflammation is maintained, the function of the affected area continues to deteriorate and leads to further tissue damage. Cyriax drew attention to such chronic types of inflammation of soft tissues that began as a result of trauma but continued long after the cause had ceased to operate self-perpetuating inflammation (see Fig. 3.16) - particularly prone to happen after a minor injury to a ligament. Occasionally it also occurs as an overuse phenomenon in a tendon. With knowledge of the inflammatory reaction in traumatized soft tissues, it is clear that lack of movement during the period of repair and remodelling which leads to adhesive scar tissue formation can be responsible for some chronic lesions. The decision whether a lesion requires rest or move ment cannot be taken by the patient, who feels pain and loss of function and interprets these symptoms as a potential threat that can be reduced by immobilization. The main goal in the treatment of musculoskeletal lesions is therefore to guide the healing soft tissues through the stages of inflammation and repair by the provision of sufficient and appropriate motion that can restore pain less function. If a chronic self-perpetuating inflammation has become established, a local infiltration of corticos teroid may interrupt the process. The scar become pain less and the tissue, no longer deprived of its functional
46
SECTION O N E - G E N ERAL PRINCIPLES
Inflammatory reaction: hyperaemia, exudation, leukocyte release, dead cell clearance
(\r�\J Self-perpetuating inflammation
'-... /
GAG content would decrease the space between colla gen fibres and thus restrict normal inter fibre movement. Random orientation of newly generated fibrils and the formation of crosslinks between newly regenerated fibrils and pre-existing collagen fibres were other findings responsible for decreased collagen mobility and restricted movements. These matrix changes are rel atively uniform in ligament, capsule, tendon or fascia. Some specific studies on collateral and cruciate liga ments have demonstrated laxity, destruction of ligament insertion site and failure at a lower load after immobi lization for 3 months.4J-43
Cartilage Several authors have also demonstrated the deleterious effects of immobilization on cartilage.43-50 •
(0 Figure 3.16 Self-perpetuating inflammation : rest initiates adhesion formation; stress applied at the inappropriate time disrupts the newly formed fibres, which starts another inflammatory response. I, inflammation; II, repair; III, remodelling.
motion and appropriate stress, starts to remodel. Another approach which helps to reduce the amount of disorgan ized scar tissue is to perform deep transverse friction followed by manipulation (see p. 54).
• • •
Muscle Muscular reactions to immobilization have also been investigated.5J,52 There is: •
EFFECTS OF IMMOBILIZATION ON H EALING Joint capsule and ligaments Disturbance of the blood and lymph stream in the syn ovial membrane influences the supply of nutrients and the scavenging of metabolic products and destroyed cells. Joint immobilization reduces synovial fluid hyaluronan concentration and is accompanied by changes in the synovial intimal cell populations.37 In a study on the effects of immobilization of knee joints of dogs, deposition of excessive connective tissue was noted.38 In the course of time, mature scar and intra-articular adhesions were found which restricted joint motion. Within the matrix a 4.4% loss of extracellu lar water and a significant reduction in GAG content (30-40%) was established. Ingrowth of new capillaries at the edge of injured tissue was diminished. Other workers studied the effects of immobilization on the knee joint of the rabbit.39,40 They confirmed the findings in the dog but also postulated that loss of water and
Shortening and thickening of fibrous articular capsule gives rise to a three-fold increase of the compression of articular cartilage, which may eventually initiate degenerative changes in the joint. Loss of water content and GAGs in cartilage decreases its elastic properties. Decreased capsular blood supply leads to a deposit of some end-products of metabolism at the joint surface. Lysosomal enzymes released from dead chondrocytes lead to an autolysis of cartilage which is proportional to the time of immobilization.
•
•
•
Decreased capillary density and muscle atrophy. Decrease in muscle strength most dramatically during the first week of immobilization. After 2 weeks in a plaster cast, there is 20% loss of maximum strength. Slow muscle fibres, with predominantly oxidative metabolism, are more susceptible to immo bilization atrophy than are fast fibres. An increased amount of connective tissue. Prolife ration first takes place in the perimysial spaces, fol lowed sometimes by the endomysial spaces. It is suggested52 that this may impair the vascular supply of muscle fibres and could facilitate degeneration and also could make regeneration more difficult. Although muscle structure, metabolism and function are severely impaired after immobilization, almost complete recovery is possible provided that the train ing programme starts with very moderate exercises and avoids maximum voluntary efforts of regenerat ing muscle fibres. Disturbance of neuromuscular coordination of muscle groups.
CHAPTER 3
The same studies drew attention to the reactions of organ systems, such as the cardiovascular, respira tory, locomotor and autonomic, which may also become disturbed.
-
CON N ECTIVE TISSUE 47
\
EFFECTS OF MOBILIZATION ON HEALING The benefit of early mobilization in most of the soft tissue lesions was advocated by Hippocrates more than 2400 years ago. Capsular circulation is increased (Table 3.2) which aids the supply of nutrients and elimination of cartilagenous debris. Physical joint movements have a beneficial effect on the assimilation of nutrients by the cartilage.53 Experimental findings12,54,55 on the influence of phys ical activity on ligaments and tendons support the view that the strength of connective tissue is increased with exercise training and decreased with immobilization, provided that the exercise programme is of an endurance nature. Trained animals have significantly heavier ;igaments, stronger ligament-bone junctions and junction strength to body weight ratios. Similar effects pertain in repaired ligaments,41,56 which show significantly higher strength values after repair is com plete if they have not been immobilized. Early mobiliza tion also considerably i nfluences the remodelli ng process and prevents formation of abnormal adhesions that may restrict joint movements.57 Another advantage of early mobilization is the posi tive effect on skeletal muscles,56,58,59 with increased circu lation, muscle strength and endurance and maintenance of proprioceptive reflexes, which ensure the active stability of the joint.
TREATMENT OF TRAUMATIC SOFT CONNECTIVE TISSUE LESIONS
The overall aim of treatment in orthopaedic medicine is to restore painless function of the connective tissue. During the last decades it has become clear that applica tion of functional movement to healing connective tissue is extremely important and should be the first and prin cipal objective for the therapist. Of course, the selection of the techniques will depend on several factors such as the stage of the lesion, the tissue involved, the severity of the lesion, the irritability of the tissue and the pain percep tion of the patient.
MUSCULAR LESIONS Delayed muscle soreness, contusion, (minor) rupture, myosynovitis and myositis ossificans are different types of lesion which can occur in skeletal muscle.
Delayed muscle soreness A delayed, specific soreness sometimes appearing 12-24 hours after intense exercise is well known in athletics and may be caused by the disturbance of metabolism, with a high concentration of lactic acid and the resulting inflammatory reactions: vasodilation, increased capil lary permeability and intercellular oedema. Swelling and oxygen deficiency may irritate free nerve endings and lead to muscle spasm. 60 Another, more recent, theory is that there is injury to sarcomeres and intra muscular collagen fibres and, in consequence, an inflammatory reaction.61
Table 3.2 Effects of immobilization and mobilization on soft tissue Tissue
Immobilization
Mobilization
Joint capsule
1. Distribution of blood and lymph flow 2. Intense synovitis 3. Loss of extracellular water and GAG content 4. Deposition of excessive connective tissue 5. Decreased collagen mobility 6. Intra-articular adhesions 7. Laxity and destruction of ligament insertion site
1. Increased circulation 2. Prevention of abnormal adhesions 3. Beneficial influence on the remodeling process 4. Increase of strength of connective tissue in ligaments
Synovial fluid
Alteration of viscoelastic properties
Cartilage
1. Increase of compression 2. Deposit of end-products of metabolism 3. Decrease of elastic properties 4. Autolysis of cartilage
1. Beneficial effect on assimilation of nutrients
Muscles
1. Atrophy 2. Decrease of strength 3. Increase of amount of connective tissue 4. Disturbance of neuromuscular coordination of muscle groups
1. Increased circulation 2. Increase of muscle strength and endurance 3. Maintenance of proprioceptive reflexes which ensure active jOint stability
48
SECTI O N O N E - G E N E RAL PRINCIPLES
Passive stretching and active contraction cause dis comfort. Pain lasts 3--4 days, gradually diminishing during the following days. Improper warm-up, unusual exertion, early season training and running before muscles are properly conditioned are some conditions that are thought to bring on the pain. The best way to avoid this condition is to stay 'in shape' between seasons. Other precautions to be advised are: • • • • •
Warm up before beginning an exercise programme. Include stretching exercises in the warm-up. Gradually increase the load and duration of the exercises. Avoid excessive tension on muscles. Allow the mu scles to dissipate waste products (warm-down).
Muscular contusion This results from a direct blow on the muscle be) ly. There is a variable degree of severity, characterized by pain and intra- or intermuscular bleeding with exten sive swelling. Intramuscular bleeding is more serious and lasts longer because of difficulty in dispersing the haematoma. Such a blow does not cause much discom fort or pain while the athlete is warm and in the middle of a game; it is late at night or the following day that stiffness and d isability set in. Active contractions against resistance cause discomfort and passive stretch ing of the muscle is painful and limited. Treatment involves aspiration of the haematoma (within 3 days), after which compression is applied immediately, using an elastic wrap. A short period of rest may be prescribed but rest should never be complete and prolonged. After a few days, treatment with gentle deep transverse frictions and active contractions with the muscle in a fully shortened position can be started (see Minor muscular tears). Minor muscular tears (or 'muscle strain injuries ') Acute lesions. These are the common 'muscle pull' or 'strain' injuries that result from sudden and overviolent effort or movement in the muscle and usually cause immediate disability. Tears occur most often during unusual contractions,62 which produce significantly higher muscle force than when the muscle is held at the same length or is allowed to shorten. It has also been shown that muscles crossing two joints, such as ham strings and gastrocnemii, are particularly at risk. The vulnerable site appears to be near the muscle-tendon junction. The immediate response to the trauma is inflammation, associated oedema and localized haemor rhage. Excessive oedema and haemorrhage should be
reduced as much as possible. Blood collections are not confined to the muscle proper but escape through the perimysium and fascia into the subcutaneous space. As a rule, the degree of pain is consistent with the extent of the rupture. Treatment. The immediate induction of local anaesthesia at the site of the lesion effectively blocks the nociceptive impulses which are responsible for muscle spasm at the site of damage. Cold therapy as an alternative has been criticized.63 Although it has a positive effect on pain threshold,64,65 physiological effects and procedures of application are still chiefly based on empirical and clini cal findings. Van Wingerden suggests that cold therapy, especially when applied in the acute phase of injury, could lead to increased oedema, inhibition of the healing process and even to increased inflammatory reactions.63 From the next day on, active or electrical contractions follow, with the muscle in a fully shortened position to maintain mobility by broadening the muscle belly. Meshwork of regenerating fibrils in the healing breach may hinder the broadening capacity of the muscle fibres during contraction. In the later stages of healing (granulation and remodelling), intramuscular formation of abnormal crosslinks takes place and the inappropri ate scar tissue will form a mechanical barrier to broad ening during contraction, a chief muscle function (Fig. 3 . 1 7) . Deep transverse friction also imitates broadening and prevents newly formed bonds from matting muscle fibres together. It should be started the day after injury, as it can be expected that repair has begun by this time. A gentle type of massage is performed daily for a short period of time (see Ch. 5). At this stage, it should not be done to an extent that interferes with the capillaries and fibrils con solidating themselves in the healing breach. Both inten sive passive stretching and resisted movements may cause damage at the site of injury and must be avoided until recovery is well established. It has been demon strated66,67 that contractile ability recovers rapidly. Once the patient is free from pain and with a full range of mobility, repetitive stretching exercises seem to make an important contribution to the future preven tion of these injuries.68-71 Return to sport can be allowed when the strength of the injured limb has been restored to within 10% of that of the unaffected leg (usually after 3-6 weeks).72 Chronic lesions. Scarring takes place in chronic lesions, matting fibres together transversely. The range of broad ening is impaired and contractions against resistance are painful. A painful spot can be palpated although it may be difficult when the lesion is deeply situated, for example the belly of biceps brachii or the extensor carpi radialis brevis. Pain probably results from overstretching
CHAPTER 3
(a)
(b)
-
CONN ECTIVE TISS U E 49
Treatment. Deep transverse friction for about 20 minutes twice a week to the site of the established scar is indi cated. The muscle fibres are teased apart, abnormal crosslinks ruptured and mobility restored. To maintain the effect of the friction, active and electrical contractions with the muscle belly in a fully relaxed position should follow. The muscle contracts to its fullest extent and this is repeated for 5 minutes at regular times. When the lesion is at the musculotendinous junction, active or electrical contractions are ineffective and treatment is by deep friction only. Steroids do not have a place in the treatment of muscu lar lesions. Recent research in an animal model indicates that corticosteroids may be beneficial in the short term but they cause irreversible damage to healing muscle in the long term, including disordered fibre structure and a marked diminution in force-generating capacity?3
Myosynovitis Myosynovitis is a painful condition described by Cyriax,74 arising from a muscle as the result of overuse. In severe cases it is accompanied by crepitus on movement. This uncommon condition seems to occur only in the bellies of the long abductor and the extensor muscles of the thumb and in the musculotendinous junction of the tibialis anterior. The last disorder is a well-known complaint in military recruits who march unaccustomed distances. Myositis ossificans This condition is characterized by progressive benign heterotopic bone formation, which may occur after severe contusion to muscle fibres, c01U1ective tissue, blood vessels and underlying periosteum. The pathogen esis is poorly understood. It is seen most often in males, aged between 15 and 30 years. Highly common sites are the brachialis and quadriceps muscles. The condition is sometimes found in the hip adductors and pectoralis major and the bony deposit is often connected to the underlying bone. There is the following triad of symptoms: • •
Figure 3.17 (a) The muscle belly broadens during contraction; (b) scar tissue and intramuscular formation of connective bridges form a mechanical barrier to broadening during contraction.
at the junction between normal and scar tissue, from local variations in tension. This explanation seems logical because pain is absent in diffuse fibrosis after sclerosing injections and in ischaemic contracture.
•
increasing pain palpable and increasing firm mass in the affected muscle gradual decrease in the range of movement of the neighbouring joint(S)?5,76
The history of severe contusion to the affected muscle is helpful in the early evaluation of these patients because radiographic changes become evident only 2--4 weeks following the trauma. The condition can mimic benign or malignant bone tumour and osteomyelitis.77,78 Specific treatment is not recommended. Bone forma tion may resorb with time but recovery may take from 1
50 SECTION ONE - GENERAL PRINCIPLES
to 2 years. Early surgery is to be avoided because it may exacerbate the bone formation. Removal can be consid ered if symptoms persist, but only after the heterotopic bone is mature and no further radiological changes occur.79,80
and fibres. In sports, a cold climate, bad equipment and wrong training procedures (e.g. lack of warm-up including absence of stretching, too progressive an increase of load and duration of the exercise programme, bouncing exercises and jerky muscle contractions) may all negatively influence the condition.
TENDINOUS LESIONS Tendons transmit power from the muscle belly to bone. In that the tendon is always less in diameter than the muscle, the load transmitted to the tendon will be much greater per unit diameter than in the muscle belly. Dysfunction may result from changes either within the tendon or in the surrounding tissues of the tendon (para tenon).
Tendinous lesions can be classified as follows:
• Overuse tendon injuries (tendinitis) • Peritendinitis (tenosynovitis, tenovaginitis) • Tendinosis • Tendinitis with peritendinitis • Local swelling of a tendon
• Complete rupture.
The inflammatory reactions in tendinitis are located not only at but also around the ruptured fibres, in the areolar tissue between the fasciculi. Here oedema, growth of capillaries, migration of leukocytes and inva sion with mesenchymal cells take place, which induces new generations of fibroblasts and leads to a large prolif eration of connective tissue around the site of the lesion.
Acute traumatic lesions. In acute traumatic lesions
48
hours after the injury, newly generated collagen fibrils start to close the tissue defect by the formation of scar
tissue. Scars may remain lastingly painful and often have an inferior tensile strength, especially if the initial inflammatory reaction was excessive and the granulation and remodelling phases inadequate. Treatment. To prevent excessive inflammation and to
stimulate better remodelling, gentle mobilization and transverse friction are used to orient the randomly dis
Tendinitis When strain on a tendon tears some fibres, it always
seems to occur in those parts of the tendon where vascu
larization is relatively poor. The insertion into bone and
tributed collagen in a fW1ctional direction. This also pre vents the formation of abnormal adhesions. Treatment starts the day after the injury and massage should be superficial and light in order not to rupture newly gener
sometimes a specific part of a tendon are such 'critical'
ated fibrils. Treatment along these lines is continued daily
vascularized zones. Good examples are a zone in the
for the first week and on alternate days for the second
Achilles tendon about 2.5 cm above its insertion into the
and third weeks. After 3 weeks, active unloaded contrac
calcaneus81,82 and the supraspinatus tendon close to its
tions can be added. A tape or bandage to support the
insertion on the major tubercle.83
structure and prevent undue movement is advisable.
tissues also decreases (ultimately by about 30%) which
activity against the degree of local reaction.
Above the age of 25, vascularization of tendinous
enhances their vulnerability.
Lesions result principally from overuse. However, the mechanical response of a tendon to a load not only depends on the amount of the externally applied force but also is closely bound up with the state of the tendon involved. Overuse may disturb the microcirculation
Careful evaluation is necessary, gauging the degree of The patient should be very cautious about returning to
full activity until the lesion is completely pain free.
Chronic (overuse) lesions Treatment. In chronic tendinous lesions, transverse
friction massage applied precisely to the exact spot may
which, especially in zones of hypovascularity, will nega
be an extremely useful technique and can often bring
tively influence metabolic processes. If this continues, a
lasting relief.
beginning of the process this is a degenerative condition
cussed in the next chapter but transverse friction aims to
process of degeneration starts, called 'tendinosis'. In the without
accompanying inflammatory reactions and
therefore clinical signs and symptoms may be totally absent.
From the moment that a normal load strains the
Modalities and effects of this treatment form are dis
achieve transverse movement of the collagen structure of the connective tissue. In this way adhesion formation is prevented and existing adhesions are mobilized. The cyclic loading and motion of the healing connective
tendon and tears some fibres, an inflammatory reaction
tissues may also stimulate formation and remodelling of
begins. Long-standing treatment with corticosteroids
the collagen.
influence the condition of collagen and lead to further
corticosteroid. This will quickly reduce the chronic
or periods of immobilization will further negatively
deterioration and decrease in the number of fibrocytes
Another approach is to infiltrate locally a low d6se of inflammatory reaction but it also affects the proliferative
CHAPTER 3 - CONNECTIVE TISSUE 51
and even the remodelling phase - the biosynthesis of col lagen)s altered by corticosteroids. For this reason, local
In specific tenovaginitis, treatment is that of the under lying disease.
steroid infiltrations should only be at the tenoperiosteal insertion and never in relation to the body of a tendon for fear of possible tendon rupture. A further disadvantage of steroid infiltration is the higher recurrence rate (about
25%) after initial therapeutic success. Persistent pain is thought to be caused by irreversible degenerative changes within the tendon. Removal by surgical treatment may then be indicated. Again treat ment may include sessions of transverse friction applied in a progressive way until the patient is free of symptoms. Thereafter a programme of rehabilitation is undertaken.
Tendinosis This is a degenerative condition of the tendon without accompanying inflammatory reactions and therefore often without clinical symptoms. The lesion is character ized by visible discolouring of the tissue and loss of the mirror-like gloss of the tendon surface. Microscopically,
tendinois
is
characterized
by
a
marked loss of collagen. The fibres show an irregular entangled course and an irregular waving pattern. Between the fibres, cavities filled with fluid loosen the tissue. T he number of fibroblasts is decreased and their nuclei transformed.
Tenosynovitis
Besides this local destruction, there are also signs of
Tenosynovitis is a well-known lesion at the ankle or the
regeneration as shown by slight fibroblast proliferation,
wrist where tendons possess a sheath. Roughening of
formation of capillary sprouts and new mesenchymal
the gliding surfaces of a tendon and the internal or vis
cells, which synthesize young collagen fibrils to fill up the
ceral layer of the sheath results from an inflammatory
tissue defect. If this process of granulation is insufficient,
reaction, commonly occupational overuse or strain.
necrosis and calcification result.
During movement, pain is evoked as the roughened sur
At the insertion (transition zone) of the tendon the
faces move against each other. In severe cases fine crepi
number of cartilage cells increases whereas fibroblasts
tus is palpable and swelling obvious. Coarse crepitus is
show signs of degeneration with swelling of their mem
a warning sign that points to rheumatoid disease or
brane. This disturbs protein synthesis and leads to radical
tuberculosis.
changes in collagen with complete loss of structure.
Treatment. This consists of deep transverse friction
whether the condition is recent or chronic but it is indi cated only in posttraumatic lesions. Friction restores the smooth and painless movement of the tendon in relation to the internal layer of the sheath. An injection of a small amount of steroid suspension between tendon and sheath is an alternative. Some lesions respond better to the massage and for others injection is the treatment of choice (see Ch.
5).
All activities that cause pain should be avoided until symptoms have ceased.
Tenovaginitis Tenovaginitis is primarily a lesion of the tendon sheath itself and is often associated with considerable swelling and tenderness but there is never crepitus. It may have a detectable cause in overuse but also occurs sponta neously. Non-specific types of tenovaginitis should be differentiated from those with a specific cause, such as bacterial infection, rheumatoid arthritis, gout and gonorrhoea.
Fibrin degeneration is always greater than that of hyalin. If regeneration is absent, calcification often results. Several authors have offered explanations for this process of calcification. Some believe that a shift of pH towards alkalosis together with a diminished metabolism creates circumstances that increase the level of calcium and phosphate ions and causes crystallization. Other investigators consider these calcifications to be the result of a tear of small parts of cartilage-bone structure away from their normal attachment showing thereafter osteo genesis in the new surroundings.
Local swelling of a tendon This is not infrequently seen in the digital flexor tendons in the palm of the hand. When these swellings are local ized at the level of the heads of the metacarpals, they engage and may become fixed in the distal part of the tendon sheath at the moment of flexion. Extension is often only possible with help. This symptom is known as 'trigger' finger or thumb. Treatment.
Infiltration
of
steroid,
to
influence
the
inflammatory component of the swelling, is sometimes
Treatment. For the non-specific types of tenovaginitis,
effective. If this fails, surgical removal of the swollen
treatment is the introduction of a small amount of steroid
tissue (scar and/ or calcium deposits) or slitting of the
between tendon and sheath, which brings quick relief. In
narrowed part of the sheath is the alternative.
persistent cases, deep transverse friction can be tried but incision of the tendon sheath is often necessary.
An overview of the localization and treatment of musculotendinous lesions is given in Figure 3.18.
52
SECTION O N E - G E N E RAL PRI N CI PLES
Complete rupture Complete rupture of a tendon usually results from indi rect trauma. It always seems to occur at the midsubstance of the tendon. Acute tears are those occurring suddenly, usually as a result of a single injury. Chronic tears are those that are insidious in onset and result from repetitive loading of a degenerated and weakened tendon. Tendinous ruptures occur predominantly at the shoulder, wrist and heel. At the shoulder, the incidence of full thickness rotator cuff tears in cadaveric populations ranges from 30% 84 to 60% 85. Ruptures of Achilles and tibialis posterior tendons are also quite cornmon. The special anatomical situations of the flexor and extensor tendons of thumb and fingers subject them to high loads which may alter their histo logical structure and finally rupture them. Healing of a ruptured tendon depends on the capabil ities of both the tendon itself as well as on reactions from the surrounding tissues. Some tendons such as the Achilles tendon have a remarkable ability to heal after rupture, whereas others do not. Rotator cuff tears for instance usually do not heal and, if they do, a permanent weakening results. Healing of a ruptured Achilles tendon does not differ from the general tissue reactions after mechanical damage: the initial stage of exudation is fol lowed by vascular granulation and fibroblast prolifera tion. Collagen synthesis begins within the first week and reaches its maximum after about 4 weeks. It then contin ues for about 3 months. Maturation and remodelling begin at the end of the third week and continue for up to 1 year after the injury.
Musculotendinous lesions
Figure 3.18
Localization
Treatment
Tenoperiosteal
Infiltration with triamcinolone or deep friction
Tendinous
Deep friction
Musculotendinous
Deep friction
Muscular
Infiltration with local anaesthetic Deep friction Active and electrical contraction
®
Tenosynovitis
Infiltration with triamcinolone or deep friction
®
Tenovaginitis
Infiltration (or deep friction)
Localization and treatment of musculotendinous lesions.
Mechanical strength of a healing tendon is related to the histological process of repair. During the second phase, strength increases but is still insufficient to prevent further stretching of the healing wound. For this reason, the region always has to be immobilized until the process of maturation has begun (about 3 weeks after injury). At that time the arrangement of col lagen fibrils is not organized and remodelling depends entirely upon the presence of repetitive tensile forces applied to the scar tissue. Several studies support the concept that controlled cyclic passive loading of the healing tendon, performed after the initial healing phase (3 weeks) is effective in decreasing the formation of abnormal adhesions and increasing the tensile strength of the healing tissue. 86--88
LIGAMENTOUS LESIONS Rationale for treatment of acute and chronic lesions Treatment regimes remain the subject of controversy and range from a policy of no treatment through early mobilization and strapping to plaster immobilization. However, experimental studies of the past decades confirm the existing clinical feeling that sprained liga ments heal better and stronger under functional loading than they do during rest. The effects of loading on healing ligaments have been studied extensively and the available evidence indicates that the remodelling of the repair tissues responds extremely well to cyclic loading and motion. 89 Long-term studies in ankle sprains have shown better results when early mobiliza tion is used.90,91 Other prospective and randomized studies also show the best results with early functional treatment (see Cyriax92 p. 8, Larsen93 and Freeman94). Because late reconstruction of ruptured ligaments at the ankle still gives very good results,95-97 there is no need for early surgical treatment and conservative treatment with early mobilization must always be tried first. At the knee joint, several studies have also demonstrated that the non-operative management of an isolated medial collateral ligament rupture gives results equally good as surgical repair but with significantly quicker rehabilitation.98-103 In spite of these findings, most physicians and sur geons dealing with the management of ligamentous rup tures reason 'anatomically': if a rupture is suspected or proven radiologically, the medical approach must be to repair the defect as soon as possible. This is achieved by partial or total immobilization or by early suture - the same approach as is taken in fractures, where the sepa rated pieces of bone are fixed in apposition. This anatom ical way of thinking does not correspond to the functional reality of connective soft tissue lesions - the
CHAPTER 3 - CO N N ECTIVE TISSUE 53
function of a ligament is in no way comparable with the function of a bone. Where bone must be strong and solid, a ligament must allow and control movements within certain limits. To serve that purpose, ligamentous tissue must be mobile enough to change its position continu ously. The same properties apply to scar tissue, which must not only be strong to prevent excessive movement but must also be mobile enough to allow sufficient move ment. If this principle is neglected and a scar becomes unduly adherent (e.g. to bone), continuous functional problems will result. Early mobilization prevents such adhesions within or around the healing structure. Tension during the state of collagen deposition aligns newly generated collagen fibrils in the direction of stress and also prevents the formation of crosslinks in a random pattern. Consequently, the scar is strong in the direction along which force is applied. Tension also prevents scar tissue becoming adherent to bone. Movement stimulates proteoglycan synthesis important in lubrication of con nective tissue and maintaining the critical distance between pre-existing fibres. It is most effective to start mobilization from the onset, before the newly generated fibrils develop crosslinks in an abnormal and irregular pattern. This may be effectively achieved by deep transverse friction and passive movements. In advocating early mobiliza tion, one common difficulty may arise: the serious trau matic inflammation and the intense pain during the slightest movement are very strong impediments to early mobilization of connective tissues. In these circumstances, Cyriax advocated the infiltration of localized lesions with small amounts of triamcinolone as soon as the patient is seen. This shortens the acute phase of the inflammatory process and therefore encour ages the patient to move the injured part at an early stage with all the associated beneficial effects. In diffuse lesions this approach is impractical, and deep transverse massage and passive movements are substituted although exercise and movement have to be modified until pain has abated. 'Sprain' of a ligament is the result of excessive joint movement with lack of muscular control. The transitional zone between mineralized fibrocartilage and bone is the site of most separations between ligaments and bones.12 However, sprain may also occur in the substance of a lig ament. A good example of this is the medial collateral lig ament at the knee, where tears are often situated in the midportion or just below the joint line adjacent to the tibia. Experiments with strength and failure characteris tics of rat medial collateral ligaments104 have shown that this especially results from a large load that is rapidly applied. The failure point is reached before significant elongation can take place. The same load applied more slowly results in failure at the transitional zone between
mineralized fibrocartilage and bone, where the connec tive structure is weakest. In accordance with the degree of the injury, ligamen tous lesions can be divided into three grades: • • •
Grade 1 : a slight overstretching with some micro-tears within the ligamentous structure Grade 2 : a more severe sprain with partial rupture of the ligament Grade 3: the ligament is completely torn across or is avulsed from the bony attachment.
This classification is rather arbitrary and, although it might be possible to distinguish a small lesion from a total separation, the difference between grades 1 and 2 is always subjective. Ligamentous lesions can also be classified according to the time that has elapsed since the causative accident: • • •
Acute: within 48 hours Subacute: 48 hours to 6 weeks Chronic: more than 6 weeks.
This classification is of importance in relation to treatment. Sprains with incomplete ligament rupture are often quite painful and accompanied by muscle spasm and pseudolocking. This makes clinical examination difficult, and diazepam or general anaesthesia may be needed to complete a thorough examination. In complete tears there is rarely pain of a significant degree and in knee and ankle sprain the patient can often walk without aid. It is a fear of 'giving way' that charac terizes the lesion and prevents the patient from doing more strenuous activities such as going up or down stairs, jumping or doing full squats. Clinical evaluation of an acutely injured joint should be carried out as soon as possible - within a few hours of the accident - otherwise pain, swelling and muscle spasm will often make it impossible to perform proper ligamentous tests. This is particularly necessary in first and second degree lesions, in which these symptoms are so evident. H istory and knowledge of the mechanism of the injury are important aids in diagnosis and point to the injured ligament(s). Tenderness and localized oedema indicate the anatomical site of the tear in most instances. Treatment. Minor ligament sprain should be treated conservatively. Ligaments will heal but it is essential not to strain them again during the first part of the granula tion stage. For example, after damage to the medial col lateral ligament of the knee joint, full extension should be prevented during the first 10 days. In the acute stage, traumatic reactions such as pain and swelling should be kept to a minimum. Therefore early application of compression and an elevated position of the extremity are most important.
54 SECTI O N O N E - G E N E RA L P R I N CI P LES
In a sprained ligament of the knee or ankle, crutches should be used if movement is necessary. The next day, physiotherapy is started. Effleurage diminishes swelling and pain, which are impediments to move ment. Thereafter transverse friction is performed to move the damaged tissue to and fro over the subjacent bone in imitation of its normal behaviour. This prevents the random orientation . of new generated fibrils and formation of abnormal crosslinks between new rege nerated fibrils and pre-existing collagen fibres. In this acute stage, really deep transverse friction will take no more than 1 minute since there is no question of breaking down strong scars. However, it should still be as gentle as is compatible with securing adequate movement of the damaged tissue. Then the joint is moved passively through its greatest possible range without causing p ain. The same movement(s) are repeated actively. There should be no attempt to increase this range in the acute or subacute stage. In a sprained joint of the lower limb, instruction on gait follows. Strapping the joint to protect it from unwanted movements is a useful additional measure, especially if the patient seems anxious. Patients treated along these lines recover most rapidly. An infiltration with a small amount of steroid at the site of the lesion is an alternative. The injection should be given during the first 48 hours - the initial and exudation stage. It reduces traumatic inflammation and prevents most structural and reflex changes. Pain also disappears, which enables the patient to move the joint in a normal way. Deep transverse friction then loses its efficacy. Steroid injections during granulation and repair may lead to fewer fibroblasts, a diminished collagen fibre formation and a weaker scar.1°5 However, these effects are not seen after a single injection.106 Overstretching a ligament often leads to permanent laxity with consequent instability of the joint. Cyriax emphasized the propensity of ligaments not controlled by muscles to develop such permanent laxity and cited the sternoclavicular, acromioclavicular, sacroiliac and sacrococcygeal ligaments, the symphysis pubis, the cruciate ligaments at the knee and the inferior tibiofibular ligaments as examples.?4 After trauma, reflex muscle spasm is not capable of stabilizing these joints. In intra capsular ligaments (e.g. the cruciate ligaments), unsuc cessful repair may also result from the synovial environment, limited fibroblast migration and reduced vascular ingrowth. The subsequent traumatic inflammation can be reduced by the means already described. To prevent laxity, it is a principle of treatment completely to avoid movements which can be achieved by immobilization of the joint or by surgical repair. Such measures are best executed within 7 days.
After recovery, minor laxity is compatible with excel lent function, whereas painful chronic laxity becomes painless in due course or can be converted into painless laxity by use of a local steroid infiltration. In joints controlled by muscles, permanent laxity is much less likely to occur. Reflex muscle spasm efficiently stabilizes the joint. Grade I and II lesions treated on the lines set out will heal adequately. The results of conser vative treatment in grade III lesions are also successful in almost all cases but it is essential that the lesion is iso lated.1°0,107 It is then advisable to immobilize the joint par tially so as to prevent any unwanted movement taking place during recovery. Lasting instability in these joints can be more or less compensated for by tautness of the muscles and tendons passing over the joint. Strength building exercises are of great importance and must be on an exact and planned basis. If necessary, strapping or braces may provide added support. In surgical repair, dense fibrous tissue is used to reconstruct the ligament - the fascia lata, part of the patellar tendon on other tendons. Following trans plantation a graft heals to the recipient tissues but never approaches the strength it had before transplanta tion. Nevertheless grafts can significantly improve the stability of joints.
CAPSULAR LESIONS Traumatic arthritis, capsulitis or synovitis all have an identical meaning: inflammation of the entire capsule as a result of a more or less recent trauma. This is invisible on X-ray and therefore this investigation cannot exclude the diagnosis. If trauma has damaged the lymph and vas cular network in the subintima, the integrity of the syn ovial membrane and therefore its cellular function will be severely disturbed. Increased permeability of small venules allows plasma to leak through and effusion results. Intra-articular swelling increases tension within the capsule and further irritates various sensory recep tors. Pain and reflex inhibition of muscles result which can further affect the joint. If the patient states that the joint suddenly became very painful and swollen, over a few minutes, haemarthrosis is suspect. The speed of appearance of the effusion and the severe pain by far exceed that caused by clear fluid. Palpation of the joint also shows it to be hot and more tense than if the effusion is clear. Blood in the joint is a strong irritant and has an erosive action on the cartilage. It must be aspirated at once, after which the remaining blood-tinged synovial effusion is removed a few days later. After injury, joints supported by muscles soon develop limitation of movement with a capsular pattern (see Ch. 4). In recent arthritis such limitation results
CHAPT E R 3 - C O N N E CTIVE TISS U E 55
from defensive muscle action which is reflexive and controls movements that could further irritate the capsule. Muscles spring into action, which can be felt (hard end-feel ) and seen on gently forcing a particular movement. In the chronic stage, inflammation is maintained by the effects of cartilagenous debris, blood elements and enzymes from destroyed cells which activate cells of the synovial membrane to produce excessive fluid of inferior quality <;:ontaining hyaluronic acid molecules that are decreased in size and concentration. Friction resistance between joint surfaces is consequently increased and inhibition of excessive collagen proliferation reduced. Contraction of the capsule occurs and restricts move ments, in the capsular pattern. In the absence of muscle spasm, end-feel then becomes rather hard, resembling leather being stretched. In joints without muscles about them to control move ments, no limitation of movement can result however severe the arthritis. Muscle spasm cannot occur and there is pain at the extremes of range only. Treatment (Table 3.3). Movements retain mobility at a joint. They have the effect of keeping a joint structure normal.92 In recent trauma, pain limits active movement and it is essential, particularly in middle-aged and elderly people, in whom posttraumatic adhesions are apt to form, to restore a full range of movement as soon as possible. Gentle assisted active and passive movement increases vascular supply, removes cartilagenous debris, resorbs oedema or joint effusion more quickly, aids in the trans port of nutrients and metabolites to and from cartilage cells, and prevents the formation of adhesions and cap sular contraction. Movements should be performed to the point of discomfort but not of pain. All possible direc tions of movement should be attempted, one by one, and a small but definite increase in range of movement should be achieved each day. If this fails, intra-articular corticosteroid injections are indicated.
In the chronic stage, stretching out the capsule requires many repetitions of a long steady push, main tained as long as the patient can bear it - say for 1 minute. Dense capsular adhesions finally yield but no increase in range of movement can be expected after the first few sessions. During the period when progress is slow, therapist and patient must show forbearance and persistence, respectively. Short-wave diathermy given for 15 minutes before mobilization diminishes the pain of capsular stretching. Symptoms and signs of activity may contraindicate forced movements. Pain in the absence of movement, especially at night, wide reference of pain and inability to lie in bed bearing weight upon the affected joint are all symptoms that indicate that the lesion is in an active stage and that forced movements will increase the problem. Local warmth, effusion and muscle spasm are signs accompanying such an event and are indications for an injection of a steroid suspension. If the patient refuses, slight distraction techniques in the neutral position of the joint are an alternative. The therapist coaxes painless distraction of minimal amplitude, inter mittently and with slight irregularity in depth and timing. Performed daily for the first week and on alter nate days for the next week(s), pain abates and range increases slowly although not in all cases of traumatic inflammation. Internal derangement at a spinal joint and at the knee joint is an exception in which forced movements are still performed despite symptoms and signs of activity. Manipulative reduction makes symptoms and signs dis appear quickly, thereby showing absence of real capsular trauma. Forced movements should not be done in traumatic arthritis of the following peripheral joints (see also Box 3.2). •
Elbow: passive mobilization for recent posttraumatic stiffness is apt to diminish rather than increase the range of movement; moreover, it is contraindicated
Table 3.3 Symptoms, signs and indications for therapy in traumatic capsulitis Inflammation stage Active
Symptoms and signs
Therapy
Constant pain
Intra-articular steroid suspension
Wide reference of pain Inability to bear weight on the joint Local warmth Spastic end-feel Chronic
No pain except on forced movement Little reference of pain Ability to bear weight on the joint Elastic capsular end-feel Resistance to passive movements is perceived before appreciable pain is evoked
} }
Alternative technique: slight distraction techniques
Capsular stretching
56 SECT I O N O N E - G E N E RA L P R I N C I PLES
• •
• •
because of the ever-present danger of setting up myositis ossificans. An intra-articular injection with corticosteroid suspension is indicated and will give quick recovery. Hip: traumatic arthritis is best treated by rest in bed. Interphalangeal and metacarpophalangeal join ts of the hand and foot: these joints respond badly to forced movements. Joints of the toes can be injected with corticosteroid suspension. Lower radioulnar joint: aggravation of symptoms can be expected even with active exercises. Joints not u nder volu ntary control: after an injury the formation of adhesions is not to be expected. Forced movements are useless and harmful. Rest, support and corticosteroid injections are then good alternatives.
Box 3.2 Contraindications of forced movements in traumatic arthritis of peripheral joints Elbow joint H i p j oint Interphalangeal and metacarpophalangeal joints Lower radioulnar joint Acromioclavicular j oint Sternoclavicular joint Sacroiliac joint
In children, adhesion formation after a sprain of a joint does not occur, hence forced movements should be avoided. Treatment of acute and chronic ligamentous lesions is summarized in Table 3.4.
Table 3.4 Treatment of ligamentous lesions Phase
Treatment (1 )
Treatment (2)
Compression Elevation
Alternative (within
Effleurage + Deep transverse massage
Controlled movements (active and passive) Gait instruction
Acute phase Joints controlled by muscles First day Following days
48 hours)
Steroid infiltration
Controlled movements (active and passive) Gait instruction
Joints not controlled by muscles
Deep transverse massage Immobilization
Infiltration (steroid or sclerosant) Immobilization
Chronic phase Adhesive scar formation
Deep transverse friction
+
(Steroid infiltration)
Manipulation
Lasting instability
Strength-building exercises Proprioceptive training
Surgical reconstruction (Infiltration with sclerosant)
REFERENCES 1 . Warwick L, Williams PL. Gray's Anatomy, 36th edn. Churchill Livingstone, Edinburgh, 1980. 2. Lewis CE, McGee JOD. The Macrophage. IRL Press, Oxford, 1992. 3. Holgate ST. Mast cells and their mediators. In: Holborrow EJ, Reeves WG (eds) Imm u noLogy in Medicine, 2nd edn. Academic Press, London, 1983:979-994. 4. Walker PS. Human Joints and their ArtificiaL RepLacements. Thomas, Springfield, 1977. 5. Kennedy JC, Hawkins RJ, Willis RB. Tension studies of human knee ligaments. J Bone Joint Surg 1976;50A:350-355. 6. Viidik A. On the rheology and morphology of soft collagenous tissue. J Anat 1969;105:184. 7. Brocklin van ]0, Ellis DG. A study of the biomechanical behav iour of toe extensor tendons under applied stress. Arch Phys Med 1 965;46:369.
8. Wyke B. The neurology of jOints. Ann R ColL Surg 1967;41:25. 9. Rowinski M. Afferent neurobiology of the joint. In: Davies GI, Gould JA (eds) Orthop and Sports: PhysicaL Therapy. Mosby, St Louis, 1985:50. 10. Ham AW. HistoLogy, 7th edn. Lippincott, Philadelphia, 1 974. 1 1 . de Morree JJ. Dynamiek van het menseLijk bindweefseL. Functie, beschadiging en hers tel. Bohn, Scheltema & Holkema, Utrecht/ Antwerp, 1989. 12. Tipton CM, Matthes RD, Maynard JA, Carey RA. The influence of physical activities on ligaments and tendons. Med Sci Sports 1975:7(3):165. 13. Henderson B, Pettipher ER. The synovial cell: biology and pathobiology. Sem Arthritis Rheum 1985;15:1-32. 14. Linck G, Porte A. Cytophysiology of the synovial membrane: distinction of two cell types of the intima revealed by their
CHAPTER 3
15.
16.
17. 18. 19. 20. 21.
22.
23. 24. 25. 26. 27.
28.
29.
30.
31. 32. 33.
34. 35. 36.
37.
38.
reaction with horseradish peroxidase and iron saccharate in the mouse. Bioi Cell 1981;42:147-1 52. Klareskog L, Forsum U, Kabelitz D et a/. Immune functions of human synovial cells. Phenotypic and T cell regulator proper ties of macrophage-like cells that express HLA-DR. Arthritis Rheum 1982;25:488-501 . Jay JD. Characterization o f a bovine fluid lubricating factor. I . Chemical, surface activity and lubricating properties. Connect Tissue Res 1992;28:71-88. Ghadially FN. Fine Structure of Synovial Joints. Butterworth, London, 1983. Sunderland S. Nerves and Nerve Injuries, 2nd edn. Churchill Livingstone, London, 1978. Harkness, RD. Mechanical Properties of Collagenous Tissue. Treatise on Collagen. Gould (ed.) Academic Press, London, 1968. Cooper RR, Misol S. Tendon and ligament insertion: a light and electron microscopy study. J Bone Joint Surg 1 970;52A:1-2 1 . Laros GS, Tipton CM, Cooper R R . Influence o f physical activity on ligament insertions in the knees of dogs. J Bone Joint Surg 1971;53A:275-286. Hunt ThK. Wound healing In: Dunphy JL, Way LW (eds) Current Surgical Diagnosis and Treatment, chapter 9. Lange Medical, Los Altos, California, 1975:97. Peacock EE, van Winckle W. Surgery and Biology of Wound Repairc. Saunders, 1980. Lehto M, Durance VC, Restall D. Collagen and fibronectin in a healing skeletal muscle injury. J Bone Joint Surg 1985;67B:820-827. Zarins B. Soft tissue injury and repair: biomechanical aspects. Int J Sports Med 1982;3:9. Kellett J. Acute soft tissue injuries: A review of the literature. Med Sci Sports Exerc 1986;18:5. Banks AR. The role of growth factor in tissue repair. In: Clark RAF Henson PM (eds) The Molecular and Cellular Biology of Wound Repair. Plenum Press, New York, 1988:2059-2079. Fox GM. The role of growth factor in tissue repair. In Clark RAF, Hensoon PM (eds) The Molecular and Cellular Biology of Wound Repnir. Plenum Press, New York, 1988:266-272. Ehrlich HP, Rajaratnam JBM. Cell locomotion versus cell con traction forces for collagen lattice contraction: an in vitro model for wound contraction. Tissue Cell 1990;22:407-417. Buckwalter JA, Crues R. Healing of musculoskeletal tissues. In: Rockwood CA, Green DP (eds) Fractures. Lippincott, Philadelphia, 1991. Stearns ML. Studies on development of connective tissue in transparant chambers in rabbit's ear. Am J Anat 1940;67:55. Frankel VH, Nordin M. Basic Biomechanics of the Skeletal System. Lea & Febiger, Philadelphia, 1980. McGaw WT. The effect of tension on collagen remodelling by fibroblasts: a stereological ultrastructural study. Connect Tissue Res 1986;14:229. van der Meulen JCH. Present state of knowledge on processes of healing in collagen structures. Int J Sports Med 1982;3:4. Hardy MA. The biology of scar formation. Phys Ther 1989; 69:1014-1023. Frank G, Woo SL-Y, Arniel D et a/. Medial collateral ligament healing. A multidisciplinary assessment in rabbits. Am J Sports Med 1983;11:379. Pitsillides AA, Skerry TM, Edwards Je. Joint immobilization reduces synovial fluid hyaluronan concentration and is accom panied by changes in the synovial intimal cell populations. Rheumatologtj 1999;38(11):1108. Akeson WH, Arniel D, Woo S. Immobility effects of synovial joints; the pathomechanics of joint contracture. Biocheology 1980;17:95-110.
-
C O N N E CTIVE TISS U E 57
39. Akeson WH. An experimental study of joint stiffness. J Bone Joint Surg 1961;43A:1022. 40. Akeson WH, Ameil D, LaViolette D . The connective tissue response to immobility: an accelerated aging response. Exp
Gerontol 1968;3:329. 4 1 . Erikson E. Sports injuries of the knee ligaments; their diagnosis, treatment, rehabilitation and prevention. Medicine Science & Sports 1976;8:133-144. 42. Akeson WH, Arniel D, Abel MF. Effects of immobilization on jOints. Clin Orthop 1987;219:33. 43. Matthiass A H . Immobilisation und Druckbelastung in ihrer Wirkung auf die Gelenke. A rch Orthop Unfall-Chir 1 966;60:380. 44. Cotta H. Pathophysiologie des Knorpelschadens. Hefte Unfallheikunde 1976;127: 1-22. 45. Dustmann HO. Knorpelveranderungen beim Hamarthros unter besonderer Berucksichtigung der Ruhigstellung. Arch Orthop Unfall-Chir 1971;71:148. 46. Giucciardi E. Some observations on the effect of blood and fibrinolytic enzyme on articular cartilage in the rabbit. J Bone Joint Surg 1 967;49B :342-350. 47. Sood Se. A study on the effects of experimental immobilisation on rabbit articular cartilage. J Anat 1971;108:497. 48. Vide man T. Connective tissue and immobilisation: key factors in musculoskeletal degeneration? Clin Orthop Rel Res 1 987;221:26-32. 49. Ratcliffe A, Mow Ve. Articular cartilage. In: Comper WD (ed) Extracellular Matrix, vol I, Tissue Function. Harwood, Amsterdam, 1 996;234-306. 50. Salter RB, Simmonds DF, Malcolm BW et a/. The biological effect of continuous passive motion on the healli1g of full-thickness defects in articular cartilage. ] Bone Joint Surg 1980;62A: 1232-1251. 51. Gerber Ch, Matter P, Chrisman OD, Langhans M. Funktionelle Rehabilitation nach komplexen Knieverletzungen. Wissenschaftliche Grundlagen und Praxis. Schweiz Z Sprtmed 1 980;28:37-56. 52. Appell H-J. Muscular atrophy following immobilization. A review. Sports Med 1990;10(1):42-58. 53. Maroudas A. Distribution and diffusion of solutes in articular cartilage. Biophys J 1 970;10:365. 54. Tittel K. Zur Anpassungsfahigkeit einiger Gewebe des Haltungs- und Bewegungsapparates an Belastungen unter schiedlicher Intensitat und Dauer. Med Sport 1973;13:147-156. 55. Robbins JR, Evanko SP, Vogel KG. Mechanical loading and TGF beta regulate proteoglycan synthesis in tendon. Arch Biochem Biophys 1 997;342(2):203-211. 56. Ehricht HG. Zur Diagnostik und Therapie der veralteten Bandruptur am oberen Sprunggelenk fibular. Med Sport 1978;18:274-280. 57. Smillie IS. Injuries to the Knee Joint, 5th edn. Churchill Livingstone, Edinburgh, 1978. 58. Cooper RR. Alterations during immobilization and regenera tion of skeletal muscles in cats. J Bone Joint Surg 1 972;54A:919-951 . 59. Jarvinen M. Healing o f a crush injury i n rat striated muscle with special reference to treatment by early mobilization or immobi lization. Dissertation Turku, 1976. 60. Vries de HA. Quantitative EMG investigation of the spasm theory of muscle pain. Am J Phys Med 1966;45:119-134. 61. Bobbert MF, Hollander Ap, Huijing PA. Factors in delayed onset muscular soreness of man. Med Sci Sports Exerc 1986;18:75-81 . 62. Stauber WT. Eccentric action o f muscles; physiology, injury and adaption. Exerc Sport Sci Rev 1989;17:157-185.
58 SECTI O N O N E - G E N E RAL P R I N C I PLES
63. van Wingerden BAM. Ijstherapie in de sport - Indicatie of contraindicatie. Kine 2000, Eur Tijdschr Kinesither 1993: 1 . 64. Travell J. Ethyl chloride spray for painful muscle spasm. Arch Phys Med Rehab 1952;32:291-298. 65. Waylonis GW. The physiologic effects of ice massage. Arch Phys Med Rehab 1 967;48:37-47. 66. Obremskey WT, Seaber AY, Ribbeck BM, Garrett WE Jr. Biomechanical and histological assessment of a controlled muscle strain injury treated with piroxicam. Trans Orthop Res Soc 1988;13:338. 67. Clanton TO, Coupe KJ. Hamstring strains in athletes: diagnosis and treatment. j Am Acad Orthop Surg 1998;6(4):237-248. 68. Beaulieu JE. Developing a stretching program. Physician Sportsmed 1981 ;9:59--65. 69. Stanish WD, Hubley-Kozey CL. Separating fact from fiction about a common sports activity: can stretching prevent athletic injuries? j Musculoskeletal Med 1984:25-32. 70. Wiktorsson-Moller M, Oberg B, Ekstrand J, Gillquist J. Effects of warming up, massage, and stretching on range of motion and muscle strength in the lower extremity. Am j Sports Med 1983;11:249-252. 71 . Garrett WE Jr. Muscle strain injuries: clinical and basic aspects. Med Sci Sports Exerc 22(4):436-443. 72. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am 1 Sports Med 1991;19(3):299-304. 73. Beiner JM, Jokl P, Cholewicki J, Panjabi MM. The effect of anabolic steroids and corticosteroids on healing of muscle contusion injury. Am 1 Sports Med 1999;27(1) :2-9. 74. Cyriax JH. Textbook of Orthopaedic Medicine, vol 1. Bailliere Tindall, London, 1982. 75. Penniello MI, Chapon F, Olivier D et al. Myositis ossificans progressiva. Arch Pediatr 1995;2(1):34-38. 76. Traore 0, Yiboudo I, Cisse R et al. Non-traumatic circum scribed myositis ossificans. Apropos of a bilateral locaJization. Rev Chir Orthop Reparatrice Appar Mot 1998;84(1):79-83. 77. Howard CB, Porat S, Bar-On E, Nyska M, Segal D. Traumatic myositis ossificans of the quadriceps in iniants. 1 Pediatr Orthop 1998;7(1):80-82. 78. Weinstein L, Fraerman S. Difficulties in early diagnosis of mYOSitis ossificans. lAMA 1 954;154:994. 79. Gilmer W, Anderson L. Reactions of the somatic tissue which progress to bone formation. South Med J 1959;52: 1432. 80. Huss CD, Puhl JJ. Myosititis ossificans of the upper arm. Am 1 Sports Med 1980;8(6):419. 81. Carr AI, Norris SH. The blood supply of the calcanean tendon. 1 Bone joint Surg 1 989;71B : 1 00-1 0 1 . 82. Ahmed 1M, Lagopoulos M , McConnell P, Soames RW, Sefton GK. The blood supply of the Achilles tendon. 1 Orthop Res 1998;16(5):591-596. 83. Katzer A, Wening JV, Becker-Manich HU, Lorke DE, Jungbluth KH. Rotator cuff rupture. Vascular supply and collagen fiber processes as pathogenetic factors. Unfallchirurgie 1997;23(2):52-59. 84. Kummer FJ, Zuckerman JD. The incidence of full thickness rotator cuff tears in a large cadaveric population. Bull Hasp It Dis 1995;54(1):30-31. 85. Milgrom C, Schaffler M, Gilbert S, van Holsbeeck M. Rotator cuff changes in asymptomatic adults. The effect of age, hand dominance and gender. 1 Bone joint Surg 1994;77B (2): 296-298. 86. Gelberman RH, Vande Berg JS, Lundborg GN, Akeson WHo Flexor tendon healing and restoration of the gliding surfaces. j Bone 10int Surg 1983;65A:70-80.
87. Takai S, Woo SL, Horibe S, Tung DK, Gelberman RH. The effects of frequency and duration of controlled passive mobilization on tendon healing. J Orthop Res 1991;9(5): 705-713. 88. Stenho-Bittel L, Reddy GK, Gum S, Enwemeka CS. Biochemistry and biomechanics of healing tendon. Part I. Effects of rigid plaster casts and functional casts. Med Sci Sports Exerc 1998;30(6):788-793. 89. Buckwalter JA. Effects of early motion on healing of musculo skeletal tissues. Hand Clin 1996;12(1) :113-24. 90. Peterson L, Althoff B, Renstrom P. Reconstruction of the lateral ligaments of the ankle joint. Proceedings of the First World Congress of Sports Medicine Applied to Football. Rome, Italy, February 1979: 141. 9 1 . Cass JR. Ankle instability: comparison of primary repair and delayed reconstruction after long-term follow-up study. Clin Orthop Rel Res 1985;198:110-117. 92. Cyriax JH. Textbook of Orthopaedic Medicine, vol II, 11th edn. Bailliere Tindall, London, 1 984. 93. Larsen E. Taping the ankle for chronic instability. Acta Orthop Scand 1984;55:551-553. 94. Freeman MAR. The etiology and prevention of functional instability of the foot. j Bone 10int Surg 1965;47B:678-685. 95. De Carlo MS, Talbot RW. Evaluation of ankle joint propriocep tion following injection of the anterior talofibular ligament. j Orthop Sports Phys Ther 1 986;8:70-76. 96. Oostendorp RAB. Functionele instabiliteit na het inversie trauma van enkel en voet: een effectonderzoek pleisterban dage versus pleisterbandage gecombineerd met fysiotherapie. Geneeskd Sport 1 987;20(2):323-329. 97. Lynch SA, Renstrom PA. Treatment of acute lateral ankle ligament rupture in the athlete. Conservative versus surgical treatment. Sports Med 1 999;27(1):61-71. 98. Fetto JF, Marshall JL. Medial collateral ligament injuries to the knee: a rationale for treatment. Clin Orthop Rei Res 1978;132:206. 99. Hastings DE. The non-operative management of collateral ligament injuries of the knee joint. Clin Orthop Rei Res 1980;147:22. 100. Indelicato PA. Non-operative treatment of complete tears of the medial collateral ligament of the knee. 1 Bone 10int Surg 1983;65A:323. 101. Jones RE, Henley B, Francis P. Non-operative management of isolated grade III collateral ligament injury in high school foot ball players. Clin Orthop Rel Res 1986;213:137-140. 102. Indelicato PA, Hermansdorfer I, Huegel M. Non-operative management of complete tears of the medial collateral liga ment of the knee in intercollegiate football players. Clin Orthop Rei Res 1990;256:174-177. 103. Kannus P, Jarvinen M. Non-operative treatment of acute knee ligament injuries. Sport Med 1990;9(4):244-260. 104. Crowninshield RD, Pope MH. Strength and failure characteristics of rat medial collateral ligaments. 1 Trauma 1969;16:99. 105. Wiggins ME, Fadale PD, Ehrlich MG, Walsh WR. Effects of local injection of corticosteroids on the healing of liga ments. A follow-up report. ] Bone 10int Surg 1995;77A(l1): 1 682-169 1 . 106. Campbell RB, Wiggins ME, Canistra LM, Fadale PD, Akelman E. Influence of steroid injection on ligament healing in the rat. Clin Orthop 1 996;332:242-253. 107. Hughston JC, Eilers AF. The role of the posterior oblique liga ment in repairs of acute medial collateral ligament tears of the knee. 1 10int Bone Surg 1973;55A:923-940.
Clinical diagnosis of soft tissue lesions
CHAPTER CONTENTS
Introduction
59
Clinical evaluation History 63 Inspection 69
63
Preliminary examination 70 Functional examination 70 Accessory tests 75 Palpation 77 Diagnostic infiltration or aspiration Technical investigations 80
Interpretation
80
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
I N TRODU CTION
As non-osseous orthopaedic disorders are one of the major causes of human suffering, they deserve accurate diagnosis. They manifest themselves with symptoms felt at a moving part of the body. Some non-orthopaedic lesions very often present with identical symptoms, which means as a consequence the orthopaedic physician is often consulted. Technical investigations are often not helpful in the diagnosis of soft tissue lesions and may even be misleading (see p. 80). Diagnosis should thus be made on the basis of the clinician's ability to interpret the symptoms and signs. The diagnosis should describe the lesion as exactly as possible. Vague phrases, such as 'rotator cuff syn drome', 'periarthritis', 'tennis elbow', 'jumper's sprain', 'painful arc syndrome', 'low back pain' and 'sciatica' are unhelpful, in that they do not answer the vital question which structure is affected? The clinician must therefore continue examination to the point at which a precise description of the lesion is achieved: for example supraspinatus tendinitis at the superficial aspect of the tenoperiosteal junction, chronic subdeltoid bursitis, lesion at the origin of the extensor carpi radialis brevis muscle, periostitis at the anteroinferior surface of the fibula, annular disc protrusion at the L4-L5 level com pressing the fifth lumbar nerve root. Such precision is essential because it accurately informs the doctor or therapist where to apply treatment. This immediate and precise approach will certainly help to speed healing. Injection, infiltration and deep trans verse massage cannot cure the patient unless applied to the exact site of the lesion. Likewise, when manipulative techniques are a possibility, the localization and type of the lesion determine whether they are indicated and what form they should take. -
CHARACTERISTICS OF S O FT TISSUE LES I O N S • The lack o f objective physical signs . • The discrepancy between the site of the symptoms and the site of the lesion.
59
60
S E CTION O N E - G E N E RAL P R I NCI PLES
There are two main obstacles to a precise diagnosis in lesions of the non-osseous tissues of the locomotor system: The lack of relevant objective physical signs In non-osseous orthopaedic lesions, the lack of objec tive physical signs is often striking. Blood examination, radiography, echography, electromyography, computed tomography and magnetic imaging are often requested but seldom of great help to the orthopaedic physician; furthermore, they too often reveal findings that are com pletely irrelevant to the lesion. Occasionally they merely confirm what is already known from the clinical findings. The group of disorders that requires further technical investigations to arrive at the diagnosis is rather small. They present with symptoms and signs that have an unusual pattern. This will put an experienced examiner on guard and make further and more thorough examina tion mandatory. (See below: Warning p. 63.) •
The discrepancy between the site of the symptoms and the site of the lesion Soft tissue lesions very often give rise to referred pain, a phenomenon that may mislead the examiner and for which the rules have already been stated (see eh. 1). Once these rules are familiar to the examiner, referred pain can be turned to advantage in that it becomes possi ble to demonstrate which structure could and which structure could not be responsible for the symptoms.
•
PRINCIPLES O F DIAGNOSTIC PROCED U RE I N ORTHOPAEDIC MEDICINE
signs that belong to the clinical picture of a certain pathologi cal disorder and that are likely to be found, more or less in a sequence which is typical for that disorder. For example: in the history, a patient with lumbar pain may mention that on some days the pain spreads down the lower limb; tennis elbow is characterized by sudden twinges when objects are picked up; and in lumbar disc lesions pain may shift from one side to the other. Functional examination can also show some inherent likelihoods. When resisted extension of the wrist hurts at the elbow, a tennis elbow is suspect and can be confirmed by positive responses to resisted extension of the wrist with the fingers held actively flexed and to resisted radial deviation of the wrist. In tendinitis at the radial insertion of the brachial biceps, apart from pain on resisted flexion and supination of the elbow, full passive pronation is also painful. In L5 sciatica, pins and needles in the medial three toes may be accompanied by numbness in the same area and by weakness of the extensor hallucis longus and peroneal muscles. The examiner who has a knowledge of what is likely to happen should recognize this and compare the pattern to the 'unlikelihoods' presented by some patients, which indicate either a non-organic lesion, a somatic but non orthopaedic problem or an unusual lesion. These inherent probabilities can of course only be recognized if the clinical examination is performed thoroughly. 2. The examiner looks for objective physical signs and, if not present, tries to objectivize the picture Examination of the moving parts is an exercise in applied
Box 4. 1 Principles of diagnostic procedure in orthopaedic medicine • • • • • • • • • •
Look for ' i n herent l i kel i hoods' Look for objective physical signs Use functional test i n g and pal pate o n l y when necessary Use the principle of 'selective tension' Use physiolog ical movements Assess the i nert tissues and the contract i l e tissues Concentrate on 'the' pain Ask for the patient's cooperation Take i nto accou nt the patient's personal ity Keep the balance between cred u l ity and excessive scept icism
• Ask for techn ical i nvestigations when necessary
1. The examiner looks for 'inherent likelihoods'
Soft tissue lesions behave in a very typical way and the examiner will there fore regularly be faced with the same history and the same response to functional testing. The symptoms and signs are closely related to the lesion present. The exam iner should therefore try to recognize 'inherent likeli hoods', a term defined as the sequence of symptoms and/or Some things are likely to happen.
The examination should include questioning (history taking) and testing which provokes or elicits symptoms and / or signs that can be assessed, judged and interpreted in as an objective way as possible. The soft tissues of the locomotor system have the advantage that their functional anatomy is well known. It is clear how joints behave, how capsules and ligaments guide and limit movements, how muscles function and what movements they provoke. Therefore, examination of the moving parts is an exer cise in applied anatomy. Each tissue or group of tissues in turn must be tested and the answer interpreted in the light of the anatomical possibilities.
anatomy.
3. The examiner uses functional testing and avoids palpation as much as possible The function of the different tissues is known.
Although
palpation is very often used as a diagnostic procedure, it is unreliable for several reasons: •
Some regions in the body are always tender to touch (e.g. lesser tuberosity at the shoulder, lateral epi condyle at the elbow, border of the trapezius muscle).
CHAPT E R 4
•
•
•
Some structures lie too deeply and cannot be reached by the palpating finger (e.g. capsule of the hip joint, cruciate ligaments at the knee). The painful area does not always correspond to the site of the lesion (referred pain) and referred dural tenderness is sometimes present. Some patients with altered perception or desire to deceive the examiner may produce misleading responses.
It is easy to understand that, in these circumstances, palpation offers no help at all or, even worse, may mis direct the examiner. Diagnosis, therefore, rests largely on the correlation of a series of semi-subjective data, obtained from a proper functional examination an indirect approach. By assess ing the function of each tissue in turn and interpreting the signs in the light of the anatomical knowledge, the examiner should be able to come to a correct description of the lesion. The patient is asked to answer some very precise questions. A patient with an organic lesion exactly describes what is felt and gives the examiner a fairly precise clinical picture. The neurotic or malingering patient will feel the need to embellish so as to give a colourful description of suffering rather than of the symptoms. -
4. Functional testing is based on the principle of 'selective tension'
The different tissues of the moving parts can be subjected to strain which may increase the pain and tests are used to elicit or influence the patient's symptoms. The possibility of making a diagnosis by selective tension depends largely on the characteristics of each tissue and on its capacity either to contract or to become stretched. Muscles and tendons may be stressed by isometric contraction of the muscle or by passive stretching in the opposite direction. By contrast, ligaments and joint capsules can be put under tension by passive stretch. If a certain test is positive, in that it provokes the symptom for which the patient consults, it establishes the relationship between the structure that becomes stretched, squeezed or contracted and the lesion. It is important to try to use movements that put tension on one structure only so that interpretation is as simple as possible. If a movement tests more than one tissue, acces sory tests or palpation may be required to obtain further information that can differentiate between potential causes. For example, when testing the lateral ligaments at the ankle, a combined movement of passive plantar flexion and inversion is performed. If this is positive and, The soft tissues can be put under tension.
-
C LI N I CAL DIAGNOSIS OF SOFT TISSU E LESIONS 61
later in the examination, passive internal rotation at the mid-tarsal joints is negative, involvement of the calcaneo cuboid ligament is excluded. In examination of the shoul der, painful resisted flexion of the elbow incriminates either the biceps or brachialis muscle; if resisted supina tion of the elbow is also positive, the lesion lies in the biceps muscle. 5. Functional testing uses physiological movements as much as possible Normal
movements
may
become
disturbed.
This
approach has some advantages: The structures that participate in the movement are well known (applied anatomy). The movements are easily controllable and repro ducible. Pain may be provoked, but also limitation can be seen and weakness is not difficult to detect. The inter- and intra-tester reliability is quite high.l-6 Patterns can be found: pain patterns, patterns of limitation and patterns of weakness. The recognition of a known pattern confirms the symptoms and signs presented.
• •
•
6. Functional testing is based on the recognition of two different groups of structures: inert and contractile tissues Soft tissues are either inert or contractile. This distinc tion is one of the pillars on which the whole system of orthopaedic medicine rests. The soft tissues of the loco motor system can be divided on the one hand into tissues that can contract (the contractile structures) and on the other hand, tissues that do not possess this capacity (the non-contractile or inert structures) (Table 4. 1). Contractile structure. The complex of muscle origin, muscle belly, musculotendinous junction, body of tendon, tenoperiosteal junction and also the bone adjacent to the attachment of the tendon are considered clinically as contractile (Fig. 4.1). The only worthwhile method of testing these struc tures is by maximal contraction against resistance. The
Table 4.1 Inert tissues
Contractile tissues
• • • • • • •
• • • • • •
Joint capsules Ligaments Bursae Aponeuroses Dura mater Dural sleeve of the nerve root Peripheral nerves
The complex of: Muscle-bone attachment (origin) Muscle belly Musculotendinous junction Body of tendon Tenoperiosteal junction (insertion) The bone adjacent to the attachment of the tendon
62
S E CTION O N E - G E N E RAL P R I N C I P LES
2
----f---tH
3
-----l'--+t:w.tll
4
Figure 4.1 Contractile structures: the musculotendinous unit: 1, tendon; 2, muscle belly; 3, musculotendinous junction; 4, insertion.
movement should be performed isometrically so that the applied tension, which causes pain, falls only on the muscle and the structures attached to it. Passive movement in the opposite direction, which stretches the contractile tissue, can also elicit the pain but cannot be used as a specific test for it because non contractile tissues are also stretched. For example, a lesion in the subscapularis tendon at the shoulder gives rise to pain on resisted internal rotation. Full passive external rotation may also hurt. This sign fits the clinical picture of subscapularis tendinitis but has no diagnostic nor localizing value because the passive movement also stretches the anterior joint capsule and the pectoralis major muscle and tendon. However, a pain elicited by resisted movement does not invariably mean that a contractile tissue is at fault. If the bone close to the tendinous insertion is affected (frac ture or other bony disorder), pain is evoked by the pull of the muscle. A contraction may also squeeze an underly ing structure such as a lymphatic gland or bursa. When such tissues are inflamed, squeezing may evoke pain. The same applies when there is a disorder adjacent to muscles, for example an abscess. This explains why, for example, contraction of the sternocleidomastoid muscle may be painful in glandular fever and why contraction of the gluteal muscles can hurt in a trochanteric bursitis.
Inert structure. An inert structure does not possess an inherent capacity to contract and relax and can thus be tested only by passive stretching or squeezing. The inert tissues are shown in Table 4.1. Active movements may also stretch or squeeze an inert structure but, because they also activate the contractile tissues, interpretation is subject to ambiguity and they cannot be used to test inert structures. For example, during active elevation of the arm, many muscles are in action (deltoid, supraspinatus, serratus anterior, trapez ius). At the same time, certain parts of the joint capsule and some ligaments are stretched (acromioclavicular, sternoclavicular, conoid and trapezoid ligaments) and other structures are compressed (subacromial bursa, infe rior acromioclavicular ligament, tendinous insertions of supraspinatus, infraspinatus, subscapularis and biceps).
7. The examiner concentrates on 'the' pain 'The' pain is that pain for which the patient consults.
When tests evoke pain, the examiner must make sure that this is the pain that is the patient's complaint. It is possi ble that some movements elicit pain in a certain area and that other tests provoke another pain in another region: one of these will be recognized by the patient as the pre senting symptom. The examiner should then concentrate on this pain alone. The situation often occurs because combined lesions are quite common. A patient may come to see tJ1e doctor with pain down the arm. If, after the history has been taken, it is not clear whether the pain originates either from the cervical spine or shoulder girdle or from the shoulder itself, the preliminary examination aims to clarify the situation. It may show some discomfort at the base of the neck when cervical movements are tested (espeCially in middle-aged and elderly people) but if only shoulder movements elicit the pain complained of, then this pain ('the' pain) is the primary problem; the other pain (' a' pain) is secondary. The arm pain will, of course, be dealt with first and only when this problem is solved is the other problem (if still present) approached. Difficulties may arise in hypersensitive patients who report every tension they experience and for which they use different words: 'it hurts, it aches, it pulls, it stretches, . . . . '
8. The examiner asks for the patient's cooperation
The patient's cooper ation is essential, and it is vital that the questions put are understood. Details are sought on what activities have an influence on the symptoms and how symptoms behave over time. Except in psychologically disturbed patients, the more precise the questioning, the easier it is to obtain
The patient knows the symptoms.
CHAPTE R 4
accurate answers. The patient must realize that, during functional examination, the examiner is looking for tests or movements that elicit symptoms. Most difficulties arise with those who are in constant pain, in that they tend to answer every question positively. It is the task of the examiner to explain carefully that movements that alter the pain are being sought. Not only tests that make the pain worse (a frequent occurrence) but also those that decrease the pain are considered important. 9. The examiner takes into account the patient's personality
The history in particular will give an idea about the patient's personality. The reaction to pain can be assessed and a picture built up of the extent of disability. The findings can then be related to what is actually found when the examination takes place. The view obtained from the history and physical examination may have therapeutic significance: for example, most patients can cope with active treatment such as manipulation or deep transverse massage but the clinician may obtain a 'perception' for those who cannot. The patient is a person.
•
•
-
CLI N I CAL D IAGNOSIS OF SOFT TISS U E LESIONS 63
but do not always prove a possible relationship with the lesion present. The value of technical procedures is either to confirm the tentative diagnosis made after the clinical exami nation or to exclude lesions for which the functional testing has not been sufficient. The positive and / or negative findings of technical examinations should be related to the findings of the clinical examination. Warning Incorporated into this system of clinical evaluation are
warning signs: certain symptoms or combination of symptoms
and signs indicate that something unprecedented is taking
place and so alert the examiner to the possible presence of a potentially serious condition. Possible warning signs are, for example, pain in the upper lumber area, deficit of more than one nerve root in the cervical spine, or a capsular pattern of the hip in children. The presence of such warning signs will put the examiner on guard and indicate accessory clinical tests, further technical investigations or reference to a neurologist, an internist, a cardiologist or an oncologist. These warning signs will be discussed further in later chapters.
10. The examiner must keep the balance between credulity and excessive scepticism
Orthopaedic medical dis orders produce symptoms and signs that may be difficult to analyse objectively. Patients who have a reason to assume disorders for some type of personal gain, therefore, commonly use clinical features in the locomotor system to try to establish their credibility (see Ch. 88 on Psychogenic Pain). Although the examiner must be on guard against feigned illness, great care must also be taken to maintain a dispassionate attitude during the clinical encounter. The diagnosis of 'psychogenic pain' must not be made too quickly. Only when many inherent unlikelihoods are encountered during the history and functional examina tion should the examiner be suspicious about the verac ity of the patient's story. Also, the discovery of a series of lesions is self-contradictory, because the development of several problems at the same time is most unlikely. Objectivity is a fair attitude.
1 1. The examiner asks for technical investigations when necessary Looking is not a substitute for thinking. Clinical testing is the first approach in orthopaediC medicine. Technical investigations, although some are able to show the soft tissues, are asked for either because clinical diagnosis is not clear, or for medicolegal reasons. •
Technical investigations are usually not valuable as a diagnostic tool. They may show anatomical changes
HISTORY
History is of prime importance in reaching a diagnosis. It is so well known as a method of determining symptoms that most examiners fail to realize how much information can be gained from it. Patients are the best source of information in that they are suffering from the lesion and can best report precisely what is felt. It is then the examiner's task to translate the subjective symptoms into anatomical and functional conclusions. Cyriax said: 'Every patient contains a truth. He will proffer the data on which diagnosis rests. The doctor must adopt a conscious humility, not towards the patient, but towards the truth concealed within the patient, if his interpretations are regularly to prove correct? History taking is a slow business that requires time, patience and concentration; the examiner must do everything possible to gain the maximal detailed infor mation. Vague, general description of the complaints should not be accepted but precise and detailed answers sought. Most patients, and certainly when they are frank, are able to provide precise answers to the examiner's questions or can spontaneously give a well-structured,
64
SECTION O N E - G E N E RA L P R I N C I PLES
detailed and chronological account. They try to be as helpful as possible and are visibly pleased to talk to an interested physician. However, taking the history becomes more difficult in those who cannot express themselves or give a disjointed story. It is the examiner's task then to make sure that the right questions are asked in order to get useful answers. The same applies to talka tive patients who try to be too helpful by adding all manner of irrelevant details. In these circumstances the examiner should concentrate on the important items only and bring the patient back to the point whenever there is a digression. Patients with a clinical presentation that may rest in non-organic causes try to escape from precise questioning. They offer a garbled story full of internal contradictions. Remarks
Questions should be asked in such a way that the account of the symptoms is given in chronological order which enables the examiner to get an idea of the duration and behaviour of the condition present. Knowledge of differ ent dermatomes and of the possible likelihoods will help in interpretation of the evolution of the patient's symptoms. Leading questions should be avoided, because they suggest to the patient what answer is expected. The questions should be neutral, so that the patient has to think about what is felt. An honest patient will have no problems in giving exact answers; one who dissembles has the opportunity to make mistakes and display inconsistencies. Examples of questions that should be recast are as follows: •
• • •
Not: does the pain spread down your leg? But: does the pain spread at all? if so, where to? Not: is it painful to cough? But: what happens when you cough? Not: is it painful to bend forwards? But: does anything bring the pain on? Not: do you feel pins and needles in your hand? But: have you got any pins and needles? and if so, where?
When there is a relationship between the patient's symptoms and rest, exertion, certain activities or certain postures, then it is probable that the patient suffers from a lesion of the locomotor system. The main exceptions are angina and intermittent claudication. Questions should therefore be asked about the movements and positions that evoke, increase or influence symptoms, for example: • •
What brings the symptoms on? What makes the symptoms disappear?
Some information can be obtained only from the history, and not from any other diagnostic procedure. For example, to ascertain the stage of shoulder arthritis, to find out whether a displaced fragment of cartilage is stable or unstable, to determine whether sciatica is caused by a primary or secondary posterolateral disc pro trusion, depends on the answers to some very specific questions. These are not only diagnostically important but also have a prognostic value and can determine correct treatment. For lesions of the knee or spine, the history is of extreme importance; the examiner must go into great detail and if this is done the diagnosis becomes appar ent. For example, a patient may mention that pain started in the centre of the back, soon spreading unilat erally towards the buttock, and later radiating down the lower limb into the lateral border of the foot and the two little toes while at the same time pain in back and buttock disappeared. After a while pins and needles began to occur in the same toes and additionally they would go numb. The patient has revealed everything: the normal evolution of a protruded fragment of disc at the L5-S1 level, compressing the first sacral nerve root, is immediately apparent. In some other joints, such as the shoulder, the history matters less but examination will disclose the lesion. TAKI N G THE H I STORY Age, sex, profession, hobbies and sports
Some disorders are confined to certain age groups so that the age of the patient may indicate diagnostic possibili ties. For example, a patient of 14 who mentions internal derangement at the knee probably suffers from osteo chondritis dissecans. The same story in a patient of 20 suggests a meniscal problem and at 60 years points to a loose body in an arthrotic joint. The same applies to the hip: trouble at the age of 5 is probably due to Perthes' disease; at 15 it could be the result of a slipped epiphysis; at 30 ankylosing spondylitis is a possibility; and at 50 arthrosis is more likely. A similar age distinction applies in root pain of cervical origin: under the age of 35 it is extremely rare that this is caused by a disc protrusion. Certain disorders are more typical for men (e.g. primary sciatica and ankylosing spondylitis) and others occur more often in women (e.g. de Quervain's disease and the first rib, thoracic outlet syndrome). The profession of the patient may sometimes give an idea about the causative strains that have acted on the affected joint. Also it may - in conjunction with hobbies or sports - have an influence on the decisions to be taken on treatment. Treatment for acute lumbago will be differ ent in an employee who sits most of the day than in a docker who has to do heavy work; a patient with regular
CHAPT E R 4
attacks of sudden backache will be advised against tennis, a sport full of quick movements.
-
C L I N I CAL D IAGNOSIS OF SOFT TISS U E LESIONS 65
Box 4.2 Evolution of symptoms • Uni nterru pted
Initial symptoms
The examiner should get an accurate picture of the moment the symptoms first appeared. The patient should be encouraged to recall that period and questions should proceed from that first instant. The onset of the symptoms has to be clear. If they came on. after an injury, a very detailed description of the accident should be elicited. The events immediately following the accident must be ascertained, in that com pensation may be claimed because of inadequate or inappropriate management. The subsequent condition of the joint may not allow complete examination and therefore an idea of the direction of the forces acting on that joint and the position in which the joint was held at the moment of the accident are essential and will give a notion of the possible structures affected. The knee is an important example. In a 'sprained' knee the inflamma tory reac�ion that follows the accident is so spectacular (swelling, limitation of movement) that proper func tional testing becomes difficult, which means that in the acute phase the examiner has to rely mainly on the history to get an idea of what has happened. If the pain is felt at the medial aspect of the joint and the patient mentions a valgus injury, the medial collateral ligament or the medial meniscus are most likely to have been damaged. Swelling of a joint after an injury may have come on immediately, in which case blood is the cause, or after a few hours, which is typically the result of a reactive effusion. When the patient mentions a spontaneous onset, thjs may be either sudden or gradual. Apart from diagnosis this distinction may have therapeutic consequences. Backache, as the result of disc protrusion, that comes on suddenly is annular and requires manipulation, whereas a gradual onset suggests nuclear displacement, which is treated with traction. The patient must exactly define the first localization of the symptoms. The area where the pain was first felt very often lies quite close to the site of lesion, referred pain usually coming on later. This does not apply to 'pins and needles'. They are mostly felt distally in the limb, from wherever along its length the nerve is affected. Questions are also asked about what influenced the symptoms. The examiner looks for a relationsillp between activities, movements or posture and the symptoms. Progression/evolution
The symptoms may be present without interruption from their onset. However, it is also possible that the patient describes a recurrence (see Box 4.2).
u nchanged d i m i n ished worsen i n g i ntermittent
• Recurrent
The progression of symptoms since their first onset is ascertained. The condition may have continued uninter rupted, in willch case details are asked about the develop ment of the severity of the symptoms and of the localization of pain. If the latter has remained unchanged from the beginning, this indicates that the lesion is quite stable and not evolving. When pain has diminished it usually indicates an improvement, although there are conditions (e.g. nerve root atrophy and certain cases of mononeuritis), in which the pain disappears long before the condition has resolved. Pain becomes worse as the condition progresses: in such circumstances it is impor tant to know the length of time for which it has been present. This has diagnostic significance: it is clear that conditions such as metastases have quite a short time course. In contrast, slowly worsening pain is characteris tic of some other conditions such as a neurofibroma. When the patient describes intermittent pain, details are sought about the occasions on which pain is felt. Nocturnal pain, for example, suggests an inflammatory condition. A very important distinction should be made between the following definitions. Reference of pain. Referred pain is a very typical feature in non-osseus lesions of the locomotor system. It is mostly segmental and thus experienced in a single dermatome, which indicates the segment in willch the lesion should be sought. Reference of pain is influenced by the severity of the lesion: the more severe it becomes, so giving rise to a stronger stimulus, the further distally does the pain (usually) spread. The reverse also holds: reduction in the distal distribution is synonymous with improvement.8,9 It is therefore always important not to forget the ques tion: 'Where was the pain originally and where has it spread since?' Shifting pain. Pain coming on in one place as it leaves another indicates a shifting lesion. Tills extremely significant phenomenon is well known in internal medicine: for example, when a renal calculus moves from the kidney down the ureter and to the bladder and urethra, the pain experienced will follow the displacement. Pain is felt in the loin first, then in the iliac fossa, later in the groin and finally in the genitals. When the pain leaves one point, it is felt in another instead.
66
S E CTION O N E - G E N E RAL P R I N C I PLES
The same happens in soft tissue lesions. A good example is central backache, which becomes unilateral, then later on shifts to the buttock and finally to the lower limb the backache has become sciatica. This shift can only be explained as follows: a structure lying in the midline and originally compressing the dura mater (backache) has shifted to one side and now compresses the dural sleeve of the nerve root (root pain). To be able to shift, that structure has to lie in a cavity and, because the pain was originally central, this has to be a central cavity. The only structure lying in a central cavity and able to change its position is the intervertebral disc: there is no other possibility (Fig. 4.2). -
This is synonymous with an expanding one that grows, for example a tumour. When it appears in another region the pain does not leave the area where it originated. It spreads, even beyond the boundaries of dermatomes. A patient may describe a pain that begins in the centre of the back and then becomes bilateral. It spreads to one buttock, and later to both, also increasing in the back. Later it spreads to one leg and even subsequently to both, while still becoming worse in the back as well as in the lower limbs. Such a course is one of expanding pain, as the lesion becomes more extensive. Expanding pain.
lesion
-
Warning
(a)
(b)
Figure 4.2 Shifting pain: posterocentral disc protrusion causing central backache (a); shifts to posterolateral position causing unilateral sciatica (b).
The same situation is encountered when a loose frag ment of cartilage moves within a peripheral joint as, for example, often happens in the knee. Dependent on the position of the loose body in the joint space, the pain can be felt at the inner aspect, anteriorly or posteriorly and on other occasions even at the lateral side. Such moving pain indicates a moving lesion.
An expa n d i n g pai n, i n which pain spreads but does not regress at the orig i nal site (in the way that a shifting pain does), is i n d i cative of an expanding lesion and is usually the manifestation of a serious condition.
Another course is recurrence. Certain disorders, such as those causing internal derangement or of rheumatoid type, have a recurrent character. Some occur suddenly, others more gradually. If the symptoms occur intermit tently, it is important to know whether the patient is or is not free of pain between attacks, because this has both prognostic and therapeutic consequences. Freedom from symptoms for a certain period of time suggests that the same may happen again. In internal derangement, regular recurrence implies that the loose fragment of car tilage or bone is unstable, in which case the maintenance of reduction will be the main concern of the therapist. A patient who is doing heavy work and who gets lumbago every 2 years must be regarded as having a stable lumbar disc which is completely different from a man with a light job who gets lumbago three times a year. In the first case reduction suffices, whereas the second will need other prophylactic measures to maintain the disc in place. The onset of pain may vary from one attack to another. Backache that starts suddenly on some occasions, but gradually on others, very strongly suggests discal trouble. The localization of the pain may also change from one attack to another: it may be felt on one side of the body or of a joint and on the next occasion on the other side. This shifting pain is very typical of internal derangement, although there are some other conditions that may present the same picture (e.g. alternating buttock pain in sacroiliac arthritis caused by ankylosing spondylitis and alternating headache in migraine). Actual symptoms
After having built up a complete picture of the patient's symptoms, information is sought about what is experi enced at the time of interview.
CHAPTER 4
Most patients consult the doctor because they have pain but other symptoms may also be described: pins and needles, numbness, limitation of movement, twinges, weakness and vertigo. These are sometimes forgotten by the patient and therefore the examiner must inquire about them. Every symptom must be given due weight and examined in detail. Pain. (Box 4.3). There are many different ways of describing pain: it is amazing how much variation patients can achieve in their vocabulary and how many different descriptive terms can be used for the different sensations perceived. The reason lies in the fact that pain is mainly an unpleasant emotional state that is aroused by unusual patterns of activity in specific noci ceptive afferent systems. The evocation of this emo tional disturbance is contingent upon projection to the frontal cortex.lO,ll The nature of the pain may have some diagnostic value: everybody knows the throbbing pain of migraine, the stabbing pain of lumbago or the burning sensation of neuralgic conditions. Although the way the patient describes the pain may sometimes point to a certain disorder, it can also indicate the emotional involvement of the patient with the lesion.
Box 4.3 Pain • Description • Character: mecha nical i nf l a m matory • Severity: therapeutic consequences • Loca l i zation: diagnostic significance
Pain may have either a mechanical or an inflammatory character (Box 4.4). Mechanical pain (e.g. in arthrosis) is characterized by pain and stiffness at the beginning of a movement; augmentation when load is put on the joint; pain at the end of the day and absence of pain at the rest although moving in bed may also be uncomfortable. Inflammatory pain (e.g. rheumatoid arthritis, gout or infectious arthritis) wakes the patient at night and gives rise to frank stiffness early in the day.12 The severity of pain may be a determinant of the type of treatment that is chosen. For example, although sciat ica without neurological deficit is not immediately an
Box 4.4 Characteristics of mechanical and inflammatory pain Mecha n i cal pain • Starting pain/stiffness • During loading • Worse at eve n i n g • Movi ng i n bed
Inflam matory pa i n • Nocturn a l • Morn i n g stiffness
-
CLI N I CAL D IAGNOSIS OF SOFT TISSUE LESIONS 67
indication for surgery, discectomy may become the treat ment of choice when the pain has become unbearable. Finally, localization has some diagnostic significance. Pain may be felt centrally (on the midline), bilaterally or unilaterally. Central and bilateral pain usually point towards a lesion lying in the midline. A bilateral lesion is another possibility, but this is much less frequent. It should be realized, however, that central symptoms do not arise from a unilateral structure. And, although some structures lie very close to the midline (facet joints, costovertebral joints, erector spinae muscles), they are still unilateral and can only give rise to symptoms felt unilaterally. Unilateral pain originates in a unilateral structure or, when dealing with the spine, in a central structure that moved to one side and compresses nerve tissue unilaterally (e.g. a disc). When the lesion is in the locomotor system, there should still be a relationship between symptoms and rest, exertion, activities, movements or posture. When cough ing, sneezing or breathing hurts in an area other than in the chest, the dura mater could very well be responsible. Dural pain can be felt in the trunk far beyond the relevant dermatome. Of special interest to the examiner are 'twinges': sudden short bouts of pain, which last only one second and are often associated with momentary functional incapacity. The occurrence of painful twinges may be the result of one of the following: • • •
Internal derangement Tendinous Neurological.
A momentary subluxation of a loose fragment of cartilage in a joint. This happens quite often in the lumbar spine, the
knee and the hip and less frequently in the elbow, ankle and subtalar joints. If there are any signs found during clinical examination, they will be articular - a non-capsu lar pattern (see p. 86). The combination of twinges and articular signs is pathognomonic of the existence of inter nal derangement. A tendinous lesion. The patient recounts that, especially when the tendon is involved in movement, there are bouts of painful momentary weakness which arrest movement. This is common in tennis elbow, where the lesion lies at the origin of the extensor carpi radialis brevis muscle from the lateral epicondyle. It also occurs, although less frequently, in tendinitis at the shoulder, especially of the supraspinatus. A neurological condition, such as tabes, post-herpetic or trigeminal neuralgia and Morton's metatarsalgia. Paraesthesia. Non-painful sensory disturbances, paraesthesia, are strongly indicative of a condition that originates in nerve (Box 4.5). They may result from an intrinsic lesion (primary neuritis or secondary
68
SECTION O N E - G E N E RA L P R I N C I PLES
Box 4. 5 Paraesthesia Loca l ization:
-----
,
m u ltisegmental
• spinal cord • central nervous disease or intern a l disorder
1
--,
.
segmental (dermatome) • nerve root
t
territory of ne rve
• p l exus • peri pheral nerve tru n k • peri pheral nerve ending
Upper extent Accompanying symptoms:
• pain • weakness
Behaviour: i.e. compression phenomenon release phenomenon
polyneuropathy) or from an extrinsic cause (compres sion). They may also vary in quality and in intensity. In orthopaedic medicine the variation lies between numb and ness real pins and needles. It is very often described as , tingling'. The moment the patient mentions the presence of pins and needles, the examiner should go into detail and ask the following questions: • • • •
What brings on the pins and needles? What makes them disappear? How far proximally do they extend? Where exactly are they felt?
In entrapment neuropathies, knowledge of what brings the pins and needles on will show whether a compression phenomenon or the release phenomenon is acting (see pp. 28-29). For example, pressure on a small distal nerve gives rise to paraesthesia and analge sia in the cutaneous area of that nerve during the time of compression (e.g. meralgia paraesthetica). However, when a nerve trunk or nerve plexus becomes com pressed, the paraesthesia are felt in a larger area, corre sponding with the territory of that nerve and occur only after the compression has ceased (e.g. thoracic outlet syndrome). Nerve root compression results in segmental pain and paraesthesia felt within the corresponding dermatome (e.g. sciatica). Multisegmental bilateral paraesthesia indicates a lesion in the spinal cord. It must be remembered that the site of compression always lies proximal to the proximal extent of the paraes thesia. They are usually felt in the distal part of the extremities. The more accurately the patient describes the area, the more distal the compression lies. A paraesthesia-like feeling, especially v.ague tingling, may be experienced in some circulatory conditions, such
as Raynaud's syndrome, but this is usually accompanied by changing of the colour of the skin in the distal part of the limb. Functional disability. Often, functional disability is complained of. It comprises limitation of movement, internal derangement, weakness and incoordination and instability. Limitation of movement. When limitation of movement is mentioned, its nature will have to be determined during the functional examination: limitation of active movements only, or limitation of both active and passive movements, and in this case whether it is of the capsular or of the non-capsular type. End-feel at the end of the passive movements and the relationship between pain and end-feel must also be ascertained (see pp.73-74). Internal derangement. Symptoms caused by internal derangement are irregular in nature. There are moments when the joint feels normal and that the patient is able to do everything, and other occasions when the joint does not work well. Typical symptoms are sudden twinges, shifting pain, giving way of the limb, locking of the joint and a feeling of insecurity. If the answer to the question 'Does the joint lock?' is positive, further inquiry should make clear in what posi tion locking occurs and how it is released. For example, a knee that locks in extension and w1locks spontaneously suggests a loose body, and one that locks in flexion and has to be unlocked manipulatively is a meniscal problem. Weakness. This symptom should lead the examiner to concentrate during the examination on both active and resisted movements to see if the weakness is physically apparent or not. If weakness is confirmed, the distinction has to be made between a lesion in the muscle itself (e.g. atrophy or rupture) or in the nervous system, which is more often the case. Incoordination and instability. These complaints are indi cations that something is amiss with either deep (proprio ceptive) sensibility, the vestibular system or the cerebellum.
Further questions
Other questions, if appropriate, are asked about similar symptoms, past or present, in other parts of the body, especially other joints (see Box 4.6). If the answer is posi tive, conditions such as rheumatoid arthritis, spondylitic
Box 4.6 Inflammatory disorders Rheumatoid pattern • Several joints • Sma l l joints • Symmetrical
Reactive pattern • Few joints • Large joints • Asymmetrical
CHAPTER 4
arthritis, Reiter's disease and gout should be suspected and further examination is required. Disorders of rheumatoid type (rheumatoid arthritis, lupus erythematosus, systemic sclerosis, dermatomyositis) are characterized by the symmetrical joint involvement, usually of the small joints (e.g. metacarpophalangeal joints). Arthritis of reactive type (e.g. peripheral joint involvement in ankylosing spondylitis, ulcerative colitis, Reiter's disease, sarcoidosis or psoriatic arthritis) affects a few large joints (e.g. shoulder, hip or knee) asymmetrically (see Fig. 4.3). Questions about the general state of health are asked to find out whether there is the possibility of a serious disorder (e.g. cancer). The patient should also reveal present medication, and a doctor or therapist who considers manipulation should make sure that the patient is not taking anticoagulants: these are a contraindication because of the danger of haemorrhage. Inquiries should also be made about previous treat ments, which may give some idea of the chance of success of the proposed therapy. Previous surgery, its timing and indication are noted - it is not impossible that the present condition is the outcome of previous intervention (see Box 4.7).
INSPECTION
Inspection, although a standard procedure, should be regarded as an especially important part of examina tion. It begins the moment the patient enters the room. If gait is disturbed, the way of walking may be diagnos tic. The examiner should have the experience and ana lytical ability to recognize, for example, the following typical patterns: a subluxated meniscus at the knee; a
Figure 4.3
Patterns of: (a) reactive arthritis; (b) rheurnatoid arthritis.
-
CLI N I CA L D I AG N OSIS OF SOFT TISS U E LESIONS 69
Box 4. 7 Summary of history 1
Age, sex, profession, hobbies, sports
2
I n i t i a l symptoms: Onset: • traumatic • spontaneous: sudden
gradual
Loca l i zation Influence
3 Progression/evol ution: Un i nterru pted Cha ng i n g : • reference of pa i n • shift i n g pa i n • expanding p a i n Recurrences 4 Actua l symptoms: Pa i n Paraesthesia Fu nctional disa b i l ity: • • • •
5
l i m itation of movement i nternal derangement weakness i ncoordi nation/insta b i l ity
Further questions
'tennis leg'; the elderly patient with arthrosis of the hip; acute lumbago; a spastic gait; the patient with parkin sonism; a Trendelenburg gait; a drop foot; a ruptured Achilles tendon; and finally the patient with a non physical condition. Further features may be noted while the history is taken. A normally seated patient should have at least 90° flexion at hip and knee which is later confirmed on func tional examination. The face may reveal the extent of pain or may disclose parkinsonism. The attitude in which a limb is held may also be diagnostic. For functional examination patients must be suffi ciently undressed so that the affected region can be seen. The way they take off clothes and shoes are removed may also provide information on disability. Deformities or deviations are easily seen: for example, in acute torticollis or in lumbago, the patient stands with the head or the lumbar spine held in deviation, usually towards one side. Real deformities can be the result of one or more fractures. Pathological fractures of a verte bral body lead to angular kyphOSiS or, if the occur at several levels, to a 'shortened' patient. Every examiner knows the typical kyphosis of adolescent osteochondro sis. Other examples are genu valgum and varum, which may be physiological up to a certain age but are patho logical in adults. The presence of a deformity is not always relevant. It is quite possible that it has nothing to do with the presenting condition. A short leg, or a long-standing scoliosis are very often seen but occur in asymptomatic as well as in symptomatic patients.
70
SECTION O N E - G E N ERAL P R I N C I PLES
Soft tissues, such as skin and muscles, may show abnormalities. The colour of the skin may be different from that of other parts of the body: red in inflammation, blue when a haematoma is present or when a venous dis order has developed, white in arterial problems. Visible muscle wasting may be obvious. If swelling is present, the examiner should ascertain whether it is general and diffuse or localized. An inflammatory condition may show quite spectacu lar signs such as redness of the skin, swelling and warmth.
Table 4.2
Movements tested in the preliminary examination of the upper limb
Root
Region
Type
C1
Neck movements
C2-C4
Shoulder movements
Active Resisted Active Resisted
C5
Arm movements Shoulder
C6-C7
Elbow
C8 T1
Wrist Thumb Fingers
Active Resisted Passive Resisted Resisted Resisted Resisted
PRELI M I NARY EXA M I N ATION
After having taken the history and amassed evidence from inspection, the examiner should have an idea of which part of the body the symptoms originate from. Regional examination follows. When the history alone is not diagnostic, so that doubt over the origin or local ization exists, a quick survey of the tissues forming the relevant segment may be necessary. This 'preliminary' examination (Fig. 4.4) includes tests for the different joints. For example, the preliminary examination for pain down the arm includes tests for the cervical spine, shoulder girdle, shoulder, elbow, wrist and hand (Table 4.2). When some tests are positive and indicate that the lesion lies about a certain joint, this joint will then be
Which joint?
1
T
Preliminary examination
IT I IJot 8 f 8 1
Accessory tests? Figure 4.4
Role of the preliminary examination.
tested more rigorously, in the sure knowledge that the lesion lies within known limits. When no abnormalities are found, i.e. no limitation of movement, pain or weak ness, the lesion clearly lies outside the moving parts. If all movements hurt, or when the patient presents a contra dictory pattern, the question of a psychogenic disorder arises.
FU NCTIONAL EXA M I N ATION
In lesions lying within the locomotor system, pain is brought on mainly by tension. Therefore, during exami nation the different tissues are selectively put under tension and the results noted. As the function of the different tissues is well known, functional testing is really an exercise in applied anatomy. This indirect approach to diagnosis is purely mechanical. The examination used is standardized, which permits a systematic search for signs in such a way that, with a minimum of tests, maximum information is obtained. Too many tests in the standard examination can confuse the examiner and make interpretation very difficult. This does not imply that the diagnosis will always be reached after functional examination. It may be necessary to add accessory tests, either clinical or technical, but this is only done as needed (see pp. 75-76). PROCE D U RE
The purpose of functional examination is to reach a deci sion on which structure is affected. However, even that may be insufficient. In a patient with a shoulder problem it is not enough to say that there is a lesion in the brachial biceps muscle: is it in the long head or the short head? In a lesion of the long head, is it localized in the bicipital groove or in its intra-articular course or at its insertion at the glenoid? Therefore, once the structure at fault is
CHAPTER 4
known, the next step must b e t o determine exactly where, within that structure, the lesion lies. Examination is usually performed on both sides. Certainly, if the range of a passive movement is assessed, it has to be compared with the contralateral normal joint. When muscle strength is evaluated, comparison with the non-affected side is again necessary. The patient as well as the examiner should adopt a good position from which to start. When passive move ments are performed, the examiner must make sure that they can be done until the end of range (if present) is reached: movement should not be limited by the exam iner's body, or by the couch or even by clothing. For resisted movements, which are done isometrically, the examiner's position must be such that the examiner can exert more power than the patient can. It may be of interest to put the patient in front of a mirror so that reactions can be observed. The movements that are used to test the different struc tures should be 'pure' ones, i.e. testing only one structure or one glOup of structures at a time. This facilitates sub sequent interpretation. Questions asked during examination should be as neutral as possible. The examiner must not impose on the patient an expected answer. Questions such as 'Does this movement hurt?' or 'Is this painful?' should be avoided. It is better to say 'How is that?' and ask the patient to report anything experienced. It must also be understood that the examiner is looking for tests that elicit the symp toms or, if they are constant, those that influence them. MOV E M E NTS
The functional examination contains active movements, which are not always necessary, passive tests and move ments against resistance. Positive tests are always repeated on the opposite side in order to compare the normal with the abnormal. Active movements
Active movements are mainly used to determine quickly the area from which symptoms originate and what struc tures to test in detail with passive and I or resisted move ments (Box 4.8). Examination by active movements goes against the principle of trying to test one structure at a time. When a limb is actively moved, muscles, tendons, ligaments,
- CLI N I CAL
D IAGNOSIS OF SOFT TISSUE LESIONS 7 1
bursae and capsule are all put under stress. In conse quence such tests are non-specific and therefore not always necessary. Howevel� they can be of interest because they suggest what the patient is able and willing to do. In most cases, they also give an idea of the range of movement possible (normal, limited or excessive) and of muscle power. They are always executed first to provide a criterion with which to compare subsequent passive and resisted movements. When a normal range is later found on passive testing and normal muscle strength is apparent when tested against resistance, there is no reason for any abnormality or restriction of active movements. Thus if, in these cir cumstances, it is claimed that the active movement cannot be done, there must be refusal, either involuntary (psychogenic) or voluntary (intention to deceive). There are, of course, organic lesions where a discrepancy exists between active and passive or resisted movement but only within certain limits. For example, a mononeuritis of the long thoracic nerve, leading to weakness of the serra tus anterior muscle, can make full active elevation of the arm impossible even though the passive range and muscle power of the shoulder are normal. A further example is total rupture of the Achilles tendon, in which resisted plantiflexion is weak and active movement impossible despite the range of passive movement at the ankle remaining unaltered. Active movements are usually required when the spine (cervical, thoracic and lumbar), the shoulder girdle and the shoulder are examined but they may also be tested at any other joints if they can supply additional information. Passive movements (Fig. 4.5) These tests are meant to examine the inert tissues. The information they give is precise, provided they are per formed correctly. The patient should completely relax the muscles and let the examiner do the movement. It is important to realize that non-inert tissues may also be stretched by the manoeuvre: if this gives rise to pain, it must be determined whether there is a 'contractile tissue pattern', in which case active contraction in the opposite direction will also be painful (see pp. 87-88). The criteria for passive testing are pain, range and end feel (Box 4.9). Pain. The patient must understand that the examiner is looking for 'the' pain - the reason for presentation - and
Box 4.8 Aims of testing active movements
Box 4.9 Aims of testing passive movements
• To ascerta i n patie nt's w i l l i ng ness and a b i l ity • To determine range • To assess m u scle power
• To assess p a i n • To determine ra nge • To cha racterize end-feel
72
SECTION ONE - G E N E RA L P R I N C I PLES
Passive movements
Excessive
1--+
L�
Too hard Too soft
I Muscle spasm Empty
I Springy block Crisp
Soggy Figure 4.5
Passive movements.
that each time this pain is evoked or influenced a response is required. When straight-leg raising is per formed in a patient with low back pain radiating down the posterior aspect of the thigh, the examiner must make sure that the sensation felt during the test is the exact pain complained of and not just a tight feeling in shortened hamstring muscles. Pain evoked by a certain movement requires the further information of exactly where it is and at what stage of the movement. Pain may come on at a certain moment but the movement is not necessarily limited. For example, straight-leg raising may become painful at 60° but continue to full range without increased dis comfort. Excessive gentleness may fail to elicit informa tion. Passive movements must be performed as comfortably as possible for the patient but, if a proper answer can only be obtained by pushing a bit harder and thus hurting the patient, this should be done. It would be a diagnostic error to interpret a perfectly full movement as being limited by a few degrees, if the movement was stopped because of pain. The same applies to a painful arc. This may be so uncomfortable that the patient cannot get beyond it by active move ment. If an arc is suspected, a harder push during passive movement may succeed and show its presence. Interpretation would be totally different: on the one
hand, limitation of movement and, on the other hand, full range with a painful arc. The presence of joint signs in root lesions is a mis leading phenomenon. When a cervical or lumbar nerve root becomes compressed as the result of a disc protru sion, passive movement in a neighbouring joint may occasionally affect the root pain. Thus passive move ments for the shoulder joint may hurt at the end of range so focusing attention on the shoulder. As pain of cervical origin is also felt down the arm the picture becomes very confused. The same occurs in lumbar root pain; passive hip movements are not limited but they may influence the pain when they are brought to full range - they are probably capable at their extreme of altering the tension on the nerve roots in a minor way, analogous to straight-leg raising. The range of movement is noted and is always compared to the unaffected side. The response should be interpreted in the light of the patient's age and general condition. Limited movement requires the examiner to ascertain whether the limitation is in all directions or only in some directions or in one direction only. If only one movement is reduced, a 'proportionate' or a 'disproportionate' limi tation may be present (see p. 86).
Amplitude.
CHAPTER 4
Pain at full range suggests that the pain is provoked by stretching or pinching of the affected structure. The local ization of the pain will very often be indicative. Excessive range may be pathological but laxity is some times purely physiological: for example, most women can hyperextend the elbow. When a joint moves further than is normally accepted, great care must be taken that the symptoms are not too readily ascribed to that phenomenon. Hypermobility with a normal end-feel is usually not of significance. End-feel. This is a term typical of Cyriax. It describes the sensation that the examiner experiences at the end of the passive movement. The hand that performs the passive movement is not only motor but also sensory. When the movement comes to the end the examiner should assess the sensation. When no limitation is present the end-feel is at the end of the normal range. When limitation exists, the end-feel is judged at the end of the possible range. End-feel is diagnostically important as it gives an idea of the structure or condition that stops the movement. In addition it has therapeutic consequences. Especially during attempted spinal manipulations, the sensation imparted to the operator's hand will indicate whether or not to proceed. Likewise, in the shoulder or hip, the deci sion whether to undertake capsular stretching depends on end-feel. For accurate judgement of the nature of end-feel, expe rience is required. Passive movement should be executed with extreme gentleness, especially during the final degrees of range. The moment resistance is first noted the rate of movement is reduced so that the feeling can be assessed before movement comes to a complete stop. In normal circumstances each joint movement has a charac teristic end-feel, which can be considered as 'physiologi cal'. In pathological conditions, end-feel may change. The examiner should know what the normal feeling of each (passive) movement of a joint is like in order to be able to judge every change in end-feel.
This can be hard, elastic or related to tissue approximation. • Hard: the movement comes to an abrupt stop, either because two bony surfaces meet (bone-to-bone end feel) or because a ligamentous structure prevents further movement (Fig. 4.6a). Extension of the elbow has a bone-to-bone end-feel, because the main factor that stops the movement is the engagement of the olecranon process in the olecranon fossa. Extension of the knee also has a hard stop, though less clearly direct than the elbow; here, the main structure that stops movement is the posterior cruciate ligament, which does not stretch. • Elastic: at the end of range the examiner feels resist ance but further stretching over a few degrees is pos-
•
-
C L I N ICAL D IAGNOSIS OF SOFT TISS U E LESIONS 73
sible (Fig. 4.6b). The feeling is one of two pieces of tough rubber being squeezed together or of a piece of thick leather being stretched. This end-feel is typical of a normal joint capsule and is felt during most rotation movements in shoulder, elbow, hip, knee, cervical and thoracic spine. The tern 'elastic' has the same meaning as 'capsular'. Tissue approximation: this end-feel is normal in those movements where extra-articular soft tissues engage against each other (Fig. 4.6c). Flexion at elbow and knee give this 'soft', 'muscular' end-feel. At the elbow the muscles of the forearm come in contact with the biceps and at the knee the calf muscles engage against the hamstrings. This 'extra-articular' end-feel does not occur in patients with poorly developed muscles: they present an 'articular' end-feel, either hard or elastic.
Pathological end-feel.
A number of types of end-feel are
pathological. •
Too hard: the normal elastic, or tissue approximation, end-feel may become harder when the quality of the tissue that stops the movement alters under the
(a)
OJ u C � IJ) IJ) OJ cr:
Hard
end
Range
(b) Elastic
OJ u c � .� U) OJ cr:
Physiological end-feel.
end
R a n ge
(c)
OJ u c '"
Tissue approximation
tl ·iii OJ cr:
Range
Figure 4.6
Hard (a), elastic (b) and soft (tissue approximation; c) end-feels.
74
•
•
•
SECT I O N O N E - G E N E RA L P R I N C I PLES
influence of pathological conditions. This change very often accompanies limitation of movement because of capsular contracture, osteophytic outcrops of bone, myositis ossificans or a malunited fracture close to the joint. Dependent on the condition, the end-feel may vary from a slight increase in hardness (early arthrosis) to a bony block (ankylosing spondylitis). The latter forms a contraindication to further stretching (i.e. during manipulation). Too soft: in those instances where a hard end-feel is expected, the movement may come to a soft stop. This is especially the case in a loose body blocking a movement as may happen at the elbow: extension is limited by a few degrees with a soft end-feel. Muscle spasm: this involuntary muscular contraction usually indicates severe disorder. The muscles contract with a sudden, vibrant 'twang' even when the move ment is performed very gently. This is reflex protec tive spasm and may happen in acute conditions, such as arthritis in the acute stage. It may also be a sign of more serious lesions such as recent fracture (e.g. scaphoid fracture at the wrist) or secondary deposits (e.g. in a cervical vertebra). Such an end-feel is always an absolute contraindication to manipulation. Empty: movement may be so painful that the patient begs the examiner to desist. The latter feels that further movement would be possible because there is no organic resistance but stops the movement because of the perceived pain or out of sympathy for the patient. Further forcing would result in active voluntary muscular contraction. This situation always indicates a serious problem. Acute bursitis, extra-articular abscess or neoplasm are some possi bilities, but there is nothing wrong with the joint itself. This end-feel may also indicate laxity in a joint or a non-organic lesion. In the latter case there is initial strong resistance, which yields to sustained pressure, disclosing a full range of motion.
I I I I I I I I I I I I
c '" a...
M ovement
Relationship between pain and end-feel.
•
•
Springy block: this finding always indicates internal derangement: when part of an intra-articular carti laginous tissue displaces, it may prevent a full range of movement which leads to a rebound at the extreme of the possible range. This commonest examples are a displaced meniscal fragment in the knee and a buckled end-plate in the lumbar spine. Crisp: this is typical for a disc protrusion and is best felt in the cervical spine. The feeling is the result of small involuntary muscular contraction at the end of the possible range, known as 'muscle guarding'. The condition is not acute, as a result of which there is no real muscle spasm. Soggy: this end-feel is seldom encountered and can be situated somewhere between a soft and an empty feeling. It is typical of rheumatoid arthritis in the upper cervical joints and is a strong contra-indication to manipulation.
Relationship between pain and end-feel. It is also important to look for the relation between the moment of appearance of pain and that of the end-feel. Usually the pain comes on at the same time as the end of range is sensed (Fig. 4.7). Earlier pain implies that the joint is in a very irritated state which has therapeutic implications.
Resisted movements
Movements against resistance are performed isometri cally. The joint is put in a neutral position and should not move when resistance is applied. This method ensures that stress on inert tissues is minimal or absent. The position of the examiner must be such that the force exerted by the patient can be resisted. A maximal contraction is asked for and held for a few seconds. Counterpressure is therefore taken by the other hand at the opposite side. For example, to test resisted extension of the neck, one hand is put on the occiput and another
i e n d of
e n d of move m e nt
S l i g htly i rritated j o i n t
Figure 4 . 7
•
c '" a...
I I I I I I I I I I I I
movement
Movement Very i rritated j o i nt
CHAPTER 4
-
CLI N I CA L DIAGNOSIS OF SOFT TISS U E LESIONS 75
I
Resisted movements
I
I
I
Pain
•
•
During repeated contraction
Caused by musculotendinous deficit
During contraction following exertion
Caused by neurological deficit
When relaxing from contraction
Caused by patient's refusal
Figure
4.8
Resisted extension of the neck.
hand on the sternum (Fig. 4.8). Similarly, to test resisted flexion, one hand is placed on the forehead and the other between the scapulae. The criteria when testing against resistance, are pain and strength (Box 4.10). Pain. In a lesion that lies in the contractile tissue, the pain should be elicited during the contraction. In mild disor ders the test may initially be negative but repetition of the movement may eventually provoke symptoms. Similarly, slight muscular or tendinous problems may give pain only during exertion and resisted movements may remain painless. If pain cannot be elicited by repetitive contractions, the patient should be seen and tested in the circumstances when pain is experienced. The resisted movements may then be found positive. There are cases of tendinitis in which the pain is only felt when the patient relaxes after muscle contraction. This is not uncommon and can also be interpreted as a positive resisted movement. A positive answer on resisted movement is usually only one, but the most important, part of a 'contractile tissue pattern' in which the passive movement that stretches or pinches the affected part is also painful. The examiner must be aware of inert tissue lesions that can become painfully squeezed or moved by muscular contraction (e.g. gluteal bursitis).
Box 4. 1 0 Aims of testing resisted movements • To assess pain • To determ i ne muscle strength
I
Strong
Painless
Figure
1
Strength
4.9
Resisted movements.
Strength. The movement should be strong, but weakness may occur and an experienced examiner will immedi ately have an idea of what is the cause. It may be the result of pain; in that instance, the examiner feels a sudden cessation of power - the patient stops the contraction when the pain is felt. This often happens in partial mus cular or tendinous ruptures when sufficient fibres are torn to diminish strength. In total contractile tissue ruptures, there will not be pain but complete absence of muscle power. This pattern is completely different from a neurological weakness. Here there still is a force that has to be overcome: the examiner is stronger than the patient and so can push the patient's limb away while still feeling continuing resist ance. The latter can vary from an almost normal sensa tion - slight paresis - to very little (scarcely detectable) force - complete paralysis. This may be the result of a lesion that has completely stopped motor innervation or it may be a consequence of the patient's refusal to undergo the manoeuvre.
ACCESSORY TESTS
After a well-balanced basic functional examination, interpretation of the pattern that emerges should, in most cases, make it possible to single out the tissue at fault. Difficulties are, of course, encountered and further accessory testing is then required to reach a precise diagnosis, to positively confirm an existing but tentative diagnosis or to disclose the precise point affected within the structure. An important feature is that a distinction should be made between standard functional examination and accessory tests. The basic examination is always done in its entirety, whereas the accessory tests are applied selectively (Box 4. 11). It is wrong to do accessory tests without a prior idea of the nature of the problem, and in the hope that more tests
76
S E CT I ON O N E - G E N ERAL P R I NCI PLES
Box 4. 1 1 Aims of accessory tests • • • • • •
I N D I FFICULT CAS E S .-
To differentiate within a group of structures To confirm a tentative diagnosis To u n ravel a difficult pattern To extend a negative exa m i nation To make a differential diagnosis To understand unusual signs
would automatically provide more complete informa tion. On the contrary, the more tests the more confusing the picture may become and in the end the 'wood cannot be seen for the trees'. Accessory tests therefore should be goal-oriented. They are performed in the following circumstances. AFTER TESTING A G R O U P O F STRUCT U R E S
When a resisted movement has tested a group of struc tures, further differentiation is sometimes necessary to find in exactly which structure the lesion lies. In 'tennis elbow', resisted extension of the wrist is painful. To find out whether the lesion lies in the exten sors of ei ther the wrist or of the fingers the test is repeated with the fingers held actively flexed, so inhibit ing the finger extensors. A negative answer implicates the wrist extensors, which can then be differentiated by executing resisted radial and resisted ulnar deviation: when resisted ulnar deviation hurts, the extensor carpi ulnaris is at fault; whereas if resisted radial deviation is painful, the lesion clearly lies in one of the radial exten sors of the wrist - true tennis elbow. Whether the ten dinitis is situated at the extensor carpi radialis longus or brevis cannot be found by further testing - palpation is called for. The same applies to the hamstring muscles. A muscu lar or tendinous lesion about the knee will give rise to pain on resisted flexion. Differentiation between either (a) the femoral biceps or (b) the semitendinosus and semimembranosus is achieved by testing resisted exter nal and internal rotation. Positive lateral rotation incrim inates the biceps and medial rotation draws attention to the other two muscles. Palpation identifies exactly where the lesion lies. TO CON FI R M A TENTATIVE DIAGNOSIS
An accessory test may help, especially in uncommon con ditions, to confirm a tentative diagnosis. For example, when the diagnosis of mononeuritis of the spinal acces sory nerve has been suspected, weakness on resisted scapular approximation will show the diagnosis to be correct.
A clinical picture can sometimes be difficult to interpret and accessory tests may then resolve doubt. When pain is thought to be due to squeezing of a structure, diagnostic traction may help to confirm this. For example, in difficult cases of internal derangement of the cervical spine, pain and / or paraesthesia can be temporarily abolished by applying manual or mechanical traction. Traction on the arm can diminish pain in subacromial bursitis. W H E N T H E FU NCTIONAL EXA M I NATION I S N EGATIVE
A negative examination does not necessarily mean that a lesion is absent. There may be a problem in a neighbour ing tissue which was not systematically tested in the stan dard examination. A negative shoulder examination, for example, invites the examiner to test the coracobrachialis muscle. In anterior knee pain a negative examination is followed by tests of the patellofemoral joint. I N D I F F E R E NTIAL DIAG N O S I S
Different conditions may give rise to similar positive answers. An accessory test can then help to elucidate which structure is at fault. For example, limitation of external rotation at the shoulder is the primary sign of anterior capsular contraction as well as of a subcoracoid bursitis. Passive external rotation with the arm held in abduction will be positive in a capsular lesion and negative when a bursitis is present. A test for distant pain can be performed when a lesion lies in a long bone. When a fracture is suspected on the dorsal aspect of a rib, pressure on the anterior aspect or on the sternum may provoke the pain. This technique can also be used to differentiate a rib problem, a lesion in an intercostal muscle or at a costovertebral joint. W H E N U N U S UAL S I G N S ARE F O U N D
Discrepancies between individual findings on functional examination may suggest an unusual and possibly serious lesion, a psychogenic problem or an attempt to deceive. In the former, the patient is sent for further spe cialized examination. When neurosis or deception is sus pected, the patient is subjected to a number of accessory tests: additional movements that cannot possibly influence the alleged symptoms or repetition of tests in other positions. The opportunity for the patient to make mistakes is thus presented, which in a positive way can confirm the examiner's suspicion (see eh. 88 on Psychogenic Pain).
CHAPTER 4
- CLI N I CA L
D IAGNOSIS OF SOFT TISSU E LESIONS 7 7
PALPATION O F TH E STATIONARY J O I NT
PALPATION
Palpation can be a very useful aid to diagnosis when per formed at the right moment. However, it is frequently done too early in the examination, with the risk of an incorrect diagnosis. When, after functional testing, the examiner has interpreted the different movements and the pattern that emerged and still thinks that more informa tion could be forthCOming about the lesion, palpation is undertaken. Abnormal sensations that are imparted to the hand in a stationary as well as in a moving joint are sought. A Palpation of the stationary joint
During palpation of a motionless joint (Fig. 4. 10a) the examiner may assess temperature (either warmth or cold), swelling, synovial thickening or structural changes. Palpation may also elicit tenderness. Warmth
Warmth is best palpated with the dorsum of the hand and may be diffuse or localized. Spurious warmth can be the result of a rubefacient ointment or of a bandage that has been removed just before examination. Otherwise,
Warm
Cold
1
Diffuse
r-C r-C1 1
Arterial Neurological Synovial fiuid Blood
Subcutaneous fiuid
Soft
Bursitis Pus (local infection)
Fluctuating
Hardish For synovial thickening
rC1
r{
For a gap
For pulsations
Mucocoele Cyst Ganglion Bony subluxation Callus
Bony
For tenderness
Haematoma
Osteophyte
Articular
Bony deformation
Tendinous
B Palpation of the moving joint
Muscular
For crepitus
Osseous
For clicking For hyper/hypomobility For end-feel
1
Bursal Scapulothoracic
1.
(I
•
__ __ __ __ __ __ __ __ __ __ __ __ __ __ __ __
'.
Figure 4.10
Physiological
r -----, a_ ath o_ lo_ 1 � 9 ic _ _ p_ 1-_ �
Palpation of (a) the stationary and (b) the moving joint.
78
S E CTION O N E - G E N E RA L P R I N C I PLES
warmth always indicates activity. The lesion may be osseous (e.g. fracture or metastases) or articular (e.g. arthritis, haemarthrosis, loose body, or a disorder of a meniscus or ligament) or tendinous (e.g. rheumatoid type tendinitis). A purely mechanical tendinitis will not cause any warmth. When the warmth occurs suddenly and twinges are also present, this indicates persistent subluxation of a fragment of cartilage. The heat may or may not diminish when the joint is kept still. Sometimes (e.g. in loose body) the warmth may be elicited merely by the examination. Cold
When the extremity feels cold an arterial problem is suspected. Palpation will then follow for arterial pulsations. Cold may also occur during an attack of sci atica, especially that which causes muscular weakness. When the foot becomes cold only after exertion, the prob able cause is an iliac thrombosis. The cause may also be neurological. Swelling
Swelling is the result of an articular reaction to a lesion and may be localized or generalized. Swelling that came on after injury may be the outcome of haemorrhage or effusion. If it is caused by bleeding, the joint fills up within a few minutes; effusion develops over a few hours. Blood also fluctuates: the swelling moves en bloc. The presence of pus is exceptional and indicates an infection with microorganisms. Periarthritic oedema may pit. In a localized swelling, its consistency should be ascertained: a soft swelling indicates subcutaneous clear fluid or a thickened bursa, a fluctuating mass may result from a haematoma or from a mucocele and a hard but still fluctuant swelling is typical of a cyst or a ganglion. When the consistency is bony the cause is usually a callus, a bony subluxation (e.g. capitate bone at the wrist or cuboid bone in the midfoot), an oeteophytic outcrop or any other bony deformity which results from a destructive process (e.g. osteitis deformans, neoplasm). Thickening of the synovial membrane
This is found in rheumatoid, bacterial or inflammatory arthritis (e.g. gout, tuberculosis, gonorrhoea, Reiter's disease, ulcerative colitis, spondylitic arthritis or psoriatic arthritis). It is absent in mechanical conditions, such as traumatic arthritis, post-immobilizational arthritis and arthrosis. To palpate capsular thickening, the examiner has to seek the reflexion of the membrane where it overlies a bony prominence. Gaps
A gap may be palpated at the site of the rupture of a muscle or tendon.
Tenderness
Palpation for tenderness is sometimes performed to determine the exact localization of a lesion. For this purpose, it is done only in a structure that has already been found, by clinical examination, to be affected and only when it is within reach of the finger. Eliciting ten derness is only necessary when, after clinical examina tion, the diagnosis still lacks precision. When a localizing sign has been fOlmd, palpation is of course superfluous. To search for tenderness is of much more value in a distal joint (wrist, hand, ankle, foot) than in a proximal joint (trunk, shoulder, hip), because the localization of the pain is much more accurate. Difficulties may arise when two tissues overlap and when no certainty exists whether the lesion lies in the superficial or a deep structure. This situation arises most in the chest and abdomen. To ascertain whether the ten derness lies in a superficial or a deep muscle or in another structure (e.g. a viscus), palpation is performed during contraction and relaxation of the superficial muscle. Greater pain when the superficial muscle is tense sug gests that the muscle is at fault, the converse that deeper structures are affected. Other misleading phenomena are the presence of either a 'referred' tenderness or an 'associated' tenderness. Localized, deep referred tenderness may occur within a painful region, for example, as the result of compression of the dura mater usually by a small dis placed fragment of the intervertebral disc. This phe nomenon is described in Chapter 1 and can be very deceptive unless the examiner is familiar with the rules of pain reference. Associated tenderness is a very well-localized tender area very close to the site of the lesion. There is a relation between the two because both pain and tenderness disap pear when the patient is cured. Associated tenderness is most common at the wrist and the elbow. In de Quervain's disease - tenovaginitis of the abductor longus and extensor brevis muscles at the wrist - the styloid process of the radius is extremely tender, as is the poste rior aspect of the lateral epicondyle in tennis elbow, espe cially when the lesion lies at the tenoperiosteal origin of the extensor carpi radialis brevis. Negative palpation does not necessarily mean that the diagnosis is wrong, except perhaps in very superficial lesions, because there are tissues that are not explicitly tender when affected (e.g. the supraspinatus tendon). Pulsation
Palpation for pulsation in the arteries may have an important diagnostic value and is indicated when symp toms are mentioned or signs are found that point to a vascular condition (e.g. claudication, a cold limb, or blue or white skin).
CHAPTER 4 - CLI N I CA L D I AG N OSIS OF SOFT TISSU E LESIONS 79
PALPATION OF TH E MOVING J O I NT
Next, the moving joint is palpated. The examiner may either experience crepitus or clicks, or can assess end-feel or mobility (see Fig. 4.10b). Crepitus
Crepitus always indicates a pathological situation. It can often be heard and can also be felt by the palpating hand placed on the moving part during active or passive move ment. There are circumstances in which the crepitus is only felt during a movement against resistance. Crepitus may be articular, tendinous, muscular, osseous or bursal. Articular crepitus. Crepitus which originates from the joint surfaces gives an idea of their ability to glide over one another. Fine crepitus indicates slight roughening and occurs in mild arthrosis or in long-standing rheumatoid arthritis. The latter gives rise to the characteristic 'silken' crepitus. Coarse grating is felt in advanced arthrosis and results from considerable fragmentation of the cartilagi nous surface. In severe arthrosis the cartilage has wholly worn through which leads to intermittent creaking of bone against bone (' cogwheel' phenomenon).
Crepitus in relation to a tendon establishes tenosynovitis. Fine silky crepitus occurs in acute mechanical cases as the result of a traumatic rough ening of the tendon surface and of the inner aspect of the tendon sheath. Coarse crepitus is felt in chronic rheuma toid or tuberculous tenosynovitis.
Tendinous crepitus.
Muscular crepitus. •
•
This is observed in two situations only.
Tenosynovitis of the two extensors and of the long abductor of the thumb in the distal part of the forearm is usually accompanied by crepitus that can be felt locally. The crepitus is, however, sometimes felt throughout the muscle bellies, possibly as far up as the elbow (see p. 524). Localized crepitus is usually felt in a lesion at the mus culotendinous junction of the tibialis anterior muscle.
Osseous crepitus. A fracture may crepitate when the limb is moved and the two ends of the fractured bone move against each other but, except in pathological fractures, an attempt to elicit crepitus usually causes so much pain that it should not be done. Bursal crepitus. Subdeltoid bursitis is the characteristic situation. Some time after a bursitis with effusion has subsided, creaking on moving the arm can be felt (see Shoulder, p. 333). Scapulothoracic crepitus. This is unique. The posterior thoracic wall can become roughened at an area just beyond the lateral edge of the iliocostal muscle, with localized crepitus felt on shoulder movement (see p. 408).
Clicks
Clicks can be produced in several ways. Certain tests on clinical examination or certain manoeuvres during a manipulative session may provoke movement of an intra articular fragment of cartilage. This often happens when a loose body is present in a joint (e.g. knee or elbow) or when a meniscus subluxates (e.g. knee or jaw) or a frag ment of disc moves (e.g. spinal joints). Clicking during a manipulative manoeuvre is of interest in that it is often associated with an improvement of the physical signs, clearly indicating that a block to movement has been removed. In ligamentous laxity (as can be seen in sublux ation of the clavicular joint, in capsular overstretching of the shoulder, or in rupture of the medial collateral liga ment at the knee), a click is produced when one bone moves in relation to its fellow. Irrelevant clicks also appear, for example painless clicking of a costal cartilage or a patellar click during active extension of the knee. End-feel
End-feel can be assessed when a passive movement comes to a stop. It is either physiological or pathological and has important diagnostic and therapeutic conse quences (see pp.73-74). Hypermobility and hypomobility
These are terms that are currently used by osteopaths and manual therapists.13-14 During their so-called 'seg mental examination' they claim to be able to feel the difference in mobility between different, mostly spinal, joints. 1S To establish hyper- or hypomobility would afford an excellent guide to the level of the lesion if it were always at the joint in which the fault lay, which is not in fact the case. Moreover, these findings are so sub jective that they are not verifiable or reproducible. It has been shown on different occasions that even experi enced osteopaths or therapists cannot agree about the findings.16-20 The main mistake, however, consists in attributing diagnostic significance to such differences in mobility. When movement in a hypomobile or hyper mobile joint strongly evokes the patient's symptoms this has to be considered as the best criterion and clearly shows where the lesion must lie. However, when the abnormal mobility does not elicit the known symptoms, the problem clearly has nothing to do with the hyper mobile joint.21-23 Furthermore, there are no universal standards to determine abnormal mobility. What is normal for one person can be abnormal for another. Hypermobility can be physiological up to a certain level, especially in women, and hypomobility can also be considered as normal, particularly in the elderly. When hypermobility gives rise to symptoms, then and then only can it be considered as pathological. The terms ' laxity' and 'instability' are then used. The end feel will add greatly to this conclusion.
80
SECTI O N O N E - G E N E RAL P R I N C I PLES
DIAG NOSTI C I N FI LTRATION OR ASPI RATION DIAG N OSTIC LOCAL ANAEST H E SIA
When faced with lesions of the locomotor system, a diagnostic infiltration with a weak local anaesthetic is extremely valuable and most effective in confirming the diagnosis. There is no other comparably effective test. By using infiltration in every suitable case, the physician makes the patient the judge of the correctness of the diagnosis. Between 2 and 10 ml of a weak local anaesthetic (e.g. procaine 0.5%) is infiltrated at the assumed site of the lesion. Five minutes later the movements that were pre viously positive are retested. This allows the patient to determine whether the infiltration has altered the pain. When the tests have become completely or partly nega tive, the exact site of the lesion has clearly been reached, confirming the diagnosis. When the tests are still as painful or as limited as before, the wrong place was infiltrated, i.e. the diagnosis is wrong. This approach is useful in the following circumstances: •
•
•
When the examiner is not certain about a diagnosis or when the examiner wants positive confirmation of a tentative diagnosis, the induction of a local anaes thetic may help. For lesions in the extremities, infiltration is particu larly useful and gives reliable answers. However, it is not useful on the posterior aspect of the trunk: paraspinal infiltrations may give temporary relief but have no diagnostic value. In difficult cases this approach may be the final ' court of appeal'.
ASPI RATION
From the diagnostic point of view it is often important to aspirate a swollen joint or a diffuse extra-articular swelling in order to ascertain what sort of fluid is present.
TECH N I CAL I NVESTIGATIONS
It should be stressed again that there still remains a huge discrepancy between discovered anatomical changes and existing pain and disability. During the last decades the medical profession has focused on and been fasci nated by techniques of imaging that can clearly show existing anatomical aberrations. However, very often, these anatomical changes are not the source of the pain because they appear to exist also in large groups of
symptomless individuals. For example, the prevalence of herniated lumbar discs in a normal asymptomatic population ranges from 35%-50% .24-30 Evidence of cervical discopathy is also found in asymptomatic subjects31-33 and there is not always good concordance between the different imaging techniques.34 In the shoul der echography can discover partial thickness and full thickness ruptures of the rotator cuff even in large asymptomatic groupS.35-38 The finding of asymptomatic anatomical changes in knee joints during arthroscopy is not uncommon.39,40 In orthopaedic medicine, technical examinations are not routinely performed but are instead used only when necessary to refine the clinical diagnosis, to exclude certain lesions or to clarify differential diagno sis. They are always undertaken when the history and ! or functional examination have revealed warning signs (Box 4. 12). The clinician should not ascribe too much diagnostic importance to technical investigations - a positive answer does not always identify with certainty the con dition present. The reverse also holds: a negative picture does not always mean that there is nothing wrong. Knowing when to ignore a positively or negatively mis leading picture comes only from proper clinical examina tion (see Box 4. 13). The latter always remains the most important of the tools available and it is far more danger ous to omit a proper clinical examination and rely on technical investigations than to do the reverse. Later chapters outline when and when not to fall back on technical investigations and complement the clinical findings.
I NTERPRETATION
Interpretation is only possible if the clinical examination has been performed correctly: a detailed history, followed by inspection and a careful functional examination. Every part of the examination may be important, and conse quently a complete examination should be carried out on each occasion. Cyriax stated 'Omission of part of this examination, because the diagnosis seems obvious or to save time, is the common source of error ' .41 Examining patients may become a routine and repetitive, with the
Box 4. 1 2 Technical investigations O n ly when necessary: • To refine the c l i n ical diagnosis
• To excl ude certa i n lesions • To cla rify different i a l diagnosis • When warn i n g signs are present
'-
CHAPTE R 4
Box 4. 1 3 Summary of functional examination 1 I nspection 2 Pre l i m i n a ry exa m i nation 3 Functio nal exami nation a) Active movements b) Passive movements: Pain: • where • when Amplitude • l i m ited • full • excessive End-feel • physiological • pathological c) Resisted moveme nts Pain Strength • normal • weak 4 Accessory tests 5 Palpation : Motionless j o i nt a) b) Movi ng joint 6 D i agnostic infi ltration or asp i ration: Diag nostic loca l a naesthesia a) b) Aspiration 7 Tech n ical investigations
same features being frequently encountered so that it is tempting to omit that part of the examination which is expected to be negative. By doing this, the presence of a double lesion can easily be overlooked or, even worse, the signs of an uncommon (possibly serious?) disorder (one of the classic 'warning signs') may be missed. The functional examination gives positive answers balanced by negative ones, the latter corroborating the former. A pattern is found, which may be capsular, non capsular, muscular or partly or fully articular, and this has to be interpreted so that logical conclusions of incon testable validity are drawn. Interpretation requires experi ence because examination is subjective and such features as weakness, end-feel and resistance can only be inter preted by comparison, which needs time and patience. In practice one of a number of patterns can emerge (see Box 4.14).
-
CLI N I CAL D IAGNOSIS OF SOFT TISS U E LESIONS 8 1
interpretation (see pp. 83-87). When the active move ment is limited, passive movement is usually also restricted although it should be possible to go a little further in the limited direction. I N C O M B I NATIO N WITH I M PA I R M E NT O F RES I STED MOVE M E NTS
When an active movement hurts and the same movement performed against resistance is also painful, the latter has to be considered as being most important (see pp. 87-89). Limitation of an active movement and not of the corre sponding passive one indicates gross weakness. The same movement performed against resistance usually also proves to be weak. Sometimes, however, other (accessory) tests against resistance must be done to uncover the lesion. I N I S O LATI O N One o r more active movements are limited but are full range on passive movement
This occurs when one or more muscles are out of action. The resisted movements aimed to test the same muscles will also be weak. Weakness is quite often encountered in orthopaedic medical disorders. It may be of organic type or functional type (Fig. 4. 1 2). Functional palsies are mostly psychogenic. Organic palsies are the result of either an anatomical patho logical condition or of a phYSiopathological (usually biochemical) lesion. The cause may be intrinsic or extrinsic. Box 4. 1 4 Patterns found in clinical examination for suspected soft tissue lesions Active movements are positive • I n com b i n ation with passive movements • In com b i n ation with resisted movements • In isolation Lim itation of active movements o n l y Presence of a painful a r c A ' s n a p ' occurs A 'crack' is heard
IMPAIRMENT OF ACTIVE MOVEME NTS IN CO M B I NATION WITH I M PA I R M E N T O F PASSIVE MOVE M E NTS
The response to active movements (Fig. 4. 11) may corre spond with that found on passive testing. When an active movement is found to be painful, passive move ment in the same direction will usually be more painful. In this case, the passive movement must be considered as the important one and the response to it is used for
Passive movements are positive • Lim itation of ra nge
The capsu lar pattern Non-capsu l a r patterns • F u l l range • Excessive range • No movement poss i b l e
Resisted movements are positive • I n co m b i n ation with passive movements • In isolation • I n co m b i n at i o n with other resisted movements No movements hurt
82
S E CTION O N E - G E N E RA L PRINCIPLES
Limited =
weakness Figure 4.1 1
Painful arc
Snap! crack
Response to active movements.
Intrinsic (myogenic) lesions are the result of either a structural disorder, such as a severe partial or a total rupture of muscle or tendon, myopathy (e.g. muscular dystrophy or myositis) or a biochemical disorder (e.g. myasthenia gravis or paroxysmal palsies). Extrinsic (neurogenic) lesions may be either central or peripheral (Table 4.3). A central palsy is the result of a lesion of the upper motor neurone (i.e. the corticospinal and/ or corticonuclear tracts), caused by a vascular condition, a tumour, trauma or disease (e.g. encephalitis or multiple sclerosis) in the region between the cerebral cortex and the spinal cord (Fig. 4. 13). Hemiplegia, monoplegia, para plegia or quadriplegia follows, characterized by muscu lar hyper tonus, hyperreflexia, disappearance of the upper skin reflexes and appearance of abnormal skin reflexes (e.g. the Babinski reflex). Because the cells in the anterior horn of the spinal cord are not affected, there is no muscular atrophy apart from some slight wasting because of the patient's inactivity. Central palsy.
Peripheral palsy. A peripheral palsy may have its origin in the cells of the anterior horn of the spinal cord
(nuclear palsy or lower motor neurone lesion). Typical anterior horn disorders are acute anterior poliomyelitis, giving rise to asymmetrical paralysis of the proximal muscle groups, and degenerative conditions such as chronic anterior poliomyelitis and amyotrophiC lateral sclerosis (ALS), which cause symmetrical bilateral paralysis starting in the distal muscle groups. Anterior nerve root lesions (radicular palsy) give rise to segmental paralysis or paresis. Nerve root palsy is usually preceded by severe segmental pain. When a peripheral nerve or nerve trunk is affected, only the muscles innervated by that nerve are weak. When a plexus is affected, the weakness is more exten-
Table 4.3
Differences between central and peripheral palsies
Central
Peripheral
Muscular hypertonus Hyperreflexia No muscular atrophy Upper skin reflexes disappear Lower skin reflexes appear
Muscular hypotonus Hyporeflexia Muscular atrophy
CHAPTER 4 - CLI N I CA L D IAGNOSIS OF SOFT TISSU E LESIONS 83
Classification of weakness
I
I
Organic
I
Disease
Total
Partial
Myopathy
I
Dystrophy
Figure 4.12
,
I
I Nerve root I
I 1
Myositis
Classification of weakness.
sive. The clinical features are muscular hypotonus, hyporeflexia and atrophy.
that also snaps on certain movements, the cause of the pain and the snapping are not always related.
A painful arc is present
A crack is heard
The moment the patient shows a painful arc the examiner knows that the lesion lies in a position that is subject to compression. Interpretation is on anatomical grounds: the examiner knows what structures can and what struc tures cannot become momentarily compressed (see later chapters on specific joints).
Joints may crack when they are brought to the end of range, either actively or passively. The cause is the momentary formation of an intra-articular air bubble from the synovial fluid as a result of the partial vacuum created by traction. This often happens in the finger joints and is also very common in the spinal facet joints during manipulation.
A snap occurs
When this is present, the patient usually mentions it as a previous occurrence is likely. It may be detected at exam ination, especially on active movements. A snap may be felt when a tendon catches against a bony prominence and then slips over it. Examples are the shoulder ('snapping shoulder'), if the long head of biceps slips in and out of the upper end of the bicipital groove as the result of rupture of the transverse humeral ligament; the ankle ('snapping ankle'), when the peroneal tendons are loose in their groove on the posterior surface of the fibula and slip forwards over the malleolus; and the hip, when the greater trochanter catches against the edge of the gluteus maximus muscle. Snapping is not necessarily painiul. Therefore when a patient complains about a joint
I M PA I R M E NT OF PASSIVE MOVE ME N TS
Positive passive movements in combination with nega tive resisted movements draw attention to the inert struc tures, although they do not unconditionally exclude a lesion of contractile tissue (see Fig. 4.14). LI M ITED RAN G E
Limitation i n the literal sense o f the word can only be detected on passive testing. Although a patient may present with limitation on active movement, this does not necessarily mean that the joint carmot move to its full
84
S E CTION O N E - G E N E RAL P R I N C I PLES
cerebral co rtex
mesencep h a l o n
pons
med u l l a oblongata
s p i n a l cord
anterior h o rn cells
Figure 4. 1 3
range. The examiner should meticulously check whether a movement really is limited. Even the slightest decrease in range has significance. When one or more passive movements are limited the major question arises: ' Is this limitation in the capsular proportions or not?' Or, in other words, ' Is there a capsular pattern present or is the pattern non-capsular?' The capsular pattern =
At the spinal joints, a similar situation is found. When the whole intervertebral joint complex is affected a full articular lesion exists which gives rise to a pattern comparable to the capsular pattern in peripheral joints. However, the lesion is not always capsular and therefore is better described as a 'full articu lar ' pattern, which covers all possible conditions. The full articular pattern.
Corticospinal tract (pyramidal tract).
The caps u l a r pattern
portion. It does not matter whether the irritation is syn ovial only (as in recent sprain or haemarthrosis), capsu lar only (as in arthrosis) or both (as in rheumatoid arthritis) - the same pattern results. This limitation of movement to a proportion typical for the joint capsule is initially caused by a protective mechanism (muscle spasm) and later by fibrous contracture. This pattern of limitation always indicates that a lesion of the whole joint is present. The condition is called capsulitis, synovitis or arthritis, the latter being the best name as it clearly indicates involvement of the entire joint. This phenomenon is easy to check in clinical daily practice but is difficult to explain. In acute cases the muscles clearly contract in a way that anticipates the situation that might be created when later the capsule 'contracts'. So there must be an in-built mechanism in the brain which acts in imitation or in correspondence with the normal evolution of the movement. The capsular pattern varies from joint to joint. It is not clear why some joints limit in certain directions and other joints in other directions. In arthritis of the shoulder it consists of a certain degree of limitation of scapulo humeral abduction, more limitation of external rotation and less limitation of internal rotation. A capsular lesion in the hip by contrast manifests itself with most restric tion of internal rotation and less limitation of flexion, abduction and extension, external rotation remaining full range. There are joints in which the capsular pattern includes complete absence of certain movements: the joint is fixed in a certain position. Examples are the sub talar joint, which fixes in full valgus, and midtarsal arthri tis in which the joints are fixed in full abduction and external rotation.
Arthritis
In a peripheral joint, a lesion of either the fibrous capsule or of the synovial membrane with which it is lined gives rise to limitation of movement, to a characteristic pro-
Joints not spanned by muscles. Where muscles are not present to cause any limitation of movement, joints are supported by ligaments only. Restriction of movement caused by irritation of the capsule (synovitis) is not pos sible. There is pain only at the extremes. This phenome non is found at the acromioclavicular, sternoclavicular, sacroiliac, sacrococcygeal and lower tibiofibular joints, and also at the symphysis pubis. Limitation with a bony block end-feel. Slight painless limitation of movement with a bony block end-feel occurs in neuropathic arthropathy. The movement causes an ache in gross osteophytosis, myositis ossificans or a mal-united fracture.
CHAPTER 4 - CLI N I CA L D IAGNOSIS OF SOFT TISSU E LESIONS 85
Passive movements positive
: •
'
.
, , , ,
LJ\AIII \ L�"'\l �___"
"'__-+-�I
• • • • • •
• • • • • • • • • • • • •
+
. ..
���i��:�ment •
Resis
,
•
• • • • •'
. . . . . . . . . . . . . . . . . . . . . . •� ----� �
Figure 4.1 4
Positive passive/negative resisted movements.
Non-capsular patterns or partial articular limitation
When the limitation of movements in a certain joint does not correspond to the capsular pattern of that joint, the lesion is clearly not capsular, which means that it does not affect the entire joint. So arthritis is not present. In contrast to the capsular pattern a non-capsular pattern is less well defined, but for each joint different patterns may occur, all of which do differ from the capsular pattern (see Fig. 4. 15).
Typical examples are the medial collateral ligament of the knee and the lateral ligaments of the ankle. At the knee, flexion is usually 10-15° limited, with pain very localized over the course of the ligament. At the ankle, the combined movement of plantiflexion and inversion
Non-capsular limitation
Partial articular pattern. In the spine the term partial articular pattern is more appropriate, indicating that only
part of the intervertebral joint complex is affected. Non-capsular conditions fall into three main categories. When a post-traumatic ligamen tous lesion heals in the absence of movement macro adhesions may form (ligament to capsule or underlying bone), which impair function. One movement is usually limited by localized pain but others may be painful at their extremes. The limitation is proportionate: slight restriction in one direction - the one that stretches the affected part of the ligament - and full range in other directions.
Internal derangement
ligamentous adhesions.
I njury in the past Slight limitation of only one movement Localized pain
Spontaneous onset Some movements blocked (asymmetrical pattern) Localized pain
Gross limitation of only one movement Localized pain or
Constant length phenomenon
Figure 4.1 5
Classification of non-capsular limitation.
86
SECTION O N E - G E N E RA L P R I N C I PLES
is slightly restricted and the tender spot lies in the affected ligament (anterior talofibular, calcaneofibular or calcaneocuboid). Internal derangement. When fragments of cartilage or bone become loose in a joint, the clinical picture is of internal derangement. The knee is the most common site followed by the spinal joints, the wrist and the jaw and less so the hip, the elbow or the tarsal joints. Displacement comes on quite suddenly and blocks part of joint movement with localized pain on one aspect and limitation of some movements but not others. Two different types of limitation occur:
When the displaced frag ment is small and lies in such a position that it does not greatly hinder the function of the joint, restriction of movement is also small by comparison with normal movement. The picture may very well mimic the propor tionate limitation in ligamentous adhesions but the absence of an injury and the short history exclude this possibility. A typical example is the loose body in an arthrotic knee: flexion is 1 5-30° limited and the pain is felt at the inner side. Proportionate derangement.
string muscles become tight, but flexion of the knee allows full flexion at the hip. Another example is Volkmann's contracture: the fingers cannot be extended without flexing the wrist. F U L L RAN G E
When n o limitation of movement exists on passive testing, the picture may be difficult to interpret. The site of pain usually helps to determine whether it is caused by stretch ing or by pinching of the affected tissue (Fig. 4.16). Pain is elicited on stretching
Pain at the extremes of several movements may be found in those joints that are not spanned by muscles. As the capsule of these joints does not have muscular protection the passive tests stretch the ligaments. When, for example, the acromioclavicular joint is affected the extremes of passive movements at the shoulder are painful. When only one passive movement causes pain as a result of stretching, the examiner should think in terms of a ligamentous, tendinous or muscular tissue being
Disproportionate derangement. A large displacement causes gross limitation of movement in some directions and full or almost full range in other directions - an asymmetrical pattern. This is a well-known clinical picture in acute lumbago. Two or three trunk movements are totally blocked and one movement, usually one lateral flexion, is scarcely limited. Extra-articular limitation. A tissue outside the joint may be damaged and prevent movement in one direction only. A disproportionate limitation is then seen: one move ment is grossly limited and all other movements are of full range. Such disproportion is only possible when the tissue that causes the limitation lies extra-articularly. In some cases it does not allow stretching, in others it is resistant to compression. Rupture of some muscular fibres (in the quadriceps or in the calf) is followed by localized muscle spasm which prevents stretching. In acute subdeltoid bursitis, gross disproportion is also found between the very limited scapulohumeral abduc tion and the slight limitation of both rotations. The 'constant-length ' phenomenon. In this phenomenon the degree of limitation of a movement in one joint depends on the position in which the adjacent joint is held. This is only possible when the structure that pre vents stretching spans the two joints. Straight-leg raising is a typical example, with the hamstring muscles span ning the hip and knee joints. The amount of flexion at the hip depends on the position of the knee: when done with the knee extended the movement stops when the ham-
Stretching pain
I
(a)
(b) Figure 4.1 6
(a) Pain on stretching. (b) pain on pinching.
CHAPTE R 4
stretched. In the last of these, resisted movement in the opposite direction is also painful - the contractile tissue pattern' (see below). However, an early arthritis in shoul der and hip may, for a short period, show pain at the end of one movement only. I
Pain is elicited on pinching
Pinching of a tender tissue may happen at the end of range or at mid-range. In both cases, the pain is the result of the same mechanism. When a passive movement elicits pain at full range but the main test result is a resis ted movement, this sign sometimes has localizing value. This is seen for example at the shoulder in supraspinatus and subscapularis tendinitis, at the elbow in biceps tendinitis, at the hip in rectus femoris tendinitis and at the heel in Achilles tendinitis. For more details, see the appropriate chapters. In other cases, logical thinking based on anatomical grounds is required to find out what structure has been painfully pinched. It may be an inert structure (bone, capsule, ligament) or a contractile structure (muscle, tendon). The latter will, of course, show with pain on resisted movements as well. Palpation may then often help to determine the exact localization and local anaes thesia can be used to confirm this. Pain felt somewhere near mid-range in a movement, either passive or active, is called a 'painful arc'. The pain is absent when the movement starts, appears at a certain moment during the movement and disappears again before the end of range is reached. To be called 'painful arc' the pain should disappear at either side of the arc. An arc indicates that the affected structure becomes momen tarily compressed between two bony surfaces. Only some structures in the body lie in a position that they can cause a painful arc. It is quite common at the shoulder and in the lumbar spine. Sometimes the painful arc can be considered a localiz ing sign: its presence shows exactly where the lesion lies. In supraspinatus tendinitis the presence of a painful arc indicates that the lesion lies at the superficial aspect of the tenoperiosteal insertion of the tendon into the greater tuberosity of the humerus, and a painful arc accompanying the signs of a subscapularis tendinitis shows the lesion to lie at the upper part of the insertion at the lesser tuberosity.
EXCESSIVE RANGE
Hypermobility is seen in capsuloligamentous laxity and is then a pathological finding. However in some circum stances excessive range can be purely physiological (e.g. passive elbow extension in most women). The matter is considered earlier in this section under palpation.
-
CLI N I CA L D I A G N O S I S OF SOFT TISS U E LESIONS 87
NO M OVE M E NT I S POSSI BLE
This is not often encountered but it may result either from a severe muscle spasm, protecting a very acute or irritated lesion or from fibrous or bony ankylosis. I M PAIRMENT OF RESISTED MOVEMENTS I N CO M BI N ATION WITH I M PA I R M ENT O F TH E PASSIVE MOVE M E NTS
If a movement against resistance is painful, passive movement in the opposite direction is usually also painful. This is the 'contractile tissue pattern'. When the lesion is tendinous there is a full range of movement. In muscular rupture, the movement that stretches the muscle may be not only painful but also limited because of a localized protective muscular spasm of the fibres around the breach. This phenomenon helps to differenti ate between a tendinous and a muscular lesion. I N I S O LATI O N One resisted movement i s positive
This indicates one muscle or one muscle group is involved. In the latter case, one or more accessory tests are necessary to find the muscle or tendon at fault. For example, resisted extension at the wrist tests the exten sors of fingers and wrist; repetition of the test with the fingers held actively flexed distinguishes between finger extensors and wrist extensors. Radial and ulnar deviation against resistance differentiates between the radial exten sors (extensor carpi radialis longus and brevis) and the extensor carpi ulnaris. I N C O M B I N ATION WITH I M PA I R M E NT O F OTH E R R E S I ST E D MOVE M E NTS Two resisted movements are positive
This can occur when two contractile structures are affected or, more probably, when one muscle is affected which combines the two functions. The brachial biceps muscle produces both flexion of the elbow and supina tion of the forearm. A lesion in this muscle leads to both movements being positive. At the shoulder, the combina tion of positive resisted external rotation and resisted adduction of the shoulder draws attention to the teres minor, which combines these functions. Three or more resisted movements are positive
When this occurs, the chance that there is a lesion in a contractile tissue is much less. It is more logical to think of either transmitted stress to a very painful
88
SECTION O N E - G E N E RA L P R I N C I PLES
space-occupying lesion, such as a tumour, metastases, abscess or very irritated bursa, or a psychogenic problem.
This excludes a musculotendinous lesion and has the same interpretive significance as multiple resistance. The examiner should also make sure that the patient does not misinterpret the questions: a hypersensitive patient may equate effort with pain and say that every movement against resistance is painful. Careful comparison of both sides is helpful in avoiding misinterpretation.
dition must be a minor lesion in a contractile structure. The possibilities are a muscular strain, a lesion at the musculotendinous junction, a tendinous problem (ten dinitis, tenovaginitis or tenosynovitis) or a lesion at the tenoperiosteal junction. Typical examples are supra spinatus tendinitis at the shoulder, lesion of the extensor carpi radialis brevis at the elbow (tennis elbow), teno vaginitis of the extensor pollicis brevis and abductor pollicis longus at the thumb (de Quervain's disease), infrapatellar tendinitis at the knee or peroneal tenosyn ovitis at the ankle.
Pain develops on repetition
Painless (or constant pain) and weak
All resisted movements are positive
Pain developing on repetition of a movement may be indicative of an arterial problem leading to intermittent claudica tion. R E LATI O N S H I P OF PAI N A N D STR E N GTH
Resisted movements test for strength and pain. The pat terns that emerge are usually a combination of strength or weakness and the presence or absence of pain. In practice, four combinations may occur (Table 4.4).
The patient is either pain-free or in constant pain. The test against resistance, although weak, does not elicit or alter the pain. This is usually the result of a nervous condition, either extrinsic or intrinsic. Dependent on the severity of the lesion the weakness detected may vary from very moderate to complete paralysis. Complete rupture of a muscle or a tendon also leads to a painless total loss of strength (see earlier). Painful and weak
Negative resisted movements - no pain and normal strength - exclude a lesion of a contractile tissue. This axiom is often neglected. For example, patients with pain and local tenderness in the trapezius area are often diag nosed as having a 'trapezius syndrome'. The clinical examination, however, shows the trapezius muscle to function normally. In this case there is no reason to incriminate the muscle. Pain and tenderness are clearly referred, usually from the cervical spine. Another example is when a patient has pain over the long head of the biceps but the tests for that muscle are completely negative, then it is apparent that the muscle is normal and the pain is referred.
This combination suggests a major lesion. The movement is painful and its strength is reduced, either because the muscle is functioning poorly or because the attempt to use it increases the pain sufficiently to inhibit full con traction. This pattern occurs in serious disorders, such as fracture or metastases. Usually there are also articular signs. When after an 'ankle sprain' resisted eversion proves painful and weak, a fracture of the tuberosity of the fifth metatarsal bone is suggested. Metastases in the upper femur or in the cervical spine give rise to weakness in resisted movements of the hip or the neck. If only one movement is painful and weak and the joint moves normally, a partial rupture of a muscle or tendon is probably present, although a severe tendinitis may cause an identical picture.
Painful and strong
POSITIVE R E SI ST E D MOVE M E NTS I N LESIONS O F
When the resisted movement causes pain but the patient is capable of exerting normal strength, the con-
N O N·CONTRACTI LE STR U CTU RES
Painless and strong
Table 4.4 Pain
Relationship of pain and strength in resisted movement Strength
Disorder
Normal +
+
Normal
Contractile tissue
Weak
Nervous lesion Complete rupture
Weak
Serious lesion Partial rupture
There are three situations in which muscular contraction causes pain in the absence of any musculotendinous lesion. The first is a bony lesion (e.g. fracture or metastases) close to the insertion of a muscle or tendon: when the muscle is tested against resistance, the contraction causes pull at the site and the test is painful and possibly associ ated with weakness. Stress fracture of the pubic bone causes pain felt on resisted adduction of the hip and in an anterior upper rib fracture contraction of the pectoralis major muscle hurts. The second is compression of a tender structure by a contracted muscle belly which is often encountered in the
CHAPTER 4
buttock where an irritated gluteal or trochanteric bursa can be compressed by contraction of the gluteus medius muscle. The third is in patients with psychological problems, when resisted movements are quite often more painfu l than passive or active ones (see Ch. 8 8 o n Psychogenic Pain).
-
CLI N I CA L DIAGNOSIS OF SOFT TISSUE LESIONS 89
Every patient with a clear pattern of symptoms in the absence of positive signs on clini cal examination should be referred for more specialized investigations.
SU M MARY
The interpretation of resisted passive movements is summarized in Figure 4.17 ABSENCE OF PAIN ON MOVEM E NT
For a given region a negative functional examination, including accessory functional tests, implies that the pain is referred. Other parts of the locomotor system from which the pain might originate are then examined. When nothing is found, the lesion is clearly non-orthopaedic, most probably nervous but possibly visceral. Also small bony lesions (e.g. osteoid osteoma) along the shaft of a long bone may cause localized pain without influencing the function of an adjacent joint.
Pain
Pain and weakness
Weakness
Figure 4. 1 7
Interpretation of resisted and passive movements.
One contractile tissue Partial rupture Fracture Space-occupying lesion Complete rupture
DIAG NOSTIC DIFFICULTIES V E RY SLIGHT PAI N
When the patient has very little pain, examination can be totally negative. Palpation is very dangerous in these cases for the reasons mentioned earlier. It is better to re examine 1-2 weeks later. If spontaneous recovery has not taken place, it is likely that some signs will have devel oped. Another way to proceed is to seek to provoke signs
Double lesion Space-occupying lesion
Space-occupying lesion
Space-occupying lesion Fracture Serious disorde r Space-occupying lesion Functional disorder
Neurological lesion: peripheral nerve or nerve root G ross neu rological lesion Functional disorder
90
SECTI O N O N E - G E N ERAL P R I N C I PLES
by having the patient exercise sufficiently to produce symptoms. Clearly a diagnosis is impossible as long as signs are absent. V E RY SEVERE PAI N
Certain conditions are so painful that i t is hard for the patient to state accurately where and when pain is felt. Functional testing and its interpretation are also difficult, either because excessive physical signs are presented or because the patient cannot move and is opposed to carrying out potentially diagnostic manoeuvres. Severe pain may interfere with the ability to cooperate so that, for example, a resisted movement cannot be done prop erly. After an injury, swelling and / or haematoma may also render palpation impossible: for example, in the first days after an ankle sprain the condition may be so acute that no clear pattern emerges on examination; lumbago may be so painful that any movement becomes impossi ble. History is then of great importance, particularly the presence or absence of warning signs. The number of conditions that can provoke such severe pain is limited and the examiner must try to interpret the symptoms in the light of the realistic possibilities.
The occurrence of a double lesion is not so uncommon and it quite often does not cause a problem, especially when the two conditions can be clearly distinguished because they cause pain in different places or show dif ferent sets of signs. Interpretation is more difficult when they lie close together or when the symptoms and signs of one clearly dominates. The examiner can make a diagnosis based on those symptoms and signs that are understood and wait until one problem is solved before attempting to interpret the remaining features. It is indeed a sound principle never to treat two conditions at the same time. The choice of which to treat first can be based on several criteria: pain, frequency, importance and the 'approachability' of the lesion. It is logical to try to improve the more painful lesion first. If doubt exists as to which structure is at fault, the condition that is statis-
Assess function
•
t
� 1
",__-j
onal examination
N O N-ORTH O PA E D I C D I S O R D E RS
Some neurological, vascular or visceral disorders may cause diffuse pain which resembles the symptoms of a lesion of the locomotor system. A patient who com plains of vague pains, especially in the trunk, but has negative findings on locomotor and soft tissue examina tion should be referred for further neurological, vascular or internal examination.
Patte:n Applied anatomy
D I F F I C U LT CLI N I CA L PICT U R E S
Conditions affecting the spinal column may give rise to vague, diffuse pain felt somewhere in the trunk. If the anterior longitudinal ligament becomes affected in ankylosing spondylitis, pain may be referred to the sternum or to the epigastrium. For those who are not familiar with the phenomenon of dural pain, the exten sive and vague radiation of multisegmental pain can be very confusing. A patient may present the symptoms and signs of a genuine, although minor, lesion which is overshadowed by psychogenic features. The picture is correct in quality, but grossly excessive in quantity. The examiner recog nizes the truth within the patient's story but finds that it is interwoven with unlikelihoods and improbable signs are mixed up with the genuine findings (see Ch. 88 on PsychogeniC Pain).
Figure 4.18
Clinical approach in orthopaedic medicine.
I
CHAPTE R 4 - C L I N ICAL D IAGNOSIS OF SOFT TISSU E L E S I O N S 91
tically more common is treated. A problem in a joint usually arthritis - is dealt with first. Finally, when it is known that one condition can be more quickly treated than anothel� this condition is treated first.
PSYC H OG E N IC PROBLEMS
The reader is referred to Chapter 88 on Psychogenic Pain.
REFERENCES 1 . Christensen HW, N i lsson N . The rel iabil ity of measuring active and passive cervical range of motion: an observer-blinded and randomized repeated-measures design. j Mal1ipulative Physiol Ther 1 998;21(5):341-347. Cyriax evaluation in assessing patients with shoulder pain. j Orthop Sports Phys Ther 1 996;23(1):34-38. B M,
rel i a b i l i ty
MacOerm id
JC,
Roth
of
the
standing
flexion
test.
Man ual
Therapy
1999;4(2) :87-93. 2 1 . Maher
2. Pellecchi a GL, Paolino J, Connell J. lntertester reli a b i l i ty of the
3. Chesworth
20. Vincent-Smith B, Gibbons P. Inter-examiner and intra-examiner
e,
Latimer J. Pain or resistance - the manual therapists'
delimma. Aust j Physiother 1 992;38:257-260. 22. Keating J, Bergman T, Jacobs G, Bradley D, Finer A, Larson K.
Inter-examiner reliability of eight evaluative di mensions of
JH,
Patterson SO.
Movement d i agram and 'end-feel' rel iability when measuring passive lateral rotation of the shoulder in patients with shoulder pathol ogy. Phys Ther 1 998;78(6):593-601 .
l u mbar segmental abnormali ty. j Manipulativc Physiol Tllcr 1 990;13:463-470. 23. Potter N, Rothstein J. l n tertester rel iability for selected clinical tests o f the sacro i l i ac joint. Phys Ther 1985;65:1671-1 675.
4. Wong A, Nansel D O . Comparisons between active vs. passive end-range assessments i n subjects exhibiting cervical range of motion asymmetries. j Mal1ipulative Physiol Ther 1992;15(3): 1 59-163.
24. MacRae DL. Asymptomatic i n tervertebral disc protrusion. Acta Radiologica 1956;46:9. 25. H i tselberger WE, W h i tten R M . Abnorm a l myelograms in asymptomatic patients. J Nellrosllrg 1 968;28:204.
5. Youdas JW, Carey JR, Garrett TR. Reliability of measurements of
26. Wiesel SW, Tsourmas N, Feffer HL, Citrin CM, Patronas N. A
cervical spine range of motion - comparison of three methods.
study of computer-assisted tomography: 1 . The incidence of
Phys Tiler 1 991 ;71(2):98-104.
positive CAT scans in an asymptomatic group of patients. Spine
6. Fritz ] M, Delitto A, Erhard RE, Roman M. An examination o f the selective tissue tension scheme, w i th evidence for the concept
of
a
caps u l a r
pattern
of
the
knee.
Phys
Ther
1 998;78(10):1 046-1 056. Tissue Lesions, 8th edn. Baill iere Tindall, London, 1982:45.
8. Donelson R, Silva G, Murphy K. Centra l ization phenomenon, its usefulness in evaluating and treating referred pain. Spine 1990;15(3):211-213.
e,
28. Weinreb
Je,
Wolbarsht LB, Cohen JM, Brown CE, Maravilla KR.
Prevalence of l umbosacral i n tervertebral d isc abnormalities on MR
images i n pregnant and asymptomatic non-pregnant
women. Radiology 1989;170 : 1 25-128. 29. Boden SO, Davis DO,
Medcalf R, Grant W. A prospective
study of centralisation of lumbar and referred pain. Spine 1997;22(10) : 1 1 1 5- 1 1 22.
Dina TS, Patronas MJ. Wiesel Sw.
Abnormal magnetic resonance scans of the lumbar spine in asymptomatic subjects. j BOlle joint Slirg 1 990;72A:403-408. 30. B u i rski G, Silberstein M. The symptomatic lumbar disc in
10. Wyke W. Neurological mechanisms in the experience of pain. AC/lpllnc Electrother Res j 1979;4:27.
patients w i th
low-back pain. Magnetic resonance imaging
appearances i n both a symptomatic and control population.
1 1 . Wyke BD. The neurology of low back pain. In: Jayson MlV (ed . ) The LU lllbar Spine a n d Back Pain, 2 n d e d n . Pitman Medical, Kent, 1980.
Spine 1993;18:1808-181 1 . 3 1 . Matsumoto M, Fujimura Y, Suzuki N , N i sh i Y, Nakamura M, Yabe Y, Shiga H. M R I of cervical i n tervertebral d iscs in asymp
12. Veys EM, Mielants H, Verbruggen G. Rewnat% gie. Omega 13. Greenman PE. Principles of Manual Medicine. William & Wilkins, Balti more, 1989:61-70.
14. Twomey LT, Taylor J R .
Physical Therapy of the Low Back.
Churchill Livingstone, New York, 1987:1 92-197. Boyling JD, Palastanga N (eds) Grieve 's Modern Manual Therapy, Col u m n .
C h u rch i l l
L i v ingstone,
E d inbu rgh,
1 994:491-501 . 16. Panzer D M . The reli a b i l ity of l u m b a r motion palpation. j Manipulative Physiol Ther 1992;15(8) : 5 1 8-524. 1 7. Matyas T, Bach T. The reliabil ity of selected techniques in clini cal arthrometics. Alist j Physiother 1 985;31 : 1 75-199. 18. Hardy GL, Napier JK. lnter- and intra therapist reliability of passive accessory movement and technique. NZ J Physiother 1991 :22-24. 19. Fjellner A, Bexander C, Faleij R, Strender L E . Interexaminer rel i a b i l i ty in physical examination o f the cer v i c a l s p ine.
I Manipulative Physiol Ther 1 999;22(8): 5 1 1 -5 1 6 .
Reli a b i l i ty of magnetic resonance imaging in pred icting d isc material posterior to the posterior longitudinal ligament in the cervical spine. A prospective study. Spine 1998;23(22):2468-2471 . 33. Kaiser JA, Holland BA. Imaging o f the cervical spine. Spine
15. Jones MA, Jones HM. Principles of the physical examination. In: Vertebral
tomatic subjects. J Bone Joint Slirg (Br) 1 998;80(1) : 1 9-24. 32. Humphreys SC, Hodges SD, Fisher DL, Eck JC, Covington LA.
Edi tions, Ghent, 1 985:21-23.
The
lumbar disc degeneration observed by magnetic resonance in symptomless women. Lancet 1 986;13:1 366-1 367.
7. Cyriax ]H. Textbook of Orthopaedic Medicine, vol 1: Diagnosis of Soft
9. Donelson R, April l
1 984;9:549-551 . 27. Powell Me, Wilson M , Szypryt P, Symonds E M . Prevalence of
1998;23(24):2701-2712. 34. Shafaie FF, Wippold FJ 2nd, Gado M, Pi lgram TK, Riew KO. Comparison of computed
tomography
myelography and
magnetic resonance i m a g i ng i n the eval u a ti on of cervical spondylotic myelopathy and radicu lopathy. Spine 1 999;24(17): 1 781-1 785. 35. Thompson WO, Oebski RE, Boardman NO 3rd, Taskiran E, Warner JJ, Fu FH, Woo SL. A biomechanical analysis of rotator cuff deficiency i n a
cadaveric model.
Alii
j
Sports
Med
1 996;24(3) :286-292. 36. Petersson CJ Ruptures of the supraspinatus tendon. Cadaver dissection. Acta Orthop Scand 1 984;55(1) :52-56. 37. Jerosch J, M u l ler T, Castro WH. The incidence of rotator' cuff rupture. An anatomic study. Acta Orthop Belg 1991;57(2):1 24-1 29.
92
SECTION O N E - G E N E RAL P R I N C I PLES
38. Kummer FJ, Zuckerman JD. The incidence of ful l t hickness rotator cuff tears in a l a rge cadaveric population. Bull Hasp Dis
1 995;54(1 ) :30-3 1 .
3 9 . Jerosch J , Castro W H, Assheuer J . Age-related magnetic resonance imaging morphology of the menisci in asympto matic individuals. Arch Orthop Tra u ma S u rg 1 996;115(3-4): 1 99-202.
40. LaPrade RF, Burnett QM 2nd, Veenstra MA, Hodgman CG. The prevalence of abnormal magnetic resonance imaging findings
in asymptomatic knees. With correlation of magnetic resonance imaging to arthroscopic findings in symptomatic knees. AIIJ ] Sports Med 1994;22(6):739-745. 4 1 . Cyriax J H . Textbook of Orthopaedic Medicille, val l: Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982: 1 5 1 .
CHAPTER CONTENTS Introduction Techniques
Principles of treatment
93 94
Deep transverse friction Mode of action 94
94
Relief of pain 95 Effect on connective tissue repair Indications 96 Contraindications 98 Technique 98 Passive movements Indications 103
102
INTRODUCTION
Manipulation of the spine Active movements
95
105
114
Simple active movements to gain or preserve normal 114 range in a j oint Isometric contractions 114 Isotonic contractions 114 Electrical contractions 115 Coordination exercises 115 Injection and infiltration
115
General principles 116 Local anaesthetics 118 Corticosteroids 121 Phenol 125
Cyriax had a straightforward opinion about treating orthopaedic problems: • • •
All pain arises from a sou rce All treatment must reach the source All treatment must exert a beneficial effect on it.
It is obvious that the method of treatment will depend largely on the existing type of disorder. In orthopaedic medicine, d isorders may be grossly categorized as follows: •
• •
an injury resulting either from one single trauma or from multiple small traumas, the so-called overuse injuries Inflammatory rheumatoid: poly- or monoarticular, infectious, traumatic Traumatic
-
-
Degenerative
- loose bodies and displ aced menisci in peripheral joints and intervertebral disc displacements in the spine Functional disorders - instability, weakness, proprio ceptive disturbances Psychogenic pain - there is no existing functional or anatomical explanation for the pain.
• Internal derangement
• •
However, most ' disorders' have a combined aetiology: traumatic inflammation or repetitive internal derange ment may lead to functional instability or to weakening of the proprioceptive reflexes; long-standing functional disorders may lead to psychogenic decompensation. Before any form of treatment is undertaken, precise diagnosis is mandatory; it is the type, extent and position of the disorder present which determines treatment. Therefore training in orthopaedic medicine must put great emphasis on how to reach a proper diagnosis. It is more difficult and requires considerable delicacy of approach to teach and learn how to diagnose and so to propose therapy chosen on logical grounds, than it is to instruct and learn treatment techniques. Other aspects must also be taken into account: how much pain can the patient bear? To what extent does the lesion interfere with normal activities? How eager is the patient to 93
94 SECTION ONE - GENERAL PRINCIPLES
receive a quick cure? And what is the patient's attitude towards certain therapeutic methods such as corticos teroids and manipulation? Orthopaedic medicine based on a detailed functional examination requires more knowledge, ski ll, time and effort from the physician than just to order technical investigations but leads to greater professional interest, more appropriate d iagnosis and a higher degree of patien t satisfaction. Clear diagnosis and consequent selection of treatment on logical grounds also leads to better understanding between doctors and therapists. Because the two groups work with the same types of patient, they must share a common approach. Therapists shou ld no longer be regarded purely as tech nicians who listen to the physician and carry out orders. On the contra ry, they shou ld be aware that they have d i agnosti c and therapeutic responsibi l ities. Their opinion must be taken seriously and is i mportant to avoid unnecessary delay in achieving a satisfactory outcome.
TECHNIQUES The treatment techniques used in orthopaedic medicine thus depend entirely on the type of d isorder. The d iffer ent types of treatment we describe are: •
•
•
•
•
Manipulation techniques (rapid, small-amplitude,
thrusting passive movement - also called 'grade C mobilization') are used to reduce small cartilaginous displaced fragments both in the spine and in periph eral joints (loose bodies). Manipulation is also called for to restore normal mobility in a joint restricted by ligamentous adhesion and in subluxation of bones. Gentle passive mobilizations (grade A and B mobiliza tions) are used to stretch capsular adhesions and to improve the function of l igaments and tendons. In the treatment of traumatic injuries they are often used in combination with deep transverse massage. Active movements and proprioceptive training are needed in the treatment of functional d isorders and instabili ty. In the treatment of minor muscular tears they are very useful in avoiding the formation of abnormal intralesional adhesion formation. Injection and infiltration techniques are used to reduce traumatic or rheumatoid inflammation. They are most valuable in arthritis, bursitis, l igamentous and tendi nous lesions and in neurocompression syndromes. Deep friction is a very useful technique in treating traumatic and overuse soft tissue lesions. The ration ale for using deep friction (which is in fact a form of soft tissue mobilization) is supported by experimental studies of the past several decades that confirm and
explain the beneficial effects of activity on the healing musculoskeletal tissues (see Connective tissue). Repair and remodelling of healing tissues respond to cyclic loading and motion.1 Early motion and loading of i njured tissues is not without risk, howevel� and excessive loading can inhibit or stop healing. Deep transverse fric tion imposes cyclic loading without bringing too much tension on the healing longitudinal structures of tendon or ligament and can therefore be considered as beneficial.
DEEP TRANSVERSE FRICTION Deep transverse friction (although the word friction is technically incorrect and would be better replaced by ' massage' ) is a specific type of connective tissue massage2 developed in an empirical way by Cyriax.3 Transverse massage is applied by the finger(s) directly to the lesion and transverse to the direction of the fibres. It can be used after an injury and for mechanical overuse in muscular, tendinous and ligamentous structure.4-6 In many instances the friction massage is an alternative to infiltrations with steroids. Friction is usually slower in effect than injections but leads to a phYSically more fun damental resolution, resulting in more permanent cure and less recurrence. Whereas steroid injection is usually successful in 1-2 weeks, deep friction may require up to 6 weeks to have its full effect. The technique is often used before and in conjunction with mobilization techniques. In minor muscular tears, friction is usually followed by active movement, in liga mentous tears by passive movement and in tendinous lesions by active unloaded movements until full resolu tion has been achieved. It is vital that transverse massage is performed only at the site of the lesion. The effect is so local that, unless the finger is applied to the exact site and friction given in the right direction, relief cannot be expected. Over the years, and unfortunately enough, the tech nique has developed a reputation for being very painful for the patient. However, pain du ring friction massage is usually the result of a wrong indication, a wrong tech nique or an unaccustomed amount of pressure. Friction massage applied correctly will quickly result in an anal gesic effect over the treated area and is seldom a painful experience for the patient.
MODE OF ACTION Transverse massage should be used empirically for what it is and what it achieves; there is no scientific proof for any postulates about the underlying mechanism of action.
CHAPTER 5 - PRINCIPLES OF TREATMENT 95
Only a few studies exist/,s and more research is urgently needed, However, experienced therapists know in what kind of soft tissues they can expect good results with transverse massage and where the technique does not work. Transverse massage either is effective quickly (after 6-1 0 sessions) or not at all. Advice on indications, contraindications and modalities of the technique that are given in this book rely solely on the experiences of the authors and not on scientific research. However, although the exact mode of action is not known, some theoretical explanations have been put forward. It has been hypothesized that friction has a local pain-d iminishing effect and results in better a lignment of connective tissue fibrils.
RELIEF OF PAIN It is a common clinical observation that application of local transverse friction leads to immediate pain relief the patient experiences a numbing effect during the friction and reassessment immediately after the session shows reduction in pain and increase in strength and mobility. The time to produce analgesia during the application of transverse friction is a few minutes and the post-massage analgesic effect may last more than 24 hours.9 The temporary reli ef at the end of a session m ay prepare the patien t for treatment with mobilization not otherwise possible, such as selective rupture of unwanted adhesions. A number of hypotheses to explain the pain-relieving effect of transverse massage have been put forward. •
•
•
•
Pain relief during and after friction massage may be the result of modulation of the nociceptive impulses at spinal cord level: the gate control theory (see Ch, 1 ) . The centripetal projection into the dorsal hom of the spinal cord from the nociceptive receptor system is inhibited by the concurrent activity of the mechanoreceptors located in the same tissues, Selective stimulation of the mechanoreceptors by rhythmical movements over the affected area thus ' closes the gate for pain afference'. According to Cyriax, friction also leads to increased destruction of pain-provoking metabolites, such as Lewis's substances. This metabolite, if present in too high a concentration, provokes ischaemia and pain.3 It has also been suggested that prolonged deep friction of a localized area may give rise to a lasting peripheral disturbance of nerve tissue, with local anaesthetic effect. Another mechanism through which reduction i n pain may be achieved is through diffuse noxious inhibitory controls, a pain-suppression mechanism that releases endogenous opiates, The latter are i nhibitory neurotransmitters that diminish the inten sity of the pain transmitted to higher centres.lO-1 2
EFFECT ON CONNECTIVE TISSUE REPAIR Connective tissue regenerates l argely as a consequence of the action of inflammatory cells, vascular and lym phatic endothelial cells and fibroblasts, Regeneration comprises three main p hases: inflammation, prol ifera tion (granu lation) and remodelling, These events do not occur separately but form a continuous sequence of changes (cell, matrix and vascular changes) that begins with the release of inflammatory mediators and ends with the remodelling of the repaired tissue (see p. 44). Friction massage may have a beneficial effect on all three phases of repair.
Friction stimulates phagocytosis It has been suggested that gentle transverse friction, applied in the early inflammatory phase enhances the mobilization of tissue fluid and therefore increases the rate of phagocytosis.13 Friction stimulates fibre orientation in regenerating connective tissue During maturation, the scar tissue is reshaped and strengthened by removing, reorganizing and replacing cells and matrix.14 It is now generally recognized that internal and exter nal mechanical stress applied to the repair tissue is the main stimulus for remodelling immature and weak scar tissue - with fibres that are oriented in all directions and through several planes - into linearly rearranged bUJldles of connective tissues. l5 Therefore, during the healing period, the affected structures shou ld be kept mobile by normal use. However, because of pain, the tissues caru10t be moved to their ful l extent This problem can be solved by friction. Transverse friction massage imposes rhythmical stress transversely to the remodel ling collagenous structu res of the connective tissue and thus reorients the collagen in a longitudinal fashion. Friction is thus a useful treatment to apply early in the repair cycle (granulation and beginning of remodelling stage): the cyclic loading on and motion of the healing connective tissues stimulates formation and remodelling of the collagen,16 Friction prevents adhesion formation and ruptures unwanted adhesions (Fig, 5,1 ) In that transverse friction aims to achieve transverse movement of the collagen structure of the cOlmective tissue, crosslinks and adhesion formation are prevented. In the early stages of proliferation when crosslinks are absent or still weak, friction must be very light so as to cause only minimal d iscomfort Therefore, in the first day or two following an injury, friction is given with slight pressure only and over a short duration, say 1 minute.
96 SECTION ONE - GENERAL PRINCIPLES
suspected spot results in diminished pain on testing immediately thereafter, so confirming the diagnosis as accurately as an infiltration with local anaesthesia.
Preparation for mobilizations and manipulation Transverse massage is often applied before and in con junction with other mobilizing techniques. In muscular lesions, friction is given before active or electrical con tractions on an unloaded muscle. The purpose is to allow broadening of the muscle and so the prevention of adhesion formation between adjacent m u scle fibres and / or bundles. For reasons of pain relief, transverse massage is usually required before manipulative breakage of liga mentous adhesions is performed. This may be indicated in chronic ligamentous lesions at knee and ankle. Deep and thorough friction also precedes manipula tion of the elbow in type II tennis elbow. The technique is used for its desensitizing and softening effect which makes the manipulation more tolerable. Therapy
Figure 5.1 Friction achieves a transverse movement between longitudinally arranged collagenous fibres.
At a later stage when strong crosslinks or adhesions have formed, more intense friction is needed to break these down. 17-20 The technique is then used to soften the scar tissue and to mobilize the crosslinks between the col lagen fibres and the adhesions between healing connec tive tissue and surrounding tissues. This, together with the local anaesthesia produced, prepares the structures for mobilizations that apply longitudinal stress to the structures and rupture the larger adhesions.
Friction induces traumatic hyperaemia Forceful deep friction produces vasodilatation and increased blood £low to the area. It may be hypothesized that this facilitates the removal of chemical irritants and increases the transportation of endogenous opiates, so causing a decrease in pain. Such a forceful friction, result ing in hyperaemia is only desirable in chronic, self perpetuating lesions.
INDICATIONS Diagnosis The reduction in pain achieved after a few minutes of localized transverse friction may be very helpful to define the exact location of the lesion. In muscular, tendinous or ligamentous lesions, a few minutes of massage on the
M uscle bel lies. Friction is given to a healing mu scle belly after contusion, in minor muscular tears and in so-called 'myosynovitis'. In minor muscular tears the friction is often part of combined treatment because it is usually applied after an infiltration with local anaesthesia and is followed by active contractions. The aim of treatment in muscular tears is to allow the torn fibres to heal in such a way that normal increase in breadth on contraction remains possible, a characteristic that can be disturbed by abnormal adhesion formation. Transverse friction aims to achieve a transverse sweep i ng movement over the longitudinal muscular fibres without pulling on the tear, so to prevent (in the early stage) or to break down (in the chronic stage) adhesion formation between the i ndividual fibres and between individual fibres and the surrounding connective tissue. It is obvious that to break down crosslinks in a chronic stage, the friction can be given forcefully and for a dura tion of 15-20 minutes, whereas in more recent lesions the technique must be applied more gently and for a shorter duration. Friction to a muscle belly is always given with the muscle well relaxed. In recent tears, especially in the large muscles of the lower limb, friction is followed by active or electrical con tractions with the muscle in a position of maximal relax ation and without weight bearing, so that tension does not fall on the healing breach. To avoid early recurrence, friction is given for 1 week after all clinical tests have become negative. During the period of treatment, all movements or activities that bring on pain should be avoided by the patient.
CH APTER 5
Theoretically, friction can be used for all muscle belly lesions. However, some lesions respond so well to local anaesthetic infiltration that friction is not used. This is the case in type IV tennis elbow (lesion at the muscle belly of the extensor carpi radialis). On the other hand, some times no alternatives exist to treatment with deep trans verse friction (Box 5.1). A lesion of the subclavius or intercostal muscles for instance can be treated only by deep transverse friction. M usculoten d i nous j u nctions. It is a common clinical experience that all musculotendinous junctions (contain ing both muscular and tendinous fibres) throughout the whole body can be treated only by deep transverse fric tion. It would seem that no al ternatives exist: local anaes thetics, so curative for some lesions of muscle bellies, and steroids, so effective for tenoperiosteal lesions, have not the slightest effect on musculotendinous lesions, whereas deep transverse friction usually has.
All overuse tendinitis can be treated by deep massage except for the tenoperiosteal origin of the exten sor carpi radialis brevis (type II tennis elbow), which is best treated by an infiltration with corticosteroid or, in refractory circumstances, sometimes by manipulations. Tenosynovitis also usually responds well to deep transverse massage. In this condition, occurring in long tendons with a sheath, inflammation and roughening of the gliding surfaces of both tendon and sheath give rise to pain and sometimes to crepitus. Friction rolls the sheath around the stretched tendon, so facilitating func tional movement between the tendon and its sheath. The technique is useful in both acute and chronic lesions. Lesions at the tenoperiosteal insertion can be treated either with corticosteroid infiltrations or with deep trans verse massage. Either one or the other will sometimes be the treatment of choice. Corticosteroid suspension quickly converts an inflamed and painful scar into one free of inflammation. However, the recurrence rate is rather high, between 20% and 25%.3 The aim of the massage is to get rid of the self-perpetuating inflamma tion by breaking up the disorderly scar tissue and adhe sion formation by converting it into properly arranged Tendons.
Box 5.1 Muscle belly disorders that can be treated only by deep transverse friction Subclavius Brachialis Su pinator Add uctors of the t h u m b Interosseus m uscles o f the hand Intercostal muscles Oblique muscles of the abdomen Interosseus m uscles of the foot
-
P R I N C I PLES OF TREATM E N T 97
longitudinal connective fibres. This takes longer but once cure is achieved there will be less tendency to recurrence. It may therefore be a policy to start treatment with infiltrations but if the trouble recurs after a few months to substitute with massage. As a rule, however, friction is always selected as the treatment of choice in athletes or when the tendon is weakened (partial rupture). It cannot be denied that repeated use of corticosteroids, even in small doses and correctly applied, temporarily weakens a tendinous structure. Steroids also take away inflammation and pain, so giving the patient the false impression of being cured. The combination of a weakened tendon and abolition of pain can be disastrous - rupture may ensue. There exist also a few conditions that seem to respond only to deep transverse friction. Steroid infiltrations are useless here. This is so in tendinous lesions of the interosseus in the hand and at the quadriceps expansion at the patella. Lesions in the tendinous body, either traumatic or resulting from overuse, are contraindications for infiltra tion with corticosteroids. Ruptures have been reported after intralesional steroid infil trations of long tendons and therefore deep frictions are the treatment of choice here.21,22 It is obvious that during the whole period of treatment of tendinitis, tenosynovitis or tenovaginitis, the patient must avoid all activities that provoke the pain, especially the loading of the affected contractile tissue. Ligaments. Transverse massage is an excellent treatment in acutely sprained ligaments, especially in ligaments of the knee and ankle. The background, mode of action and technique differ considerably and depend on the stage of the lesion. It has been explained (see p. 46) that early mobilization is extremely important for swift and ful l recovery of liga mentous sprains. However, in advocating this, one main difficulty is encountered: the intensity of the initial inflammatory reaction. The slightest movement causes pain which forces the patient to immobilize the joint and the ligaments. However, during immobilization regener ating fibrils quickly start to form randomly organized scar tissue, leading to crosslinks and adhesion formation. This problem can be solved by gentle transverse frictions. RhythmiC movement across the inflamed l igament eases the pain and the tissue can be moved to and fro in an imitation of its normal behaviour. In these recent cases the friction need not last long nor be very vigorous - 1 or 2 minutes of daily gentle trans verse sweeping movement over the regenerating fibrils is enough. As pain diminishes over subsequent days the intensity of friction is progressively increased to about 4-5 minutes for 2 or 3 days and finally to a full duration
98 SECTION ONE - GENERAL PRINCIPLES
of 1 5-20 minutes. From the third day, friction is followed by passive and active movements within the limits of pain to maintain normal gliding of the ligament over adjacent bones. When the lower limb is involved, the patient should be instructed to walk as normally as possible but withou t provoking too much pain. In chronic ligamentous lesions, frictions are also used but in a totally di fferent way. Here adherent scar tissue has been allowed to form abnormal attachments as the resu lt of healing during a period of insufficient move ment. As a result of the reduced mobility of the ligament, vigorous use of the joint resprains the ligament and i n due course leads to recurrent sprains. Treatment will consist of rupturing the adhesions by manipu lation, for which vigorous deep friction to the site of the adhesions prepares the ligaments. The massage weakens and desensitizes the structure, making the forced movement practicable and painless. Experience has shown that particular ligamentous lesions can be trea ted only by friction. This is the case for the posterior carpal l igaments at the wrist and the tibio talar ligaments. Deep transverse friction can be applied to the capsules of the trapezium-first metacarpal joint, the temporomandibular joint and the cervical facet joints. The indication is traumatic arthritis or osteoarthrosis. Resul ts are fa ir, provided the arthrosis is not too advanced. Indications and contraindications to friction are outlined in Table 5 . 1 . Joint capsu l es.
CONTRAINDICATIONS Extensive ossification in muscles, tendons, ligaments or capsules is a bar to all active treatment. However the minor calcifications that may occur after a sprain can be managed by friction. In supraspinatus tendinitis, calcification is regarded as responsible for complaints Ossification a n d calcification of soft tissues.
Table 5.1
Indications and contraindications to friction
Indications
Contraindications
Diagnostic difficulties Preparative massage Therapeutic massage: • To muscle bellies • To musculotendinous junctions • To tendons • To ligaments • To joint capsules
Ossification and calcification of soft tissues Bacterial and rheumatoid-type tendinitis, tenosynovitis and tenovaginitis Skin problems such as ulcers, psoriasis or blisters Neighbouring bacterial infection Bursitis and disorders of nerve structures Haematoma, if large
when the insertion is very tender to touch and a radi ograph shows calcification. These findings are a contra indication to friction. In contrast, when calcification is present in the absence of severe tenderness, transverse massage can be given. Bacterial and rheu matoid-type ten d i n itis. tenosynovitis.
All types of bacterial and rheumatoid dis orders, no mater at what stage of inflammation, are absolute contraindications to friction. tenovag i n itis.
Skin problems such as u lcers. psoriasis and
blisters.
When normal skin has been abraided - sometimes by friction - massage should not be given. In skin disorders, it must be abandoned when stable skin-finger contact becomes impossible and friction aggravates the skin problem. Neighbouring bacterial i nfection. Because these may be reactivated by or may extend if friction is used, it must be postponed u ntil the infection has resolved. B u rsitis and d isorders of nerve structures. When bursitis is m istaken for a tendinous or ligamentous disorder and friction is given the problem will either increase or, at best, the pain will remain unchanged - it certainly will not improve. Friction to a nerve is also harm ful. Haematoma. A haematoma in a muscle belly or after an ankle sprain is not a contraindication to friction. Even if the haematoma is the result of deep friction, treatment may be continued unless the effusion is large.
TECHN IQUE Introduction Transverse massage is not an easy technique. In order to produce results, three conditions must be satisfied. First, the therapeutic movement should be applied to the exact site of the lesion which may occupy only a very small volume of tissue. In other words, an identification of the site to within 1 cm must be achieved which relies entirely on clinical diagnosis and palpation of the lesion, based in turn on anatomical knowledge. In some instances it will be necessary to palpate carefully the entire structure at fault so as to find the point that reproduces the patient's pain. Secondly, friction shou ld be appl ied transversely across the longitudinally orientated fibres, with sufficient sweep to reach all the affected tissue and firmly enough to produce movement between the individual connective tissue fibres of the affected structure. Third, the movement can only reach deeply seated structures if the deep friction technique of Cy riax is used; that implies attention must be paid to different elements such as the position of the patient and of the
CHAPTER 5
therapist's hand, which fingers are used, the amount of pressure, the du ration and frequency of the sessions. The patient's skin and the therapist's finger must move as one, so that the deep layers of the skin move over the affected fibres. Therefore all cream, ointments, powder or any other procedure, such as previous heat, that makes the skin sweat, must be avoided . Six to 12 treat ments are normally necessary. Except in acute ligamen tous di sorders they are not given more often than every other day because otherwise the site of the lesion may still be too tender from the previous treatment to perm it adequate massage.
Position of the patient The patient's position must be comfortable because it must be maintained for up to 15-20 minutes. Sitting or lying is preferable. The lesion must be brought within finger's reach. In some structures this can be easily attained but others such as the supraspinatus insertion and the anterior aspect of Achilles tendon, require more specific positioning of the patient. In addition, positioning must place the affected struc tu re under the required amount of tension. Full relaxation is necessary for a muscle belly in order not only to treat its surface but also to access a deeply seated lesion. Tendons with a sheath most be kept taut otherwise friction will be ineffective between tendon and sheath. The same applies in ligamentous lesions, which are also placed in tension but within the limits of pain. Position of the therapist and the hands The bodily position of the patient should be the most comfortable and least tiring for the therapist. Working height is of chief importance, so an adjustable high-low couch is ideal. To have some economy of effort the thera pist should adopt a position that utilizes body weight to a maximum. Usually this is standing and with the patient on a slightly lower plane. The therapist should avoid flexed positions. The shoulder should also not be in abduction because this quickly leads to pain and cramp in the neck and shoulder girdle. Massage is performed by the whole arm and is not just an activity of hand and digits. Movement is generated in the shoulder and conducted via elbow and forearm to the digits. One set of muscles is used to apply force and another to provide movement, for example pressure with the fingers, movement with the arms. Digits, hand and forearm should generally form a straight line and are kept parallel to the direction of movement. The majority of friction techniques are performed in two phases: an active movement, usually as a result of flexor muscular activity and a passive movement, when the arm and hand are returned to the starting position. At the end of the passive phase there should also be a
-
PRINCIPLES OF TREATMENT 99
moment of rest during which the therapist fully relaxes the muscles. There exist a variety of ways the hands can be used depending on the tissues to be treated and the surface worked on. The wrist and metacarpophalangeal joints should be kept in an almost neutral position. The inter phalangeal joints are slightly flexed to avoid traumatic arthritis. Three main techniques can be distinguished. These are used in the treatment of dense, round or flat collagenous bundles (tendons or ligaments) and in the treatment of tenosynovitis. The active phase is a sweep with the tip(s) of one or two digits across the tendinous structure. During the passive relax ation phase the finger is returned to the starting position, without losing contact between finger and skin. Movement i s with the arm; friction is given by use of the pulpy part of the finger (Fig. 5.2). In la rge lesions, as in
To-a n d-fro moveme nts.
Figure 5.2
Friction to the supraspinatus tendon: counterpressure is by the thumb.
100 SECTION ONE - GENERAL PRINCIPLES
peroneal tendinitis, two or three adjacent fingers are used together. In deep-seated lesions as in tendinitis of the long head of biceps in the bicipital groove or at its inser tion on the radius or in infraspinatus tendinitis, the thumb performs friction. Counterpressure is usually provided to enable a good sweep. The finger(s) applying coun terpressure and sta bilization are most important in bringing those applying friction into the right position and also determining the direction of the friction. The thumb is used (to give counterpressure) when the sweep is performed by a movement of the index rein forced by the middle finger or the middle finger aided by the i ndex finger. When the thumb does the massage, counterpressure is from the fi ngers (Fig. 5.3). The most common way of applying friction around a round edge on a flat surface is to use the index rein forced by the middle finger. Sometimes the opposite is done: the middle finger is reinforced by the index. Sometimes counterpressure is not given, for example in friction to the quadriceps expansion or inter costal muscles. Pronation-supination. This technique is often used where the lesion is difficult to reach: the anterior aspect of the Achilles tendon, popliteus tendon and the dorsal interossei of the metacarpals. Massage is performed with the pulpy part of the third finger (long finger), reinforced by the index finger. The long finger is used because its long axis is the prolongation of the axis of pronation-supination rotation of the forearm (Fig. 5.4). The active phase is usually on supination. No counter pressure is given. Caution is taken not to move the finger on the skin but rather to move the skin and the fingertip as a whole. The passive phase is the pronation movement that brings the frictioning finger back to the starting position without losing contact with the skin. Pinch g rip. This is the normal technique for a muscle belly. The pinch is between the thumb and the other fingers. The muscle is fully relaxed. The fingers are placed at one side of the affected area and the thumb at the opposite side (Fig. 5.5). By drawing the fingers upwards over the affected area, the therapist feels the muscle fibres escape from the grip until only skin and subcutaneous tissue remain. During the passive phase the fingers are slightly relaxed and moved downwards into the previous deep position where the same movement starts again. Sometimes the same technique is used in tendinous lesions, for example, at the sides of the Achilles tendon.
No movement between finger and skin is allowed Deep friction can only be effective when skin and sub cutaneolls fascia are moved over tendon ligaments or
Figure 5.3
Friction to the infraspinatus tendon: counterpressure is by the fingers.
muscles. No movement is allowed between the thera pist's finger and the patient's skin. If movement occurs between finger and skin, blistering soon takes place and usually indicates faulty technique. Sometimes it can be avoided by keeping the skin dry by the use of 95% alcohol in water and / or by placing a piece of cotton in between the finger and the skin. In the obese, subcutaneous soreness and / or ecchy mosis may occasionally occllr and sometimes a nodule may form. For this reason the finger should not be i n continuous contact with the same area but should
CHAPTER 5
(a) (a)
-
PRINCIPLES OF TREATMENT 101
(b)
(b)
Figure 5.4 Active phase of pronation-supination friction technique to the anterior aspect of the Achilles tendon. A, starting position; B, end of supination (active) movement.
displace the skin slightly to one or other side, before pressure is applied .
Direction of friction must be transverse to the tissue fibres Longitudinal massage improves the circulation of blood and lymph but has no effect on musculoskeletal lesions. On the contrary, because lesions of tendons, muscles and ligaments are normally caused by a longitudinal force, longitudinal massage can possibly be harmful in that it may separate the ruptured ends further. To restore and / or maintain full mobility of a lesion, massage must be given across the fibres, so moving all fibres in relation to each other. To achieve this, the therapist must have a good anatomical knowledge of the direction of the fibres. Sweep The main goal of friction is to move fibres in relation to each other and adjacent structures. Enough sweep must be given to the friction for this purpose, so the frictioning
Figure 5.5 Pinch grip friction to the Achilles tendon. A, starting position; B, end of active phase.
finger starts at the far side of the lesion, glides over it and ends at the near edge. Pressure alone, however hard and painful it may be, is totally ineffective. Adequate sweep is sometimes limited by the amount and elasticity of the overlying skin. Initial displacement of skin over the lesion from the near to the far side may help increase sweep and reduce the risk of blistering.
102 SECTION ONE - GENERAL PRINCIPLES
Amount of pressure Over recent decades, friction has been held in some dis repute i n that it was perceived by some as synonymous with very pai nful treatment. Though it cannot be claimed as wholly pain-free, the pain should not be unbearable. When excessive pain is provoked, this is usual ly the result of a fai lure to understand the meaning of the term 'deep', which means 'as deep as needed to reach the lesion'. Many therapists misi nterpret this in such a way that they feel that they always have to work hard physi cal ly, which obviously leads to pain and may do more harm than good . The amount of pressure applied depends on three elements. tha t friction must al ways reach sufficient depth to move the affected fibres in relation to their neighbours and sometimes the underlying bone or capsule, increased pressure must be applied to deeper structures. The 'age' of the lesion: recent sprains and injuries require only preventive friction because crosslinks or adhesions have not had time to form. In long standing cases more pressure i s needed to get rid of these. However, pressure should always be associated with movement and should not replace it because pressure alone is both painful and ineffective. The tenderness of the lesion: in severely inflamed lesions that are very tender to touch, friction with the usual amount of force may be very painful . Pain can be avoided by starting with a minimal amount of pres sure - just enough to reach the lesion - and progres sively increasing the force as treatment proceeds.
Treatment is stopped once the patient is pain-free during daily activities and functional tests are totally neg ative. Local tenderness may persist longer but disappears spontaneously because it is the outcome of repetitive hard pressure. However, in a minor lesion of a muscle belly, massage is continued for 1 week after full clinical recov ery to preven t recurrence (see Table 5.2; see also Box 5.2).
Box 5.2 Summary of deep friction technique 1
• The depth of the lesion:
•
•
In order to avoid painful sessions of deep transverse friction it is good practice to grade its application. Begin with a sweep that is gentle and continue this for a few minu tes; some numbness of the treated area foll ows which a llows sl ight intensification of the amount of pressure, which in turn leads to more numbness. Finally, it will be possible to give effective massage that is practica lly pai nless to the patient.
Duration and frequency Friction is usua lly given for about 1 0-20 m inutes and, because of tenderness, on every second day. The ideal timing of the next treatment is when local tenderness caused by the previous session has resolved. If tender ness persists after 2 days, the pressure used during fric tion should not be diminished but the i n terval between sessions must be increased. Massage im mediately after a l igamentous sprain or a mi nor muscular rupture may be applied daily for the first week but should be of very low intensity and short duration.
Position of the patient must: Be comforta ble B r i n g lesion wit h i n fi nger's reach Be a p p ropriate for the type of structure at fault: • tendon/l igament under tension • musc le bel ly: relaxed
2 Position of the therapist must: Be comforta b l e Facil itate economy o f effort: • a lternati n g active and passive ph ases • usi n g l a rge muscles 3 Use of the hand: To-an d-fro movement Pronation/supi nation Pinch g r i p
4 Use of the fingers: Counterp ressure Friction usi n g the fingers
5 Other points: F i n gers a n d ski n move as one unit D i rection of friction must be transverse Sufficient sweep must be used The pressure must be a p p ropriate Duration and frequency must be ap propriate
PASSIVE MOVEMENTS Treatment by passive movement is otherwise known as mobilization. It cannot be performed by the patient and requires the i ntervention of a therapist. Depending on its velocity and the range of movement that is aimed for, it can be graded as A, B and C mobilization. • •
•
Grade A mobilization is a passive movement performed within the pain-free range. Grade B mobilizations are passive movements performed to the end of the possible range. The latter i� indicated by a n end-feel (see p. 43). All stretching and traction techniques are grade B mobil izations. Grade C mobilization is a mini mal thrust with a high velocity and over a small amplitude. It is performed at the end of the possible range, i.e. the moment the therapist has reached the end-feel . Another word for grade C mobilization is manipulation.
CHAPTER 5
Table 5.2
-
PRINCIPLES OF TREATMENT 103
Transverse massages/modalities
Indication
Duration (min)
Pressure
Frequency
Diagnostic Acute ligamentous Subacute ligamentous Chronic ligamentous Ligamentous adhesions Tendinitis - tenoperiosteal Tenosynovitis Musculotendinous Myosynovitis Muscular tear - acute
1 5-20 30 sec 3-1 0 1 5-20 1 5-20 1 5-20 1 5-20 1 5-20 1 5-20 5-1 0
High Very low Low High High Grading Grading Grading Grading Low
Once Daily Daily-3tlw 3t!week Once 3t!week 3t!week 3t!week 3t!week Daily
Muscular tear - chronic Capsular lesions
1 0-1 5 1 5-20
High Grading
3t!week 3t!week
Combined treatment
Effleurage before and active movement after the treatment Passive grade B movements after Passive grade B movements after Before manipulation (grade C mobilization) Relative rest - unloaded active movement Relative rest - unloaded active movement Relative rest - unloaded active movement Relative rest - unloaded active movement Procaine infiltration before and active unloaded contractions after treatment Active unloaded contractions after treatment
3Vweek. three times per week
INDICATIONS Grade A mobilizations Passive movements within the pain-free range are usually called for in the treatment of injured connective tissue. A com prehensive literature evaluation and meta-analysis of experimental studies of the past several decades have demonstrated that regeneration of injured connective tissue is significantly better with the application of con tinuous passive motion. If the healing tissues are not loaded, regeneration results in unstructured scar tissue. Under fu nctional load, the collagen fibres are oriented in a longi tudinal direction and the mechanical properties are optimized.23 Grade A mobilizations are therefore applied early i n the treatment o f sprained ligaments t o promote orienta tion of the regenerating fibres. They are given in conjunc tion with gentle transverse massage and within the pain-free range. Care should be taken not to bring the fibres under longitudinal stress in order not to d isrupt the healing breach . The movements are of short duration but repeated often.
To promote hea l i n g of i n j u red con nective tissue.
Distractions at the shoulder. Grade A mobilizations are also used on the capsule of the shoulder in stage III arthritis when stretching and intra-articular steroids are contraindicated (see p. 309). In this condition, long-stand ing stimulation of the nociceptors has increased neuro sympa thetic activity, giving rise to vasoconstriction, muscle spasm and pain. Gentle and rhythmical grade A movements are per formed in such a way that the fibres are stretched longi tudinally, stimulating the mechanosensor mechanisms i n the joint and s o inhibiting somatosympathetic reflexes
that are co-responsible for the increased inflammation of the joint. Some cases of lumbago show per sistent spinal deviation even after the pain has ceased . A quick thrust manipulation so effective in relief of pain is not effective in correcting the remaining deformity but sustained translatory gliding in the opposite direction is most helpful. The movement is performed slowly and care is taken to keep the gliding within the pain-free range (see p. 890).
Deformity correction.
Red uction of an i ntra-a rticular d isplacement i n a periph
When a meniscus or some other piece of intra articular cartilage (with or without an osseous nucleus) becomes displaced and locks a joint, the logical treat ment is either to remove it or manoeuvre it into such a position that the joint can again move freely over a normal range. The technique needed for the latter is usually a series of manipulative movements which nor mally contain elements of traction combined with move ments of rotation and flexion or extension. In general, these are first performed in the less painful direction of movement and repeated several times with progres sively increasing force. Unlike manipulations in the spine, the manoeu vre to reduce an intra-articular loose body is not a grade C mobilization because the movement is not performed at the end of range nor does it contain a 'thrust' element. The flexion-extension movement is over a wide range and stops before the end-feel is reached. The rotation movements are performed to the end of range where end-feel is sensed by the therapist. T he ' manipu lation of an intra-articular d isplacement in a peripheral joint' is therefore a combination of grade A and grade B mobilizations. eral j o i nt.
104 SECTION ONE - GENERAL PRINCIPLES
Grade 8 mobilizations normal range at the j o i nt. Paralysed muscles may lead to a loss of normal range of motion of the corresponding joint. This can be avoided by gently stretching the capsule, starting as soon as possible after the onset of paralysis. The approach should also be con sidered for joints that have been injured or subjected to surgery. In such circumstances, there may be the paradox that immobilization is needed for a fracture to heal but that movement is required to prevent loss of capsular elasticity. Often the problem can be solved by adapting the technjque of capsular stretching so that it does not influence the site of the fracture. To m a i nta i n a
Grade B mobilizations may be required to stretch the joint capsule in non-acute arthritis and in early osteoarthrosis. The techruque will be further referred to as capsuLar s tretching. Capsular stretch ing is particularly u seful in shoulder and hip joints but is applicable in all 'non-irritable' capsulitis. The condition is characterized by: To stretch the capsule of a joi nt.
• •
a limitation in the capsular pattern (see p. 84) demonstration of a hard-elastic end-feel to restricted movements (see p. 85).
In the very beginning of an arthritis, muscle spasm forces the joint to be held in a position of ease, so restricting movement in some d i rections more than i n others (see Capsular pattern, p. 84). Immobilization and infla m mation cause d isordered deposition of collagen fibres in the joint capsule and lead to the formation of capsular adhesi ons, which in turn are responsible for more restriction of movement and pain. Stretching aims at restoring mobility and function by breaking mi cro-adhesions and producing elongation of the short ened capsu le. To be applicable, however, the ligamen tous end-feel must be reached before the protective muscle spasm begins. To be successful, the therapist should therefore be able to d ifferentiate between an elastic and a spastic end-feel. The technique is a slow and steady pressure, per formed at the end of range over about 30 seconds to 1 m inute with as much force as is reasonable for the patient to bear. Tension is slightly diminished for a few seconds, so affording the patient some respite, and then again increased. From time to time the procedure is completely i n terru p ted . If tension i s released too qui ckly, some pain may be felt and it is therefore wise to bring the limb back into neutral position under traction. The technique is not painless. The stretching causes some m icro-ruptures, which result in an inflammatory response and after-pain that lasts for a few hours. Normal ly, capsular stretching is given for 15-20 minutes, three times a week. The therapeutic effect is slow.
Capsular stretching can be preceded by application of heat, either through short-wave diathermy or ultrasound. This can relieve some pain and seems to lower the viscosity of the collagenous tissue, allowing more move ment for less force. In vivo studies on the effects of heat on ligament extensibility have shown that sustained force applied after elevating tissue temperature produced sigruficantly greater residual elongation.24, 25 Marupulation of a joint capsule u nder anaesthesia is a grade C mobilization and is only considered for post operative intra-articular adhesions. A joint that has been marupulated under anaesthesia requires daily intensive mobil ization immediately afterwards in order to prevent the formation of new intra-articu lar adhesions. Children with short calf muscles can be helped by sustained stretching. The procedu re consists of a series of alternating passive stretchings and active contractions. Stretching is maintained for about 8-10 seconds and is followed by full relaxation and active con traction of the muscle. These alternating movements are performed six to eight times per session, preferably daily but at a m irumum of three times a week. The earlier the stretching is started, the better the result. Above the age of 1 5 not much improvement can be expected.
To stretch a muscle.
Traction is u sed to separate articular su rfaces from each other and can be e mployed in two ways: as an accessory to manipulation or as the sole treatment. Reducing a d isplaced fragment is obviously easier when the bone ends between which it lies are pulled apart. If the fragment projects beyond the articular edge, tauten ing of the l igaments and capsule also provides a centri petal force. In that traction diminishes the pressure on the fragment, pain decreases, which allows the patient to relax the muscles moreY In the cervical and thoracic spines, traction is a bui lt-in safety measure for protect ing the spinal cord during manipulation (see below) a lthough the use of traction for this purpose and at these sites does not imply that manipulation can be per formed on a basis of ' try and see what happens' wi thout a proper diagnosis.26 I n the spine, traction is used as the sole treatment only in nuclear d isc protrusions, willch are rare at the cervical and thoracic levels but are more common in the lumbar area. Spinal traction is a lways mechanical and is performed with the help of a harness (lumbar or low thoracic) or a sling (cervical or upper thoracic). Spinal traction d istracts the intervertebral disc spaces. It also pulls the apophysial joints apart and slightly widens the intervertebral foramina .26-3o At the same time, negative intradiscal pressure is produced with centripetal 'suction' on any protrusion. The posterior longitud inal ligament is tightened, willch may help reduce a displaced fragment. All these elements are helpful in the progressive reduc-
Traction.
CHAPTER 5 - PRINCIPLES OF TREATMENT 105
tion of a nuclear disc protrusion. Reduction of herniated bulges has been demonstrated on epidurography30-32 and on CT scan33 during and after traction. The effect of traction depends on the amount of force applied, the length of time per session, the interval between two sessions and the total number of sessions.34
Grade C mobilizations Grade C mobilizations or manipulations are forceful passive movements, performed at the end of range. Spinal manipulations are mainly to interrupt discodural or discoradicular contact. At the peripheral joints the purpose of a manipulation is to rupture unwanted adhesions between bone and ligament or bone and tendon or to reduce small bony subluxations in wrist or foot. Rupture of l i g a me ntous a d hesions. Small ligamentous adhesions sometimes develop between a healing liga ment and bone. They usually result from a sprained lig ament that has been immobilized during the healing process. The usual presentation is at the lateral liga ments of the ankle and at the medial collateral ligament of the knee. The clinical features are local pain during exertion and a small limitation of movement in one direction only. The adhesions can be ruptured by a high velocity, small-amplitude thrust manipulation, after preparation of the affected ligament with intensive deep transverse friction. The joint is stretched as far as possible in the limited direction and manipulated with a single firm thrust, during which a typical 'snap' is often heard. Harm is not caused to the ligament nor to the other parts of the joint because the adhesions bear the brunt of the force. The manipulation is almost painless and after-pain is not to be expected. A successful manipulation should achieve an immediate result. Active movements during the fol lowing days to maintain function should be highly encouraged .
In type II tennis elbow (tendinitis of the attachment of the extensor carpi radialis brevis), an adherent and disorganized scar tissue causes a self-perpetuating inflammation. The manipula tion aims to rupture the adhesions and produce a permanent elongation of the tendon. The high-velocity manoeuvre is preceded by thorough deep transverse fric tion in order to numb and to weaken the spot. The manipulation is performed only once per session; 1 0-15 sessions may be required to achieve result. Rupture of tenoperiosteal adhesions.
A subluxation of one of the carpal bones or of the cuboid bone can easily be reduced by digital pressure combined with translatory movement during traction.
To reduce a bony subl uxation.
Spinal manipulative therapy is a major part of treatment techniques in orthopaedic medicine and will be discussed thoroughly later in this chapter.
Manipulation o f the spine.
Contraindications to forced movements Contraindications to spinal manipulations are discussed later in this chapter. Capsular i nfla m m ation. Forced movements should not be performed when signs and symptoms of capsular inflammatory activity are present. These are spontaneous pain, pain especially at night, wide reference 'of pain, inability to lie on the affected side at night or to bear weight on the affected side. Local warmth and effusion are other pointers of a highly inflamed joint. However, if these symptoms and signs are present but the rest of the clinical examination demonstrates internal derangement (e.g. knee, hip, ankle), manipulation is indicated and can safely be performed. M uscle spasm. Grade C mobilizations should never be applied to a joint that is protected by a muscle spasm. Grade B mobilizations may be used unless the end-feel of the movement that is intended to be forced through is also spastic.
Grade B mobilizations, for instance stretching of the shoulder or hip joint in elderly people, should always be carried out with caution for fear of fracturing the humerus or the neck of the femur.
Severe osteoporosis.
J o i nts a n d
l i g a m e nts
n ot
u n d e r v o l u nt a ry t e n s i o n
Mobilization is also contraindicated for those joints and ligaments on which the tension is not under voluntary control. This is the case for the acromioclavicu lar, the sternoclavicular and the sacroiliac joints and the sacrococcygeal ligament. control.
MANIPULATION OF THE SPINE Introduction Spinal manipulative therapy includes all procedures of mobilizing or adjusting the spine by means of the hands. As in the peripheral joints, grade A and B mobilizations are movements of low velocity with varying amplitude but remaining within physiological limits and within the patient's tolerance and control. A manipulation or grade C mobilization usually implies a single thrust of high velocity performed at the end of a passive movement after the 'slack' has been taken up, and over a small amplitude. It goes beyond the physiological limit but remains within the anatomical range. Precision of the movement and control of the applied force are reguired.35 Spinal manipulative therapy is a valuable method in the treatment of mechanical
106 SECTION ONE - GENERAL PRINCIPLES
spinal disorders. Although it has not been scientifically validated, some studies have shown beneficial effect.36-39 However, its potential benefit should not be overesti mated and the indications must be well defined and based on a sound clinical diagnosis. It must never be done as a test to see if it is effective. Therefore it should not be used on all those with back and neck pain although it may well cure a proportion who actually require it. To use McKenzie's words: Even if you have a hammer in your hand not everything you see is a nail. Therefore indiscriminate use of spinal manipulative therapy must not be made if the criticisms that have been justifiably levelled at chi ropractice and osteopathy are to be avoided. The development of postgraduate courses in manipula tion is welcome, al though some have overvalued the benefits of manipulative therapy. All who undertake man ipulation have experienced the feeling of pride and joy in producing cure. It is the duty of those who have more experience of the benefits and limitations of manipu lative therapy to moderate the understand able enthusiasm of those entering the field - a few successes may quickly lead to the temptation to manipu late every patient for any d isorder.4o M a nipul ation ei ther helps quickly or not at a l l . Therefore if improvement does not occur after one o r two sessions, manipulation is not likely to be successful and it is pointless to continue with it.
Historical note Manipulation is as old as medicine and embraces both medicine and mankind in general. In recent times, the medical aspect has become structu red and d ifferent methods have been developed which are subject to con troversy and competition. The concept of osteopathy was introduced by T. Still (1 828-1 9 1 7) and developed out of frustration with traditional medicine. His ideas were based on two principles: ( 1 ) the body has within itself the processes to combat all disease, and (2) the cause of all disease is dis located bones, abnormal ligaments or contracted muscles with consequent mechanical pressure on blood vessels and nerves. Diagnosis is mainly based on palpation for restricted spinal mobility and treatment consists of a manipulative system in which joints are forced by a distant leverage. Cure is sought for all kinds of disorders of both visceral and musculoskeletal nature.26 Osteopathy.
This method was started in 1 885 by D Palmer. It is based on a revision of techniques that origi nated with Hippocrates and is also i n fluenced by osteopa thy. Chiropraxy was long regarded as maintain ing osteopathic dogma in its most primitive form and having a strong commercial cha racter.
Chiropraxy.
Chiropractors also claim to cure visceral diseases via the musculoskeletal system. Diagnosis is made on palpa tion for vertebral displacement and manipulative pres sure is applied directly to the bone. This term describes the system of d iagnosis and treatment of musculoskeletal lesions in tro duced by J.H. Cyriax. It is the system on which this book is based. Diagnosis rests on careful history and functional examination. Treatment depends mainly on the type of lesion, and manipulation is applied only when indicated. In spinal manipulation, Cyriax proposed a fixed set of high-velocity, small-amplitude thrusts performed at a certain distance from the lesion and, characteristically for this method, usually under strong traction. The objective of Cyriax's spinal manipul ative techniques is to alter the discodural or discoradicular interaction by moving a dis placed cartilaginous fragment away from the sensi tive dura mater and dural nerve sleeve. Spinal rotation manipulations apply a torsion stress throughout a whole part of the spine, not only at just one level. With an intact posterior longitudinal ligament and annulus fibrosus, some of this torsion force exerts a centripetal force by suction on the protruding disc material.41 This effect is not confined to one level and fu ll reduction is not absolutely necessary for pain rel ief, in that when contact between dura and disc has ceased the problem is fre quently solved. Orthopaed ic medicine.
Treatment is characterized by rhythmic repeated movements within the physiological range. Oscillatory techniques had already been used by E. Cyriax (father of J.H. Cyri ax) bu t were more widely employed by Maitland and later slightly changed by the different schools of manual therapy (Cyriax:3 p. 40). Pressure is applied to what is believed to be the appro priate level.
M a n u a l therapy.
Orthopaedic medicine technique Before any manipulation is done an exact diagnosis must be made. The decision to manipulate is followed by choice of the right manoeuvre. The patient is put in a comfortable position and the manipulator adopts a stable stance. The floor and shoes shou ld not be slippery, so that there is no risk of inappropriate movement. Attention must be given to the following general matters, which are important for all manipulations. d u r i n g m a n ipulation . Most types of spinal manipulation in orthopaedic medicine are performed u nder traction. For the cervical and thoracic spine, trac tion is applied by the manipulator with the help of a fixing belt or by one or two assistants. At the lumbar level, traction is usually already built in in the ma noeuvre. Traction facilitates the reduction of a displaced
Traction
CHAPTER 5 - PRINCIPLES OF TREATMENT 107
fragment and provides an important safety element against the possibility of a protrusion contacting the spinal cord during manipulation. All spinal manipula tions are performed over only a small ampli tude. Therefore all 'slack' must be taken up by moving the ver tebral joints passively to the end of the normal passive range of movement. At this stage it is absolutely neces sary to have a clear idea of the end-feel, which is nomi nally elastic for the entire spine. An end-feel that does not correspond with this - muscle spasm, or hard or empty end-feel - is an absolute contraindication to any manipu lation and the manoeuvre is not continued. End-feel o n taking u p the 'slack'.
Final thrust. Immediately after the slack has been taken up in the surrounding tissues, a minimal amplitude, high-velocity thrust is given to affect the target tissue. The velocity is of great importance because tissues loaded quickly are stiffer so that the manoeuvre will affect only the displaced fragment of disc and will not damage lhe surrounding structures.42 The amount of force used for the final thrust depends mainly on the patient and manipulator in that a tall manipulator will have to use less force in a small patient and vice versa.43 The length of the lever (see l ater) is also important. The force should always be kept reasonable and may be progressively increased, according to the immedia te resul t. The manipulation thrust is often accompanied by an audible 'pop' .28,44 Although it is a common belief that pops or clicks are provoked by the formation of a tempo rary vacuum, as occurs in small peripheral joints put under traction,4S-47 this is not definitely established for the spine. An alternative and more likely explanation is movement of cartilaginous fragments, as may be heard during manipulation for a loose body in the knee or hip. If the clicks were simply the result of the collapse of a vacuum they should also be - but are not - heard during mechanical traction, in which the traction force is much higher.
The patient and not the manipulator is the arbi ter.48 Depending on the immediate outcome, the therapist decides whether to repeat the same manipulation, proba bly with increased strength, to try another manoeuvre or to refrain from further manipulation. It should be appreciated that after successful manipu lation the anatomical lesion is still present: a piece of cartilage although put back in place or into a neutral position persists and may redisplace. For this reason, those who undertake mani pulation should note the results obtained and what manipulations were used, in case the patient returns w ith recurrence. Figure 5.6 outlines the assessment of spinal lesions and their manipulation.
Selectivity of a manipulative treatment Selectivity must be considered both in d iagnosiS and therapy. Osteopaths and manual thera pists claim to have developed both the cl inical skills to localize by palpation the exact site of fixation or by locking - the so-called hypomobile segment - and are able to perform the manipulation at the required level. Diagnosis is mainly based on segmental mobility tests: joint play, springing test or tests of passive physiological movements. Movement can be tested by exerting local pressure at one side of a vertebra while counterpressure is applied to the contralateral side of the vertebra above or below. For the lumbar spi ne, it can be done with the patient on the side with both hips flexed to 90°. Small Selectivity of d i ag nosis.
Is the lesion discodural or discoradicular? Is the lesion an indication for manipulation? Are there contra indications? Does the patient have a positive attitude?
Leverage. The amount of force used depends on the length of the lever. If for example a rotation of the lumbar spine is forced via the shoulder and pelvis, the lever offered by the shoulder is the same length as that offered by the pelvis, so an equal amount of force must be used by both hands. But if the femur is used instead of the pelvis, the length of the pelvic lever doubles. The hand on the shoulder must apply double the amount of force that is used on the knee. The longer the lever, the less force is needed.
After each manoeuvre the patient is assessed, the criteria of success being the absence of symptoms and the restoration of pain-free movement.
Technique Take up the slack Check end·feel Thrust Reassess
Reassessment.
Figure 5.6
Spinal manipulation
108 SECTION ONE - GENERAL PRINCIPLES
movements of the thighs cause the lumbar spine to flex or extend which can be detected by palpation of the spinous processes. Other practitioners look mainly for palpable soft tissue changes, such as local subcutaneous thickening or exqui site tender spots (trigger points) in muscles, ligaments (iliolumba r, sacroi liac) and over bony prominences. All these are considered to be important diagnostic and therapeutic factors. The great variability in the extent of spinal stiffness between subjects, or at different levels within the one subject, makes the determination of areas of abnormally increased stiffness difficult. Increased stiffness may in fact be a normal variant and bear no relationship to the patient's presenting symptoms. Few of those advocating segmental mobility tests have seriously examined the value of their tests. They have generally presumed that the tests were useful because their patients got better.49 However, several studies have failed to demonstrate the rel iability of these tests.50-{;] Therefore it must be made clear that judgement of small changes in the range of movement of a segment, in the absence of full restriction of movement, remains a very subjective find ing, which depends mainly on the personal conviction of the exam iner rather than on objective measurements. Moreover, in soundly based tests, findings must be reproducible and must show correspondence when performed by other investigators. In the establishment of 'joint play' the inter-observer discrepancy is too large to be acceptable.62 In 1 973, Cyriax attended a demonstration in which five therapists, all of whom specialized in mobility testing, examined over a period of a few minutes a patient with a neck problem. There was no agreement between these specialists about the level of the lesion (C2, C3, C4, C5, C6 or T2), or about the direction of restriction (see Cyriax:63 p. 1 08). Simil arly, a patient who had congenital fusion of the sacroiliac joints was examined by 10 manipulators. Each had his own diagnosis, such as left anterior sacrum, right anterior sacrum and bilateral posterior sacrum, although 'the tests were very positive' for all of them (see Maigne64 and Cyriax:63 p. 363). Even if it were possible to identify with certainty local ization of the hypomobile segment, the question remains as to whether this is also the site of the lesion. Studies have shown that frequently the lesion does not lie at the joint where motion is restricted but at one which appears to be norma].54 Moreover, other disorders such as osteo phytOSiS, congenital fusion and ankylosing spondylitis all give rise to restricted movement which is usually painless. Sel ecti v i t y o f m a n i p u l at i o n. Manipulation is often accompanied by i mmediate relief of symptom s and signs which, since success has been obtained, is logically
taken as absolute confirmation of the precision of diag nosi s and treatment. Such a deduction may be - and often is - totally wrong. The only thing proved is that the manipul ation was effi cacious. The erroneous reasoning that su ccessful manipulation necessarily confirms the diagnosis has been and is still today an important argument for the false belief of some schools that manipu lation can cure all kinds of disorders even including visceral diseases. A typical example is pec toral pain, resulting from a thoracic discodural interac tion which is misd iagnosed as angina. The patient goes to an osteopath who manipulates the thoracic spine and the pectoral pain ceases immedi ately. Both patient and mani pulator, mi sled by the wrong diagnosis, will believe that the manipulation has al tered autonomic tone and cured the angina, whereas what it actually did was interrupt the d iscodural interaction. In orthopaediC medicine most manoeuvres used are non-specific long-lever manipulations. These include all procedures in which a force is exerted on a part of the body some distance away from the area where it is expected to have its beneficial effect. Levers may include the shoulder, transverse processes and parts of the skull, pelvis or thigh (Frymoyer et al:44 p. 1 594). Although some criticize the crudity of long-lever high-velocity manipula tion it should be realized that it is not elegance, impres siveness, specificity or technical difficulty which count but effectiveness and safety. Fu rthermore, the use of a lever enables the manipulator to reach the lesion more effectively. During the preparative phase - on taking up the slack - all the normal joints are brought to their anatomical end position except for the joint that is blocked. When the add itional thrust is given, the final extra pressure falls inevitably first and to the greatest degree on the deranged joint. The manoeuvre thus becomes specific even though in general the techniques are regarded as non-specific. Long-lever manipulations are in full contrast to what are called 'specific' short-lever high-velocity manipula tions. Here the goal is to act specifically at what is believed to be the level of the lesion. The spinal segment and the facet joints adjacent to the lesion are locked by moving the spine to the physiological limit of passive movement and a high-velocity small-amplitude thrust is given to the short vertebral lever (transverse process or spinous process) in the specific direction that will liber ate the restricted movement. However, it is technically not possible to lock all other joints and then to manipu late at just one level (Cyriax:63 p. 1 08). It was even demonstrated that by mobilizing the sacroiliac joints after locking of the lumbar spine, the largest movement took p lace between L4 and L5.65 Furthermore, if diagno sis fails to be absolutely right, how can there be certainty as to the exact level of the lesion to work on? Fortunately
CHAPTER 5 - PRINCIPLES OF TREATMENT 109
for those who employ 'specific' short-lever manipula tions these are much less specific than they think, because the manipulations actually cover a much larger part of the spine and so unintentionally also include the lesion. Specificity is a false attribute. The methods that claim to lead to specific localization in both diagnosis and treat ment are scientifically unacceptable. Claims of specificity only add to the p restige of manipulators who claim to feel something that cannot be felt. Manual therapists, chi ropractors and osteopaths over-complicate their teaching and often create excessive patient dependency, instead of providing the patient with independence. Indeed, patients are encouraged to return at regular intervals for pointless prophyl actic adjustment.4o We support R . McKenzie's conclusion that demystification o f spinal manipulative therapy is an urgent priority.4o Chiropraxy, manual therapy and osteopathy, however, thrive by cre ating the impression that there is something complex and exclusive about the practice of passive end-range motion that only experts in these practices can understand or have the skills to feel. The belief is strong that expertise in the understanding and delivery of spinal manipulative therapy requires 3 or 4 years' training. The main advan tages of the methods discussed in this book are that the manipulations are much simpler and at least as effective as those advocated by chiropractors, osteopaths and manual therapists. Non-specific long-lever manipula tions are quickly effective, do not take long to perform and are simple to learn. Moreover, they take only about 180 hours of tuition, provided that the student has already passed through a school of medicine or physio therapy.
Mode of action of spinal manipulation To date, the mode of action of manipulation has not been totally clarified, although many different models have been put forward. All pose unsolved questions, lack objective confirmation and a re subject to d ispute. Different attitudes towards spinal disorders determine theories and explanations. 66 Those who believe in ' posterior facet joint' syndrome as a frequent source of back pain, believe that manipu lation corrects a posterior joint dysfunction, in which either a minor subluxation of a facet together with an entrapment of the synovial fold, or of part of a small intra-articular meniscus, is held responsible, both of which may give rise to a blocked vertebral joint (Kirkaldy-Willis:28 p . 296; Mathews and Yates67 . ) Others suggest that manipulation ruptures periarticular connective tissue adhesions or that it abolishes a muscle spasm.68 In our opinion, a manipulation does not directly affect muscle spasm; instead, the latter disappears second arily when the underlying problem is solved.
It has also been su ggested th at manipulati ons influence the mechanism of cu taneou s pain tolerance as the result of release of endorphins, or th at stimulation of mechanoreceptors of the facet joint capsules, ligaments and annulus fibrosus infl u ences the neurophysiological gate that controls the perception of pain.69 This cou ld conceivably abolish pain immediately after manipula tion but does not explain longer term improvement. Some believe that mani pulation may move an inflamed nerve away from the herniation7o or that relief is achieved via a return to normal of neurogenic reflex activity.41 ,71 We strongly believe that spinal pain is the result of disc protrusion that gives rise to a conflict between the posterocentral or posterolateral rim of the disc and the pain-sensitive dura mater or dural nerve sleeve, and that a displaced fragment of an intervertebral disc can be moved by manipulation.4 1, 72-75 This was the hypothesis of Cyriax3 (see his pp. 38-50) and Maigne76 and has been supported by the observa tions of Mathews and Yates,67 who have shown by epidu rography that in acute lu mbago small lumbar disc protrusions diminished in size after manipulation. Manipulative interruption of contact, moving the dis placed cartilaginous rim away from sensitive stru ctu res, is the objective for relief of pain and is best obtained by a non-specific long-lever, high-velocity manipulation.
Indications for spinal manipulation Spinal manipulation is useful for all annular disc protru sions in the absence of any contraindications or of any signs or symptoms that indicate that manipulative reduc tion would not succeed. All these factors may vary for the cervical, thoracic and lumbar spine, and the indications are discussed in detail in later chapters. Contraindications to spinal manipulation All effective treatments are potentially dangerous and therefore possess contraindications. Although manipu la tive techniques are not hard to learn, years of experience are needed to learn when to manipulate, when not, and what sort of manoeuvres to use. Contraindications to manipulation a re bleeding disorders, softening of bone, rheumatoid conditions, neurological deficit and danger to the spinal cord. B l e e d i n g d i so rd e rs a n d a nt i c o a g u l a nt u s e . When normal clotting of blood is not guaranteed, as in con genital or acquired (liver disease) b leeding disorders or because of the administration of anticoagulants spinal manipulations are potentially dangerous (see Box 5.3). Disastrous results can follow, such as intraspinal h aem orrhage with the formation of a h aematoma that may lead to sensory and motor deficit, to paraplegia, qu adri plegia or death?7 For this reason, a coagulopathy is an
110 SECTION ONE - GENERAL PRINCIPLES
absolute contraind ication to spinal manipulations. Manipulation can be safely performed only after blood clotting tests have returned to normal . Spinal tumours, u nstable fractu res, verte bral i nfections
(see Grieve: 26 p. 829). These all result in weakening of bone with risk of further damage by manipulation. Long-lever manipulation is not safe in severe osteoporosis.
and severe osteoporosis
Rheumatoid
arthritis,
psoriatic arthritis,
Reiter's syn
The first three of these may be associated with ligamentous laxity and gross destruction of the joint with subsequent instability. Manipulation must not be undertaken. The same applies for the inflammatory stage of ankylosing spondylitis. In the unlikely event of a patient with this disorder devel oping a disc lesion, manipulation is not at all safe, espe cially in the cervical spine, where luxations, fractures and cord compression have been described.78 drome and a n kylosing spondylitis.
N e u ro l o g i c a l
deficit
and
spinal
cord
c o m p ress i o n.
Segmental neurological deficit is characterized by distur bance of either motor function, with unpaired reflexes and / or muscular weakness, or sensory function, with di minished sensibility. The two may be combined . Segmentally referred pins and needles due to compres sion of the sensory fibres of a nerve are not regarded as neurological deficit and are therefore not a contraindica tion. In neurological deficit manipulation is usually without value because deficit suggests a large protrusion that cannot be reduced. This opinion is not universally supported/9,8o and some still manipulate when minor neurological signs are present. However, in all instances where progressive neurological deficit is present, manip ulation must not be done. A similar rule applies in cord compression or caud a equina syndrome when a very large posterocentral pro trusion threa tens the spinal cord or the cauda equina. This is true not only for obvious signs but also in the presence of even the slightest symptoms, such as extrasegmental pins and needles or pain in the S4 dermatome.
Box 5.3 Anticoagula nts contraindicate spinal ma nipulation '-
Coumarin derivatives: • Heparin
• Warfarin • Phenprocoumon • Acenocou m a ro l Indandione derivatives: • D i phenadione • Phen i ndione
Hy permobil ity. In several schools of thought on manip ulation, too much emphasis is placed on hypermobility. Although it is true that special attention must be given to hypermobility in the cervical spine, it is not impor tant elsewhere. A hypermobile joint may move further than an ordinary joint, but once extreme range is reached it stops in exactly the same way as does an ordi nary joint. More often the disc fragment itself is hyper mobile, which may lead to frequent recurrences. This circumstance does not contraindicate manipulation but calls for extra measures to achieve stabilization, for example by infiltration with ligament sclerosant (see Cyriax:3 p. 38). For the cervical spine a history of frequent disc prob lems, alternating from one side to another, may be suggestive of hypermobility. When doubt exists the following tests may be useful: spinal flexion with putting the palms flat on the floor with knees straight, passive apposition of the thumb to the flexion aspect of the forearm, passive hyperextension of the fingers parallel to the external surface of the forearm and hyperextension of the elbow and / or of the knee of 1 0° or more. If one or several of these are positive hypermobility is likely.8l Also, when the end-feel on passive rotation, extension or on preparation for a straight-pull manipulation, is too elastic, further manipulation must cease.
Spinal manipu lation should never be done in an unconscious patient. First, anaesthesia is unnecessary. Second, the final warning of potential danger offered by increased pain or abnormal end-feel on taking up the slack is completely lost, as is clinical assessment after each manoeuvre. Consequently, complications arc more frequent after manipulation under anaesthesia.82 Patients who have difficulties in relaxing during manipulation may benefit from being given diazepam before a session. Spinal m a n i pu lation u nder a naesthesia.
Evaluation of the effectiveness of spinal manipulation Although several studies, mainly done on the lumbar spine, support the view that many patients benefit from spinal manipulation,38-40,83-86 agreement on the effec tiveness and the role of manipulation in spinal disorders is still lacking. Reports from clinical trials are not always clear and the effects of manipulation are often difficult to interpret8? because of a small number of patients and their selection by symptoms rather than diagnosis. To make trials scientifically valuable a precise definition of manipulation is necessary, a record of which types of technique have been used and for what type of di sorder and its d uration. It should also be said that a double blind randomized trial on spinal manipulation is not
CHAPTER 5 - PRINCIPLES OF TREATMENT 1 1 1
possible because of the absence of a placebo and the obvious knowledge by the patient and operator of what is being done. Sims-Williams published a clinical trial on 94 patients with non-specific lumbar pain, who took part in a trial in which placebo physiotherapy was compared to Maitland mobilization and manipulation. Studies mainly showed that manipulation hastened improvement chiefly in those patients whose severity and duration of symptoms did not require specialist referra1?9,88 Bergquist-Ullman and Larsson,89 Coxhead et al80 and Farrell and Twoney38 found a significantly shorter dura tion of complaints in patients receiving manipulation. Chrisman et al90 stated that half of those suffering from sciatica showed clinical improvement after manipulation, but the improvement could not be objectively confirmed by myelography. Hadler et al85 compared the results of spinal mobiliza tion to high-velocity thrust manipulation in patients with acute, uncomplicated low back pain and tried to exclude all elements of chronicity or compensation insurance. Patients treated by manipulation improved to a significantly greater degree and more rapidly than those treated by mobilization. In one study, in which rotational manipulation was compared with simulated short-wave diathermy, those who received the former fared better immediately after the session.9] However, when pain relief was compared 7 days after treatment there was no significant difference between the two groups. In another study, 24 patients with complaints of less than 3 weeks' duration were followed. It showed that 92% of those treated by rotational manipulation were cured in less than 2 weeks.92 Of those who received diathermy, only 25% got better in the same period of time. A further trial in acute disc herniation compared conventional physiotherapy with manipulation and showed that the manipu lative group scored signifi cantly better.93 All manipulated patients were able to return to work, whereas only 26% of the physiotherapy group could do so. In a randomised clinical trial Koes et al compared the effectiveness of manipulative therapy, physiotherapy, treatment by the general p ractitioner and placebo therapy in 256 patients with non-specific back and neck complaints of at least 6 weeks' duration. They concluded that manipulative therapy showed a faster and greater improvement in physical functioning compared to the other three therapies.94,95 Controlled studies performed by Mathews et al clearly demonstrated that manipulation treatment for low back pain scored significantly higher in the subgroup with limited straight leg raising.96,97
Generally it can he concluded that manipulation and mobilization hasten both pain relief and the resolution of objective signs such as limitation of straight leg raising and of articular movement. Manipulation with high velocity thrust seems to work better and quicker than more gentle mobilization technique. The results are also better in recent-onset cases than in those of longer dura tion. Manipulation helps either quickly or not at all, which means that manipulative therapy continued over a long period of time is not appropriate.
Complications of spinal manipulation Genera l considerations. Manipulation is, as with any thing in medicine, not without danger and it must be admitted that even in experienced hands accidents may happen. Therefore manipulative treatment must never be undertaken recklessly, or on a 'hit or mi ss' basis. 3 Although it is p robable that more accidents have occurred than have been reported, the risks must not be overstressed. 39,98 So far, fewer than 1 00 serious cases h a ve been reported, mainly in the cervical spine (Frymoyer et al44 p. 1 588). In 30 years of clinical practice Kirkaldy-Willis28 (their p . 293) did not have one patient who was made worse by a manipulation. Dvorak and Orelli estimated that in l out of 400 000 manipulations severe neurological damage results, and in l out of 40 000 slight neurological signs appear.99 It should not be forgotten that traditional treatment with non-steroidal anti-inflammatory d rugs is a lso not without complica tions, in that they may give rise to severe gastrointesti nal problems (mucosal bleeding, or reactivation of previous ulcers or initiation of new ones), haemolytic anaemia, leukopenia, thrombocytopenia and even fatal agranulocytosis, salt and water retention, album inuria, nephritis, acute renal insufficiency, or to allergic reac tions in all degrees of severity. No matter what treat ment is given there will always be an inherent risk, but this should be reduced to a minimum by taking all necessary precautions. Complications of manipulation can range from a tem porary slight increase in pain to severe neurological deficit and death.
Immediate postmanipulation pain - which is usually not severe and is present in the whole area - can be relieved by using special techniques at the end of a manipulation session such as a lateral glide at the cervical spine or the rhythmic extension technique in the lumbar spine. A degree of pain for a short d uration - due to stretch ing of the muscles and ligaments - is normal in the elderly. It disappears spontaneously wi thin 1 or 2 days. To avoid undue anxiety, patients should be warned of this. For the same reason, in older patients some Postma nipulation pain.
1 1 2 SECTION ONE - GENERAL PRINCIPLES
manipula tion-free days must be planned between two sessions. Worsening of the condition immediately after a manipulative manoeuvre is manifest by either an increase in original pain or by its movement more later ally. The implication is that the protrusion has been further d isplaced. This may occasionally occur in a manipulation which was perfectly performed and does not necessari ly mean a poor technique. Further worsen ing can usually be avoided by performing a different manoeuvre, very often by changing the direction of rota tion. The same course is adopted when, after manipula tion, pain moves to the other side - an indication that overcorrection has occurred. Increased pain.
Fracture. Exceptionally, manipulation may be compli cated by a rib fracture, sternal fracture or fracture of a transverse process. These usually occur in the elderly and can be avoided by not using certain techniques in patients 'above 60 years of age. Onset of neurological deficit. Sometimes uncompli cated root pain becomes complicated by neurological deficit, and it may occur after a manipulation that was correctly performed. What has happened is that the pro trusion has moved further laterally or that compression has increased. This event must be considered when root pain does not improve. Neurological reassessment must be done and, as a consequence, further manipulations will cease and, if necessary, epidural injections or sinu vertebral nerve blocks may be given. It is very seldom th at the problem is so severe that neurosurgical inter vention is needed . Vascular interference and cord compression. Most severe problems arise from compression of blood vessels result ing in temporarily or permanent ischaemia of the cere brum, brainstem or spinal cord, or as a result of direct compression of the spinal cord by a disc fragment or as a sequel to vertebral fracture or luxation. Para- or tetraplegia may follow, sometimes leading to death. These complica tions are usually encountered in the cervical spine and are extremely rare at the thoracic level. When they occur at the lumbar spine, they may give rise to a cauda equina syn drome, often followed by definite neurological features. Risks in relation to level. The risks involved in manipu lation differ at the cervical, thoracic and lumbar levels. Cervical level. Serious neurological complications have been reported after manipulation of the cervical spine. They are mainly the result of a dislocation of the atlas, giving rise to vascular disturbance with occlusion of the vertebral-basilar arteries and to cord compression.lOO Vascular injuries are usually the result of cervical hyper extension manoeuvres accompanied by excessive rota-
tion44,1 01.102 which may cause vertebral artery dissection and lead to brain infarction with permanent neurological deficits.86-89, 1 03-1 07 During a recent inquiry over a period of 2 years among 468 Californian neurologists, 55 strokes follow ing osteopathic cervical manipulation were surveyed. Most of the patients continued to have persistent neuro logical deficits 3 months after the onset and about one half were marked or severe. Nearly all of th.e strokes involved the posterior circulation and almost one-half were angiographically proven.J08 A Danish survey reported the incidence of cerebrovas cular incidents (CVI) after chiropractic manipulation to be about 1 for every 1 20 000 cervical treatment sessions, manipulation to the upper neck being about four times more commonly associated with CVI than treatment of the lower neck.109 Exceptionally vascular injuries are the result of already existing but undetected anomalies such as atlantoaxial subluxations or congenital disorders of the arteries. Thoracic level, Complications at this level are usually due to vertebral metastases or to severe osteoporosis resulting in fractures of vertebrae, ribs or stern:.Jm.
The main complication is compression of the cauda equina because of a massive posterior sequestration of a lumbar disc.I 1 O Compression of the cauda equina complicating lumbar manipulations without anaesthesia is extremely rare, when it is consid ered that in the US in 1 975 about 124 mil lion office visits to chiropractors took place. Between 1911 and 1992 only 13 cases were recorded .l11 This potential complication should never be taken as contraindication to manipula tion. However, anyone who manipulates must be able to recognize the syndrome immediately, so that no time is lost before surgical decompression is performed. Lumbar level.
M easures to prevent complications. Although complica tions may occur and cannot be totally excluded by any means, each manipulator should try to reduce the even tuality to the lowest possible degree. It would be wrong to condemn the manipulator simply because a mishap or a complication occurred. If this was done it would mean that, instead of getting on with his work, the practitioner would forever be ' looking over his shoulder' . It is not possible to arm oneself against unpredictable events. Even if they do occur occasionally, this argument should not be used to condemn manipulation.111 Obviously all measures must be taken to decrease the risks as far as possible. In orthopaedic medicine the nec essary steps are taken during the whole procedure, start ing with the h istory, through clinical examina tion, technical investigations and ending with the manipula tion itself. Safety measures and acknowledged warning
CHAPTER 5
signs are incorporated in each stage. These are discussed in detail in the relevant chapters and are only briefly out lined here. History taking. Before any manipulation, history taking must be sufficiently thorough to elicit information on drug intake (anticoagulants) and the existence of other (visceral-rheumatoid ) diseases. Severe pain in the absence of movement or pain worse at night may indicate that the lesion - whatever it may be - is in a highly inflamed state and unsu itable for manipulation. Expanding pain, excessive weight loss and recent opera tions may indicate metastases and must always be excluded. All these are severe warning signs. Cervical root pain of more than 2 months' duration or root pain at lumbar level for over 6 months (unless there is still scapular or lumbar pain influenced by cervical or lumbar movements) do not respond to manipulative reduction. Hence no attempt to manipulate should be made. Clin ical examination. A complete clinical examination must a/ways follow. In particular, in relation to the cervi cal spine, fu ll attention must he paid to the end-feel on passive rotations and on extension. Even if the clini cal examination suggests an ordinary d isc lesion, if the end-feel shows muscle spasm is empty or if it comes to a bony hard stop, manipulation should not be done before serious disorders have been excluded. Muscle or empty end-feel may point to a disorder such as metas tases, fracture or infection. A bony b lock end-feel implies that it is im possible to increase the range beyond this point, and therefore the lesion is unsuitable for manipulation. A patient suffering from acute lumbago or sciatica usually cannot put weight on the joint, may suffer from constant pain day and night and on clinical examination may be fowld to have deviation and muscle spasm. When more severe d isorders such as metastases, rheuma toid arthritis and ankylosing spondylitis have been excluded, a disc lesion is most likely and manipulation can be safely performed. A protrusion of disc substance larger than the aperture from which it emerged - usually characterized by a neu rological deficit - means that reduction is impossible. The same accounts for nuclear protrusions, which require traction. Manipulation should never be used simply because 'no contra-indication has been discovered, no one can think what else to try, and a friend was recently relieved by this means' (Cyriax:ll2 p. 3 1 ). If the diagnosis is unclear or if too many inconsistencies are found, manipulation should be avoided. Once again it should be stressed that manipulation follows only if the diagnosis of a disco dural or discoradicular interaction has been established.
-
PRINCIPLES OF TREATMENT 1 1 3
For safety, the following must be added: 'If the diagnosis is established but it is uncertain if manipulation will work, then try. I f the diagnosis is uncertain and it is unclear whether or not manipulation is safe, do not try.' (Cyriax3). Ra diographic appearances. Radiological changes are signs of structural alterations that usually cannot be treated, though it is of first importance to find out if they are relevant to the symptoms present. Osteoarthrosis of the spine cannot be cured by mani pulation, but a manip ulation can easily reduce a displaced disc fragment even in an osteoarthrotic spine. Although the diagnosis of tumours of the lumbar spine is largely dependent on radi ography examina tions, it must be remembered that 30% of the osseous mass of a bone must be destroyed before this type of lesion becomes radiologicall y evi den t . l l 3 Therefore radiographs do not reveal early disease, and too much reliance on negative radiographic appearances can give rise to a false feeling of security. Radiographs that show no evidence of bone disease should not be taken to indi cate that manipu lation is safe (Cyriax:63 p. 292). A deci sion to manipulate because the radiograph is normal carries a high risk of worsening the patient's condition and may even lead to d isaster. The diagnosis of lesions in bone in the early stage is mainly dependent on history and clinical examination. Special attention must be paid to ' warning signs' . In several d isorders, such as early invasion of bone by a secondary neoplasm, the clinical signs may precede the radiographic findings. In doubtful cases, w hen rou tine radiography fa ils to support the clinical impression, a radioisotope scan must be obtained. Appropriate te chnique. Manipulative tech niques contain important safeguards against possible acci dents. This is chiefly so for the cervical spine, in which dangerous techniques such as extension in combination with rotation should never be used.35, 1 1 4, 1 J 5 Those with special interest i n musculoskeletal disorders should not only read textbooks but must be prepared to take courses in order to collect the necessary theoretical and practical skills before undertaking manipulation. Once a manipulation has sta rted, the operator must always concentrate on the type of tissue resistance (end-feel) while taking up the slack just before the final thrust is given. If the end-feel is abnormal, he must stop immediately and must not manipulate. To push through m uscle spasm protecting a joint should never be attempted. ] 16 To prevent compression of the spinal cord all manipu lations must he performed under traction. The major aim of manipulation should always be to gain maximal benefit with the use of minimal force.
1 1 4 S E CT I O N O N E - G E N ERAL P R I N C I PLES
Therefore it is good sense to start gently and progres sively to increase the force if needed . Each manipulation must always b e followed by re assessment. If the patient is worse, the same manoeuvre should not be repeated but another manoeuvre can be tried. If the latter also increases signs or symptoms, further manipulations should be abandoned. Once symptoms and signs have cleared, treatment must be stopped. There is no sense in asking the patient to come back at regular intervals for ' prophylactic' manipulations. Box 5.4 summarizes measures to prevent complications.
Avoidance o f o vertrea tment.
ACTIVE MOVEMENTS The effects of immobilization on skeletal muscle, tendon, ligament, joint capsule and articular cartilage are dra matic and have been described thoroughly in Chapter 3. Physical activity is also the primary stimulus for the repair of musculoskeletal tissues. Therefore, most thera peutic modalities that are advocated in this book are in conjunction with movement. Active movements are defined as those undertaken by the patient via muscular contraction. In orthopaediC medicine they are not so often used as a sole therapy; their main role is in combination with other therapeutic techniques. However, there exist a few situations (both therapeutic and prophylactic) where active movements play a particular role.
SIMPLE ACTIVE MOVE MENTS TO GAIN OR PRESERVE NORMAL RANGE IN A JOIN T A few examples make the above clear. Immobilization of the shoulder leads to the development of an arthritis with limitation of all movements in a capsular way if the shoulder is not brought daily through a full range of movement. Total rupture of the infraspinatus tendon lead s to limitation of external rotation of the shoulder if the patient is not performing daily lateral rotations. Treatment of sprains is essentially treatment with movement (see p. 52). Although the first measure is fric tion, passive and active movements within the limits of pain to maintain normal gliding of the ligament over adjacent bones should be encouraged. When the lower limb is involved, the patient should be instructed to walk as normally as possible but without provoking pain. Ligamentous adhesions that have developed as the consequence of a chronic sprain at ankle or knee need to be ruptured manually: the joint is forced through its normal range of movement by a high-velocity, short amplitude thrust manipulation (see p. 105). After the manipu lation and in order to retain the mobility achieved, the patient should repeat the same movement
Box 5.4 Measu res to prevent complications H i story • Exclude a nticoa g u l a nts • Check for warn i n g signs • Ascertain d u ration of root p a i n C l i n i cal exa m i nation • Check for warn i n g signs • Assess en d-feel • Excl ude n e u rological deficit Radiograp h ic appearances • Exc l u d e structural a lterations • Do not re ly on radiography a l one; negative radiography does not g u a rantee absence of d isease When m a n i p u lating • Avoid dangerous techniques • Check end-feel • Use traction • Start gently • Reassess after each m a n i p u lation • Do not overtreat
actively and on a daily basis. After rupturing of adhe sions under anaesthesia, active movements in addition to passive ones are also necessary to maintain the range that has been regained. They should be performed several times a day.
ISOMETRIC CONTRACTIONS Isometric contraction is the development of tension within a muscle without significant change in its fibre length. Joint motion or work is not achieved. In orthopaediC medicine isometric contractions are mainly performed to strengthen stabilizing muscle groups. The main example is in treatment of shoulder instability: in order to provide a firm foundation for the scapula, the muscles of the shoulder girdle (trapezius, serratus anterior, rhomboids and pectoralis minor) are strengthened by isometric training.
ISOTON IC CONTRACTIONS Isotonic exercise is classically defined as the movement of a load at constant resistance through an arc of motion. In orthopaedic medicine, isotonic contractions are per formed in the following situations: after the lesion has been pre pared by gentle transverse friction (see p. 96). The con tractions are carried out with the muscle in a position of maximal relaxation and with minimal resistance so that no tension falls on the healing breach. They begin as soon as possible after the injury and are preceded by an infiltration with local anaesthesia and by transverse
• In m inor muscular tears
CHAPTER 5
•
•
friction. The idea is to promote movement between adjacent muscular fibres to prevent abnormal forma tion of adhesions because these can disturb the normal increase in breadth on contraction. To strengthen weakened m uscles as in arthritis or after local or generalized immobilization. If passive move ments are limited, say by the arthritis, the isotonic exercises should be performed within the painless range to avoid increase of synovial inflammation. To strengthen muscles so they can protect joints or inert structures from being painfully overstretched. One example is the strengthening exercises of the short plantiflexor muscles and the lumbricals of the foot i n the treatment o f splay foot a n d chronic metatarsalgia. Strong muscles that contract properly at each step will take most of the body weight and relieve the metatarsal heads.
ELECTRICAL CONTRACTIONS In some circumstances a strong voluntary muscle con traction is not possible. Muscles can be (temporarily) paralysed or they are affected by severe injury. In such a situation, daily application of electrical stimulation (ES) may retard the loss of muscle strength or even improve it in already weakened musculature. The gains are not long-lasting, however, and electrical stimula tions should only be used temporarily while awaiting neurological recovery. ES can then be replaced by a good exercise programme.
COORDINATION EXERCISES During the last decades it has become clear that rehabili tation should not be restricted solely to procedures that improve mobility, strength and endurance but also that functional exercises allowing a better coordination of par ticular muscle groups should be included i n the rehabili tation programme. This kind of training is particularly important in the treatment of problems of instability (e.g. in shoulder, knee and ankle). The ability to control the position of a joint during active motions (proprioception) and to produce a volun tary muscular contraction to stabilize the joint and / or to alter the joint position so as to prevent excessive joint dis placements is referred to as reactive neuromuscular control. Proprioception is a specialized sensory modality that gives information about extremity position and direc tion of movement: stretch-sensitive mechanoreceptors within skin, capsular ligaments and tendons (see p. 36) are activated by tension, thus producing a muscular contraction to protect these structures at the extreme of motion.l17 This type of afferent sensory feedback is extremely important in mediating muscular control
-
PRINCIPLES OF TREATMENT 1 1 5
over joints and thus preventing them from overstretch and (sub )luxation.ns Numerous authors have recommended the training of proprioceptive skills and proper muscular coordination to re-establish the reactive neuromuscular control abili ties in the joints at risk and to create a functional joint stability.119- 123 Several techniques exist, from the see-saw block or tilting board in the treatment of functional insta bility of the ankle to the use of dual channel electro myography biofeedback systems in the treatment of patellofemoral dysfunction124 and glenohumeral instabil ity.125 However, most functional training techniques used to re-establish the proprioceptive skills make use of eccen tric training.126 Eccentric activation refers to the situation in which the muscle-tendon unit is lengthened while active. Small weights and multiple repetitions of the movements are used. Proprioceptive neuromuscular facilitation (PNF) tech niques can also be used to gain or improve neuromuscu lar stability at a joint. PNF techniques may be of value in the prophylaxis of recurrent periarticular shou lder lesions. PNF may be defined as a method promoting or hastening the neuromuscular mechanism through s tim ulation of the proprioceptors. Hence, PNF refers to the improve
ment of flexibility through stimulation of the nerves and muscles internally. The technique involves the use of the principles of reciprocal innervation and the stretch reflex: as a muscle is passively or actively stretched, it is brought to a point of limitation before pain develops. This is the point at which the proprioceptive organs send a message to the central nervous system to terminate the movement before further elongation occurs. At this point the muscles being stretched (antagonist) are contracted for a few seconds at an intensity of 50% of maximum. This contraction allows for the inhibition of the muscle spin dles and Golgi tendon organs and a subsequent initiation of the stretch reflex of the stretch receptors. After releas ing the contraction, the muscle is stretched to a new point of limitation and held for another few seconds. The interested reader is referred to Alter ' s 'Science of stretchings', 127 that offers over eight PNF techniques and exercises.
INJECTION AND INFILTRATION Musculoskeletal disorders such as tendinitis, minor muscular ruptures, ligamentous sprains and arthritis can usually be treated by infiltration. For an optimal effect the product administered must he put directly into the lesion and not in its surroundings. The descriptive terms 'injec tion' and ' infiltration' are used; each has a well-defined meaning and expresses a different way by which the product is administered. In injection the tip of the needle
1 1 6 S E CT I O N O N E - G E N E RA L P R I N C I PLES
is placed in exactly the right place and all the product is deposited at one single push, as is done in an ordinary intramuscular injection. This technique is mainly used for intra-articular and caudal epidural i njections. Once the tip of the needle has been brought within the joint or the epidural space, the full amount of product is put in. Local administration of a drug into a structure, as in bursitis, tendinitis, tenosynovitis, tenovaginitis, lesions of a muscle belly and also in ligamentous problems, is usually performed by infiltration. In this, maximal beneficial effect is obtained when all the different areas within the lesion receive some of the product. This can only be achieved if the tip of the needle is displaced several times while injecting a small amount of the product at each point. An infiltration is therefore a series of injections, given at sligh tly different places, within the lesion. Al though the aim of all infiltrations is the same, the specific technique may vary depending on the type of lesion and its location. In orthopaedic medicine three types of product are used : local anaesthetics, corticosteroids and sclerosant solution. Each of these has its own specific indications, contraindications and side effects. Although, in each group, several agents are available, it is better to use only one as this leads to optimal therapy.
GENERAL P RINCIPLES To obtain maximal benefit with minimal side effects the following general rules must be observed.
Exact diagnosis Any treatment must reach the lesion. Infiltrations, like deep friction, need a diagnosis accurate within a milli metre or two and must be directed to the precise site of the lesion. The steroids used in orthopaedic medicine are all suspensions of insoluble particles, so their action is mainly confined to the place where they are adminis tered. An exact preliminary diagnosis must be made, together with proper localization of the lesion.128 Choice of product Many different products are used in musculoskeletal dis orders. Local anaesthetics and corticosteroids are most frequently used but occasionally a sclerosant solution containing phenol, glycerol and dextrose is needed. The type of the product, i ts concentration and volume depend on the structure affected, the nature of the lesion, the degree of inflammation and other additional elements such as age, activities and the general condition of the patient. Of main importance are increased liability to - or the presence of - general or local infections and allergy to the products. A lesion of the muscle belly can be treated by infiltration of a local anaesthetic, usually procaine, whereas steroid is
never used. Musculotendinous insertions do not respond to any product and therefore are never therapeutically infiltrated but are best treated by deep transverse friction. Procaine is of no curative value in tenoperiosteal insertions or periosteal attachments of ligaments; for these, steroid is used or friction is given. In lesions of the body of a tendon, steroid is never infiltrated into the tendon itself, but is put at the surface along the tendon. For optimal results the appropriate agent at the indi cated dose and concentration must be used. For example, 20 mg of triamcinolone at a concentration of 10 mg / ml means that a total volume of 2 ml is administered. This is not the same as 0.5 ml of a 40 mg / ml suspension, as the steroid administered in this way will be concentrated over a much smaller area and may not be sufficient in volume to reach the whole lesion. Moreover, a strong concentration of steroid spread over too small an area may cause an increased risk of tendinous or ligamentous rupture.
Equipment If a certain amount of product is indicated, it should always be put into a syringe of the corresponding volume. If this is not done, infiltration may fail because of counterpressure offered by the tissue. Care should be taken to fit the needle firmly to the syringe because an infiltration into a ligamentous or tenoperiosteal insertion may demand considerable pressure on the plunger, which could lead to detachment of the syringe. The needle to be used must be of appropriate length and be as thin as possible. These characteristics are always indicated throughout the text in subsequent chap ters. An appropriate needle enables the therapist to rec ognize the type of tissue by the resistance it offers as the needle penetrates the structure: for example, ligaments and tenoperiosteal junctions have a totally different resistance from that of a muscle belly. Moreover, the thinner the needle the easier it is to recognize differences in resistance on the plunger during infiltration. Both types of resistance are important in giving a good indica tion of the localization of the tip of the needle. The main characteristics of the needle types referred to in this book are given in Table 5.3. Table 5 3
Main characteristics of needles used
Needle typeG
Preparation
2.5 em 3 em 4 em 5 em 7 em Spinal
'Terminology used in this book.
19 25 22 21 22 20 22
Gauge mm
1.1 0.5 0.7 0.8 0.7 0.9 0.7
Length mm inches
1� 1 1t 1� 2 2% 3�
40 25 30 40 50 70 90
CHAPTER 5
Position of the patient Before any attempt is made to infiltrate, the patient is positioned in the way that renders the lesion most acces sible. For each injection, the ideal positions from which to start are presented in later chapters; positions are usually the same as for deep friction. For intra-articular injec tions, different positions have been described. We present those which are the most simple to perform and which offer the least risk in relation to other neighbouring struc tures. The landmarks required and sometimes also the affected structure should be palpated and, if necessary, should be marked on the patient's skin. Aseptic care Careful aseptic precautions are always necessary i n order to avoid, for example, a suppurative arthritis. The possi bility of an unintentional intra-articular injection when infiltrating a tendon or a bursa in the neighbourhood of a joint should not be overlooked. Although infrequently encountered, septic arthritis is usually the result of con tamination during preparation of the equipment. Technique of infiltration Two major teclmiques are considered here: dynamic infiltration, in which the product is injected during move ment of the needle, and a static infiltration, in which the product is administered with the needle at rest.
-
product is infiltrated b y a series o f partial withdrawals and reinsertions at a slightly different angle. infiltra tion . This technique is simi lar to conewise infiltration but is two-dimensional. It is used in subacromial bursitis. The needle is directed towards the centre of the deep part of the subdeltoid bursa and to its full length. By a series of partial withdrawals and rein sertions in a horizontal plane, to the left and to the right from the centre (Fig. 5.8), the full amount of product is applied during withdrawal. Fan wise
Cylin drica l in filtra tion. A cylindric infiltration is used to place the agent along the surface of a tendinous body. The tendon is first stretched to provide a stiff flat surface. The needle is tangentially inserted along the tendon between the tendon and its sheath, until the tip reaches the far edge of the lesion. During partial withdrawal as the needle traverses the surface of the tendon, constant pres sure on the plunger maintains flow of the suspension. The needle is then reinserted parallel to its first position but 2 mm to one or the other side and the manoeuvre repeated (Fig. 5.9). This is repeated four or five times u ntil the full amount has been given.
Dynamic infi ltration . This is used mainly when large amounts of product have to be administered in extensive lesions. Three different techniques are used, mainly conewise, fanwise and cylindrical infiltration. A further technique is used for static infiltration. Conewise in filtra tion. This is the usual technique for a lesion of a muscle belly. The limb is brought into such a position that the muscle is well relaxed. The tender part is pinched between the thumb and fingers and the needle is inserted obliquely in between them until its tip passes beyond the farthest edge of the lesion. Some of the product is now administered while the needle is withdrawn until the tip is at a point j ust beyond the nearer border of the lesion. It is then reinserted at a slightly different angle and more product is infiltrated while the tip is again withdrawn (Fig. 5.7). This is repeated several times u ntil the entire lesion h a s received some o f the product. During the whole proce dure, the fingers that hold the lesion verify and control the infiltration. Cone infiltration is also used in bursitis lying within the reach of the fingers. After the lesion has been carefully defined, the needle is directed to the centre of the tender area and towards the underlying bone. The site of ten derness usually cannot be kept between the fingers. The
P R I N C I PLES O F TREAT M E NT 1 1 7
Figure 5.7
Conewise infiltration.
Figure 5.B
Fanwise infiltration.
1 1 8 SECT I O N O N E - G E N ERAL P R I N C I PLES
Figure 5.9
Cylindrical infiltration.
This technique is mainly used to put a small amount of fluid into a well-delineated area. It is indicated for tend inous insertions and ligamentous attachments to bone. These offer considerable resistance to depression of the plunger. Hence the smallest syringe must be used to provide enough purchase to force the product into the structure. When the tip of the needle lies at the exact site, a typical counterpressure is felt during insertion, just before its point hits the bone. Now a few droplets are injected with the tip of the needle in bony contact. The needle is then five to ten times partly with drawn and inserted at slightly different angles and depths (Fig. 5.10) until the full amount has been adminis tered and the whole lesion has been treated. The tech nique is sometimes referred to as peppering. During the entire infiltration a typical resistance is felt, much more marked than during infiltration of a muscle belly or a bu rsa, where resistance is minimal. Static i nfi ltration.
Follow-up and after-care For maximal benefit, all infi ltrations in any part of the contractile structures are followed by relative rest for 1-2 weeks. If full activity is continued without this rest, relapse is likely. When tendinous structures are infi ltrated by steroid there is a second reason for rest, in that the agent may temporarily weaken the tendon. The patient should be reassessed after 14 days and, if pain still remains, a second infiltration is given. A partial ru pture of a muscle belly offers an exception to this in that it is infiltrated only once, followed next day by deep transverse friction, active exercises and electrical stimu lation in the position of maximal relaxation of the muscle. Stress at the site of healing is avoided for about 3 weeks. After infiltration into a sprained ligament, the joint is immediately used as fully as possible, allowing move ments within the limits set by pain but avoiding stretch ing of the damaged structure. This leads to good functional results in a short period of time.
Figure 5.10
Static infiltration.
The advantage of this type of treatment is its rapid effect but on some occasions it may lead to recurrence in tendinous lesions. Recurrences are best treated by deep transverse friction.
LOCAL ANAESTHETICS Cyriax first started using procaine purely for diagnosis. If the suspected lesion is infiltrated by local anaesthetic, the pain on functional testing should disappear almost immediately, so confirming the diagnosis. He was most surprised when some of those patients came back some time later and claimed persistent improvement. He con tinued to use procaine because he felt that the thera peutic results were better than the alternative local anaesthetics. Nowadays local anaesthetics are still used for both diagnostic and therapeutic purposes. Because prolonged action of the anaesthetic is never needed in orthopaedic medicine, adrenaline (epineph rine) is not added. In addition, vasoconstriction restricts the spread of the agent so diminishing any beneficial effect.
Types of local anaesthetic Two major types of local anaesthetic are available: procaine and those belonging to the amide group (e.g. bupivacaine, lidocaine (lignocaine)) (Table 5.4). Proca i n e. Procaine is an ester of para-aminobenzoic acid and was first synthesized in 1 904 by Einhorn. Until 1943 it was the only anaesthetic available.129 It is quickly and locally metabolized by an esterase, giving rise to the acid itself, which may act as an allergen. Its effect begins after 5-10 minutes and lasts approximately 45 minutes. The maximum dose used is 250 mg, which corresponds to 50 ml of a 0.5% concentration. Although classical texts emphasize the hazard of aller gic reactions, we have used procaine several times daily for over 20 years without any problems. Cyriax estimated the risk as 1 per 500 000 administrations.
C H APTE R 5
Table 5.4
-
P R I N CI P LES OF TREAT M E NT 1 1 9
Local anaesthE;iics and their effects 130
Name
Strength
Toxicity
Maximum dose (mg)
Latency (min)
Duration (min)
Procaine Lidocaine (lignocaine) Prilocaine Mepivacaine Bupivacaine
1 4 4 4 16
1 2 1 , 5/4 2 8
500 200 400 350 1 50
5-- 1 0 2 2 1 2-5
45 60 60 1 00 360
The usual concentrations employed are 0.5 and 2% . Indications for 0.5% procaine are lesions of muscle bellies, most cases of chronic bursitis and caudal epidural injection. Procaine 2% is used to dissolve calcifications in tendons and bursae and in sinuvertebral nerve blocks.
full explanation of what is to happen. If symptoms do occur, the patient is immediately placed in Trendel enburg's position (head and thorax low, legs up) and oxygen given. The patient usually improves promptly after 1-2 minutes.
Amides. Newer local anaesthetics are the amides. They are metabolized in the liver and seldom give rise to aller gic reactions. We use local anaesthetics, such as lidocaine (lignocaine) and prilocaine, to anaesthetize only certain structures so al lowing other interventions. For this reason, they are used to anaesthetize the skin and the interco rnual ligament before inserting an epidural needle, and for skin and tenoperiosteal anaesthesia before a tenotomy in type II tennis elbow. Because their local anaesthetic effect is stronger and comes on more quickly than that of procaine, they are also used for diagnostic infiltrations around nerves and in tendons, ligaments and bursae. In countries where procaine is not available, or there is allergy, bupivacaine 0. 125% is an alternative. The maximal dose used is 60 mg, which corresponds to about 50 ml of a concentration of 0.125%. The immediate effect starts after 2-5 minutes and continues over 3-6 hours.
Toxic reactions These are dose-dependent side effects rela ted to the amount of product that reaches the blood circulation.132 They may be the result of unintentional intravascular injection, absolute overdose, swift absorption or delayed elimination of the drug. 133 If local anaesthetics are used at the indicated dose, which is usually less than half of the maximum dose allowed, and in a proper way - taking care during the administration that it is not directly intravascular - toxic reactions should never occur. However, if they do occur during an injection, administration must stop at once.
Side effects Side effects of local anaesthetics are traditionally divided into three groups: • • •
Psychogenic reactions Toxic side effects Allergy.
Psychogenic side effects These minor side effects are mainly caused by somatosym pathetic reactions on pain and fear and are not related to the drug as such. Nevertheless the symptoms may be quite similar to those of real toxic reactions: pallor, cold sweat ing, dizziness, nausea, yawnings, palpitations and vaso vagal collapse with syncope all may be present.l31 They should be taken seriously because if the patient is not placed supine quickly, cerebral hypoxia may follow, with unconsciousness, tremor and convulsions. To avoid these effects, all patients who require an infiltration should at least sit or lie down and be given a
Toxic side effects can be divided into two groups. They may be related to the central nervous system or to the cardiovascular system or to both.
Types of reaction .
(eNS). Although local anaesthetics may provoke stimulation or depres sion of both cortex and medulla, stimulation is the more frequent but is less severe than depression. Normally the depression period is preceded by a stimulation stage, but it may come on at once without a prior stage of excitement.134 Some stimulation of the cerebral cortex and the upper centres may sometimes occur even with a low dose. It is characterized by anxiety, excitement, logorrhoea, hypertension, headache, dizziness, tinnitus, diminished hearing, disturbed vision, metallic taste, muscular fascic ulations around the mouth and tremor. None of these symptoms is severe as such, but they are all signs of the presence of a toxic reaction that could lead to cardio vascular collapse. Further stimulation may be followed by convulsions, which indicate that severe cortical stimula tion is present and may progress to postconvulsive depression.1 34 Stimulation of the emetic centre causes nausea and vomiting. Stimulation of the cardiovascular centre in the medulla may cause tachycardia and hyper tension; respiratory stimulation is characterized by an increased depth and frequency of breathing. Effects on the cen tral nervous system
1 20 SECT I O N O N E - G E N E RAL P R I N C I PLES
The fi rst feature that draws attention to depression of the cortex is sleepiness, together with dysarthria and a feeling of coldness. If injection is not stopped at once and the necessary measures instituted, the outcome may be coma and death. Depression of the medulla may suppress vasomotor control resulting in pallor and hypotension, later followed by syncope and cardiac arrest. Respiratory depression is first characterized by irregular breathing with periods of apnoea and dysp noea and often cyanosis. Finally, total respiratory arrest may resul t. A depressive effect is far more dangerous than is stimu lation. Effects on the cardiovascular system. A direct peripheral effect on the blood vessels causes vasodilatation, leading to hypotension. Local anaesthetics have a depressive effect on the myocardium, which can lead to bradycardia, arrhythmia and cardiac arrest. In patients with already weakened myocardium, heart failure may result. Local anaesthetics can alter the blood pressure in differ ent ways. Stimulation of the CNS leads to hypertension, depression to hypotension. Hypotension may be intensified via a direct vasodilatory effect on the blood vessels and by direct myocardial depression. Furthermore, in lumbar epidural injection, hypotension may be due to blockade of the sympathetic nerves.13S Cl i n ical appearance. Toxic side effects may clinically appear in two ways:136
may occur within 5-30 minutes after the infiltration. This is the most frequent reaction and is due to slow absorption u ntil a toxic level is reached. It usually first gives rise to stimulation of the cortex before respiratory symptoms and cardiovascu lar collapse occur. For this reason the patient should al ways remain under supervision du ring the first half hour following an injection. An immediate reaction may occur within seconds to minutes of the administration, with all toxic reactions coming on at once. It is usually the result of intra vascular injection or of swift absorption. Collapse may occu r very quickly and death may follow rapidly if resuscitation is not begun at once.
• A delayed reaction
•
The most important measures, even if only minor signs of CNS or cardiovascular involvement are present, are to stop further infiltration at once and to administer oxygen. These may be sufficient to stop further development towards more severe conditions. The rest of the treatment should be in relation to the degree of toxic reaction. Treatment.
are best treated by intravenous diazepam (5-10 mg). Cerebral signs - tremor and convulsions - require immediate administration of 1 00% oxygen via a
• Fear or anxiety attacks •
•
• •
mask. Small intravenous doses (5-10 mg) of diazepam may be given. Barbiturates and short acting muscular relaxants should only be used by the experienced and should always be preceded by the administration of oxygen.133 Hypotension: the patient is put into the Trendelenburg position. If this is not sufficient, administration of vasoactive drugs such as dopamine or noradrenaline may be required.132 In circulatory depression, intra venous fluid must also be given. Bradycardia can be treated by atropine. Cardiac arrest: oxygen and external cardiac massage are given. Respiratory depression is treated by oxygen and artificial respiration (intubation) (see Box 5.5).
Allergic (anaphylactic) reactions Side effects not related to dose can occur even after the administration of small amounts of the agent. Previous exposure and sensitization to the active product or preservatives (methylparaben) or any other accessory material present is an essential precondition. Two types of allergic reaction may occur: an anaphyl actic reaction, which may be life threatening, and a local reaction presenting as dermatitis from local contact with the skin. The latter is usually encountered only in profes sionals who use the product, rather than in patients. Although allergic reactions are frequently mentioned in relation to local anaesthetics they are in fact rare. 136 According to Cyriax, anaphylactic reactions occur in
Box 5.5 S u m mary of treatment of side effects of local a n aesthetics Always: Stop further i nfi ltration Give oxygen at once Tremors and convulsions: 1 00 % oxygen via mask D iazepam i .v. 5- 1 0 mg Vascular collapse: Hypote nsion: Trend e l e n b u rg position Vasoactive d rugs i.v. (dopa m i ne, isuprena l i ne hydrochloride, adre n a l i n e (ep i n e p h ri ne» F l u i d i.v. B radycardia: Atro p i n e Card iac arrest: External cardiac massage Respiratory depression: G ive oxygen Artifici a l respiration (i ntubation)
CH APT E R 5
1 / 50 000 procaine infiltra tions, though they are more frequently encountered with procaine than with the amides. 133,135,137 In that an anaphylactic reaction may be very dramatic, with a mortality rate of about 3.4%, one must always be aware that it is possible.l38 Before local anaesthetics are admini stered the patient must always be asked for evidence of an allergic constitution. If a patient claims to be allergic to local anaesthetics, a careful and detailed history must be taken because 99 out of 100 reactions are due to toxic or psychogenic side effects and not to an allergy as such. 136 An intradermal test with a small amount of agent can be useful but is not 100% reliable.1 36 An anaphylactic reaction may come on immediately after the injection or some time later, up to about 30 minutes. It is the immediate type which is often dra matic. The initial feature of an anaphylactic reaction is often flushing occurring w ithin 20 minutes after adminis tration. This may be quickly followed by dyspnoea due to bronchiolar constriction and localized oedema of the larynx and glottis. It may end in respiratory obstruction which is the main cause of death. The respiratory symptoms are accompanied by vasodi latation which leads to hypotension and shock. Occasionally other anaphylactic reactions such as urticaria and angioneurotic oedema may also present immediately, but are far less dramatic. Treatment is different for immediate and delayed allergic reactions. The treatment is outlined in Tables 5.5 and 5.6. Treatment.
Immediate reaction. Even when only minor signs of anaphylactic reaction are present 0.3-0.5 ml of adrenaline (epinephrine) 1 / 1000 (0.3-0.5 mg) is immediately a dmin istered by the subcutaneous route to provoke vaso constriction, bronchiolar dilatation and resorption of oedema. In that adrenaline (epinephrine) is broken
Table 5.6
-
P R I N CI PLES OF TREAT M E NT 1 2 1
Table 5.5
Classification of anaphylactic reactions of increasing severity and their treatment Severity
Symptoms
Treatment
Urticaria Red conjunctivae Fever
Antihistamine
Hypotension Dyspnoea Tachycardia Nausea Diarrhoea
Trendelenburg position 1 00% oxygen Adrenaline Antihistamine Corticosteroid Aminophylline
III
Shock: Circulatory collapse and angioneurotic oedema Life-threatening spasms of the bronchi
Trendelenburg position 1 00% oxygen I ntubation Infuse: Adrenaline (epinephrine) Antihistamine Corticosteroid Aminophylline
IV
Cardiac arrest Respiratory arrest
Heart massage Artificial breathing
down quickly, it should be repeated every 20 minutes. Subcutaneous administration of adrenaline can only be done i f the general circulation is intact. When blood pressure is too low it must be carefully administered intravenously. In this event 3-5 ml of adrenaline (epi nephrine) 1 / 1 0 000 must be administered in repeated shots of 1 ml (0.1 mg) until effect has been attained. 1 39 Small repeated shots are necessary since there is fear of ventricular fibrillation. Some also advise inhalation of a 1 / 1 0 000 adrenaline (epinephrine) solution via aerosol in case of laryngeal oedema. S teroids inhibit allergic reactions but act too slowly in this situation. Oxygen shoul d also be given but may be of little value if the airway is severely obstructed. In the latter case, amino phylline should also be injected.
Medication used in anaphylactic reactions
Drug
Dose
Notes
1 /1 000, 0.3-0.5 ml s.c. 1/10 000, 3-5 ml i.v. 1/1000, 0.01-0.03 ml/kg s.c.
To be repeated every 20 min 1 ml per shot
2 mg i.m.li.v.
Every 6 h for up to 24 h
4-8 mg i.v.
Every 6 h for up to 24 h
Adrenaline (epinephrine)
Adults Normal blood pressure Severe hypotension Children Antihistamine
(clemastine)
Corticosteroids
(dexamethasone)
Aminophylline
Adults, initial dose Children Initial dose Follow-up dose
240 mg. i.v. 5 mg/kg i.v.li.m. 0.4 mg/kg/h i. v.
1 22 SECT I O N O N E - G E N E RAL P R I N C I PLES
The patient should remain under supervision during the first few hours after the anaphylactic reaction. Delayed reaction . If the allergic reaction comes on only after 30 mi nutes, administration of an antihistamine drug is sufficient.
CORTICOSTEROIDS The adrenal corticosteroids are classified into two groups: mineralocorticoids such as aldosterone, with sodium retaining activity, and glucocorticoids, which influence the intermediary metabolism (nitrogen catabolism, i ncreased glucogenesis) and have a strong anti-inflam matory and anti-allergic effect. The ability to suppress inflammation has made the glucocorticoids very useful but also potentially harmful. Administered in high dose they may cause Cushing's syndrome.14o A ll corticosteroids used in orthopaedic medicine are glucocorticoids. The first was hydrocortisone, extracted from the adrenal cortex by Kendall in 1936, and first intra-articularly injected by Thorn in 1 950.141 Since then many other steroids have been synthesized. Efforts to increase the anti-inflammatory effect and to diminish the influence on metabolism have remained largely u nsuccessful so far. Thus, u nnecessary use should be avoided. The ideal steroid should meet the following criteria: li ttle discomfort to the patient during and after injection, a low level of absorption into the systemic circulation (if absorption does occur, it should be slow), together with a prolonged local effect without general and local side effects.142 Some preparations are formulated specifically for local use and are available as a crystalline suspension. The less water soluble they are, the less they are absorbed into the general circulation. As a consequence they have a more prolonged local effect and fewer general side effects. Intrasynovial administration has the advantage of a maximal local benefit with minimum systemic side effect.143 The agent we use most often is triamcinolone ace toni de, in a concentration of 10 mg / ml. Throughout this book, this is the product and concentration intended, unless indicated otherwise in the text. It has a mean dura tion of activity of about 14 days, whereas triamcinolone hexacetonide has more prolonged activity.J44 Normal doses used are 5 mg for small joints, 20 mg for medium sized joints and 50 mg for the hip and knee. Therapists who prefer another type of corticosteroid should always administer the dose equivalent to the one indicated in the text (see Table 5.7).
Effects of local corticosteroids Corticosteroid injected locally has a local anti-inflamma-
tory effect due to stabilization of the lysosomal mem brane with decreased liberation of cytotoxic enzymes. Steroids also impair the proliferation of fibroblasts and decrease the rate of production of mature collagen. They decrease plasma fibrinogen as well and have an increased fibrinolytic activity.145 Furthermore, corticos teroids reduce oedema formation and the escape of plasma protein across the capillary membrane, and diminish the number of leukocytes in exudate at an inflammatory site. All these effects lead to reduction of pain and fibrosis.146- 150 When injected into a joint, steroid is partly broken down by enzymes from the synovial membrane and is partly resorbed into cells of the synovial fluid and cells of the synovium. A small amount enters the general circulation.
Indications for local corticosteroids Joints. Beneficial effects occur in traumatic arthritis, monoarticular steroid-sensitive arthritis, rheumatoid arthritis, crystal-induced arthritis (gout and pseudogout), ankylosing spondylitis, lupus erythematosus and psoria SiS.142 Steroids are ineffective in Reiter's disease (Cyriax:3 p. 52). Monoarticular steroid-sensitive arthritis is of sponta neous onset without any other signs of rheumatological disorders and resolves equally spontaneously over months or years. The joints affected are the gleno humeral, the elbow, the knee, the hip, the ankle and the temporomandibular. The treatment of choice is intra articular steroids. Usually, the joint must be kept under continuous anti-inflammatory influence for some time. Hence a specific sequence of injections must be observed. Improvement is subjectively felt by the patient in that pain and stiffness diminishes, and objectively shown by a decrease of local heat and effusion together with improved function. Patients should be warned against
Table 5.7
Costicosteroids
Product
Anti·inflammatory effect
Hydrocortisone Cortisone Prednison Prednisolone Methylprednisolone
0.8 2.5 4 4
Triamcinolone
5
Betamethasone Dexamethasone Beclometasone
28 28 40
1
C HAPT E R 5
overactivity at weight-bearing joints for the first days after injection for fear of further destruction of carti lage.151 Moreover, the efficacy of an injection is greater with relative rest. In arthrosis, lasting improvement is not to be expected.152 Some authors even suggest, although this has never been scientifically proven, that it may acceler ate the degenerative process. l5l If synovitis complicates arthrosis, intra-articular injection may well be beneficial. Steroids may be i ndicated i n tendinitis, tenosynovitis and tenovaginitis. It is often used in ten dinitis of the supra- and infraspinatus tendons and the subscapularis tendon at the shoulder. The same applies for type II tennis elbow and for golfer'S elbow at the tenoperiosteal insertion. In the lower limb, steroid injec tion is mainly used in supra- and infrapatellar tendinitis and for tendinitis of the peroneal tendon. Infiltration should be at the tenoperiosteal insertion or between tendon and tendon sheath, never into the body of the tendon for fear of rupture. 151 ,153- 156 Ruptures have been reported mainly after intratendinous infiltra tion with agents of high anti-inflammatory effect or at too high a concentration or when too frequently admin istered. When the rules are respected as set out in this chapter, no danger of rupture need be entertained.
Te n d o n s.
Ligaments. In the acute stage - within 24 hours of the injury - of a ligamentous sprain at the ankle or tarsus or of the medial and lateral collateral ligaments at the knee, a steroid infiltration quickly helps but should only be done at the ligamentous insertions. Because the inflammatory reaction ceases shortly after administra tion, the ligamentous lesion can heal in the presence of movement. This leads to better functional results and to absence of adhesions, which are later often the reason for chronic pain. In sprain of the cruciate ligaments of the knee, steroid infiltration is the only possible treatment, no matter what the stage of inflammation. Steroid infiltration is also an important part of the treatment in sprains of the radial and ulnar collateral ligaments of the wrist and in plantar fasciitis.157
Depending on the type and location of bursitis, steroid is used at once or after an infiltration with procaine has been found to be unsuccessful. Pain, local tenderness and functional impairment are all reduced .158 Bursae.
Nerves. Compression of the median nerve in the carpal tUlmel of the ulnar nerve at the ulnar sulcus or of any nerve root by an unreducible disc protrusion all usually benefit from an infiltration with triamcinolone around the nerve. 159
-
PRI N CI PLES O F TREAT M E NT 1 23
Local side effects Unwanted side effects of local corticosteroids are minimal compared with those of even low doses of oral steroids.H2 They are traditionally divided into local and general side effects. M usculoskeletal side effects. A number of musculo skeletal side effects of local injection of corticosteroids exist.
This complication is the most feared although i t is seldom encountered. The incidence varies from author to author: it follows in between 1 / 1 000 and 1 / 40 000 injections.142,1 60 The usual organism is S taphylococcus aureus; less often, Gram negative organisms are involved.161 The condition should not be regarded as a real side effect caused by the steroid but is due rather to inadequacy of aseptic care or contamination, chiefly occurring during preparation of the syringe. Patients who suffer from diabetes, or who are receiving oral steroids or are immunosuppressed (leukaemia, AIDS, drug abuse) are more vulnerable. 162 Suppurative arthritis may often lead to therapeutic d ifficulties, and death may follow. 163 Obviously this complication should be avoided by good antiseptic care, especially when the injection is made into a high-risk patient and when infiltrating in the neighbourhood of a joint or in the joint itself. Although skin lesions in psoriasis are highly colonized by bacteria, it has not been documented whether intra-articular injec tions given through such plaques increase the likelihood of an infectious arthritis. Iatrogenic in fectious arthritis.
Destruction o f joint cartilage and evolution of steroid
It has been suggested that intra-articular steroids may hasten the process of arthrosis by a deleteri ous effect on cartilage, leading to changes that closely resemble a Charcot-like neuroarthropathy. Steroid depresses the synthesis of collagen and proteoglycans, which may result in a loss of stiffness of the cartilage. In non-weight-bearing joints this has little or no effect. In weight-bearing joints it may result in fissure formation at the surface of the cartilage and cystic degeneration in the middle zone.1 64-1 67 However, rapid progression to degen eration has not been proved with certainty. 1 60,168 Cases have been reported of multiple intra-articular injections in some joints not leading to any abnormalities on later radiography.169,170 Often effects of local steroid camlot be differentiated from those caused by general administra tion of the product,1 71 prompting the question whether it is a local or general effect. Because it is difficult to differ entiate the possible destructive effects of the steroids from the natural progression of the osteoarthrosis, even though the risk may appear small, it is a good habit to avoid frequent injections. Moreover, injection into arthropa thy.
1 24 S E CT I O N O N E - G E N ERAL P R I N C I PLES
cartilage should never be done. When too much counter pressure on the plunger is present, the tip of the needle �.ust be replaced. It is also wise to rest weight-bearing JOints for 24-48 hours after an injection.128 During the first 48 hours after an intra-articular injection of a crystalline suspension, a synovitis may flare up as response to the c:� stals. The mechanism is the same as in gouty arthritis. An equally painfu l inflammatory reaction is occasionally encountered after a local tenoperiosteal infiltration. Normally it d isappears within 1 2-48 hours. If the reaction is prolonged, iatrogenic infection must be excluded . Flare up of crystal-induced arthritis.
Rup ture of ligament or tendon. Tendon ruptures have been described after one or multiple infiltra. . 55' 1 72, 173 Infiltrati' on 0f sterol' ds Into 1 ns. 1 acutely Injured ' fo ligaments in the rat significantly impaired the healing process relative to a non-injected ligament at 10 days and at 3 weeks after injury.174 However, after 6 weeks the tensile strength (the ultimate stress) of the ligaments that had been injected with the steroids returned to a value that was equal to that of the controls that had not received an injection.175 Although other studies have not confirmed these findings,176, 177, 178 infiltration into the tendon body should never be done. In tenosynovitis, steroid can safely be infiltrated between tendon and tendon sheath and at the tenoperiosteal insertion, although multiple repetitive infiltrations must be avoided.
Punctate calcifications of joint capsules and pericapsular calcifications are common after intra articular and periarticular injections. Steroid paste can be found on the surface of infiltrated tendons. These observations are not clinically important. Calcifica tion.
c o m p l i ca t i o n s . Direct i ntrafasci cular injection of steroid in peripheral nerves may provoke permanent damage, whereas extrafascicular injection does not appear to be harmful.182 The mechanism of injury i s multifactorial and can be related to direct trauma with the needle, to ischaemia and to a neuro toxic effect of the steroid or of the buffer agents and add itives su ch as polyethylene glycol and benzyl alcohol . The first features are severe radiating pain and numbness or paraesthesia in the sensory territory of the nerve, together with motor deficit. The pain usually responds poorly to narcotics and may persist for many years.183 As to the steroid itself, triamcinolone hexacetonide and hydrocortisone are most hazardous and dexamethasone causes minimal damage, whereas triamcinolone acetonide is intermediate.182, 184 Damage to the nerve should be treated conservatively for abou t 12 weeks. If the neurological deficit does not im prove after thi s time, neurological consultation is necessa ry. N e u rovas c u l a r
Dermatological side effects. Fat necrosis, atrophy of skin and subcutaneous tissue and depigmentation of the skin may be encountered. These are due to a faulty injection technique or to leakage of the product after an intra articular injection. The latter occurs often in smaller � oints . if the volume injected is excessive. Consequently, If reSIstance during the injection increases markedly, the injection should be stopped.
General side effects Although injected intra-arti cularly or into the soft tissues, corticosteroids do enter the circulation . The causes are leakage and absorption. Therefore general side effects depend on the admini stered dose, the frequency of injections, the number of joints injected and the aqueous solubility of the agent. The greater the aqueous solubility, the higher the absorption rate. Less soluble m icrocrystalline suspensions remain within the joint for longer. Administration of a given dose equally divided between two joints produces more general side effects than if the same amount was injected into a single joint - the result of a larger absorptive surface . 161 The majority of the more severe systemic effects can be avoided if no more than two joints are treated at the same time, using a maximum of 40 mg triamcinolone and allowing an interval of 1 month between two injec. hons. 185 If treatments are performed as recommended in this book general side effects are extremely rare. E n docrinolog ical side effects. There are five categories of potential endocrinological side effects. Disturbance of hormonal equilibrium. This can result in either hyperglycaemia or suppression of the adrenal cortex via depression of plasma cortisol levels.
glucocorticoids have an important influence on the intermediary metabolism. They increase circulatory glucose via stimulation of gluco neogenesis and decrease the intracellular use of glucose. Therefore it is wise to advise diabetic patients to check their blood sugar more closely for the first few days after the use of steroid .
• Hyperglycaemia:
•
Suppression o f the adrenal cortex vin depression of plasma cortisol levels: small doses of steroid may provoke
some suppression of the adrenal cortex.186 This seems to occur not only when steroids are adminis tered orally but also after intra-articular injections.18? Prolonged administration renders the adrenals atrophiC and provokes suprarenal insufficiency with symptoms such as hypotension, anorexia, fever and generalized joint or muscular pain. The full syndrome with weight gain, depression, insomnia, amenorrhoea,
Iatrogenic Cushin g 's syn drom e .
C H APTE R 5
diminished libido, thinned skin, muscular weakness, polyuria and polydypsia is seldom encountered after local use of steroids . 169 Occasionally facial hirsutism and acne may be seen. Flushing. In the first few days after an intra-articular injection, some patients suffer from erythema and warmth in face, neck and chest. This is a totally benign but rather frequent sensation which is more common after the use of triamcinolone.
Very rarely patients suffer from chilliness and shaking after the use of steroid, a reaction that normally abates within 24-48 hourS.143
Shaking and chilliness.
Interference with the menstrual cycle. In female patients repeated injections with steroid may lead to dysfunc tional uterine bleeding. Steroids may also interfere with hormonal contraceptives. There is no evidence for a teratogenic effect.18S
In addition to the local musculoskeletal side effects already mentioned, there can be systemic musculoskeletal effects. Musculoskeletal side effects.
Osteoporosis a n d increased risk of fra ctures. It is difficult to estimate the exact incidence of osteoporosis provoked by corticosteroids. Nevertheless, special care should be taken when administering them to post menopausal females because of the increased likelihood of these side effects. 1 85,189 Steroid myopathy, spontaneous tendon ruptures and
Any of these may occur, although they are all very rare. 1 90
• •
•
-
P R I N C I PLES O F TREAT M E NT 1 2 5
Prolonged use of steroids may provoke changes in personality and mood. In patients who have previously suffered from peptic ulcer and pancreatitis, steroids should he cautiously used. After long-term use of steroids some patients m ay complain of worsening of vision. This may be due to glaucoma or cataracts.196
Indications for and contraindications to local corticosteroids The indications for corticosteroid injection are given in Box 5.6. Contraindications may be divided into absolute and relative (Box 5.7).
PHENOL Introduction Chemical agents such as phenol and dextrose injected into ligaments are used to cause the formation of strong, thickened fibrous tissue. The solution is used to treat weakened ligaments that cause instability and pain. Because of its proliferative effect on connective tissue, the technique is called prolotherapy. Product The original solution, used by Hackett and consisting of zinc sulfate and carbolic acid, provoked painful reac tions and was not totally risk free. 197 The mixture used
aseptic necrosis.
Suppression of the inflam matory mechanism sometimes leads to a disappearance of symptoms in non-injected joints. Chronic use of steroids may increase the liability to infections. An allergic reaction to steroids is not expected because they all have an immunosuppressive and anti-inflamma tory activity. However, a number of well-documented allergic anaphylactic (type I) reactions to corticosteroid medications have been reported.191 Recent reports have warned of potential (though rare) anaphylactic reactions after intra-articular or intralesional injection of triamci nolone acetonide.192, 193, 194 One recent study indicates that the triamcinolone ace tonide component responsible for the patient's reaction is the suspending agent carboxymethylcellulose.195 It is therefore suggested that care be taken and component testing eventually considered when patients experience allergic-type reactions to drugs.
Box 5 .6
Indications for corticosteroid injection
I m m u n ological s i d e effects.
M iscel laneous s i d e effects . Central nervous system, gastrointestinal and ophthalmological side effects have been reported.
Tendons • Te n d i n itis at a tenoperiosteal j u nction • Te nosynovitis/tenova g i n itis: i njection betwee n tendon and tendon sheath, never i nto tendon
Joints • All non-supportive types of synovitis • Exception: Reiter's d isease Bursae • Acute su bdeltoid b u rsitis • Retroca lcaneal bursitis • Isc h i a l b u rsitis • B u rsitis i ntracta b l e to local a n aesthetics Ligaments • Acute stage of a spra i ned l i g a ment • P l a ntar fasciitis • Spra i ned cruciate l igaments at the knee • Sprain of rad i a l and u l na r co l l ateral l iga ment at the wrist Spinal d isc lesions • E p i d u ra l i nject i o n : i n patie nts i ntracta ble to local a naesthesia • S i n uvertebral block
1 26 SECTION O N E - G E N E RA L P R I N C I PLES
Box 5.7
Contra ind ications to corticosteroid injection
Absolute contra indications • I nfection of a j o i nt • Severe i nfection of neig h bo u r i n g s k i n • Osteomye l itis i n n e i g h b o u r i n g bones • Bacterae m i a • Bacterial endocarditis • Active tuberculosis and herpes corneae • I m m une deficiency (leukaemia, AI DS) • All ergy to steroid or its veh icle • Osteochondral fracture • J o i nt prosthesis • U ncontro l led clotting d isorder Relative contra indications • Anticoagulant treatment: the risk of b l eed i n g from the need le p u ncture is s m a l l , but cl otti ng should not be excessively delayed160 • Haemarthrosis • Reiter's d isease • M a rkedly u nsta b l e j o i nt • Poorly controlled d i a betes • Adjacent a braded s k i n : cha nce of i nfection is real
nowadays is the one chosen by Ongley which has a safe reputation as it was regularly used to sclerose varicose veins. It is formulated as described in Table 5.8 and is mentioned u nder the name P2G. 198
Mode of action The infiltration produces a local inflammatory reaction which is followed by an increased proliferation of fibro blasts with production of new collagen fibres. The final outcome is tightening, reinforcement and loss of normal elasticity of the ligaments. Liu et a/199 and Maynard et a/200 studied the histologic effect of injections with a sclerosant. B iopsies of infiltrated medial collateral ligaments of the knee of the rabbit showed not only increase i n ligamentous mass and strength but also a normal alignment of the fibres. In other words, the newly produced connective tissue did not have the chaotic appearance of scar but appeared much the same as normal tissues, except that they were thi cker, stronger, and contained fibres of varying thickness. Klein et a/201 performed biopsies of posterior sacroiliac ligaments in three patients with chronic low back pain
Table 5.8
Phenol preparation for injection (P2G)
Component
% by weight
Phenol Anhydrous dextrose Glycerol Water
2 25 30 43
both before and after prolotherapy injections. After six injections at intervals of a week they found an increase in the average ligament diameter measured by electron microscopy from 0.055 micrometres to 0.087 micrcme tres. Light microscopy showed an increase in collagen producing fibroblasts. The ligament orientation was organized and linear, as in normal ligaments. In addition to the effects on fibrous tissue, phenol also has a neurolytic effect. When injected in or around the medial branches of the posterior ramus, it provokes a chemical denervation. This may explain the quick relief (sometimes from the day after the injection) obtained by a number of low back pain patients, treated with sclerosant injection.202
Indications The main indication for sclerosant therapy is at the lumbar spine. In recurrent disc protrusions or in chronic backache from postu ral ligamentous pain, a series of infiltrations is made in all the dorsal ligaments of L4-L5-Sl motion segments. Sclerosing injections are also used in treating sacroiliac strains. Infiltration is always at the ligamentoperiosteal junction. The technique may also be required in partial liga mentous ruptures, such as are present in recurring carpal subluxations or in the inferior tibiofibular liga ment. Infiltration is into the remains of the ligament at the ligamentoperiosteal attachment. The injections can also be used in the treatment of recurrent subluxations and strain of the acromioclavicular joint. Local reinforcement is aimed for in type II tennis elbow in which previous infiltrations with steroid have given poor or only temporary relief. Also recurrent supra- or infraspinatus tendinitis can be treated with pro liferant infiltrations. Again the injections should be given tenoperiosteally. Phenol can also be used for pain relief in intractable backache of the lumbar spine because of its neurolytic effect. The agent is infiltrated around the lateral or medial branch of the posterior ramus. If the right level has been chosen, pain relief of months' and years' du ra tion can be obtained and the injection can be repeated if necessary. Side effects and complications Infiltration of a sclerosant is quite painful. Therefore 25% of a strong local anaesthetic should always be added to the sclerosant solution. After an hour and up to 2 days thereafter there is considerable after-pain, sometimes to such an extent that the patient needs strong analgesics. Apart from the after-pain there are very few reported side effects.
CH APT E R 5 - PRI N CI PLES OF TREAT M E NT 1 27
In 1993 Dorman published a survey of prolotherapy injections performed on a total of 494 845 patients.203 Of these, 343 897 were treated for low back pain. Only 66 minor complications were reported. These included 24 reports of allergic reactions and 29 instances of pneu mothorax. All of these resolved without serious prob lems. There were also 14 reports of major complications, defined as the patient needing hospitalization or having transient or permanent nerve damage.
Results A double-blind controlled study of prolotherapy was published in the Lancet in 1987. 1 98 The investigators used
a strict set of criteria (such as no litigation, long-standing pain, no severe medical illnesses and a diagnosis of liga mentous back pain). One half of a group of 81 patients received prolotherapy injections with a solution of dex trose, phenol, l i docaine ( lignocaine) and glycerin, while the others were injected with saline. The average length of time of symptoms was 8.98 years in the treatment group and 10.72 years in the placebo group. The resu lts showed a statistically significant difference in the two groups, with the prolotherapy group showing a marked decrease in subjective pain as compared to the saline groups (p
REFERENCES 1. Buckwalter JA. Effects of early motion on healing of musculo
skeletal tissues. Halld Ciill 1996;12(1):13-24. 2. Carreck A. The effect of massage on pain perception threshold .
2 1 . Stannard J P, Bucknell AL. Rupture of the triceps tendon
associated with steroid injections. Alii ' Sports Med 1 993;21 (3): 482-485. 22. Clark SC, Jones MW, Choudhury RR, Smith EN. Bilateral
Mallip Pllysiotller 1994;26: 10-16. 3. Cyriax J. Textbook of Orthopaedic Medicille, vol II, 1 1 th edn.
Bai lliere Tindall, London, 1984. 4. Gobelet C, Rostan A, Mourre R. Tendinite chez Ie sportif: traite ment par massage transverse profond et glace. Schweiz Ztschr Sportllled ] 982;30:21-23. 5. Woodman R, Pare L. Evaluation and treatment of soft tissue
lesions of the ankle and forefoot using the Cyriax approach.
patellar tendon rupture secondary to repeated local steroid injections. 1 Accid Elllerg Med 1995;12(4) :300-301 . 23. Lynch SA, Renstrom PA. Treatment of acute lateral ankle ligament rupture in the athlete. Conservative versus surgical treatment. Sports Med 1999;27(1):61-7l . 24. Warren CG, Lehmann J F, Koblanski I N . Heat and stretch proce dures: an evaluation using rat tail tendon. Arch Phys Med Rehabil 1976;57(3):122-126.
Phys Tiler 1982;62:1144-1147.
6. Cyriax J. Deep massage. Physiotherapy 1977;63:60-6 1 . 7. Houbben R . La tendinite du tendon rotulien chez Ie sportif pa r Ie massage transversal profond . Mel1l Fin d 'E tl/de, Fleron,
25. Reed B, Ashikaga T. The effects of heating with ultrasound on
knee joint displacement. Ort/wp Sports Phys Ther 1997;26(3): 131-137. 26. Grieve G. Modeme Mall uele Therapie VnJI de Wervelkololll, vol Il,
1989. 8. Van Lauwe L. Diepe dwarse fricties bij weke delen letsels.
Stedelijk hoger instituut voor paramedische beroepen stad Gent, 1988. 9. De Bruijn R. Deep transverse friction: its analgesic effect. Int f
editor, Lochem, 1988. 27. Yates D. Indications and contra-indications for spinal traction. Physiotherapy 1972;53:55-57. 28. Kirkaldy-Willis W. Managing Low Back Pain, 2nd edn. Churchill
Livingstone, London, 1988.
Sports Med 1984;5:35-36. 10. Kaada B, Torsteinbo O. Increase of plasma beta-endorphins in
connective tissue massage. Cell PharmacoI 1989;29(4):487-489. 11. Field TM. Massage therapy effects. Am Psychol 1998;53(12): 1270-1281. 12. Goats Gc. Massage - the scientific basis of an ancient art: Part 2.
Physiological and therapeutic effects. Br 1 Sports Med 1994;
29. Harris P. Cervical traction. Review of literature and treatment
guidelines. Phys Ther 1977;57(8):910-914. 30. Deets 0, Hands K, Hopp S. Cervical traction: a comparison of
sitting and supine positions. Phys Ther 1977;57(3):255-261 . traction. Physiotherapy
3 1 . M a thews J . The effects o f spinal 1972;53:696-697.
32. Gupta R. Epidurography in reduction of lumbar disc prolapse
28(3):1 53-1 56. 13. Evans P. The healing process at cel lular level, a review.
by traction. Arch Phys Med Rehab 1978;59:322-327. 33. Onel 0, Tuzlaci M. Sari H, Demir K. Computed tomographic
Pllysiotherapy 1980;66:256-259. 14. Buckwalter JA, Crues R. Healing of musculoskeletal tissues.
investigation of the effect of traction on lumbar disc herniations.
In: Rockwood CA, Green DP (eds) Fractu res. Lippincott, Philadelphia, 1991. 15. Hardy MA. The biology of scar formation. Phys Ther
Spine 1989;14:82-90.
16. Buckwalter JA. Effects of early motion on healing of musculo skeletal tissues. Halld Ciill 1996;12(1):13-24 17. Walker H. Deep transverse frictions i n ligament healing. , Orthop Sports Phys Ther 1984;6(2) :89-94. 18. Winter B. Transverse frictions. S Afr f Physiother 1 968;24:5-7. 19. MacGregor M. Manual treatment at the knee. Physiotherapy
treatments. Physiotherapy 1989;75(3) :445-453. 36. Spitzer W et al. Scientific approach to the assessment and man
agement of activity-related spinal disorders: a monograph for clinicians. Report of the Quebec Task Force on Spinal Disorders. Spille 1987;12: 1-59. 37. Hoehler F, Tobis J, Buerger A. Spinal manipulation for low back
pain. lAMA 1981;245 : 1 835-1838.
1971 ;57:207-2 1 1 . Sports Phys Ther 1982;4:16-22.
58-63. 35. Grieve G. Contra-indications to spinal manipulation and allied
1989;69: 1014-1023
20. Chamberlain G. Cyriax's friction massage: A review.
34. Hickling J. Spinal traction technique. Physiotherapy 1972;58:
1
Orth
38. Farrell J P, Twomey LT. Acute low back pain. Comparison of two
conservative treatment approaches. Med f A ustr 1982;1:160-164.
1 28 S E CT I O N O N E - G E N E RAL P R I N C I PLES
39. Haldeman S, Rubinstein S. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1 992; 17(12):1 469-1473. 40. McKenzie R. A perspective on manipulative therapy. Physiotherapy 1989;75(8). 4] . Sandoz R. Some physical mechanisms and effects of spinal adjustments. Anll Swiss Chil'o Assoc 1 976;6:91-1 4 1 . 42. Threlkeld AJ. The effects o f manual therapy o n cOlmective tissue. Phys Ther 1 992;72:893-902. 43. Triano J, Schultz AB. Loads transmitted during l umbosacral spinal manipulative therapy. Spille 1997;22(17) : 1955-1964. 44. Frymoyer J, Ducker T, Hadler N, Kostuik J, Weinstein J, Whitecloud T. The Adult Spine. Raven Press, New York, 1 99 1 . 45. Roston J, Wheeler H a i nes R. Cracking in the metacarpo phalangeal joint. ] Anat 1 947;81: 1 65. 46. Unsworth A, Dowson D, Wright V. Cracking joints, a bioengi neering study of cavitation in the metacarpophalangeal joint. A IIII RheulI/ Dis 1 971 :30:348. 47. Herzog W, Zhang YT, Conway pJ, Kawchuk GN. Cavitation sounds during spinal manipulative treatments. J Manip Physioi Ther 1993;1 6(8):523-526. 48. Cyriax J. Textbook of Orthopaedic Medicine, vol 1, 1 1 th edn. Baill iere Tindall, London, 1984:41 . 49. Maher C, Latimer J. Pain or resistance - the manual therapist's dilemma. Aust Physiother 1992;38(4):257-260. 50. Binkley J, Stratford P, Gill C. Inter-therapist reliability of lumbar accessory motion mobility testing. Proceedings IFOMT, Vail, 1993. 5] . Potter N, Rothstain J . Intertester reliability for selected clinical tests of the sacro-iliac joint. Phys Ther 1 994;6:2. 52. Matyas T, Bach T. The reliabi l i ty in selected techniques in clini cal arthrometrics. Aust ! Physiother 1 985; 1 : 1 75. 53. Gonella C, Paris S, Ku tner M. Reliability in evaluating passive intervertebral motion. Phys Ther 1982;62:437. 54. Panzar D. The reliability of lumbar motion palpation. ] Manip Physiol Ther 1 992;15(8):51 8-524. 55. Keating J, Bergman T, Jacobs G, Bradley D, Finer A, Larson K . lnter-examiner reliability of eight evaluative dimensions o f lumbar segmental abnormality. ! Manip Physiol Ther 1990;13: 463-470. 56. Potter N, Rothstein J. Intertester reliability for selected clinical tests of the sacroiliac joint. Phys Ther 1985;65:1671-1675. 57. Mann M, Glashee-Whray M, Nyber R. Therapist agreement for palpation and observation of i liac crest heights. Phys Ther 1984;64:334-338. 58. Hardy G, Napier J. Inter- and intra therapist reliability of passive accessory movement technique. ] Physiother 1991;Dec:22-24. 59. Van Deurson L, Patijn J, Ockhusyen A, Vortman B. The value of some clinical tests of the sacroiliac joint. J Manual Med 1 990;5:96-99. 60. Carmichael J. Inter- and intraexaminer reliability of palpation for sacroiliac joint dysfunction. I Manip Physiol Ther 1987;10:164-171 . 61 . Hellsing A, Nordgren B, Schele R, Ahlborg B. Predictability of back pain around the age of 20. Reproducibility of examination variables. Proceedings of the Tenth I n ternational Conference of the World COllfederation for Physical Therapy, Sydney, 1987: 1 85-189. 62. Haldemann S. Functional and palpatory examination. Presented to the Illtemational Socieh} for the Study of the Lu mber Spille,
Zi.irich, 11 May 1 99 1 . 63. Cyriax J H . Textbook of Orthopaedic Medicine, v o l I, 8th edn. Baill iere Tindall, London, 1 982. 64. Maigne P. Newsletter of North AlIlericall Academy of Manipulative Medicine 1 972;3(2). 65. Winkel D. Orthopedische Gelleeskllllde en Manuele Therapie, vol 4a, Wervekolol1l. Bohn Stafleu Van Loghum 1 991 :79.
66. Rahlmann J. Mecllanisms of intervertebral joint fixation: a literature review. ] Mallip Physiol Titer 1987;10(4):177-187. 67. Mathews jA, Yates AH. Reduction of lumbar disc prolapse by manipulation. BM] 1 969;3:695. 68. Paris Sv. Spinal manipulative therapy. Clin Orthop Rei Res 1983;179:119-231. 69. Vernon HT, Dami MSI, Howley TP, Annett R. Spinal manipula tion and beta-endorphin: a controlled study of the effect of a spinal manipulation on plasma beta-endorphin levels in normal males. J Manip Physiol Titer 1 986;9(2):115-123. 70. Troisier O. Techniques. Masson, Paris, 1973:282, 290. 71 . Armstrong JR. Lumbar Disc Lesiolls. Churchill Livingstone, Edinburgh, 1965. 72. De Seze S. Les accidents de la deterioration structurale du disque. Semill Hop Paris 1955;1:2267. 73. De Seze S. Les attitudes antalgique dans la sciatique sicoradicu laire commune. Semin Hop Paris 1955;1:2291. 74. Sandoz R. Newer trends in the pathogenesis of spinal disorders. Anll Swiss Chil'O Assoc 1971 ;5:93-180. 75. Troisier O. Semiologie et Traitelllellt des Aigies Discales et Ligal1lentaires du Rachis. Masson, Paris, 1973:290. 76. Maigne R. DOlileurs d'Origille Vertebrale et Traitell/ents par Manipulatiolls, 3rd edn. 1974. 77. Dabbert 0, Freeman D, Weis A. Spinal meningeal hematome, warfarin therapy, and chiropractic adjustment. JAMA 1970;214(11):2058. 78. Schmidley J, Kocll TH. The noncerebrovascular complications of chiropractic manipulation. Neu rology 1984;34:684-685. 79. Sims-Williams H, Jayson M, Young S, Baddely H, Collins E. Controlled trial of mobilisation and manipulation for patients with low back pain in general practice. BM] 1 978;11 Nov:703-701i. 80. Coxhead C, Meade T, Inskip H, North W. Multicentre trial of physiotherapy in the management of sciatic symptoms. Lancet 16 May, 1 98 1 . 8 1 . Larsson L-G, B a u m J , Mudholkar G , Srivastava D. Hypermobility: prevalence and features in a Swedish popula tion. Brit J Rheum 1993;32:1 1 6-119. 82. Haldeman S, Rubinstein S. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spine 1 992;17(12): 1 469-1473. 83. Hoehler F, Tobis J, Buerger A. Spinal manipulation for low back pain. lAMA 1981;245:1835-1 838. 84. Lankhorst GJ. Manuele therapie, capita selecta. Ned Tijdscltr Geneeskd 1987;131(21). 85. Hadler N , Curtis P, Gillings D, Stinnet S. A benefit of spinal manipulation as adjunctive therapy for acute low back pain: a stratified controlled trial. Spine 1 987;12(7):702-706. 86. Haldeman S. Manipulation and massage for the relief of pain. In Wal l PD, Melzack R (eds) Textbook of Pain, 2nd edn. New York, Churchill Livingstone, 1989:942-951 . 87. Nachemson A. A critical look at the treatment for low back pain. In Goldstein M (ed) The Research Status of Spinal Manip"latioll Therapy, 1975. 88. Sims-Williams H, Jayson M, Young S, Baddely H, Collins E. Controlled trial of mobilisation and manipulation for low back pain: hospital patients. BMJ 1979;24:1318-1320. 89. Bergq uist-Ullman M, Larsson U. Acute low back pain in industry: a controlled prospective study with special reference to therapy and confounding factors. Acta Orthop Med 1 973;5:191-196. 90. Chrisman OD, M ittnacht A, Snook GA. A study of the results following rotatory manipulation in the lumbar intervertebral disc syndrome. ] Bone Joill t SlIrg 1964;46A:517.
CHAPT E R 5 - P R I N C I PLES O F TREAT M E NT 1 29
9 1 . Glover j, Morris J, Khosla T. Back pain: a randomized clinical
1 1 3. Edelstyn G, Gillespie P, Grebbel F. The radiological demon
trial of rotational manipulation of the trunk. Br ] Industr Med
stration of skeletal metastases: experimental observations. Ciill
1974;31 :59-64. 92. Ramussen G. A randomized clinical trial of manipulation:
diagnostic criteria and treatment techniques. In: Buerger AA, Greenman PE (eds). Empirical Approaches to the Validation of Spillal Manipulatioll. Thomas, Springfield, 1985:1 74-178. 93. Nuruga V. Relative therapeutic efficacy of vertebral manipula tion and conventional treahllent in back pain management. Alii J Phys Med 1982;61:273. 94. Koes BW, Bouter LM, van Mameren H et al. Randomised
95.
96.
97.
98
clini.cal trial of manipulative therapy and physiotherapy for persistent back and neck complaints: results of one year follow up. BM] 1992;304(6827):601-605. Koes BW, Bouter LM, van Mameren H et at. The effectiveness of manual therapy, physiotherapy, and treatment by the general practitioner for nonspecific back and neck complaints. A randomized clinical trial. Spine 1 992;17(1):28-35. Mathews J, Mills SB, Jenkins VM et al. Back pain and sciatica: controlled trials of manipula tion, traction, sclerosant and epidural injections. Br J RhelllllatoI 1987;26:416-423. Mathews W, Morkel M, Mathews J. Manipulation and traction for lumbago and sciatica. Physiotherapeutic techniques used in two controlled trials. Physiother Pract 1988;4:201-206. Gorr:1an P. Cardiac arrest after cervical spine mobilization. Med
J AlIst
1978;12(2) :1 69-170.
99. Dvorak j, Orelli F. Wie gefiihrlich ist die Manipulation der
Halswirbelsai.ile? Fallbericht und Ergebnisse einer Umfrage. Mall uelle Medizin 1982;20:44.
J. Vertebral artery occlusion follow ing manipulation of the neck. NZ Med 1 1978;88:441-443. 101 . Schellhas KP, Latchaw R, Wendling L, Gold L. Vertebrobasilar injuries following cervical manipulation. lAMA 1 980;244(13): 100. Parkin P, Wallis W, Wislon
1450-1453. 102. Mueller S, Sahs A. Brain stem dysfunction related to cervical
manipulation. Nell rology 1976;26:547-550. 103. Nyberg-Hansen P, Loken A, Tenstad O. Brainstem lesion with
coma for five years following manipulation of the cervical spine. 1 Nell roI 1978;218:97-105. 104. Daneshmend T, Langton Hewer R, Bradshaw J. Acute brain stem stroke during neck manipulation. BM] 1984;288:189. 105. Simmons K, Soo Y, Walker G, Harvey P. Trauma to the verte bral artery related to neck manipulation. Med ] Aust 1982;Feb 20:1 87-188. 106. Lyness S, Simeone F. Vascular complications of upper cervical
spine injuries. Orthop Ciin North Alii 1978;9(4) : 1 029-1038. 107. Hufnagel A, Hammers A, Schonle PW, Bohm KD, Leonhardt
G. Stroke following chiropractic manipulation of the cervical spine. 1 NellroI 1 999;246(8) :683-688. 108. Lee KP, Carlini WG, McCormick GF, Albers Gw. Neurologic complications following chiropractic manipulation: a survey of California neurologists. Neu rology 1995;45(6):1213-1215. 109. Klougart N, Leboeuf Y de C, Rasmussen LR. Safety in chiro practic practice. Part II: Treatment to the upper neck and the rate of cerebrovascular incidents. 1 Manipulative Physiol Ther 1996;19(9) :563-569. 110. Hooper J. Low back pain and manipulation. Paraparesis after
treatment of low back pain by physical methods. Med J Aust 1973;March 17:549-557.
RadioI 1 967;18:158. 1 1 4. De Kleyn A, Versteegh C. Uber verschiedene formen von
Meniere's syndrome. Deutsche Zschr Nerventh 1 933;132:57. Kleyn A, Nieuwenhuyse P. Sch windelanfalle und Nystagmus bei einer bestimmten Stellung des Kopfes. Acta
115. De
Otolaryng 1927;11:155-157. 1 1 6. Maigne
G. Manipulatie van de Wervelkololll ed itor De Tijdstroom, Lochem-Poperinge, 1 981 :209. 1 1 7. Terry GS, Hammon D, France P, Norwood LA. The stabilizing function of passive shoulder restraints. Am J Sports Med 1991;19:26-34. 1 1 8. Warner JJ, Lephart S, Fu FH. Role of proprioception in patho
etiology of shoulder instability. Ciin Orthop 1 996;330:35-39. 1 1 9 . B arrack RL, Skinner H B, Brunet DW. joint lax ity and
propr i oception
in
the
knee.
Physician
Sports
Med
1983;11 (6) : 1 30-135. 1 20. Freedman L, Mmlro RL. Abduction of the arm in the scapular
plane. J Bone Joint S u rg 1 966;48A : 1 503-1 5 1 0 . 1 2 1 . Kennedy JC, Alexander I}, Hayes KC. Nerve supply of the
knee and its functional Significance. Alii ] Sports Med 1982;10:329-335. 1 22. Newton RA. Joint receptor contributions to reAexive and
kinesthetic response. Phys Ther 1 982;62:22-29. 123. Rowinski MJ. A fferent neurobiology of the joint. In: Gould jA,
Davies GJ (eds) Orthopaedic alld Sports Physical Therapy, 2nd ed n. CV Mosby, St Louis, 1985;50-64. 124. Le Veau B, Rogers C. Selective training of the vastus medialis muscle using EMG biofeedback. Phys Ther 1 980;60(11 ) : 1410-1415. 125. Beal l MS J r, Diefenbach G, A l len A.
Electromyographic biofeedback i n the treatment of voluntary posterior instability of the shoulder. Aln ] Sports Med 1987;15(2):1 75-178. 126. Fyfe 1, Stanish WD. The use of eccentric training and stretch ing in the treatment and prevention of tendon injuries. Ciill Sports Med 1 992;11(3):601-624. 127. Alter MJ. Science of S tretching. Human K inetics, Champaign,
IL, 1988:90-120. 128. Brand C. Intra-articular and soft tissue injections. At/st Falll Physician 1 990;19(5):671-675, 678, 680-682. 129. Jenkner F. Nervenblockaden auf Pharmakologischel1l Weg, auf Elektrischem Weg, Nervenblockaden . 3rd edn. Springer Verlag, Wien, 1980. 130. Deconinck R, B isschop P, Ombregt L, Van de Velde A. Workbook in Orthopaedic Medicine. Belgian Scientific Society of Orthopaedic Medicine, De Haan, Belgium, 1989. 1 3 1 . Eriksson E. Illustrated Handbook ill Local Anaesthesia 2nd edn. Schultz Forlag, Denmark and AB Astra Lake-medel, Sweden, 1979:17. 132. Kerkkamp H, H asenbos M, Crul J. Ongewenste reacties op
lokale anaesthetica en de behandeling daarvan. Ned Tydsch Geneeskd 1985;(129)49:2353-2358. 133. Van Kleef J. Lokale anesthetica, fundamentele werkings
mechanismen en klinisch gebruik. Ned Tydsch Gelleeskd 1982;(126)42 : 1 8 1 6-182 1 . 134. Meyers F, Jawetz E , Goldfien A. Review of Medical Pharmacology,
2nd edn. Lange Medical, Los Altos, California, 1974:194. 135. Sitsen J, Besse T. Toepassing van middelen voor plaatselijke
1 1 1 . Schi6tz E, Cyriax J. Mallipulation: Past and Present. Heinemann,
verdoving anno 1985. Geneesllliddelellblll/etilJ 1985;19(14): 61-66.
London, 1975:129. 112. Cyriax j. Textbook of Orthopaedic Medicine, vol II, Treatmellt by Maniplliation, Massage and injection, 10th edn. Bailliere Tindall, London, 1984.
136. Rolly G. Nevenwerkingen en gevaren van locale anesthetica. Tijdschr v Geneeskd 1 9 78;3. 137. Fisher M, Pennington J. Allergy to local anaesthesia. Br J Allaesth 1982;54:577-603.
1 30 SECTION O N E - G E N E RA L PRI NCIPLES
1 3 8 . Fisher M, More D. The epidemiology and clinical features of
165. Anderton JM, Orth MCH, Helm R. Multiple joint osteonecro
anaphylactic reactions in anaesthesia. Allaesth lnte/lsive Care
sis following short-term steroid therapy. ] Balle loillt SlIrg
1981;9:226-234. 139. Fisher M. Treating anaphylaxis with sympathomimetic drugs.
1 982;64A(l) : 1 39-141 . 166. Sweetnam DR, Mason RM, Murray RO. Steroid arthropathy of
the hip. BMJ 1960: 1 392-1394.
BM/ 1992;305:11 07-1 108. 1 40. Schwarz F. Klinische toepassing van cortico-steroiden. Stafleu 's
1 67. Bentley G, Goodfellow W. Disorganisation of the knees fol
lowing intra-articular hydrocortisone injections. I Balle loillt
wet lIitg IIrnatsch 1968. 1 4 1 . Cyriax J. Hydrocortisolle ill Orthopaedic Medicine. Diagnostic Criteria alld Techllique. Cassell, London, 1956.
S u rg 1969;51B:498-502 168. Van der Korst JK. lntra-articulaire toediening van corticos
142. Strandberg B. Intra-articular steroid therapy. Acta Rheulllatol
teroiden: een poging tot herwaarding. Ned Tijdschr Gelleeskd
Scalld 1964;10:29-54. 143. Gottlieb N, Riskin W. Complications of local corticosteroid
1984;128(47):22-34. 169. Gray R, Tenenbaum J, Gottlieb N. Local corticosteroid injec
tion treatment in rheumatic disorders. Semill Arthrit Rhelllll
injections. lAMA 1980;243(15) :235-263. 144. Glick E, Rigby P. Intra-articular use of triamcinolone hexa 145. 146. 147. 148.
cetonide. Arthritis Rheum 1971 ;14(3) :383-384. De Schaepdryver A. Medische Fanllakologie. Gent, 1976. Blacow N (ed) Martilldale: The Extra Pharlilacopoeia, 26th edn. The Pharmaceu tical Press, London, 1975:496. Crisp E, Kendall P. Treatment of periarthritis of shoulder with hydrocortisone. BMI 1955;1 : 1 500-1501 . Weiss J, Ming Ting Y. Arthrography-assisted intra-articular injection of steroids i n treatment of adhesive capsulitis. Arcll
1 981 :10:231. 1 70. Gibson T, Burry H, Poswillo 0, Glass J. Effect of intraarticular
corticosteroid injections on primate cartilage. AIIII Rhelllll Diseases 1976;36:74-79. 1 71 . Shaw N, Lacey E. The influence of corticosteroids on joint
tissues. J Bone Joint S u rg 1970;52B(1). 1 72. Clark Sc, Jones MW, Choudhury RR, Smith EJ. Bilateral
Pll IIS Med Rehab 1978;59:285-287.
173.
injections of depot corticosteroids. A rch Phys Med Rehab
1 74.
149. St� inbrocker 0, Argyros T. Frozen shoulder: treatment by local 1974;55:209-213. ] 50. McCarty D. Treatment of rheumatoid joint inflammation with
triamcinolone hexacetoni de. Arthritis RheulII 1 972;15(2):
1 75.
157-173. 151 . Fitzgerald R. Intra-synovial injection of steroids. Use and
abuses. Mayo Ciill Proc 1 976;51.
1 76.
152. Curran J, Ellman M, Brown N. Rheumatologic aspects of
painful conditions affecting the shoulder. Ciin Orthop Rei Res 1983;173:27-37. 153. Kolind-Sorensen V. Treatment of trigger fingers. Acta Orthop Scnnd 1970;41:428-432. 154. Lapidus P, Guidotti F. Stenosing tenovaginitis of the wrist and
fingers. Ciill Orthop Rei Res 1 972;83:87-90. 155. Freiberg R, Weinstein A. The scallop sign and spontaneous
rupture of finger extensor tendons in rheumatoid arthritis. Ciill Orthop Rei Res 1972;83. 1 56. Clark 0, Ricker J, McCollum M. The efficacy of local steroid
injection in the treatment of stenosing tenovaginitis. Plastic Recollstr S u rg 1973;Feb : 1 79-180. 157. Furey G. Plantar fasciitis. I Bone joillt S u rg 1975;57A(5): 672-673. 1 58. Valtonen E. Triamcinolone hexacetonide and methylpred
nisolone. Scnlld j Rheumato/ 1978;(suppI 16):3-13. 159. Schuchmann J, Melvin J, Duran R, Coleman C. Evaluation of
local steroid injection for carpal tunnel syndrome. A rch Phys Med Rehab ] 971;June. 1 60. Gray R, Gottlieb N. Intra-articular corticosteroids. An updated
assessment. Ciill Orthop Rei Res 1983;177:235-263. 1 6 1 . Leslie B, Harris J, Driscoll D. Septic arthritis of the shoulder in ad u l ts. I Balle loillt S u rg 1989;71A(10) : 1 5 1 6-1522. 162. Hughes RA, Rowe I F, Shanson 0, Keat AC. Septic bone, joint and muscle lesions associated with human immunodeficency virus infection. Br j RheulilatoI 1992;31(6);381-383. ] 63. Gardner GC, Weisman M H . Pyarthrosis in patients with rheumatoid arthritis: a report of 13 cases and a review of the l i teratu re from the past 40 years. Am I Med 1990;88(5): 503-5 1 1 . 164. Behrens F, Shepard N, Mitchell N . A l teration of rabbit articu
lar cartilage by intra-articular injections of glucocorticoids. I Balle loillt Surg 1975;57A(1):11 57-1 1 60.
1 77.
patellar tendon rupture secondary to repeated local steroid injections. Accid Emerg Med 1995;12(4) :300-301 . Stannard JP, Bucknell AL. Rupture o f the triceps tendon associ ated with steroid i njections. Alii I Sports Med 1993;21(3):482-485. Wiggins ME, Fadale PO, Barrach H, Ehrlich MG, Walsh WR. Healing dlaracteristics of a type I collagenous structure treated with corticosteroids. Am J Sports Med 1994;22(2):279-288. Wiggins ME, Fadale PO, Ehrlich MG, Walsh WR Effects of local injection of corticosteroids on the healing of ligaments. A follow-up report. I Balle ]oill t Surg 1995;77A : 1 682-1 691 . Noyes F, Nussbaum N, Torvik P, Cooper S. Biomechanical and ultrastructural changes in ligaments and tendons after local corticosteroid injections. I Balle joillt Surg 1975;57 A:876. Kennedy J, Wil lis B. The effects of local steroid injections on tendons: a biomechanical and microscopic correlative study. Amer I Sports Med 1976;4(1).
1 78. Coonrad R, Hooper R. Tennis elbow: its course, natural
history, conservative and surgical management. J Balle loil l t S u rg 1973;55A : 1 1 77-1 182. 1 79. Campbell RB, Wiggins ME, Cannistra
LM, Fadale PO, Akelman E. I n fluence of steroid injection on ligament healing in the rat. Clin Orthop 1996;332:242-253. 180. McWhorter JW, Francis RS, Heckmann RA. Influence of local steroid injections on traumatized tendon properties. A bio memanical and histological study. Alii ] Sports Med 1991;19(5): 435-439.
1 8 1 . Read MT. Safe relief of rest pain that eases with activity in
achillodynia by intrabursal or peritendinous steroid injection: the rupture rate was not increased by these steroid injections. Br I Sports Med 1999;33(2):1 34-1 35. 182. Mackitulon S, H udson A, Gentili F, Kline 0, Hunter D.
Peripheral nerve injection injury with steroid agents. Plastic Reconstr S u rg 1982;69(3):482-489. 183. Preston 0, Logigian E. Iatrogenic needle-induced peroneal
neuropathy in the foot. AIII1 in tern Med 1988;109(11 ):921-922. 184. McFarland R, Dugdale T, Gerbino P, N ielsen R. Neurovascu lar
complications
resul ting
from
corticosteroid
injections.
Physician Sports Med 1990;18(7) :89-9 1 . 185. Geusens P, Dequeker J. Locomotor side effects of corticos
teroids. Bailliere's Ciill RhellmatoI 1991 :5(1) :99-118. 186. Meikle W, Tyler F. Potency and duration of action of glucocor
ticoids: effect of hydrocortisone, prednisone, dexamethasone on human pituitary-adrenal function. Am J Med 1977:63. 1 87. Shuster S, Williams 1. Adrenal suspension due to intra articular corticosteroid therapy. Lancet 1961 : 1 7] -172.
C HAPTER 5 - P R I N C I PLES O F TREATM E N T 1 3 1
188. Thierry M. Gynecologie. ObstetriCil. Omega, Gent, 1984:563. 189. Lems W, Jacobs J, Raymakers J, Bijlsma J. Botontkalking door
corticosteroiden. Ned Tijdschr Geneeskd 1992;136:1595-1599. 190. Veys E, Mielants H, Verbruggen G. Reumatologie. Omega, Gent, 1985.
V, Leynadier F et al. Systemic allergic reactions to corticosteroids. I Asthllla 1991;28(5):329-339. 192. Gonzalo FE, Montagut LB, Vecina ST. Anaphylactic shock caused by triamcinolone acetonide. A n n Pharl11acother
1 9 1 . Murrieta-Aguttes M, Mid1elen
1994;28(11):1310. 1 93. Larsson LG. Anaphylactic shock after i.a. administration of
triamcinolone acetonide in a 35-year-old female. Scand J Rlleulllato/ 1989;18(6):441-442. 194. Downs AM, Lear JT, Kennedy CT. Anaphylaxis to intra
dermal triamcinolone acetonide. Arch Dermatol 1998;134(9): 1 1 63-1164. 195. Patterson DL, Yunginger JW, Dunn WF, Jones RT, Hunt LW.
Anaphylaxis induced by the carboxymethylcellulose compo nent of injectable triamcinolone acetonide suspension (Kenalog). Anll Allergy Asthma Imll1unoI 1 995;74(2) : 1 63-166. 196. Vaughan D, Asbury T, Cook R. General Ophthalmology, 6th edn. Lange Medical, Los Altos, 1971 :255.
197. Hackett
G.
L igalllent
and
Telldoll
Relaxatioll
Treated
by
Prolothernphy, 3rd edn. Thomas, Springfield, 1958. 198. Ongley M, Klein R, Thomas A. A new approach to the treat
ment of chronic low back pain. Lallcet 1987;2: 1 43-146. Y, Tipton C, Matthes R et al. An in situ study of the influence of a sclerosing solu tion in rabbit med ial collateral l igaments and its junction strength. COlllleet Tissue Res
199. Liu
1983;11:95-102. 200. Maynard J, Pedrini V, Pedrini-Mille A, Romanus B, Ohlerking
F. Morphological and biochemical effects of sodium morrhu ate on tendons. f Orthop Res 1985;3 :236-248. 201 . Klein R, Dorman T, Johnson C. Proliferant injections for low back pain: histologic changes of injected ligaments and objec tive measurements of lumbar spinal mobility before and a fter treatment. J Neural Orthop Med SlI rg 1989; 1 0 : 1 23-126. 202. Silvers H . Lumbar percutaneous facet rhizotomy. Spille 1990;15:36-40. 203. Dorman T. Prolotherapy. A su rvey.
J
Ortllop Med 1993;15:
28-32. 204. Klein R, Eek B, DeLong B, Mooney V. A randomized double
blind trial of dextrose-glycerine-phenol injections for chronic, low back pain. J Spinal Disord 1993;6:23-33.
THIS PAGE INTENTIONALLY LEFT BLANK
SECTION TWO
The cervical spine
SEalON CONTENTS 6. Applied anatomy of the cervical spine
Bones 135 Intervertebral discs Joints 137 Ligaments 139 Muscles 142 Nervous structures Nerve roots 144 Blood supply 145
Infections 216 Intraspinal tumours 217 Neurological conditions with positive signs on neck examination 218 Visceral conditions 219 Shoulder girdle disorders causing cervicoscapular
135
137
pain
142 11.
Uncoarterioradicular junction
219
Headache and vertigo of cervical origin Headache
146
Vertigo 7. Clinical examination of the cervical spine
History 147 Inspection 151 Functional examination Technical investigations
227
147 12. Whiplash-associated disorders
152 161
8. Interpretation of the clinical examination
165
Interpretation of the history 165 Interpretation of the functional examination Interpretation of the neck movements 169
169
239
Definition 239 Incidence 240 Classification 240 Pathology 241 Medicolegal consequences 241 Psychological problems 242 Diagnosis 242 Natural history Chronicity
Interpretation of the shoulder girdle movements 172 Interpretation of the arm movements
223
223
243
243
Therapeutic approach
243
172 13. Treatment
9. Mechanical disorders
247 Treatment of discodural and discoradicular
175
Degeneration and anatomical changes
176
Ageing of the cervical spine 176 Pathology 177 Disorders of the disc: disc displacements 177 Stages of disc displacement 178 Degenerative disorders 197 Capsuloligamentous disorders 204 Disorders causing pain on resisted movements of the neck 204 Disorders causing symptoms on active and/or resisted shrugging of the shoulders 205 10. Non-mechanical disorders
211
Warning signs 211 Classification 211 Osseous disorders 211 Rheumatoid arthritis and ankylosing spondylitis
215
interactions 247 Manipulation 247 Traction 263 Injection at a nerve root Epidural injection 266 Collars 266 Prophylaxis 266
265
Awaiting spontaneous recovery 267 Surgery 267 Treatment of other, non-discogenic lesions Manipulation/capsular stretching 267 Deep transverse friction 269 Injection/ infiltration 270 Collar 271 Surgery 271
267
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Bones
Upper cervical spine Lower cervical spine Intervertebral discs Joints
Applied anatomy of the cervical spine
135 135 136
137
137
Occipitoatlantoaxial joints Joints between C2 and C7
137 138
139
Ligaments
Liga'ments of the occipitoatlantoaxial complex Ligaments of the lower cervical spine 141 Muscles
BONES
142
Nervous structures
142
The cervical spine has seven vertebrae, which may be divided in two groups that are distinct both anatomically and functionally: the upper pair (C1 and C2, the atlas and axis) and the lower five (C3-C7) (Fig. 6.1).
Related structures 142 Spinal membranes 143 Nerve roots
144
The dural sheath 145 The parenchyma 145 Innervation of the cervical spine Blood supply
140
The anatomy of the cervical spine is complex and unique. To understand the diagnosis and treatment of the multiple disorders affecting this vital region, a thorough knowledge of the anatomy is necessary.
145
Uncoarterioradicular junction
146
145
UPPER CERVICAL SPINE
The upper cervical spine has the first and second verte brae - the atlas and axis - and forms a unit with the occiput.
The atlas The atlas (Fig. 6.2) does not have a vertebral body - this has been absorbed into the axis vertebra, to form the odontoid process (Fig. 6 3). A thick anterior arch remains, .
Figure 6.1
Anterior view of the cervical spine 135
136 SECTION TWO - THE CERVICAL SPINE
(a)
(b) 2
Figure 6.3 The axis (C2): 1, odontoid process (dens); 2, transverse foramen; 3, spinous process.
LOWER CERVICAL SPINE
Figure 6.2 The atlas (C1). (a) Superior view, (b) inferior view: 1, posterior arch; 2, anterior arch; 3, transverse foramen.
extending into and joining the two lateral masses, on which are the superior atlantal joint facets, which articu late with the occipital condyles; and the inferior joint facets of the axis. The posterior arch is thinner than the anterior arch and forms the posterior junction of the lateral masses. The large vertebral foramen thus formed has a larger diameter in the transverse than in the sagittal plane. The transverse processes contain a transverse foramen through which the vertebral artery passes before it loops back above the upper surface of the posterior arch, which sometimes contains an arterial groove, although anatomical anomalies are frequently encountered. The posterior aspect of the anterior arch has a facet for articulation with the odontoid process of the axis, which is held in place by the transverse ligament, spanned between two tubercles, which project from the inner sides of the lateral masses.
The lower cervical spine is composed of the third to the seventh vertebrae which are all very similar. Each verte bral body is quite small (Fig. 6.4). Its height is greater pos teriorly than anteriorly and it is concave on its upper aspect and convex on its lower. On its upper margin it is lipped by a raised edge of bone. The anteroinferior border of the vertebral body projects over the antero superior border of the lower vertebra. Anterolateral (in the upper vertebrae) to posterolateral (in the lower vertebrae) on the upper surface of the body, two uncinate processes project upwards and articulate with the lower notches (or anvils) of the upper vertebra to form the joints of von Luschka or uncovertebral joints. (a)
3
The axis The second cervical vertebra is the axis (Fig. 6.3). Its ver tebral body is formed by fusion with the vertebral body of the atlas to form the odontoid process (or dens), which is completely separate from the atlas. The laminae of the axis are very well developed and blend into a bifid spinous process. Both transverse processes have a transverse foramen for the vertebral arteries. The superior articular facets of the axis articulate with the inferior articular facets of the atlas. The inferior articular facets of the axis articulate with the superior articular facets of the third vertebra.
(b)
Figure 6.4
A lower cervical vertebra. (a) Superior view, (b) anterior view: 1, posterior tubercle; 2, anterior tubercle; 3, transverse foramen.
CHAPTER 6
Figure 6.5
- APPLIED ANATOMY OF THE CERVICAL SPINE 137
The seventh cervical vertebra.
Laterally, the transverse processes have an anterior and a posterior tubercle, which are respectively the rem nants of an embryonic rib and transverse process. The spinal nerve lies in the groove between the two tubercles. The transverse process also has a transverse foramen for the vertebral artery and vein. This is not so at C7, where the foramen encloses only the accessory vertebral vein. The intervertebral foramina are between the superior and inferior pedicles. The articular processes for the artic ulation with the other vertebrae are more posterior. The two laminae blend together in a bifid spinous process (at C3, C4 and C5). The spinous processes of C6 and C7 are longer and taper off towards the ends. C7 has a large spinous process and is therefore called the vertebra prominens (Fig. 6.5).
Figure 6.6
The intervertebral discs.
Table 6.1 Differences between the cervical and lumbar discs Cervical
Lumbar
Contained by vertebral bodies Thicker anteriorly than posteriorly Annulus thicker posteriorly Nucleus in anterior part of disc
Not contained by vertebral bodies Equal height Annulus weaker posteriorly Nucleus in posterior part of disc
INTERVERTEBRAL DISCS
There are six cervical discs, because there is no disc between the upper two joints. The first disc is between the axis (C2) and C3. From this level downwards to the C7-Tl joint they link together and separate the vertebral bodies. Each is named after the vertebra that lies above: e.g. the C4 disc is the disc between the C4 and C5 vertebrae (Fig. 6.6). The disc, comprised of an annulus fibrosus, a nucleus pulposus and two cartilaginous endplates, has the same functions as the lumbar disc, and so will not be discussed in detail (see Applied Anatomy of the Lumbar Spine). There are, however, some differences (Table 6.1). At the cervical spine the discs are more effectively within the spine than they are at the thoracic or lumbar levels because of the superior concavity and inferior convexity of each vertebral body. They are also about one-third thicker anteriorly than posteriorly, which gives the cervi cal spine a lordotic curve that is not related to the shape of the vertebral bodies. The annulus fibrosus is also thicker in its posterior part than it is in the lumbar spine.
The further down the spine, the more the nucleus pulpo sus lies anteriorly in the disc, and it disappears earlier in life than it does in the lumbar spine. For both these reasons, nuclear disc prolapses are uncommon after the age of 30.
JOINTS
The cervical spine is more mobile than the thoracic or lumbar. Its structure allows movements in all directions, although not every level contributes to all movements. OCCIPITOATLANTOAXIAL JOINTS
The occipital condyles are arcuate in the sagittal plane and fit into the cup-shaped superior articular surfaces of the atlas (Fig. 6.7). These joints only allow moderate flexion-extension (13-15°) and lateral flexion (3-8°) movements (Fig. 6.8). Axial rotation is not possible at these joints.
138 SECTION TWO - THE CERVICAL SPINE
(a)�
Figure 6.7
The occipitoatlantoaxial joint complex: 1, occiput; 2, atlas; 3, axis.
At the joint between C1 and C2 extensive rotation movement is possible (45-50°) which represents about 50% of rotation in the neck (Fig. 6.9). There is a moderate flexion-extension excursion (10°) but lateral flexion is impossible. JOINTS BETWEEN (2 AND (7
Most flexion-extension takes place at the joints C3-C4, C4-C5 and especially C5-C6. Lateral flexion and axial rotation occur mainly at C2-C3, C3-C4, C4-C5. Mobility is less in the most caudal segments and cou pling of movements is present (Fig. 6.10a). This phenom enon is the result of the position of the articular surfaces of the facet joints (see p. 139). Lateral flexion is always combined with ipsilateral rotation. So, for example, lateral flexion to the left is accompanied by rotation to the left. This is greatest at C2-C3 and coupling rotation decreases towards the caudal aspect of the spine. The clinical importance of this becomes clear during exami nation: specific articular patterns may occur as its result. Movement takes place at two sites. First, in the anterior part of the lower cervical spine, which contains the inter vertebral joints (with their intervertebral discs) and the uncovertebral joints and, second, in the posterior part where the facet joints, the arches and the transverse and spinous processes are found.
(e)
\
+
Anterior aspect Intervertebral joints. The intervertebral joint is the complex of two vertebral bodies and the intervertebral disc between them (Fig. 6.11). The disc has several func tions: it permits greater mobility between the vertebrae; it helps distribute weight over the surface of the verte bral body during flexion movements; and it acts as a shock absorber during axial loading. The joints are mainly stabilized by the anterior and posterior longitu dinal ligaments. Uncovertebral joints (Fig. 6.12). These develop during childhood when fissuring occurs in the lateral aspect of
Figure 6.B
The occipitoatlantal joint and its movements: (a) flexion, (b) extension, (c) lateral flexion.
the intervertebral disc, leading to the formation of a cleft in the adult spine. They do not contain articular cartilage or synovial fluid and must therefore be considered as pseudojoints, although they do undergo degenerative changes. These secondary 'joints' add to lateral stability.
CHAPTER 6 - APPLIED ANATOMY OF THE CERVICAL SPINE 139
I \ �I \� I \ \
Figure 6.9
(a)
The atlantoaxial joint and its rotation.
Posterior aspect and facet joints Posteriorly the vertebrae are held together by the liga ments between the spinous processes (ligamentum nuchae and interspinous ligaments) and between the laminae (ligamentum flavum), and they articulate via the facet joints. The facet joints are classified as diarthrodial joints: the articular surfaces are covered with cartilage; there is a synovial membrane and a fibrous joint capsule with con tained synovial fluid. The joint line is oblique: it courses from anterosuperior to posteroinferior, along an angle of 45° at the level C2-C3, which decreases to 10° at C7-Tl (Fig. 6.13). Because the joint line is oblique and the capsule is lax, more movement is possible than at the thoracic and lumbar levels. Rotation is always combined with ipsilateral side flexion. During rotation to the left the lower facet of the upper vertebra at the left side glides backward on the upper facet of the vertebra below. The opposite happens at the right. During extension of the neck, the vertebral body of the upper vertebra glides backwards (Fig. 6.14a). The lower facets not only glide backwards and downwards but also tilt backwards, which results in opening in front and closing behind. The reverse happens during flexion: the lower facets of the upper vertebra glide forwards and upwards and tilt forwards, which opens the joint at the back and closes it in front (Fig. 6.14c).
(b)
LIGAMENTS
The cervical spine has a complex ligamentous system. Ligament function is to maintain normal osseous rela tionships. Clinically, however, they are not so important because ligamentous lesions in the cervical spine are not
Figure 6.10 Combined flexion and rotation in the lower cervical spine (a), and lateral view of disc movements (b), upper: extension; middle: neutral position; lower: flexion.
140 SECTION TWO - THE CERVICAL SPINE
(a)
Figure 6.11
The intervertebral joint (coloured).
Figure 6.12
The uncovertebral joint (boxed). Figure 6.14
Movements at the facet joints: (a) extension, (b) neutral, (c) flexion.
LIGAMENTS OF THE OCCIPITOAT LANTOAXIA L COMP LEX
These are strong structures that stabilize the upper cervi cal spine. First, there are the ligaments connecting the occiput to atlas and axis: the anterior atlanta-occipital mem brane, the posterior atlanta-occipital membrane and the tecto rial membrane (Fig. 6.15). A second ligamentous complex connects the axis to the occiput: the apical ligament, the longitudinal component of the cruciform ligament and the alar ligaments (Fig. 6.16). Third, there is the complex of lig aments that connect axis to atlas: the lateral component of
Figure 6.13 The facet joints, showing the decrease of the obliquity of the joint line towards the lower part of the spine.
that common and, when they occur, it is difficult to find out where exactly the problem lies. Two distinct sets of ligaments can be recognized: the ligaments of the occipitoatlantoaxial complex and those of the lower cervical spine.
Figure 6.15 The occipitoatlantal ligaments: 1, anterior atlanto-occipital membrane; 2, tectorial membrane; 3, posterior atlanto-occipital membrane.
CHAPTER 6 - APPLIED ANATOMY OF THE CERVICAL SPINE 141
Figure 6.16 The occipitoaxial ligaments: 1, apical ligament; 2, cruciform ligament; 3, alar ligament.
the cruciform ligament (the transverse ligament), the two accessory atlantoaxial ligaments and the ligamentum flavum (Fig. 6.17). Finally, the ligamentum nuchae (Fig. 6.18) is attached above to the external occipital protuberance, lies in the sagittal plane and merges with the interspinous ligaments and supraspinous ligament, which becomes an individual ligament from the spinous process of C7 downwards. This ligament contains much elastic tissue
Figure 6.18
The ligamentum nuchae.
and is stretched during neck flexion. Because of its elastic ity it helps to bring the head back into the neutral position. LIGAMENTS OF THE LOWER CERVICA L SPINE
The anterior longitudinal ligament (Fig. 6.19) is closely attached to the vertebral bodies, but not to the discs. By contrast the posterior longitudinal ligament (Fig. 6.20) is firmly attached to the disc and is wider in the upper cervical spine than in the lower. Both ligaments are very
Figure 6.19
The anterior longitudinal ligament.
Figure 6.20
The posterior longitudinal ligament (posterior view).
(b)
Figure 6.17 The atlantoaxial ligaments: (a) cruciform ligament: 1, longitudinal component; 2, lateral component ( transverse ligament); 3, accessory atlantoaxial ligaments; (b) ligamentum flavum. =
142 SECTION TWO - THE CERVICAL SPINE
3
Figure 6.21
The supraspinous (1), interspinous (2) and intertransverse (3)
ligaments.
Figure 6.22
Flexor muscles: 1, scalenes; 2, longus colli; 3; longus capitis.
Figure 6.23
Superficial extensor muscles: 1, trapezius; 2, levator scapulae;
strong stabilizers of the intervertebral joints. The lateral and posterior bony elements are connected by the liga mentum flavum, the intertransverse ligaments and inter spinous ligaments and the supraspinous ligament (Fig. 6.21).
MUSCLES
Muscular action at the cervical spine is dependent on a combination of activities of a great number of muscles and whether or not they contract bilaterally or unilater ally. There are three functional groups: flexors; extensors; and rotators and lateral flexors. Most muscles do not have clinical importance, in that lesions of them hardly ever occur. However, they can sometimes indirectly involve other (non-contractile) structures. On examination a resisted movement (muscu lar contraction) or a passive movement (whereby the muscle is stretched) may influence a lesion lying outside the muscle in, for example, an inert tissue. It should be noted that the function of many of the muscles is multiple and depends on the mode of action employed. For example, bilateral action of the sterno cleidomastoids is involved in flexion-extension, but unilateral action results in ipsilateral lateral flexion and contralateral rotation (Fig. 6.25). Unilateral action of the flexors results in either pure rotation or lateral flexion, or a combination of both, some times ipsilaterally and sometimes contralaterally. Many of the extensor muscles have other functions as well as extension, the latter occurring when they act bilaterally. The muscles of the neck are illustrated in Figures 6.22-6.25.
3, splenius cervicis; 4, splenius capitis.
NERVOUS STRUCTURES RE LATED STRUCTURES
Spinal canal In the cervical spine, the spinal canal is commodious compared to that of the thoracic and lumbar spine. Its outline is oval in the transverse plane and the average anteroposterior diameter is 17 mm, although this varies with movement: flexion increases it and extension decreases it. During extension there is a backward movement of the upper vertebra in relation to the lower
CHAPTER 6
Deep extensor muscles: 1, longissimus capitis; 2, semispinalis capitis; 3, spinalis cervicis; 4, multifidus; 5, longissimus cervicis; 6, iliocostalis cervicis; 7, suboccipital complex. Figure 6.24
-
APPLIED ANATOMY OF THE CERVICAL SPINE 143
Figure 6.26 The intervertebral foramen: s, sensory fibres; m, motor fibres. 1, articular facet; 2, vertebral body; 3, uncinate process; 4, dural sleeve.
and anterocaudaI15°. The anterior border is the uncinate process and vertebral body and the articular facet is pos terior. The diameter of the foramen is reduced during a combined movement of extension and ipsilateral rotation. SPINA L MEMBRANES
Figure 6.25
Functions of the sternocleidomastoids.
because of the obliquity of the facet joints (Fig. 6.14). As the anteroposterior diameter of the spinal cord at midcer vical level is about 10 mm, there is however a large margin of safety.
Intervertebral foramen The intervertebral foramen lies between adjacent pedicles and through it the spinal nerve emerges from the spinal canal (Fig. 6.26). The foramen continues across the bifid transverse process and is orientated anterolaterally 45°
The dura mater is firmly attached to the rim of the foramen magnum and its fibres blend with the peri osteum within the skull. In the spinal canal it is not attached to the vertebral arches, because of the presence of protective fat tissue in between. The arachnoid is a membrane which lies in close contact with the dura. The subarachnoid space is quite wide. The third layer, the pia mater, covers the spinal cord (Fig. 6.27). A number of dentate ligaments pass between a fold of the pia mater which extends longitudinally and the anterior and pos terior nerve roots. These ligaments are attached to the dura and suspend the spinal cord in the cerebrospinal fluid.
Mobility of the dura mater The dura mater can move considerably without influence on the cord. This is an interesting feature, in that the cer vical spine lengthens approximately 3 cm during neck flexion. Consequently the dura mater, attached above and below, migrates within the spinal canal. It thus moves forwards and can be dragged against any space occupying lesion within the canal (e.g. a disc protrusion).
144 SECTION TWO - THE CERVICAL SPINE
4
;.,..".....� ... � 8 7'....,'!IlIf!�_�- 7
Figure 6.27 The dura mater and exits from the spinal canal: 1, dural membrane; 2, pia mater; 3, dentate ligaments; 4, spinal cord; 5, dorsal root; 6, ventral root; 7, dural sheath; 8, spinal ganglion.
Figure 6.28 The sinuvertebral nerve and its related structures: 1, anterior longitudinal ligament; 2, sympathetic trunk; 3, rami communicantes; 4, ventral ramus of spinal nerve; 5, dorsal ramus of spinal nerve; 6, posterior longitudinal ligament; 7, spinal ganglion; 8, anterior root; 9, sinuvertebral nerve.
As a consequence the mobility of the dura can be hin dered, increasing tension and resulting in pain, because the dura is also sensitive.
Sensitivity of the dura mater The anterior aspect of the dura mater is innervated by a dense longitudinally orientated nerve plexus consisting of different fibres of the sinuvertebral nerves originating at several levels (Fig. 6.28). Distal to the spinal ganglion the sinuvertebral nerve detaches and passes back into the spinal canal to innervate the anterior structures within the posterior longitudinal ligament, the anterior aspect of the dural sac and the dural sheath around the nerve root, the anterior capsule of the facet joints and also the vascular structures (Fig. 6.27). This could be an explanation for the dural pain' that occurs when the anterior part of the dura is compressed (see p. 17). The pain is multisegmental, which means it is felt in several dermatomes at a time. The mobility and sensitivity of the dura mater are described in detail on page 715. I
NERVE ROOTS
The nerve root contains motor and sensory branches formed by the convergence of rootlets emerging from the ventral and dorsal aspect of the spinal cord. The branches
Figure 6.29 The anterior part of the 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, spinal ganglion of nerve root; 4, sinuvertebral nerve; 5, posterior longitudinal ligament.
CHAPTER 6
-
APPLIED ANATOMY OF THE CERVICAL SPINE 145
remain completely separated until their fusion in the spinal ganglion - sensory above and motor below - but are surrounded by the continuation of the dura - the dural sheath. Just outside the intervertebral foramen the root divides into a dorsal and ventral branch - the dorsal ramus and the ventral ramus, the latter joined by the cervical sympathetic chain.
o
C1 C2 C3
THE DURAL SHEATH
C4
The dural investment surrounds the nerve root from the point where it leaves the spinal cord to the lateral border of the intervertebral foramen (Fig. 6.27). It is sensitive and slightly mobile, which means that some migration is possible.
C6
Mobility of the dural sheath
C7
At the cervical spine the nerve roots are not as mobile as in the lumbar spine. The dural sleeve is tethered to the transverse process" especially at the mid-cervical level. Therefore it is more difficult to use tension tests during clinical examination.
C5
C8 Figure 6.30 The mainly horizontal course of the nerve roots and the relationship between roots and discs.
Sensitivity of the dural sheath The dural sheath is sensory-innervated by its own sinu vertebral nerve. Pain that originates from the dural sheath is therefore strictly segmental and felt in the corresponding dermatome.
THE PARENCHYMA
Irritation of the parenchyma, for instance as the result of external pressure, results in paraesthesia. These are also segmental and felt in the same dermatome as the 'dural sheath pain'. Further irritation and destruction of the neural fibres lead to impaired conduction, which results in motor and/or sensory deficit Except for the nerve roots C6 and C7, which are slightly more oblique, the course of the root is almost directly lateral and thus horizontal, in contrast to the oblique course found in the lumbar spine. There are eight cervical nerve roots. The C1 root emerges between occiput and atlas, and the nerve root C8 between the seventh cervical and the first thoracic vertebrae. The result of this is that, for instance, a nerve root C7 can only become compressed by the disc C6 (the disc between the vertebrae C6 and C7) (Fig. 6.30).
INNERVATION OF THE CERVICAL SPINE
That part of the cervical spine which lies anterior to the plane of the intervertebral foramina is innervated by the anterior primary rami and their branches - the sinuverte-
braI nerves. The posterior aspect of the spine is inner vated from the posterior primary rami.
BLOOD SUPPLY
The main blood supply to the cervical spine and related structures is from the vertebral arteries which originate from the subclavian arteries and finally join to form the basilar artery. During their course they give off branches to the spine and to the spinal cord (anterior and posterior spinal arteries). The vertebrobasilar system is a 'closed' circuit (Fig. 6.31), starting below in the subclavian arteries and ending above in the arterial circle of Willis. The verte bral arteries run parallel on both sides of the spinal column through the canal formed by the successive transverse foramina, and are the main blood supply for the cervical spine, the spinal cord and the brain stem. Between the axis and atlas the arteries curve backwards and outwards and run over the posterior arch of the atlas. They curve upwards again and run cranially. Inside the skull they join to form the basilar artery which then splits into a left and right posterior cerebral artery. These arteries communicate with the internal carotid artery from which the anterior cerebral arteries branch off. For a detailed description see pp. 228-230.
146 SECTION TWO - THE CERVICAL SPINE
anterior cerebral artery
anterior cerebral artery
anterior communicating artery
middle cerebral artery
middle cerebral artery
posterior communicating artery �I-I-_
_
basilar artery
-------+1---4-
posterior cerebral artery internal carotid artery
external carotid artery
external carotid artery
Ii--f-f--- vertebral artery
common carotid artery
common carotid artery
subclavian artery--'--''-: subclavian artery
brachiocephalic trunk
aortic arch Right Figure 6.31
Left
The vertebrobasilar system.
Intervertebral foramen
UNCOARTERIORADICULAR JUNCTION Inferior articular process
There is a close connection between the uncovertebral joint, the vertebral artery and the nerve root. The artery is between the uncinate process and the nerve root. The latter lies behind the artery and just anterior to the facet joint. Degenerative changes leading to osseous, cartilagi nous or capsular hypertrophy may result in compression of artery or nerve root. The uncovertebral joint is the main threat to the vertebral artery, the facet joint to the nerve root. Movements such as rotation, combined with either extension or flexion, also influence these structures (Fig. 6.32).
Superior articular process
Vertebral artery
Figure 6.32
The uncoarterioradicular junction.
Nerve root
CHAPTER CONTENTS History
147
Pain 147 Paraesthesia 150 Vertigo or symptoms related to the vertebral artery Incoordination and spasticity 151 Medication 151 Inspection
151
Clinical examination of the cervical spine
151
Functional examination 152 Neck movements 152
Scapular movements Arm tests 157
155
Technical investigations
161
HISTORY
History taking in patients with problems in neck, trapez ius or shoulder region should be as detailed as possible and great care should be taken to define every symptom precisely. Especially when a controversial treatment, such as manipulation, is to be considered, it is vital that nothing has been forgotten that could constitute a contraindication. Age may be important, because some disorders do not occur before or occur typically at a certain period of life. For instance, torticollis in a baby is probably congenital. The same clinical picture in a 5-year-old child is more likely to be caused by contracture of the sternocleido mastoid muscle after, for example, glandular swelling or abscess formation. During and after adolescence it is more probably the result of a disc protrusion. The same argument applies to root pain. Under the age of 35 it is scarcely ever caused by a disc except after trauma, in which it may occur from 30 years upward. Radicular pain in a young person is usually the result of a neurofibroma, while in the elderly it is commonly the result of compression by an osteophyte or invasion from secondary deposits in the spine, rather than a disc protrusion. Early morning headache is typical in the elderly and is often the result of contracture in upper cervical liga ments. Headache from temporal arteritis also occurs late in life. Whenever symptoms appear in a patient of the 'wrong' age group, further investigation should be requested in order to exclude more serious disorders. The patient's work, hobbies or preferred sport may give an idea of postures, movements or strains that may be causative or provocative. Cervical sp.ine lesions may lead to the following symp toms: pain, paraesthesia, vertigo or symptoms related to the vertebral artery, and incoordination and spasticity. PAIN
Pain is the most common symptom. Its localization may give an idea as to the position of the lesion. Details about 147
148
SECTION TWO - THE CERVICAL SPINE
its evolution and behaviour help to determine the nature of the disorder. If this is the patient's first presentation with a problem in the cervical spine, questions are asked about the current complaints (see below). In a recurrence, a detailed and chronological reconstruction of the past history should be made. The patient may present with acute, subacute, chronic or recurrent pain. Acute and subacute episodes are characterized by difficulty in moving the head without exacerbation of the pain. Except in young people with torticollis or after injury, acute lesions are not as common as more chronic complaints. Chronic lesions come and go for months or years without any tendency towards spon taneous recovery. Most problems in the cervical spine however are recurrent, which implies that the course is characterized by definite attacks of short duration. The examiner should then find out whether the patient is totally free from pain in between the attacks, for how long the symptoms last and whether the pain is always felt on the same side. Onset
Next, the following questions are asked about the onset of the pain. •
Where did it start?
Pain of cervical origin very otten starts at the cervical spine but otten spread or shifts to another region quite quickly, so that the cervical source may pass unnoticed. Interscapular onset of pain is typical for a lower cervical disc lesion that compresses the dura (see p. 150). In contrast, it is very unusual for pain to begin in the arm. Should this occur, the possibility of a neurofibroma, compressing a nerve root, has to be con sidered in young people. In the elderly, an osteophyte or even a malignant process is more probable. •
When did it start?
Pain of cervical origin may occur in discrete attacks, especially when a disc lesion is responsible. It is important to try to get the patient to recall the first episode and to ask for a chronological account. In discal root pain, a normal period of spontaneous relief should be recognizable. Root pain that persists is sug gestive of a more serious cause. • How did it start?
The origin may be spontaneous, either acute or chronic but may also be the consequence of injury. In the latter, more details should be sought about the type of injury (e.g. a fall or whiplash). It is then nec essary to seek further investigations to exclude the fractures or luxations.
Evolution
More detailed information is then obtained about the development of the complaints in relation to localization, duration and intensity. The localization may change, either because the pain shifts to another place or because it spreads. Pain shifting from the scapular area to the upper limb is very indica tive of a disc lesion: the fragment of disc substance first displaces posterocentrally and compresses the dura mater which results in central, bilateral or unilateral scapular pain; it then moves laterally and impinges on the dural investment of a nerve root. The scapular pain disappears and is replaced by a radicular pain down the upper limb.
Mechanism of dural pain. In order to interpret correctly the pain distribution described by the patient the mecha nism of dural pain should be understood. Because of the innervation of the anterior aspect of the dura mater by a dense network of branches of sinuverte bral nerves originating at several levels, extrinsic com pression and subsequent irritation of the dura may give rise to pain felt in several dermatomes - multisegmental pain (see Ch. I, p. 17). Because the dural investment of the nerve root is innervated from its own recurrent nerve, the same mechanism here results in pain felt in the corre sponding dermatome - segmental pain. This pain is iden tical to segmental pain referred from any other soft tissue lesion (see Ch. I, p. 10). (Chapter 48 The Dural Concept, p. 743 gives more detailed information.) The same logic applies to the duration of pain. Root pain as the result of a disc protrusion lasts for a variable but limited period and then ceases as spontaneous remis sion takes place. Root pain which lasts longer than 6 months should arouse suspicion of another and possibly progressive cause. Most benign cervical disorders are intermittent and if pain progressively worsens then the presence of an irreversible lesion such as metastases must be borne in mind, particularly in the elderly. Because cervical disorders are frequently episodic, the patient should be asked to describe the different attacks in as detailed a way as possible. Often a recurrence can be ascribed to instability of the affected structure. Once an intervertebral disc fragment has displaced, it may do so again, because the cartilage remains unhealed. Further displacement may be in a different direction and it is thus possible that the pain is variable and not on the same side. Pain that changes sides from one attack to another very strongly suggests the presence of a disc lesion. The duration of the previous attacks may have prog nostic value and can give an idea of how long the present symptoms may be expected to last. Previous treatment should be ascertained because, if the present episode is a
CHAPTER 7
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 149
recurrence, it is very likely that it will respond to the same treatment. It would therefore be quite logical to start with the same approach that has proved to be effective in the past. Further questioning will also show whether the patient has been totally free of pain between attacks. Freedom from symptoms indicates that the patient went into com plete remission and this result could be obtained again. Failure of complete remission requires a search for the reason: possibly previous treatments have not been com plete; alternatively, age can be a factor in that some con ditions have a tendency to become more persistent as age advances. Current symptoms
After the patient has given a thorough description of the behaviour of the pain, the moment has come to ask for details about current symptoms.
localization. The localization may vary: headache, pain in the face, pain in the neck, pain in the scapular area, pain in the pectoral area or pain down the upper limb. Headache. If headache is referred from the cervical spine, the patient will usually mention an association between the symptoms and certain postures and/or movements. The pain may be bilateral, or unilateral and can be either segmental or multisegmental. Segmental pain (Fig. 7.1) originates from the upper cervical segments (C1 and C2). Disorders at the joints between occiput and atlas, or between atlas and axis may give rise to pain felt to start at the centre of the upper neck, spreading to the occiput, to the vertex (C1) and/or to the temples and forehead (C2). The pain is not neces sarily felt in the upper neck. Localization to the head can divert attention from the cervical spine. Multisegmental headache (Fig. 7.2) results from com pression of the dura at any cervical level. The pain often radiates from the midneck up to the temple, the forehead and behind one or both eyes but rarely to the bridge of
Figure 7.2 Multisegmental headache.
the nose. If, apart from this distribution, there is also downwards reference of pain to the scapular area, the dural origin is clear. Some types of headache can be recognized by atten tion to the history. Early morning headache in elderly patients is a typical example: the patient wakes every morning with headache and/or occipital pain. After some hours the symptoms ease and have completely disappeared by . midday. Symptoms do not recur until the next morn mg. The sequence is repeated daily without fail and, as the years go by, pain tends to last longer into the day. This type of headache responds spectacularly to manipulative treatment (p. 268). Migraine is another typical history. Symptoms usually start during adolescence and may go on for many years. The vascular origin of this disorder has been widely accepted and the following features are well know� : an . 'aura' which frequently includes visual hallucmatIOns, photophobia, nausea, vomiting and other bizarre �xperi ences, often precedes an attack; pain is severe, umlateral and well localized though may change sides for each attack and may be described as throbbing or bursting. Cluster headache is very severe, more common in men, and occurs on a regular basis. The pain is always felt on the same side, mainly above the eye and may be accom panied by a partial Horner's syndrome. Pain in the face.
Figure 7.1 Segmental headache.
This may have either a local origin or be
referred. Local lesions are sinusitis, dental problems, a temporo mandibular lesion, a lesion of the facial bones (such as fracture, neoplasm, abscess or osteitis deformans), neur� logical problems, (e.g. trigeminal and postherpettc neuralgia), and finally arteritis. Referred pain is also a possibility and may have a seg mental basis originating from the C2 level, or multiseg mental basis as the result of compression of the dura mater at any level. Such pain should always be borne in
150
SECTION TWO - THE CERVICAL SPINE
Table 7.1 Pain in the neck Pain
Local origin
Upper cervical
Unilateral or bilateral pain: Ligaments/tendons/ facet joint
Lower cervical
Cervical origin Multisegmental origin
Unilateral or central/bilateral pain with wide reference: Discodural conflict
1
Scapular pain ...._..
Localized unilateral pain: Facet joint
mind because, if a local cause is not found, treatment to the cervical spine may be curative. Local pain in the upper neck is usually the outcome of a local lesion: ligaments of the upper cer vical segments or one of the upper facet joints (Table 7.1). Rarely, the muscular insertions on the occiput are respon sible. However, upper cervical pain may also have multi segmental origin in the lower cervical dura mater. Mid- or lower cervical pain is most often caused by a mid- or lower cervical lesion possibly in contact with the lower cervical dura mater. Unilateral pain prompts a search for a cause on the same side. Well-localized pain can originate from a facet joint. If the pain is felt centrally or bilaterally, the lesion usually lies in the midline and a disc protrusion is very probable. Pain in the neck.
This is the most common local ization. A cervical origin is usual, in which case it must be considered as being multisegmental (Fig. 7.3), although upper scapular pain may also be segmental, i.e. C4. Other possibilities are a thoracic lesion or a scapular lesion (Fig. 7.4). Again the pain may be felt unilaterally, bilaterally or centrally between both scapulae and, depending on the patient's age, it may be intermittent or constant. Pain in the scapular area.
Pain in the pectoral area. Another rare manifestation of multisegmental reference of pain is pain in the pectoral area as the result of a cervical problem. Because the pain is usually felt deeply, this localization makes the patient feel that angina is a possibility.
Figure 7.4
Origins of multisegmental scapular pain.
Pain down the upper limb. When present, this is always segmental. Distribution within a dermatome indicates the cervical segment in which the lesion must be sought. If the lesion lies in the cervical spine, and certainly if it is to be a disc lesion, the normal time sequence of the symptoms must be appreciated: neck pain followed by unilateral scapular pain and finally root pain. It is there fore important to ask whether or not the arm pain has been preceded by scapular pain. If not, non-spinal origin of the pain is a differential diagnostic possibility.
Exacerbation of pain by a cough. This is uncommon in cervical lesions but may occur in a disc prolapse, when the pain is usually felt in the scapular region. Pain in the arm on coughing is more likely to be the consequence of a neuroma. PARAESTHESIA
Paraesthesia is a very common symptom which may originate from any nerve fibre in the cervicoscapular area or in the arm (Table 7.2). Paraesthesia is often experienced as a 'pins and needles' sensation. In other instances, the patient may describe the feeling as 'numb ness'. The moment the patient mentions the presence of
Table 7.2 Paraesthesia Level
Cause/site of cause
Symptoms
Cervical
Myelopathy: Intrinsic
No pain Multisegmental paraesthesia on neck flexion Lhermitte's sign
Extrinsic
Figure 7.3
Multisegmental scapular pain.
Nerve root
Pain Segmental paraesthesia Compression phenomenon
Shoulder girdle
Brachial plexus
Vague paraesthesia Release phenomenon
Arm
Nerve trunk
Defined area of paraesthesia Specific tests
Nerve ending
Cutaneous analgesia (Paraesthesia)
CHAPTER 7
such symptoms, the examiner should carefully determine how proximal they are because, as has been explained in Chapter 2, the point of compression always lies proximal to that of the paraesthesia. The lesion may lie at any one of a number of different levels but the more vague the distribution of the pins and needles, the more proximally the lesion needs to be sought. At the cervical spine
Spinal cord. The spinal cord can be responsible. Early myelopathy, either intrinsic or as the result of external pressure, is characterized by painless paraesthesia felt distally in the upper and I or lower limbs in a multiseg mental distribution. The paraesthesia comes and goes in a wholly irregular way, most marked by day. Neck flexion can increase the symptoms. Lhermitte's sign may be present: an electric shock sensation in the trunk and I or upper limbs following forceful passive flexion of the cervical spine. Differential diagnosis has to be made from other extraspinal disorders, such as pernicious anaemia, dia betes and peripheral neuritis. Nerve root. When a nerve root is affected, paraesthesia appears distally in the corresponding dermatome. The pins and needles come and go by day or night in an erratic fashion and do not actually last more than an hour at a time. Pain may precede or accompany the paraes thesia, which indicates that external pressure is being exerted on the dural sleeve. At the shoulder girdle
Lesions of the brachial plexus at the thoracic outlet give rise to paraesthesia in one or both hands and affect all digits. When there is external pressure and because of the release phenomenon, pins and needles are only felt after the compression has ceased. They are often nocturnal, waking the patient after some hours' sleep. In the arm
When one of the peripheral nerves in the upper limb is involved, paraesthesia (and sometimes pain) is felt in the territory of that nerve (radial, median or ulnar). The well known distribution of paraesthesia (three and a half radial, or one and a half ulnar fingers) often gives a clue. The cause is usually obvious. Some specific tests in order to elicit the pins and needles exist (e.g. Tinel's test in carpal tunnel syndrome). In lesions at the distal extent of a peripheral nerves the pins and needles are accompanied by cutaneous analgesia, which may be pronounced.
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 15 1
VERTIGO OR SYMPTOMS RELATED TO THE VERTEBRAL ARTERY
It is well known that vertigo may be the consequence of vertebrobasilar vascular insufficiency. However, cervical disorders without any impairment of the vertebral artery can also give rise to vertigo. The explanation is that the cervical spine, together with the eyes and the labyrinths of the ear, is an important source of proprioceptive infor mation that influences the sense of balance. When vertigo is a dominant symptom, the examiner must carefully look for its origin. The decision on the nature of treatment will depend on the diagnosis (see p. 236). IN COORDIN ATION AND SPASTICITY
These complaints are indications that something is amiss with either deep (proprioceptive) sensibility, the vestibu lar system or the cerebellum. MEDICATION
Current medication may have a bearing on both diagnosis and management and should be carefully ascertained, especially because anticoagulants are contraindications to manipulative therapy (see Ch. 5). A summary of history taking is given in Box 7.1.
INSPECTION
The examiner stands behind the patient and looks at the neck and scapular region. The neck may be held in flexion, in lateral deviation or in a combined position of lateral deviation and rotation. The lateral tilt as well as the rotation can be towards or away from the painful side. Lateral flexion towards the pain combined with rotation to the other side indicates a spasm of the sternocleidomastoid muscle - the so-called 'blackbird's sign'. In acute torticolis the head is usually deviated in lateral flexion away from the painful side. There is no fixation in rotation. A deviation in flexion is less common but suggests a block at the back of an intervertebral joint and is most common after whiplash injuries. If the deviation of the neck is localized in the upper cervical spine, adolescent scoliosis, a cervical rib and Klippel�-Feil syndrome must all be considered. The scapular and deltoid areas are surveyed. Deviations are noted in the position of the scapulae and in the muscular contours of the scapular and shoulder muscles.
SECTION TWO - THE CERVICAL SPINE
152
Box
7.1
Summary of history -
Age
felt; and where? The next step is to determine whether the following tests have any influence on the symptoms present or evoke other symptoms.
Work, hobbies, sport Pain
N ECK MOVEMENTS
1 Where? 2 When? 3 How?
Active movements are tested first and then repeated passively; after this, resisted movements are tested.
Evolution 1 Localization
Active movements
Onset
2 Duration
Current symptoms
1 Localization a Headache Segmental/multisegmental ii Typical histories • early morning headache • migraine • cluster headache b Pain in the face i Local lesions ii Referred pain • segmental • multisegmental c Pain in the neck Upper neck • local lesion • multisegmental ii Mid- or lower neck d Scapular pain i Segmental ii Multisegmental iii Thoracic lesion iv Scapular lesion e Pectoral pain: multisegmental f Arm pain: segmental i Spinal origin ii Non-spinal origin 2 Influence of coughing Paraesthesia
Lesion at the cervical spine 1 Spinal cord 2 Nerve root
Lesion at the shoulder girdle (brachial plexus) Lesion in the arm (peripheral nerve) Vertigo or symptoms related to vertebral artery Incoordination and spasticity Medication
The movements are first performed actively. The patient is asked to flex, extend, rotate the head to right and left and tilt in both directions (Fig. 7.5). The amplitude of each movement is noted and the patient indicates whether it is painful and, if so, where. Neck flexion must be considered not only as an articu lar test for the cervical spine but also as a dural test for the thoracic spine in that it stretches both the cervical and the thoracic dura. Hence, if pain is elicited in the upper thoracic region, it may be the consequence of a dural impingement either at p. cervical or at a thoracic level. A decision about the level of the lesion will depend on which other movements are painful- cervical or thoracic. After active movements have been performed, the examiner notes whether the patient presents either a symmetrical pattern - the full articular pattern (Fig. 7.6) or an asymmetrical pattern - a partial articular pattern (Fig. 7.7). The full articular pattern of the cervical spine is: some or great limitation of extension, equal degree of limitation of both rotations and both lateral flexions and no limita tion of flexion. Passive movements
After testing active movements, the same movements are performed passively. It is not always necessary to carry out all the movements passively. Flexion and lateral flexion to both sides may be omitted and are done in doubtful cases only when all possible information may be needed. Passive extension and passive rotation to both sides are always executed. It is noted whether they are painful and whether they are limited, and the end-feel is also assessed. The normal end-feel is capsular. Abnormal end · feels are: muscle spasm, bone-to-bone, crisp, empty, soggy and elastic rebound. They point towards certain pathological entities (see p. 73).
FUNCTIONAL EXAMINATION The movements
During the examination the examiner is looking for artic ular signs, root signs, cord signs and also for alternative causes for pain down the upper limb. Before the examination starts, the examiner asks the patient if anything can be felt at that moment. If the answer is yes, the supplementary questions are: what is
Primary tests: extension and rotation. These are illus trated in Figure 7.8. Extension. The examiner asks the patient actively to extend the neck. Both forearms are then placed against the patient's scapulae with the fingers on the patient's
CHAPTER 7
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 153
(a)
(b)
(e)
(d)
(e)
( f)
Figure 7.5 Active movements: flexion (a), extension (b), rotation (c, d) and lateral flexion (e, D of the head.
154
SECTION TWO - THE CERVICAL SPINE
Left
Right
flexion side flexion
side flexion
extension
Figure 7.6
(a)
The full articular pattern.
Left
Right
flexion
side flexion
side flexion
(b) extension
Figure 7.7
Example of a partial articular pattern (colour indicates pain).
forehead. Simultaneous radial deviation of both hands tests the end-feel in extension. By executing the test very gently, hard axial pressure is avoided. Rotation. The patient turns the head in rotation, first to
one side, then the other. To avoid trunk movements, the examiner stabilizes the patient's body using the forearms. One is placed against the patient's scapula at the side towards which the patient turns the head and the other at the anterior aspect of the other shoulder. The hand of the arm that overlies the scapula moves into ulnar deviation and grasps the patient's forehead on the contralateral side. The other hand moves into radial deviation and grasps the patient's occiput on the side
(c)
facing the examiner. Movement is performed by a simul taneous action of both hands. As the head turns, end-feel is again noted.
Figure 7.8
Primary passive movements: extension (a) and rotation
(b, c).
CHAPTER 7
Secondary tests: lateral flexion and flexion.
These are
illustrated in Figure 7.9. Lateral flexion. The examiner places the ipsilateral hand laterally against the patient's shoulder. With the other hand placed above the ear at the opposite side, gentle side flexion is undertaken.
(a)
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 155
Flexion. The patient bends the head and the examiner slightly increases pressure with the hand placed on the patient's occiput. Excessive pressure should be avoided.
Resisted movements
After testing the active and passive movements, resisted movements are tested. Both rotations suffice and an isometric test is appropriate. Other movements are necessary only in cases of doubt and for the purpose of differential diagnosis. Rotatory movements give addi tional information on motor conduction in the first cervi cal nerve root. The movement may be painful, weak, or painful and weak. Muscular and tendinous lesions are extremely uncom mon at the cervical spine. Interpretation of positive resis ted movements must be done in the light of the overall clinical picture. The response can be obscured in acute lesions, where the slightest effort augments the pain as the result of transmitted stress.
Primary test: rotation. The patient holds the head in the neutral position. The examiner places the forearms against both scapulae with the fingers just above the patient's ears and the fingertips pointing forwards so that they lie on the temples (Fig. 7.10). The patient is asked to rotate the head and the movement is resisted with the fingertips. Secondary tests: extension, flexion and lateral flexion. These are illustrated in Figure 7.11. Flexion. The examiner stands beside the patient and places one hand on the upper interscapular area and the other hand on the forehead. The patient is asked to push the head forwards and resistance is provided.
The examiner stands beside the patient. One hand is placed laterally on the sternum and the other on the occiput. The patient is asked to pull the head backwards and resistance is provided. Extension.
(b)
The examiner stands behind the patient. One hand is placed laterally on the opposite shoulder and the other above the ear. The patient is asked to push the head against the hand. Resistance is exerted. Lateral flexion.
SCAPULAR MOVEMEN TS
Scapular movements are performed to establish the mobility of the scapula in relation to the thorax. They are also part of shoulder girdle examination and of tests of the thoracic dura. Active movement (c)
Figure 7.9 Secondary passive movements: lateral flexion (a, b) and flexion (c).
The patient is asked to elevate his shoulders (Fig. 7.12) and the examiner notes if the movement is painful or limited. In addition to an assessment of the mobility of the scapula on the thoracic cage, the integrity of the acromioclavicular
156
SECTION TWO - THE CERVICAL SPINE
Figure 7.10 Primary resisted movement: rotation.
(a)
(b)
(e)
(d)
Figure 7.11 Secondary resisted movements: extension (a), flexion (b) and lateral flexion (c, d).
CHAPTER 7
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 157
patient this should be impossible: the patient's move ment is stronger than the examiner's. ARM TESTS
Arm movements test the integrity of the muscular system. If pain is elicited, alternative causes of pain down the upper limb should be sought. When one or more movements are weak a neurological problem is respon sible. The pattern presented will indicate the possible level. Active elevation
Figure 7.12 Active elevation of the shoulders.
joints, the sternoclavicular joints and the joints between the first ribs and the vertebral column is assessed. Any pain or limitation suggests the need for shoulder girdle examination (see pp. 395-399).
The patient is asked to elevate both arms sideways, as high as possible (Fig. 7.14). This is a global test for the shoulder girdle but also enables the examiner to ascertain if the shoulder itself is involved. Pain and limitation are noted. If this test is positive and the presence of a shoulder lesion is possible, a complete shoulder examination should follow (see pp. 295-302).
Resisted movement
This tests motor conduction in C2-C4. The patient holds the shoulders elevated. The exam iner puts his or her hands on top of both shoulders and tries to pull them downwards (Fig. 7.13). In a normal
Figure 7.13 Resisted elevation of the shoulders.
Figure 7.14 Active elevation of the arms.
158
SECTION TWO - THE CERVICAL SPINE
(a)
(b)
Figure 7.15 (a) Resisted abduction of the shoulder tests the C5 nerve root and the abducter muscles. (b) Resisted external (or lateral) rotation of the shoulder tests the C5 nerve root and the external (or lateral) rotators.
Resisted movements
Isometric resisted tests are done bilaterally, so that strength may be compared. These are mainly tests for motor conduction and so strength is noted but, if the test elicits pain, the possibility of a local lesion should be con sidered. The tests are illustrated in Figures 7.15-7.18. Detailed execution of the different tests is discussed in the relevant chapters on the shoulders, elbow and wrist.
Resisted abduction of the shoulder. This tests the C5 nerve root and the abductor muscles of the shoulder (deltoid and supraspinatus). The test is performed with the arm hanging down, a few degrees of abduction being permitted. The patient is asked to resist the examiner's attempt to push the arm inwards. Resisted external rotation of the shoulder. The C5 nerve root is tested as well as the external rotators of the shoul der (infraspinatus and teres minor). The patient is asked to bend the elbow to a right angle and to hold it firmly into the side. The examiner's attempt to push the forearm medially should be resisted. Resisted flexion of the elbow. This test examines both the nerve roots C5 and C6 and at the same time the flexors of the elbow (biceps, brachialis and brachio radialis). The patient holds the elbow in 90° flexion and
supination and resists the examiner's attempt to extend the elbow.
Resisted extension of the elbow. This tests the nerve root C7 and the extensor of the elbow (triceps). The elbow is also held to a right angle and the examiner's attempt to bend the patient's elbow is resisted. Resisted extension of the wrist. The C6 nerve root is tested as well as the extensors of wrist (extensores carpi) and fingers (extensor digitorum communis). The elbow is held in extension. The patient resists the examiner's attempt to flex the wrist. Resisted flexion of the wrist. This test examines the nerve root C7 and the flexors of wrist (flexores carpi) and fingers (flexores digitorum). The elbow is held in extension. The examiner's attempt to extend the wrist is resisted.' Resisted extension of the thumb. The C8 nerve root is tested as well as the extensors of the thumb (extensores pollicis). The examiner's attempt to flex the thumb is resisted. Resisted adduction of the fifth finger. This tests the T1 nerve root and the intrinsic muscles of the hand, i.e. the adductors of the little finger. The patient squeezes the examiner's finger between the fourth and fifth fingers. The examiner assesses the strength.
CHAPTER 7
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 159
(b)
(a)
Figure 7.16 (a) Resisted flexion of the elbow tests the C5 and C6 nerve roots and the elbow flexors. (b) Resisted extension of the elbow tests the C7 nerve root and the elbow extensors.
(a)
(b)
Figure 7.17 (a) Resisted extension of the wrist tests the C6 nerve root and the wrist and finger extensors. (b) Resisted flexion of the wrist tests the C7 nerve root and the wrist and finger flexors.
Sensory conduction
The examiner passes his fingers over the patient's skin in the different dermatomes (Fig. 7.19). The patient is asked if the sensation is the same over all areas.
One arm is compared with the other, and each dermatome is compared with the others in the same limb.
160
SECTION TWO - THE CERVICAL SPINE
(a)
(b)
Figure 7.18 (a) Resisted extension of the thumb tests the C8 nerve root and the thumb extensors. (b) Resisted adduction of the fifth finger tests the T1 nerve root and the intrinsic muscles of the hand.
Figure 7.19 Testing sensory conduction.
Figure 7.20 Testing the biceps reflex: C5 and C6 nerve roots. The reaction is elbow flexion.
Testing reflexes
The main reflexes are tested and it is noted if they are normal, diminished, absent or inverted. Each side is always compared with the other.
Biceps reflex. The patient's elbow is held to a right angle and well relaxed. The tendon is stretched by the pressure of the examiner's thumb on which the hammer is tapped. The C5 and C6 nerve roots are tested. The reaction is elbow flexion (Fig. 7.20). Brachioradialis reflex. The patient's elbow is held to a right angle and well relaxed. The hammer taps on the distal end of the radius. This tests the C5 nerve root. The reaction is elbow flexion (Fig. 7.21). Triceps reflex. The patient's elbow is 90° flexed and well relaxed. The hammer strikes the triceps tendon, just ProX-
imal to the olecranon. The C7 nerve root is tested. The reaction is elbow extension (Fig. 7.22).
Plantar reflex. In testing the plantar reflex, using the sharp end of the reflex hammer the examiner strokes the sole of the patient's foot, starting at the lateral aspect of the heel, moving along the lateral border of the foot to the base of the fifth metatarsal bone and then onwards to the base of the big toe at the medial aspect of the foot. The normal reaction, as described by Stri.impell, is flexion of the toes and withdrawal of the foot. The pathological reflex - Babinski's sign - is a slow extension of the big toe, combined with spreading of the other toes and flexion of knee and hip. The presence of Babinski's sign indicates a (severe) central disorder (Fig. 7.23).
CHAPTER 7
Figure 7.21 Testing the brachioradialis reflex: C5 nerve root. The reaction is elbow flexion.
-
CLINICAL EXAMINATION OF THE CERVICAL SPINE 161
Figure 7.23 Testing the plantar reflex: central nervous system. The reaction is flexion of the toes.
Summary of functional examination Neck movements 6 active movements: painllimitation 3 (or 6) passive movements: pain/limitation/end-feel 2 (or 6) resisted movements: pain/weakness-Cl
Scapular movements Active elevation pain/limitation Resisted elevation (2-C3-C4
Shoulder girdle examination?
Arm tests
Tests for neurogenic integrity and alternative causes of arm pain
Active elevation: pain/limitation Figure 7.22 Testing the triceps reflex: C7 nerve root. The reaction is elbow extension.
A summary of the neurological deficit at each level is given in Box 7.2.
TECHNICAL INVESTIGATIONS
Technical investigations have become for several reasons a routine measure in the evaluation of patients with pain originating in the cervical area: in the hope of reach ing a diagnosis; to complement the clinical diagnosis; to meet the patient's question for 'radiography'; or for medicolegal reasons. There is a tendency to reduce the time for history taking and clinical examination and to proceed immediately
Resisted movements? (tests for motor conduction): shoulder: • abduction-CS • external rotation-CS elbow: • flexion-CS/C6 • extension-C7 wrist: • flexion-G • extension-C6 thumb extension-C8 little finger adduction-Tl Sensory conduction Reflexes: biceps-CS/C6 brachioradiaIis-CS triceps-G plantar-CNS
-+
Shoulder examination?
162
SECTION TWO - THE CERVICAL SPINE
Box 7.2 Neurological deficit at each level -
C1-(2
C3
C4
C5
C6
C7
C8
T1
T2
Compression of the C1-C2 nerve roots produces tingling in the occipitoparietal region. Muscular weakness is rare. Involvement of the C3 nerve root causes paraesthesia or numbness at the lower pinna, the posterior part of the cheek, the temporal area and any part of the lateral aspect of the neck, with a forward projection along the chin. Weakness is clinically not detectable. Cutaneous analgesia is uncommon, but would occupy any part of the lateral aspect of the neck. Interference of conduction in the C4 root causes a horizontal band of cutaneous analgesia along the spine of the scapula, the mid-deltoid area and the clavicle. Muscular weakness is not detectable and paraesthesia does not occur. Compression of C5 has the following clinical signs: weakness of the supraspinatus, infraspinatus, deltoid and brachial biceps muscles. Paraesthesia and sensory deficit do not occur. The biceps and brachioradialis jerks may be sluggish or absent. Involvement of the C6 nerve root results in paraes thesia felt in thumb and index fingers. There is weakness of the biceps, brachialis, supinator brevis and the extensores carpi radiales muscles. Cutaneous analgesia may be found at the tips of thumb and index fingers. The biceps jerk is sluggish or absent. Compression of the C7 nerve root shows paraesthesia in index, middle and ring fingers. The weak muscles are the triceps and the flexor carpi radialis. Cutaneous analgesia is found at the dorsal aspect of the index and middle fingers. The triceps jerk is seldom affected. Interference of conduction in the C8 nerve root results in paraesthesia in the middle, ring and little fingers. The weak muscles are both extensors of the thumb, the extensor carpi ulnaris and the flexor carpi ulnaris, the adductor pollicis, the common extensor of the fingers and the abductor indicis. Cutaneous analgesia is found at the little finger. Compression of the T1 nerve root results in weakness of the intrinsic muscles of the hand. Paraesthesia and cutaneous analgesia are felt at the ulnar aspect of the hand. Paraesthesia, motor and sensory deficit are very uncommon.
towards technical investigations in the hope of detecting anatomical changes which might be responsible for the patient's symptoms. It has been shown in different studies - although more extensively in the lumbar spine - that there is often no relationship between the clinical picture and radiological changes as the result of degeneration of the spine. Radiography may be helpful if the clinical examination suggests bony disorders such as fractures or luxations but has no value for instance in the diagnosis of disc displacements. Even computed tomography (CT) scan and magnetic resonance imaging (MRI) give rise to a certain number of false-positive findings. Boden et all mention a figure between 14 and 28% and Teresi et al2 a figure of 23%.
Technical procedures may be of great help to comple ment the clinical findings, i.e. to confirm a tentative diag nosis or to exclude serious disorders. It should, however, be remembered that the picture is not always clear from the beginning. It is important not to get a false feeling of security when an examination turns out to be negative. The examiner should avoid sending the patient through a whole battery of machines but should, on the contrary, ask for the examination that has the greatest chance of answering the examiner's questions. Radiography may show congenital anomalies but these are quite often not clinically significant. The same applies to degenerative disorders,3 which are present in sympto matic as well as in asymptomatic subjects. Radiography is often the first and most easy approach in posttraumatic cases. The American College of Surgeons suggests routine lateral views in all patients with major trauma.4 Fractures and luxations may be detected, although if there is clinical suspicion of fracture and the radiological picture is inconclusive the patient should be sent for CT scanning.5,6 Although there have been some studies dis cussing7-9 the value of this approach, EI-Khoury et a[1o conclude in a review article that routine radiography should remain the first choice in cervical trauma. They state however that computed tomography is the best approach to detect possible fractures. Computed tomography scanning because of its superior depiction of osseous anatomy - certainly is a good diag nostic tool for bony disorders, such as fracturesll and lux ations - where it is often more effective than MRI12 - and also for osseous neural foramina I stenosis, bone destruc tion or bone proliferation and ossification of the posterior longitudinal ligament. Also, for example, it is effective for detecting cranial migration of the odontoid process in rheumatoid arthritis patients with involvement of the upper cervical spine.13 Magnetic resonance imaging - because of its superior depiction of soft tissue anatomy - is to be preferred in soft tissue disorders,I4 such as pre- or paravertebral haemorrhage or oedema, ligamentous lesions, disc her niationsl5,16 although it has a low sensitivity for predict ing free disc material posterior to the posterior longitudinal ligamentY It very well shows spinal cordIS or nerve root injuries.l9 It appears to be the most reliable imaging study for diagnosing spinal infection20,21 and tumours.22,23 It also adds additional information when compared to conventional imaging methods in patients with advanced stages of degenerative disease.24 Dynamic functional MRI may provide additional infor mation in patients with rheumatoid arthritis.25 The tech niques of MRI scanning have further improved, for example since the emergence of volume 3-D gradient echo scanning in the axial plane, which allows a better evaluation of foraminal anatomy. -
CHAPTER 7
-
CLINICAL EXAMINATION OF THE CE RVICAL SPINE 163
importance of a complete and thoughtful clinical evalu ation cannot be stressed enough. 28
Scintigraphy is most useful for the detection of quanti tative changes in the skeleton in case of bone metastases and inflammatory and metabolic bone diseases. 26 Electromyography has a low sensitivity and specificity and is therefore only secondary in the diagnosis of cervi cal nerve root palsies, which can easily be detected by clinical testing. It can be of certain importance in cases with medicolegal implications. Decisions about treatment procedures should be made on clinical grounds, but may be influenced by specific findings on the imaging pictures. It is not because the images show great precision that the examiner should omit or reduce the clinical approach. The presence of anatomical and morphological changes does not auto matically imply causality.27 Technical evolution cannot be stopped and certainly has great advantages but the
CON CLUSION S • • • • •
Technical investigation should not replace clinical examination. The results must be evaluated with great care and only in the light of the clinical picture. They may be used to clarify the clinical picture or to exclude serious disorder. Treatment decisions should never be taken on the outcome of imaging studies alone. In doubtful cases, clinical evaluation will be more important than technical investigations.
REFEREN CES 1 . Boden SO, McCowin PR, Davis DO, et al. Abnormal magnetic
1 5 . Matsumoto M, Fujimura Y, Suzuki N, et nl. MRl of cervical inter
resonance scans of the cervical spine in asymptomatic subjects.
vertebral discs in asymptomatic subjects. ] Bone joint S u rg (Br)
1998;80(1) : 1 9-24.
J Bone joint Surg (Am) 1990; 72: 1 1 78-1184.
16. Dai L. Disc degeneration and cervical instability. Correlation
2. Teresi LM, Lufkin RB, Reicher MA. Asymptomatic degenerative disc disease and spondylosis of the cervical spine: MR imaging.
of magnetic
Radiology 1987;164:83-88.
1998;23(16):1 734-1 738.
resonance
imaging
with
radiography.
Spine
3. Kim KS, Rogers LF, Regenbogen V. Pitfalls in plain film diagno
1 7. Humphreys SC, Hodges SD, Fisher DL, et nl. Reliability of mag
sis of cervical spine injuries: false positive interpretation. S u rg
netic resonance imaging in predicting disc material posterior
NeuroI 1 986;25:381-392.
to the posterior longitudinal ligament in the cervical spine. A prospective study. Spine 1998;23(22) :2468-2471 .
4. American College of Surgeons Committee on Trauma. Advanced Trauma Life Support Course for Physicialls. American College of
1 8. Muhle C, Metzner J, Weinert D, et al. Classification system
Surgeons, Chicago, 1984.
based
puted
tomography of nonvisualized C7-Tl cost-effective? ] Spinal
tomography myelography and magnetic resonance
and radiculopathy. Spine 1999;24(17) : 1 781-1785.
Oisord 1999;12(6):472-476. cervical
imaging in cervical spondylitic
imaging in the evaluation of cervical spondylotic myelopathy
20. Rothman SLG. The d i agnosis of infections of the spine
7. Badami JP, Norman D, Barbaro NM, et al. Metrizamide CT in
MR
19. Shafaie FF, Wippold FJ 2nd, Gado M, et al. Comparison of com
1 998;23(24) :2701-2712. 6. Tan E, Schweitzer ME, Vaccaro L, Spetell AC. Is computed
myelography
on kinematic
myelopathy. Am J NeuroradioI 1998;19(9) : 1 763--1771 .
5. Kaiser JA, Holland BA. Imaging of the cervical spine. Spine
myelopathy
and
by
radiculopathy:
Correlation with conventional myelography and surgical findings. Am j Neuroradiol 1985;144: 675-680.
8. Bernhardt M, Hynes RA, Blume HW, White AA. Current concept reviews. Cervical spondylotic myelopathy. ] Bone Joint
Surg (Am) 75: 1 1 9-128. 9. Benzel EC, Hart BL, Ball PA, et al. Magnetic resonance imaging for the evaluation of patients with occult cervical spine injury.
] Neurosurg 1996;85:824-829. 10. El-Khoury GY, Kathol MH, Daniel Ww. Imaging of acute illjuries of the cervical spine: Value of plain radiography, CT and MR imaging. Am ] Roentgenol 1995;164:43-50.
1 1 . Katz MA, Beredjiklian PK, Vresilovic EJ, et al. Computed tomo graphic scanning of cervical spine fractures: does it influence treatment? ] Orthop Trauma 1999;13(5) :338-343.
12. Klein GR, Vaccaro AR, Albert TJ, et al. Efficacy of magnetic res onance imaging in the evaluation of posterior cervical spine fractures. Spine 1 999;24(8) :771-774.
1 3 . Ostensen H, Gudmundsen TE, Haakonsen M, et al. Three dimensional CT evaluation of occipito-atlanto-axial dislocation in rheumatoid arthritis. Scand J RheumatoI 1998;27(5):352-356.
14. Katzberg RW, Benedetti PF, Drake CM, et al. Acute cervical spine injuries: prospective MR imaging assessment at a level 1 trauma center. Radiology 1999;213(1):203-212.
modern
imaging
techn iques.
Orthop Ciin
North
Arn
1996;27:15-3 1 . ,
2 1 . Friedman DP, Hills JR. Cervical epidural spinal iniection: MR imaging characteristics. Am ] Roentgeno/ 1 994;163:699-704.
22. Algra PR, Bloem JL, Tissing H, et al. Detection of vertebral metastases: Comparison between
MR imaging and bone
scintigraphy. Radiographics 1991;11:219-232.
23. Carmody FT, Yan pJ, Seeley GW, et al. Spinal cord compression due to metastatic disease: Diagnosis with MR imaging versus myelography. Radiology 1989;173:225-229.
24. Muhle C, Metzner J, Weinert 0, et al. Kinematic MR imaging in surgical management of cervical disc disease, spondylosis and spondylotic myelopathy. Acta RadioI 1999;40(2) : 146-153 .
2 5 . Allmalm K H , Uhl M, Uhrmeister
P,
et al. Functional MR
imaging of the cervical spine in patients with rheumatoid arthritis. Acta Radiol 1998; 39(5):543-546.
26. Ono K, Okada K, Nakashima H, Yamashita K. Scintigraphy and selective angiography. In: The Cervical Spine Research Society (eds): The Cervical Spine. Lippincott, Philadelphia,
1989 : 1 77. 27. Modic MT, Ross JS. Morphology, symptoms, and causality. Radiology 1990;175:619-620. 28. Kaiser JA, Holland BA. Imaging of the cervical spine. Spine 1998;23(24):2701-2712.
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Interpretation of the history Pain 165 Paraesthesia
165
168
Interpretation of the functional examination Interpretation ofthe neck movements
169
169
Cervical spine: interpretation of the clinical examination
169 Active and passive movements are positive 171 Active and resisted movements are positive Interpretation ofthe shoulder girdle movements 172
Interpretation of the arm movements 172 Active elevation ofthe arm is positive 172 Resisted arm movements are positive
173
Because the clinical examination is standardized, the examiner can easily recognize differences between differ ent patients. He is able to distinguish the 'usual' from the 'unusual', to recognize possible 'warning signs' (see p. 211), to differentiate neck, shoulder girdle and shoulder and will realize - if necessary - when and where to send the patient for more specialized examination. This 'func tional' examination also enables the examiner to make the distinction between 'mechanical' conditions - disc lesions, degenerative disorders, muscular and capsulo ligamentous lesions - and 'non-mechanical' conditions osseous, rheumatological, infections, intraspinal, neuro logical, visceral and psychoneurotic disorders, as well as some non-cervical soft tissue lesions that give rise to pain in the cervicoscapular area.
INTERPRETATION OF THE HISTORY
History-taking leads to the patient presenting a variety of symptoms: pain, paraesthesia, numbness and dizziness, but other features such as diminished mobility and weakness may be mentioned. The former are purely sub jective and cannot be controlled. Detailed questioning and interpretation by the examiner will therefore be necessary. The latter are more objective elements (signs): they have to be controlled during the functional examination (see Interpretation of the functional examination, p. 169). PAIN
Pain is the symptom for which the patient most fre quently consults. Other symptoms may be present as well and if they are not mentioned the examiner should enquire for them. Questions about localization, onset, evolution, factors that influence the pain, accompanying symptoms and duration are answered and these answers interpreted in the light of known clinical pictures and of the signs shown in the examination. Localization
The localization of the pain may give a rough idea of where to look for the origin of symptoms. Pain may be 165
166 SECTION TWO - THE CERVICAL SPINE
quite localized and is then usually felt in the neighbour hood of the lesion but it often radiates and if it does it mostly refers distally (see p.16). Looking at the area where pain presents may help to make a first classification which can then be compared to the findings on functional examination. The first question that arises is: Is the pain referred or is it felt locally? If the pain is referred, to where? Following the rules of referred pain (see Fig. 8.1), it should spread into a dermatome - segmentally - but radiation into several adjacent dermatomes at the same time is quite common and indicates a multisegmental type of reference. Multisegmental pain reference may be the result of multi radicular involvement but this is extremely uncommon in the cervical spine and should immediately arouse suspi cion (see Warning signs, p. 211). It is frequently the result of a discodural interaction in which case other dural symptoms may also be found and the functional exami nation should show a clinical picture of internal derange ment in the intervertebral joint (see p. 178). Dural symptoms are mostly discogenic but may occur in any space-occupying lesion in the spinal canal interfering with the sensitivity or the mobility of the dura mater. Dural pain may spread upwards to the head, the face and the upper neck but it usually radiates downwards and the typical and most common localization is from the lower neck to the trapezius area and the upper scapular region, either central, unilateral or bilateral. Pectoral and axillary localizations of pain are less common. Segmentally referred pain is often monoradicular in origin but may also result from any soft tissue lesion in the region of the neck. If a nerve root is involved, it is � ost often a mid- or lower cervical one giving rise to pain 10 the shoulder area (C4) or in the upper limb (C5-T2). It often indicates a discoradicular interaction and is then accompanied by other root symptoms as well as articular symptoms.The clinical picture must be compatible with a disc problem (see p. 185). If not, other causes for root pain should be considered, including the degenerative conditions or any space-occupying lesion in the radicular canal (lateral recess). When no nerve root is involved segmentally referred pain points towards a soft tissue lesion.In theory any soft tissue in the neck region may be the seat of a lesion: joint capsules, ligaments, muscles, tendons, nerves and vascu lar tissues.They must present with a clinical picture that is recognizable. The same rules apply as for the periph eral joints: this means that the symptoms can be elicited by putting several tissues under tension, either by stretching them passively (inert tissues) or by making them contract (contractile tissues). Local pain in the neck can be felt anywhere but is mostly unilateral and mostly the result of a local soft tissue lesion. Upper cervical pain is less common than
Pain
, Referred
I Soft tissuel
Figure 8.1
Bone
Reference of pain.
lower cervical pain but it is more often localized.It makes the examiner think of the occipitoatlantoaxial complex with its bones, joints and ligaments, the zygoapophyseal joints in the upper and mid-cervical area (espeCially C2-C3 and C3-C4) and the muscular attachments at the occipital bone. In the lower part of the neck local pain is less common than referred pain but if it occurs one should look, for example, for a possible facet joint lesion. The functional examination will complete the picture. The only tissue that does not give rise to referred pain . IS bone. Bony lesions give rrse to pain felt locally. When, after some time, the pain spreads it is the result of a con dition affecting bone and the surrounding soft tissues, for example, metastatic disorders. Bony disorders may give rise to indirect signs: compression pain or pain as the result of contraction of a muscle which is attached to that bone. Onset (Fig.8.2) Pain may come on suddenly, gradually or as the result of an injury. Pain that starts suddenly often has an articular
Figure 8.2
Onset of pain.
CHAPTER 8
cause. It is a manifestation of sudden internal derange ment of an intervertebral joint, mostly the result of the displacement of a discal fragment. It is then usually accompanied by sudden twinges when moving.It comes and goes in an irregular way and tends to recur. It is clearly activity-related. On functional examination articu lar involvement is demonstrated. A common example is acute torticollis. Pain that comes on graduaLLy is not very informative because many different conditions begin in that way. It may again indicate a discal lesion which must show a similar picture on further examination but it may also result from any other disorder. If the pain is related to specific activities, a mechanical condition (see p. 175) is probable and, if this relation between symptoms and movements or postures is not found, a non-mechanical condition should be considered (p.211). If an injury is responsible for the development of the patient's symptoms, further technical investigation will be necessary to exclude serious disorders such as frac tures and luxations. Evolution (Fig. 8.3) Pain may spread but if it does it will always be within well defined boundaries, most often the dermatome, indicating either a soft tissue lesion or a nerve root involvement. If the pain radiates beyond the boundaries of a certain der matome, thus becoming multisegmental, it is either dural in origin or the result of a disorder affecting several nerve roots or several soft tissues, possibly serious disorder. Pain may shift from one place to another, mostly from the centre of the neck to one side or from the cervico trapezioscapular area to the upper limb. The significance
Figure 8.3
Evolution of pain.
-
INTERPRETATION OF THE CLINICAL EXAMINATION 167
is the same: the pain shifts because the lesion shifts. There are not that many lesions that may change their place: a loose fragment of disc is one of the few possibilities. In that disco dural or discoradicular interactions occur in episodes, pain may also shift from one attack to another. Pain may also expand, which means that it increases in extent and also in intensity. This indicates an expanding lesion, for example a tumour. In instances of discoradicular interactions, pain starts proximally in the neck, trapezius and / or scapular area and then shifts to the upper limb. Pain that starts in the arm from the beginning can be the result of a primary posterolateral disc protrusion but the possibility of a neurofibroma must be considered. In elderly people osteophytic or metastatic root compression is among the possibilities. Factors influencing pain
The questions: What brings the pain on? and What makes the pain disappear? are necessary to find out whether or not the condition is related to activity or posture. The type of activity that has an influence on symptoms may help in determining the possible type of lesion. Disc lesions suffer from certain movements, especially towards kyphoSiS, as well as from certain postures, whereas liga mentous conditions are mostly purely postural. In that case maintenance of positions will aggravate pain and altering the position relieves the pain. Most disorders are activity-related - of the mechanical type: discodural or discoradicular interactions, degenerative conditions, muscular and capsuloligamentous lesions. When the con dition is non-activity-related it is of the non-mechanical type and suggests bony lesions, rheumatOid-type condi-
168 SECTION TWO - THE CERVICAL SPINE
tions, iniections, intraspinal or neurological disorders or visceral pathologies. Accompanying symptoms Coughing or sneezing causing pain in the trapezius or scapular region is a common symptom in discodural or discoradicular interactions although any space occupying lesion in the spinal canal may elicit such symptoms. Pain in the arm on coughing is considered as unusual and indicates a closer look: the patient could be suffering from a neurofibroma. Twinges - sudden bouts of pain as the result of a movement of the head - are a typical articular symptom. They very much suggest internal derangement in the intervertebral joint - a disc protrusion. Morning pain is typical for arthrotic and rheumatoid type conditions such as ankylosing spondylitis. It also occurs in capsuloligamentous contracture following degeneration ('the elderly man's matutinal headache see p.197). Nocturnal pain is generally accepted as being of the inflammatory type although mechanical pain may occur when the patient has a poor sleeping posture whereby the head is put into a painiul position.
Duration of pain
Except in acute torticollis, which recovers spontaneously within a maximum of 10 days, neck pain has no tendency to spontaneous recovery.It may improve after some time but it may continue. If the cause is internal derangement it usually does improve but tends to recur, certainly in young people.In the elderly the tendency to spontaneous remission is inclined to diminish. Neck pain that con tinues and at the same time increases in intensity, is very suggestive of malignancy. Root pain as the result of a discoradicular interaction has a spontaneous remission over a period of 3--4 months reckoned from the moment of the 'shift': the pain appears in the arm and the scapular pain disappears. Root pain that has not diminished after several weeks is probably the result of another condition, either degenerative or malignant.
PARAESTHESIA
Paraesthesia is the major differential diagnostic feature between nervous tissue and other structures. This may vary from real 'pins and needles' to 'numbness' and may evolve towards a sensory deficit. If paraestheSia is men tioned and is clearly related to the lesion, a nervous dis order or a lesion affecting a nervous structure is present. The problem may be intrinsic ('neuritis') or extrinsic ('entrapment') (see Fig.8.4).
Infectious Toxic Metabolic ViI. B 12 absorption deficiency Vascular Iatrogenic
Disc Degeneration Injury Tumour, abcesses Soft tissue compression
Proximal extent Localization Behaviour: Spinal cord Nerve root Nerve trunk Nerve ending
Figure 8.4
Paraesthesia.
Intrinsic neuritis may result from iniectious (mononu cleosis), toxic (ethyl alcohol or lead poisoning), metabolic (diabetes mellitus) or vascular conditions (arterioscler osis), may have an iatrogenic cause (injection) or follow vitamin B12 absorption deficiency. When the lesion is the result of external pressure on the nerve, the cause must be sought in the intervertebral disc (discoradicular interaction), degenerative conditions (lateral recess stenosis), injury (fractures or luxations), space-occupying disorders (tumour, abscess, haematoma, aneurysm) or other soft tissue compression (fibrous bands, scars). In nerve tissue compression the three major features have to be interpreted: proximal extent, localization and behaviour. The patient has to clearly understand the difference between pain and paraesthesia, because both behave differently. The lesion which is responsible for the development of the pins and needles always lies proxi mal to their proximal extent or, in other words, the area of paraesthesia is always felt distally to the site of compression. The localization of the paraesthesia is defined to a multisegmental area (spinal cord), to a segmental area (nerve root) - dermatome - or to the territory of a periph eral plexus or nerve. The behaviour of the symptoms depends on which part of the nervous system is involved and subsequently which mechanism is active: spinal cord, nerve root, nerve trunk or nerve ending (see complete information on pressure on nerves in Ch. 2, p. 23).
CHA PTER 8
INTERPRETATION OF THE FUNCTIONAL EXAMINATION
The functional examination of the cervical spine does not cause technical problems. Active, passive and resisted movements are used.The movements are easy to perform, because they are purely physiological. The patient has no difficulties executing the active movements. The examiner knows how to do the passive and resisted movements. The tests are easy to assess: the patient reports if they are painful and the examiner can easily detect even the slight est limitations, either because it is visible or because the end-feel has changed, and also the slightest degree of weakness. Interpretation rests on the physical findings, positive as well as negative, and must be done in the light of the findings from the history and of the recognition, or not, of certain (known) patterns (see below). Because the examination comprises tests at three different levels neck, shoulder girdle and arm - it is possible to find out at what level the lesion should be sought (see Fig. 8.5). If signs are found at the three levels, it is logical to look for the lesion 'half-way', i.e.in the shoulder girdle. If the neck movements - active, passive and/ or resisted - are clearly disturbed the problem must lie in the neck. When, on the contrary, they are totally negative a lesion in the neck is excluded.A neck that moves perfectly well in all directions, actively as well as passively, with a normal end-feel, cannot have an articular problem. The passive movements being normal - full range and pain less - indicate that the structure is not being painfully stretched, thus excluding a lesion of an inert tissue. Negative isometric tests show that the contractile tissues, rarely affected, are also functioning well and that there is nothing wrong with the bone to which they are attached.
Neck problem
..
- INTERPRETATION
OF THE CLINICA L EXAM INATION 169
Pain in the absence of any positive test must therefore be referred or at least of the non-mechanical type, for example inflammatory. Positive scapular movements usually point towards a lesion in the shoulder girdle, although it is not impossible to find slight positive signs in a disorder of the cervical spine. If a shoulder girdle problem is suspected, a complete shoulder girdle examination should follow (see p.396). Positive arm tests may occur in cervical disorders such as spinal cord or nerve root palsy but if they provoke pain felt in the arm, they usually indicate a local lesion in the upper limb - shoulder arthritis, subdeltoid bursitis or tendinitis. They are thus also used to detect alternative causes of pain down the upper limb.Peripheral nervous lesions will also show on examination of the arm. If nec essary the appropriate local examination - shoulder, elbow or wrist - has to be done.
INTERPRETATION OF THE NECK MOVEMENTS
Neck movements can be disturbed in two ways: active combined with passive, or active combined with resisted movements (Fig. 8.6). If the three sets of tests give posi tive findings the examiner should be careful: an acute lesion could be present, a serious condition or just a common condition; but in the last case one or the other passive or resisted movement - must dominate. ACTIVE AND PASSIVE MOVEMENTS ARE POSITIVE
On active testing it will be clear whether movement is limited or not. Painless limitation is usually not a reason for consultation unless it interferes with certain activities, for example backing a car. Painful limitation will disclose a certain pattern, which can be confirmed by passive testing: the same limitation will be found and the end-feel will be informative about the structure that might cause this restriction. Two main 'patterns of limitation' may be recognized: the full articular pattern or any other pattern that deviates from the full pattern. Disturbance
-------04
Active
X passive
Active
X resisted
Figure 8.5
Cervical examination.
Figure 8.6
Interpretation of neck movements.
Tests
170 SECTION TWO - THE CERVICAL SPINE
Left
flexion side flexion
Right
side flexion
Limited movement: a suspicious partial articular pattern Warning The partial articular pattern in which side flexion away from the painful side is the only painful movement is an important sign (Fig. B.B).
A displaced fragment of disc is very unlikely to disturb side flexion while leaving all other movements free. During side flexion, several tissues may be painfully stretched and therefore any costoscapuloclavicular lesion or a lesion in the apex of the lung must be considered. •1
II
Full range: 'partial articular patterns' extension
Figure 8.7
The full articular pattern.
Limited movement: the full articular pattern
The full articular pattern at the cervical spine is no limi tation of flexion, equal degree of limitation of side flexion and rotation and some or great limitation of extension (variable) (see Fig.8.7). Painless limitation with a hard end-feel in an elderly person indicates that the patient has arthrosis of the cer vical spine.Apart from stiffness and possibly some vague ache, this condition doe not really lead to any important symptoms. Painful limitation usually points towards a more serious condition, such as ankylosing spondylitis, rheumatoid arthritis, recent fracture or luxation, postconcussional syndrome, bone disease or a lesion of the upper cervical complex. The history together with the end-feel is most informative and these cases quite often require further investigations in order to obtain sufficient information.
The same 'pain patterns' may occur in the absence of any clinically detectable limitation. This usually has the same significance although the examiner has to be even more careful because a non-activity-related condition could easily be responsible.As long as the findings are consistent, there is no reason to doubt the patient's honesty. Full range: no specific 'pattern'
End-range pain is difficult to interpret. Pain can be elicited by stretching the affected structure or by pinching it. Anatomical knowledge helps to find out what the possibilities are. The first situation typically occurs in patients with capsuloligamentous problems, possibly adhesions at the upper cervical levels. Stretching pain may also present as part of the 'contractile tissue pattern', in which isometric contraction in the opposite direction must be positive as well (see p. 204).
Left
flexion side flexion
Right
side flexion
Limited movement: partial articular patterns
A partial articular pattern is a common finding.It often indicates an internal derangement and then suggests dis placement of a disc fragment - discodural or discoradic ular interaction - in the intervertebral joint.The complete clinical picture must, of course, be compatible: right history and right findings on examination. The clinical picture of disc disorders described in Chapter 9. Specific types of partial articular pattern are occasion ally found: the convergent type - a combination of move ments towards the painful side or the divergent type - a combination of movements away from the painful side. These patterns may indicate a lesion of a facet joint (see p. 198) although it is not impossible that the same pattern arises in an ordinary disc lesion.
extension
Figure 8.8
A suspicious partial articular pattern (colour indicates pain).
CHAPTER 8
ACTIVE AND RESISTED MOVEMENTS ARE POSITIVE
Isometric testing - movements are performed against maximal resistance - may cause pain, weakness or a com bination of both. The muscular contraction augments the pressure in the intervertebral joints. It is therefore not totally impossible to find positive resisted movements in an articular lesion, especially when the condition is in an acute or subacute stage, e.g. acute torticollis, or when there is a high degree of inflammation. The passive tests however should still dominate. When a clear contractile tissue pattern is found - pain on isometric testing in one direction but also on active and passive stretching in the opposite direction - the possibil ity of a lesion of a musculotendinous structure, although not so common, should be considered. When resisted
Discodural or disco radicular interaction
Ankylosing spondylitis Rheumatoid arthritis Recent fracture/luxation Postconcussional syndrome Bone disease Lesion upper cervical complex
Figure B.9
Neck movements positive.
�•••
-
INTERPRETATION OF THE CLINICAL EXAMINATION 171
movements are clearly more positive than the active and passive ones or when the pattern includes weak move ment(s) it has to be considered as a warning sign. Vertebral metastases, fracture of the first rib, glandular fever, wedge fracture of a vertebral body, postconcus sional syndrome and retropharyngeal tendinitis or abscess are the most important possibilities. Warning • Isometric contraction being more painful than active or passive movements warrants a closer look. • Painless weakness and certainly painful weakness of one or more neck movements indicates a serious disorder. Further investigations are necessary to confirm or to exclude such a condition.
....
Musculotendinous lesion
Vertebral metastases Fracture of the first rib Glandular fever Wedge fracture of vertebra Postconcussional syndrome Retropharyngeal disorder
172 SECTION TWO - THE CERVICAL SPINE
When no clear pattern of pain and/ or weakness is detected or when the pattern is inconsistent, the patient should be re-examined or sent for further investigations. In these instances diagnosis on clinical grounds is extremely difficult. An overview of positive active and passive and active and resisted neck movements is given in Figure 8.9.
INTERPRETATION OF THE SHOULDER GIRDLE MOVEMENTS
Shrugging the shoulders may be positive. This move ment involves quite a number of different structures: acromioclavicular joint, sternoclavicular joint, upper rib joints, costo- and coracoclavicular ligaments, costocora coid fascia, upper lung, brachial plexus and muscular structures - elevators are at work, depressors become stretched (see Fig. 8.10). Pain when the shoulders are shrugged may occur in a lesion in the region of the shoulder girdle that becomes painfully stretched, for example sternoclavicular arthritis, healed apical tuberculosis and lesions of the first or second thoracic nerve root, subclavius, costocoracoid fascia or of the first costotransverse joint (see Ch. 23). It must be remembered that this test also stretches the tho racic dura mater: pain in the thorax is elicited in a thoracic discodural interaction. Painless limitation shows that the mobility of the scapula in relation to the thorax is impaired, for example in contracture of the costocoracoid fascia, or that there is limitation of movement at either the sternoclavicular or acromioclavicular joint.
Contracture costocoracoid fascia Sternoclavicular or acromioclavicular limitation
Figure 8.10
Shoulder girdle movements.
Painful limitation is rare and is indicative of a lesion, such as a haematoma in contact with the costocoracoid fascia, an apical pulmonary neoplasm or a severe sterno clavicular lesion. Pins and needles in one or both hands on sustained movement suggests the thoracic outlet syndrome. Crepitus indicates roughening of the posterior thoracic wall. See Chapter 23 for more extensive information.
INTERPRETATION OF THE ARM MOVEMENTS ACTIVE ELEVATION OF THE ARM IS POSITIVE
Elevation may show pain, painless or painful limitation. The movement is considered painful when it elicits or influences the pain for which the patient consults. When active elevation is painful but not limited, the examiner should ascertain where the pain is felt. If positive neck signs have been found and the shoulder movement hurts in the neck region, this is probably the result of 'trans mitted stress' and thus irrelevant. If the movement hurts in the shoulder and lor arm region the problem is local and the appropriate examination - shoulder, elbow or wrist - should follow. Active elevation being painful and limited is probably the result of a local condition in the shoulder girdle or in the shoulder. The pain is not felt in the neck but either in the shoulder girdle or in the arm. Local examination follows and discloses the lesion. A number of conditions limit active but not passive elevation of the arm. Apart from more generalized neuro-
Sternoclavicular arthritis Healed apical tuberculosis T1-T2 nerve root lesions Lesion of the subclavian muscle Lesion of the costocoracoid fascia Lesion of the 1 st costotransversejoint
Costocoracoid haematoma Apical pulmonary neoplasm Severe sternoclavicular lesion
CHAPTER 8
logical disorders, the following lesions can be respons ible: mononeuritis of the long thoracic or spinal accessory nerves, osteophytic or traumatic root palsy of CS. Tendinous ruptures, especially of the supraspinatus tendon, may also limit arm elevation, as does fracture of the first rib or of the spinous process of C7 or n. Psychoneurosis is another possibility.
RESISTED ARM MOVEMENTS ARE POSITIVE
Resisted movements of the arm can be painful, painful and weak or just weak. When one or more isometric tests of the arm are painful and/ or weak the lesion must be local - in shoulder, elbow or wrist. This can be diagnosed by doing the appropriate local examination. Weakness is sometimes difficult to detect. The patient is asked to do a maximal contraction and the examiner assesses the strength. This can be difficult, especially when the weakness is very slight or when the patient does not understand exactly what has to be done. A good test follows specific questions such as, for example: Prevent me from pushing your arm inwards.
Weakness may vary from ordinary paresis, typical for nerve root compression by a fragment of disc, to com plete paralysis, as found in more serious disorders or in complete tendinous rupture.
Mononeuritis -long thoracic nelVe -spinal accessory nelVe NelVe root palsy C5 -traumatic - osteophytic Rupture rotator cuff (i.e. supraspinatus tendon) Fracture - first rib - spinous process C7lf1 Psychogenic
Figure 8.11
Arm movements.
Local examination (shoulder, elbow, wrist)
-
INTERPRETATION OF THE CLINICAL EXAMINATION 173
The examiner should be able to find out whether the condition is intrinsic (myogenic) or extrinsic (neuro genic). Neurological conditions either have a central cause - upper motor neurone lesion - or are the result of a lesion of a peripheral nerve, including the brachial plexus. A peripheral nerve lesion may show as a lower motor neurone lesion, a nerve root lesion or as a lesion of a peripheral nerve. Painless myogenic weakness is probably the result of a complete rupture of a tendon. Neurological weakness may also be the result of a local peripheral nerve lesion. In both instances local examina tion should follow. When the weakness has a neurologi cal origin, but is segmentally distributed, or when the distribution is more extensive, the problem must lie in the cervical spine or in the central nervous system. The most common condition causing weakness down the arm is nerve root compression - usually C7 by a displaced fragment of disc. In orthopaedic medicine the most important non discogenic causes for weakness down the arm are mono neuritis of the suprascapular nerve, vertebral metastases, n nerve root lesion, neuralgic amyotrophy, osteophytic root palsy, traction palsy of CS and neurofibroma. In more generalized neurological conditions (e.g. dis eases of the central nervous system and cerebrovascular accidents), the weakness is more extensive (see Fig. 8.11 for an overview of positive arm movements). -
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Degeneration and anatomical changes Ageing of the cervical space 176 Pathology
176
Mechanical disorders
177
177 Disorders of the disc: disc displacements Stages of disc displacement 178 Degenerative disorders 197 Capsuloligamentous disorders 204 Disorders causing pain on resisted movements of the neck 204 Disorders causing symptoms on active and/or resisted shrugging of the shoulders 205
Mechanical disorders of the cervical spine affect the structures belonging to the locomotor system. They are very often related to the consequences of the ageing spine. The degenerative changes at the level of the inter vertebral discs lead to the possibility of disc displace ments but also have anatomical and biomechanical consequences for the other structures: ligaments, cap sules, nervous tissue, vascular structures. Apart from the degeneration being responsible for the development of certain disorders, injuries and overuse may lead to soft tissue lesions in the region of the neck (Box 9.1). Mechanical disorders are activity-related which means that their symptoms are influenced by movement and / or posture. Questions in the history-taking such as 'What brings your symptoms on?' or 'What makes your symptoms disappear?' elicit answers that may suggest the type of condition from which the patient suffers.
Box 9.1 Mechanical d isorders of the cervical spine • Disc disorders
•
• •
•
Discodural interactions D iscoradicular interactions Degenerative disorders With localized pain - Arthrosis at the upper two cervical joints, leading to ligamentous contracture: morning headache in the elderly - Subacute arthritis of the atlantoaxial joint - Arthrosis at a facet joint - Traumatic osteoarthrosis With radicular pain: osteophytic root compression Compression phenomenon: the mushroom phenomenon Cervical spondylotic myelopathy Capsuloligamentous disorders Disorders causing pain on resisted movements of the neck Musculotendinous lesions - Lesions of the semispinalis or splenius capitis muscle - Lesions of the longus colli muscle (retropharyngeal tendinitis) Serious disorders Disorders causing symptoms on active and/or resisted shrugging of the shoulders: shoulder girdle lesions 175
176 SECTION TWO - THE CERVICAL SPINE
From middle age nearly all people have a degenerating spine. This is not necessarily symptomatic and diagnoses such as 'degeneration', 'athrosis', 'osteophytosis', 'spondylosis' or 'spondylarthrosis' are still too easily made. Throughout the literature, a discrepancy between the discovery of structural changes and the presence of symptoms is a consistent finding.1-7, 1 2
flatten. Degenerative changes at this level threaten the spinal nerve and the vertebral artery. From the fifth and sixth decades on, the disc tends to collapse, further diminishing its height. The borders of the vertebral bodies come in apposition with, as a reac tive result, the formation of hyperostOSiS and osteo phytes. The osteophytes increase the articular surface area which promotes the development of circular disc displacement and thus new osteophytes. The spine stiffens and the articular segments stabilize again. See Chapter 50 for an extensive explanation of the function and behaviour of the lumbar disc, which is very comparable to the situation in the cervical spine.
AGEING OF THE CERVICAL SPINE
As the result of weight-bearing in the bipedal man the axial spine is submitted to increased forces acting on the different structures. The disc, being entirely avascular, suffers most from this situation and degeneration starts quite early in life and goes on until the stage of spondylo sis is reached. In this degenerative process the other structures of the spine - bone, ligament, capsule, zygapophyseal joints - are also involved and end up in a state of spondylarthrosis.
AGEING OF THE CERVICAL DISC In healthy individuals the intervertebral disc in the cervi cal spine has a structure which is very similar to the lumbar disc - an annulus fibrosus which contains a nucleus pulposus. As long as the disc is not submitted to excessive asymmetrical forces, the hydraulic mechanism within the disc functions perfectly. It becomes deficient as the result of excessive forces, occurring during everyday activities, or following absence of movement. The annular fibres become strained and sprained and the nucleus starts to dry out. This is a characteristic sign of disc degeneration. It has been shown that in the first two decades of life, lateral tears occur in the annulus fibrosus. They tend to develop joint-like structures - the uncovertebral joints that then begin to undergo transformation.s In the second and third decades, the lateral tears enlarge towards the medial part of the disc, often ending in a complete transverse splitting of the disc into equal halves. These anatomical changes cause instability of the disc and favour the possibility of cartilaginous displacements, either of the annulus fibrosus or of the nucleus pulposus (see below: disc displacements). In the fourth and fifth decades, the nucleus pulposus dries out further, because of the loss of proteoglycan matrix, with, as a result, diminution of the height of the intervertebral space and flattening of the lordotic curve. The uncovertebral joints start to bear weight and tend to
CONSEQUENCES OF THE AGEING OF THE DISC FOR THE SURROUNDING STRUCTURES Effects on the ligaments
Instability of the intervertebral joints results in instability of the entire segment. Movements of the related vertebrae become excessive and irregular. The facet joints and the ligamentous structures become more easily submitted to excessive forces which may result in sprains and strains of capsules and ligaments. The whole segment becomes vulnerable to trauma. Spur formation at the anterior and posterior borders of the vertebral body indicates lifting of the ligaments as the result of excessive movement. Effects on the facet joints
Diminution of the height of the disc and the subsequent reverse from lordosis to kyphosis result in a greater trans mission of shearing forces to the facet joints. They start to bear weight and this furthers the degenerative process, also leading to loss of cartilage. Osteophytes develop in the posterior part of the vertebra which accompanies uncovertebral joint and facet arthrosis, which may result in zygapophyseal joint hypertrophy. The facets are richly innervated with the result that degeneration may be a potential cause of pain.9 Later in life when the facets continue to degenerate subperiosteal osteophytes with periarticular fibrosis develop. This will result in gross decrease in mobility at the facet joints. Together with the stabilizing changes in the disc it results in a more stable segment in the elderly. Effects on the spinal canal and intervertebral foramen
Circular disc displacement, as happens when the disc becomes totally degenerated, may further the develop ment of osteophytic outcrops at all sides, and thus also in the spinal canal threatening the spinal cord. As the outcome of excessive compression forces because of the
CHAPTER 9
diminution of the intervertebral distance, osteophytic excrescences may form at the level of the uncovertebral joint, at the level of the zygapophyseal joint or at both. Once the bony parts formed by the uncovertebral joints touch each other, further loss of height can only happen anteriorly. Because of the decrease in height in the anterior column of the cervical spine the cervical lordosis may diminish and even disappear resulting in the typical posi tion of the degenerated neck - the chin projected forwards. The association of diminished intervertebral space, osteophyte formation at both the uncovertebral and zygapophyseal joints and hypertrophy of the facet joint capsules causes diminution of the intervertebral foramen and eventual neural foraminal encroachment. Retrolisthesis in the mid-cervical area (C3-C6) is a common finding in spondylarthrosis. The oblique posi tion of the facet joints is responsible for the upper verte bra sliding backwards as it approaches the lower one following diminution of the intervertebral space. In this situation extension of the neck further narrows the spinal canal. Anterolisthesis follows arthrotic changes in the intervertebral joint.lO
RADIOLOGICAL CHANGES Degenerative changes of the cervical spine are common in both symptomatic and asymptomatic adults. At the age of 50 spondylosis is visible on plain X-rays in more than 50% of asymptomatic people. The clinical question is whether the patient's symptoms are caused by the changes that are seen.ll Uniortunately, even the most sophisticated imaging studies do not show pain but only structural abnormalities that may or may not be the cause of the patient's symptoms. Disc degeneration shows on a radiograph with disc space narrowing, osteophyte formation at the anterior and posterior margin of the vertebrae and sclerosis of the end plates. It occurs most often at the levels C5-C6 and C6-C7, followed by C4-C5.12 It is not abnormal to find a loss of lordosis or even kyphosis of the cervical spine in younger people or in elderly people with severe spondylosis. 9% of asympto matic people seem to have an actual cervical kyphosisY
DISORDERS OF THE DISC: DISC DISPLACEMENTS
Symptomatic disc displacements in the cervical spine are more common than is generally believed. They can occur at any age from childhood onwards but present with dif"
-
MECHANICAL DISORDERS 177
ferent clinical syndromes, depending on the age group. Cartilaginous displacements are most frequent at the C6-C7 and C5-C6 joints.13-1 7 They are occasionally found at the C4-C5 or C7-Tl joints, and rarely at the C2-C3 or C3-C4 joints. Nuclear prolapses are very uncommon, except in young people. It was to Cyriax's credit that he recognized the clinical pictures of a disc protrusion and made an inventory of symptoms and signs. A distinction can be made between posterocentral and posterolateral displacements resulting respectively in disco dural and discoradicular inter actions. It should be remembered that the diagnosis of a disc protrusion is often made on a purely clinical basis, fol lowing the patient's history and the signs found during functional examination. Technical investigations very easily lead to misinterpretation because the results are mostly findings that have nothing to do with the actual complaint.18 They can sometimes be used to confirm a diagnosis, rather than to make one.
POSTEROCENTRAL DISPLACEM ENT Posterior migration of disc tissue beyond the posterior limits of the intervertebral joint space causes pressure on the posterior longitudinal ligament and via the ligament on the anterior part of the dura mater. This produces multisegmental pain with dural reference, mostly in the trapezius and scapular area but possibly towards the head and / or pectoral area (see p. 166). The pain is the result of a discodural interaction: irritation of the anterior structures in the spinal canal is responsible for the dural symptoms. Pure posterocentral compression gives rise to pain felt centrally and / or bilaterally. Compression just laterally from the midline will result in pain felt unilater ally but still multisegmental. The internal derangement in the intervertebral joint provokes articular signs demonstrable on functional examination.
POSTEROLATERAL DISPLACEMENT If the extruded disc material runs into the nerve root canal, discoradicular interaction occurs. This postero lateral migration of disc tissue causes pressure on the nerve root which results in a series of symptoms: first segmental pain following compression of the dural sheath (root pain ), then segmental paraesthesia and / or neurological deficit as the result of the parenchyma becoming pinched. The disc displacement may be primary or secondary. Secondary posterolateral displacement
This is the most frequent situation. The patient has suf fered from a few posterocentral displacements with neck,
178 SECTION TWO - THE CERVICAL SPINE
trapezius or scapular pain in the past. During the most recent attack, as the disc fragment moves from the centre to one side, the pain shifts from the neck to the upper limb, segmental root pain developing as the multi segmental neck pain disappears. Primary posterolateral displacement
From the beginning the pain starts in the forearm. There has been no previous neck pain because originally there was no compression of the dura mater but immediately of the nerve root. The segmental pain can be accompa nied by paraesthesia and I or neurological deficit. Because this condition is rather uncommon, differential diagnosis should be made with non-discal nerve root compression or with intrinsic conditions of the nervous system.
STAGES OF DISC DISPLACEMENT
In the evolution of a disc protrusion during a patient's lifetime, Cyriax13 (p. 77) recognized different possible stages. Each is characterized by a typical history.
Stage 4
The patient, over 35, may find the pain shifts from the scapular region towards the upper limb: severe root pain develops and increases during the first 2 weeks then remains unchanged over the next 4-8 weeks and gradually recovers. Pain may be accompanied by paraesthesia and a neurological deficit may also develop. There is sponta neous recovery in the course of a few months. The situa tion is analogous to the lumbar spine, in which backache develops into sciatica although spontaneous cure takes much longer (6-12 months) than in the cervical spine. Stage 5
In elderly patients, a bilateral protrusion may cause aching in both upper limbs and paraesthesia in all the fingers. Stage 6
Constant bilateral aching in head, neck and scapulae may be experienced in elderly patients as the result of a fixed posterocentral protrusion that leads to constant disco dural interaction. Stage 7a
Stage 1
Adolescents or young adults are apt to suffer attacks of acute pain in the neck, which totally immobilize the patient's head and fix it in a certain deviation. This so called 'acute torticollis' is the result of a large discodural interaction, usually of the nuclear type, and undergoes spontaneous cure within 10 days.
The disc compresses the spinal cord. This results in aching in both upper limbs and paraesthesia in the hands and I or feet. Stage 7b
Secondary to the posterocentral protrusion, an osteophyte has formed in the spinal canal and may obliterate the anterior spinal artery, leading to progressive paraplegia.
Stage 2
Patients in their late 20s or older. They describe bouts of intermittent scapular pain, which is mostly unilateral but not always on the same side. The symptoms may last several weeks. Remission is the result of spontaneous reduction of disc material. Stage 3
When the patient is over 50, the pain tends to become more constant (Fig. 9.1). The increasing stiffness of the neck prevents the spontaneous reduction of the disc material.
c '" 11.
FINDINGS ON EXAMINATION The symptoms and signs in cervical disc conditions are very unlike those found in an arthrotic spine. The pain is periodic and between attacks the patient may be com pletely pain-free. The pain is very often felt unilaterally and may shift from one side to the other during the same attack or from one attack to another. On examination some movements may be found painful and I or limited, whereas other movements are painless and full range. The end-feel is either elastic or crisp and not at all the bone-to-bone feel that one would expect in spondylosis. It is obvious that a narrowed disc and osteophytosis cannot give rise to symptoms that vary that much. The findings on examination differ from one stage to another and are the result of the position, size and behav iour of the protruded fragment and its relation to dura mater or nerve root. Dural symptoms
Figure 9.1
Attacks of pain from disc placements in different age groups: pain becomes more constant over the age of 50.
When a fragment of disc (at any level) protrudes postero centrally, it may compress the dura mater either in the
CHAPTER 9 - MEC HANICA L DISORDERS 179
midline, which results in central or bilateral pain, or slightly to one side, leading to pain felt unilaterally. The dura mater, being a multisegmentally innervated tissue, translates this compression into multisegmental pain, which may spread up to the head and down to the midthoracic region but may be felt anywhere in this area (Fig. 9.2). The pain is most commonly experienced in the region of the trapezius and the scapula or may spread upwards towards the ear (Fig. 9.3a). Occasionally it may be felt in.the pectoral area or in the axilla (Fig. 9.3b). The patient very often mentions that there is a tender spot, usually somewhere in the suprascapular part of the trapezius, which is identified as the source of symptoms. On palpation the examiner indeed finds localized tender ness but this phenomenon has no localizing nor diag nostic value as it is only an evidence of multisegmental tenderness, one of the dural symptoms, resulting from dural compression at any level. This will be positively confirmed when, later in the examination, movements designed to test the trapezius muscle are found to be neg ative. Fur thermore, the tender spot may shift during neck manipulation and disappears when a full and painless range is obtained. The tenderness is clearly a referred phenomenon (see Ch. 1).
Figure 9.2
The boundaries of multisegmental reference of pain of cervical origin.
In contrast to a lumbar discodural problem, a cough seldom hurts. Occasionally swallowing may be uncom fortable, although the mechanism causing this symptom is unclear (see Box 9.2). Dural signs are not found on examination. Although neck flexion stretches the cervical dura mater, the pain very often experienced during this movement must be regarded as an articular sign rather than a dural one. Neck flexion can only be regarded as being a dural test if it stretches the cervical dura from a distance, which is not the case here. There is also no equivalent to the straight leg raising test in the lumbar examination where a simple movement (hip flexion with an extended knee) allows differentiation between dural pain, root pain and mus cular tightness. Some nerve roots (C4-C6) are tethered to the gutter of their respective transverse process, but Box 9.2 Dural symptoms and signs in the cervical spine
Symptoms • Multisegmental pain • Multisegmental tenderness • (Pain on coughing) • Pain on swallowi n g
Signs There are no dural signs in the cervical spine. (ULTT?)
Figure 9.3 Multisegmental pain: (a) the most common distribution involves trapezius and interscapular area; (b) less commonly pain is felt in the pectoral area and the axillary area.
180 SECTION TWO - THE CERVICAL SPINE
apparently not to the foramen.19 Some authors have developed and discussed 'upper limb tension tests' (ULTT) as a valuable examination procedure for patients with neck problems with or without radiation down the upper limb.20--32 The aim would be to create stress, trans mitted to the structures in the spinal canal, via the peri pheral nerves (median - radial - ulnar). The peripheral nerves in the upper limb, however, have, unlike those in the lower limb, a more complex course. It is therefore more difficult to do 'pure' movements and a great number of structures are stretched during the execution of the dif ferent tests. Their development is nevertheless interesting to follow. If further experience shows any to be valuable tools in the neurological evaluation of the upper limb, this will certainly be recognized in the future. However, until their use becomes more evidence-based they remain hypothetical and they are not integrated into the standard functional examination of the cervical spine. They can of course be used as accessory tests.
(a) Left
flexion s i d e flexion
Right
s i d e flexion
extension
(b)
Articular symptoms and signs
The patient describes the symptoms as activity-related: pain is elicited or influenced mostly by movements and / or activity and occasionally by posture, i.e. in flexion. Because a disc displacement causes an internal derange ment in the intervertebral joint, twinges may occur during movement of the neck. The partial articular pattern of internal derangement is found on examination. Some active movements provoke considerable pain and may either be limited or cause pain at the end of range. Others are negative or clearly less positive. An asymmetrical pattern occurs, which may vary from very slight, with hardly any limitation, to very pronounced, some movements being completely blocked, possibly forcing the head in a deviated position. A minimal partial articular pattern (Fig. 9.4a) is seen where the internal derangement is minor, either because the posterocentral displacement is small or because the pro truded fragment lies partly outside the intervertebral joint (posterolateral displacement). A severe partial artic ular pattern is the result of a gross internal derangement following a severe disco dural interaction (Fig. 9.4b). Passive movements usually hurt more than active ones but cases may be encountered in which passive move ments ease the pain. Resisted movements are negative, except perhaps resisted flexion, which may slightly increase the pain in more acute cases, presumably as a result of the conse quent compression strain on the affected joint. When neck flexion elicits pain in the upper thoracic area, further examination of the neck, the shoulder girdle and the thorax must differentiate between a cervical lesion with pain reference to the upper thorax and a lesion in the shoulder girdle or upper thoracic spine. The movement - an articular sign for the cervical spine - is
extension
Figure 9.4
Examples of partial articular patterns: (a) minimal; (b) severe (colour indicates pain).
regarded as a dural sign for the thoracic spine. During neck flexion the dura mater is stretched and drawn forward against an eventual upper thoracic protrusion. A painful arc may be found on active or. passive testing. This sign sometimes occurs during rotation movement in patients with unilateral symptoms and during extension in patients with central or bilateral pain and is pathognomOnic of a disc lesion. If only one movement proves positive, it is usually rota tion towards the painful side. Caution must be taken when
the only painful movement seems to be sideflexion away from the painful side. T his sign may occur in any costoscapulociavicular lesion, or may suggest that a lesion at the apex of the lung is being painfully stretched. Further investigations are necessary. In discodural problems either the normal leathery end feel is expected or, in more severe cases, the more typical
CHAPTER 9
-
MECHANICAL DISORDERS 181
Box 9.3 Articu lar symptoms and signs in the cervical spine -
Symptoms • Pain on movement, activity or posture • Twinges on movement
Signs • Deviation • Partial articular pattern • Painful arc • Crisp end-feel
end-feel of muscle guarding ('crisp'). This is clearly unlike the fairlyhard end-feel of arthrosis or the empty or muscle spasm end-feel of more serious disorders (see Box 9.3). Root symptoms and signs
By analogy with the lumbar spine, where backache may evolve into sciatica, cervicoscapular pain may be replaced by brachial pain. The original multisegmental cervicoscapular pain dis appears and severe and purely segmental pain down the arm supervenes. The examiner must be aware that patients sometimes omit to mention the original pain in the trapezius area but concentrate only on the severe symptoms at presentation. This change in pain localization is the result of the disc moving laterally (Fig. 9.5). Pressure on the dura mater ceases and the dural sleeve of the nerve root becomes compressed. As the structure causing the lesion has shifted, the site of pain will also move. When the nerve root compression become more severe, symptoms and signs are found that point towards the nerve fibres themselves and paraesthesia or numbness develops, felt (mostly) in the distal part of the correspon ding dermatome. When the pressure increases even more, conduction may become impaired, leading to neurological deficit, which can manifest as a minor motor palsy (paresis), a sensory palsy (cutaneous analgesia) or both. Some reflexes may become sluggish or absent. Because the cer vical nerve roots emerge horizontally, the symptoms and signs are strictly monoradicular, in contrast to the situa tion in the lumbar spine where the nerve roots have an oblique course, and more than one may become com pressed by the same disc. The C6 and C7 nerve roots have a slightly more oblique course and may sometimes pass two discs. Biradicular compression is not totally impossible at this level. Further analysis will show whether the 'upper limb tension tests' are valuable in the examination of the dif ferent nerve roots (see also: Dural symptoms and signs and Box 9.4).
Figure 9.5
Pressure on the dura mater (a) ceases when the disc moves laterally and compresses the nerve root (b).
Box 9.4 Root symptoms and signs i n the cervical spine
Symptoms
Signs
• Segmental pain Segmental neurological deficit • Segmental paraesthesia • Motor (weakness) • Sensory (cutaneous analgesia) • Segmental numbness • Diminution of reflexes • (ULTI?)
disturbance will soon supervene. If pain is also present, the cause is compression of the dura mater. Where pain is absent, compression of the dura has clearly provoked localized ischaemia so that it is insensitive. In more severe cases, the gait will become disturbed, the plantar reflex may become positive (Babinski's sign) and the patient may develop spasticity, incoordination and extensive weakness in the lower extremities (see Box 9.5).
Cord symptoms and signs
In posterocentral disc protrusion, the spinal cord may become compressed. Pressure on the cord itself is not painful. It leads to multisegmental paraesthesia, usually felt in both hands and / or feet and very often provoked or influenced by active or passive neck flexion. Sensory
COMMON SYNDROMES The following clinical pictures can occur in the cervical spine. They are all caused by a cervical disc protrusion and indicate different stages in its evolution.
182 SECTION TWO - T HE CERVICAL SPINE
Box 9.5 Spinal cord symptoms and signs in the cervical spine
Symptoms • Multisegmental paraesthesia • Increase of paraesthesia on
neck flexion • Sensory disturbance
Left
flexion
Right
Signs An extensive picture may develop with i.e.: • Gait disturbance • Spasticity - clonus • Incoordination • Extensive multisegmental weakness • Positive plantar reflex (Babinski's sign)
Acute torticollis: unilateral pain with asymmetrical picture
Unilateral acute torticollis, caused by a discodural inter action, is very rare before the age of 12 years but is quite common between 15 and 30. History. Most patients wake in the morning with a stiff neck. As soon as they get up and the weight of the head has to be borne by the neck, they find that they have great difficulty in moving the head. Any attempt to do so results mostly in unilateral pain, felt in the neck and radiating to the trapezius or upper scapular area. Occasionally the symptoms come on suddenly as the result of a certain movement (e.g. bending over a wash basin), a minor incident causing trivial trauma (e.g. a blow to the head33) or coughing. Neck movements make matters worse, and even arm movements may cause considerable pain. The pain dimin ishes when lying down with the neck supported but it may be very difficult to change position and the patient has to hold the head firmly between the hands to do so. Previous attacks, not necessarily with symptoms on the same side, may be mentioned. Many patients feel giddy during an attack of acute torticollis, the vertigo ceasing as soon as manipulative reduction becomes complete. Inspection. The patient holds the head in an asymmetri cal position. The examiner should note whether the devi ation is a pure lateral tilt or also contains an element of rotation. The head may be held deviated towards or away from the painful side. In acute torticollis that results from a disc lesion, the deviation is usually purely lateral, often away from the painful side and without any rota tory component. Slight deviation in flexion occasionally occurs. Exa m i nation . On examination, gross and obvious articu lar signs are found: marked pain and limitation of one rotation and one lateral flexion towards the same side, usually the painful side. Often no movement is possible in either of these directions (Fig. 9.6). The other move-
extension
Figure 9.6 The partial articular pattem in acute torticollis (colour indicates pain).
ments are much less painful and scarcely limited, except possibly extension. At the end of range an empty feel or one of severe muscle guarding is noticed. Resisted movements are sometimes painful and even weak. Muscular contraction and subsequent release cause a momentary increase or decrease of pressure in the intervertebral disc, leading to augmentation of the pain. The patient therefore immediately stops the contraction. Arm movements may also be impaired. On active ele vation of the ipsilateral arm, a false painful arc may be present and in very acute cases the patient may be unable to bring the arm up voluntarily above the horizontal. Some resisted movements of the arms may also increase the pain. These secondary signs are clearly the result of transmitted stress and will disappear as soon as the con dition improves: when the arm reaches the horizontal, the muscular effort is at its greatest and secondary taut ening of the cervical muscles takes place, leading to such pain that the arm falters and a false shoulder sign appears. There are no root or cord signs. D i a g n osis. The pattern of limitation is diagnostic. Acute torticollis is the most striking example of a partial articular pattern, which indicates that part of the joint is blocked by an intra-articular displacement. In most instances the displacement is nuclear : the nucleus has oozed out slowly during the night, while the patient has lain for some hours with the neck in side flexion or rotation. The dura mater becomes compressed and irritated, which causes the cervicoscapular pain. A sudden onset suggests an annular displacement. Acute torticollis occurring in patients over 30 is usually of the annular type.
CHAPTER 9
Differential diagnosis. This is not very difficult. There are, nevertheless, a number of conditions in the head or neck which may provoke a more or less pronounced deviation or asymmetrical position of the head. Congenital torticollis. Some babies are born with a pain less contracture of one sternocleidomastoid muscle. The neck is fixed in side flexion towards the affected side and rotation away from it. This may occur in combination with congenital anomalies of the atlas,34 such as hemi atlas, partial atlantic aplasia,35 partial atlanto-occipital fusion36 and asymmetry of the lateral masses of the atlas.37 When conservative treatment fails, biterminal open release is a possible surgical treatment.38 Acute torticollis in children. Acquired torticollis in chil dren is a symptom that may be the consequence of one of a number of underlying causes, some of which are severe and life threatening. Musculoskeletal, ophthalmological, infectious, neurological and neoplastic conditions may present early with torticollis only.39 Benign paroxysmal torticollis is relatively uncommon and a self-limiting condition occurring during infancy. I t resolves by the age of 2-3 years. Periodic episodes of torticollis may randomly alternate from side to side and be associated with other symptoms. The aetiology is unknown and no treatment is effective.4o Fixation of the head may also be the result of reflex spasm of the sternocleidomastoid muscle. This contraction follows irritation from swollen glands lying under it. Differential diagnosis from a disc lesion causing devia tion has to be made. In a disc lesion, the deviation is purely in lateral flexion or flexion or a combination of both. When a spasm of the sternocleidomastoid muscle is responsible, the neck is held in flexion, side flexion towards and rotation away from the painful side ('black bird's sign'41). This occurs in the following conditions:42 •
•
•
•
Recent tonsilitis: is seen in children aged between 5 and 10 years, usually after a sore throat, who have suddenly developed a stiff neck. The condition is not particularly painful but the head is held in deviation (as described above). The resisted neck movements may be slightly painful. On palpation, glands are felt, especially on the contracted side. Anginal variety of glandular fever: the glandular enlarge ment leads to real fixation of the neck in side flexion towards and rotation away from the painful side. Grisel's syndrome: an atlantoaxial subluxation as the result of ligamentous laxity following parapharyngeal inflammation43 or other conditions including upper res piratory tract infection, sinusitis, tonsilitis, otitis media, parotiditis, mastoiditis and acute rheumatic fever.44 Trochlear palsy: a lesion of the trochlear nerve (IV) leads to weakness of the superior oblique muscle of the eye.
-
MECHANICAL DISORDERS 183
Two other conditions give rise to a greater degree of limitation of movement: •
•
Afebrile otitis media: occasionally the first symptom may be pain felt in the neck. In the first 2 weeks, the head is fixed in an asymmetrical position. Any attempt to move the head results in muscle spasm and obstruction by the pa tient. Retropharyngeal abscess: may also start in the same way and gives rise to swallowing problems or airway obstructions.45
'Ocular torticollis': febrile infection may lead to unilateral palsy of the abducens (VI) nerve involving the lateral rectus muscle of the eye. The eye is fixed in the medial corner of its socket and the child has to turn the head in order to look sideways. The limitation of the movement clearly lies in the eye, not the neck.J3 The lesion usually regresses spontaneously after 1-3 months. Postviral torticollis in adolescents. Stiffness and diffuse aching of the neck may be the first symptom of glandular fever. These symptoms occur even before the patient begins to feel unwell. Active movements are uncomfort able and sometimes even limited. The passive move ments have a normal range and a normal end-feel. Resisted movements are often painful. On palpation, glandular swelling is found and fever follows. Spasmodic torticollis. The inspection is diagnostic. The patient is seen to rotate the head suddenly, always in the same direction, by an apparently irresistible active move ment. This involuntary movement can be prevented by manual pressure which can also be used to overcome the muscles and rotate the head back into the neutral posi tion. The muscles give way in a manner that suggests neurological hypertonus. Therapy of spasmodic torticollis should be started with methods such as biofeedback,46 behavioural therapy and anticholinergic drugs. When these procedures are not successful, local application of botulinum toxin offers a new and highly effective technique.47 Surgical treat ment, such as neurotomy, rhizotomy or stereotaxic oper ation, should be restricted to otherwise i ntractable cases.
In this rare disorder, the head is held fixed in rotation and side flexion in the same direction. To bring the head back to the neutral position takes a strong voluntary effort on the patient's part. The spasm abates in the lying position. Neurosurgery is often required.48,49 Spastic torticollis.
Hysterical torticollis. The patient keeps the head and scapula fixed i n an impossible position, which immedi ately demonstrates its non-organic nature: the head is held in side flexion towards the alleged painful side and the scapula at the same side is kept hunched. No organic lesion exists which leads to fixation of the head in side
184 SECTION TWO - THE CERVICAL SPINE
flexion and whereby the patient is obliged to keep the scapula elevated. On examination, all active and passive movements are very painful and limited. Resisted movements are painful and weak. This again is a hysterical manifestation. The end-feel discloses active muscular contraction but sus tained passive pressure during persuasion quite soon leads to full range of movement and confirms the diagnosis. Parkinsonism. The neck may become gradually stiff and painful, because of muscle rigidity as the result of increased extrapyramidal tone.so Identification that the passive range is much larger than the active one affords the clue and inspection of the facies is confirmatory as are other typical findings (e.g. tremor, gait).
The presence of a compensating thoracic curve following cervical scoliosis indicates the possibility of adolescent scoliosis, unilateral cervical rib, Klippe-Feil deformitysl,s2 or a past thoracoplasty. Cervical scoliosis.
The differential diagnosis is not very difficult. In meningitis, the patient develops acute pain in the neck with headache. There is nausea and sometimes vomiting and fever. The neck is deviated into extension. On exam ination very pronounced dural symptoms and signs are found: even straight leg raising is positive (Kernig's sign [drawing up of legs]; Brudzinski's sign [flexion of hip and knee upon testing for meningism]). Meningitis.
Natural history. Untreated the pain is constant and severe for 2 or 3 days and the condition recovers spontaneously in the course of the next week. Treatment. Treatment is by manipulation. The technique will be adapted according to the clinical picture. Acute torticollis in patients under 30 very often behaves in a nuclear manner: these patients should be treated with 'nuclear ' techniques - progressive sustained rotation and / or lateral flexion, whereby an attempt is made to persuade the displaced nuclear material slowly back. The less frequent cases that are clearly annular should be treated with the normal 'annular' manipula tion techniques (see Ch. 13). See Box 9.6 for a summary of unilateral acute torticollis.
Unilateral pain in the neck, trapezius or scapular area
This is the most common of neck complaints. The symp toms may start from the late 20s on and can occur at all ages. It has recurrent character with varying localization and may in the end become more or less chronic. History. The patient describes periods of unilateral cervicoscapular pain, sometimes radiating to the head (occipitofrontal headache), which may come on sponta neously or after minor trauma. The pain may be quite local ized, usually at the mid- or lower neck, but there is often
Box 9.6 S u mma ry of u n ilateral acute torticollis --
Definition
Acute torticollis is a sudden attack of severe cervicoscapu!ar pain, owing to a large posterior shift of disc material, compressing the dura mater and resulting in a discodural i nteraction. Onset
Sudden: annular (age > 30) Slow: nuclear (age < 30) Symptoms
Articular (Twinges) Pain on active movements Dural Dural pain: large reference Signs
Deviation in side flexion (or flexion) Gross partial articular pattern Treatment
> 30 years: manipulation under traction <30 years: progressive sustained movements Spontaneous recovery: takes
7-10 days
reference of pain to the trapezius area, upper scapular area or shoulder region. Because this multisegmental radiation shows the pain to be dural, it has no localizing value. The pain varies in an irregular manner and may last some days to several weeks. There is no pain between episodes. The symptoms are not always felt on the same side. Over the age of 50, pain tends to become more constant but is still made worse by certain movements. A common complaint is difficulty in twisting the head to one side so as to reverse a car. The pain is felt on certain movements only and there is usually no pain at night, except on turning in bed. Certain postures, especially flexion maintained for a certain time (e.g. reading), may increase the pain. Examination. On examination, a mild partial articular pattern is found (Fig. 9.7). Common patterns are that two, three or four movements out of the six are painful, and four, three or two prove painless. Minor limitation of some movements may be present and a painful arc may be found on active or passive testing. Passive movements are usually more painful than active ones. The end-feel is rather crisp, indicating the muscle guarding typical of a disc lesion but it is not uncommon to find a normal, capsular end-feel. In the painful area, the typical tender spot is found, usually unilaterally at the base of the neck or in the proximal trapezius muscle. Root and cord signs are absent. Diagnosis. The diagnosis is based partly on the history, in which the patient describes periods of pain, coming and going without any specific reason. The pain is dependent
CHAPTER 9
(a) Left
flexion
Right
-
MECHANICAL DISORDERS 185
Box 9.7 Summary of u n i lateral pain in the neck, trapezius or scapular area Definition
An attack of moderate pain in the cervical, trapezial or scapular area as the result of a posterior shift of disc material intermittently compressing the dura mater and resulting in a discodural interaction. The pain is usually unilateral, but may change sides. Onset
Sudden: annular Slow: nuclear Symptoms
Articular Pain on movements Dural Multisegmental pain reference possible Signs
extension
Moderate or slight partial articular pattern Crisp end-feel
(b) Left
flexion side flexion
Right
side flexion
Treatment
Manipulation (Traction) Prevention
Differential d i a g n os i s. The differential diagnosis includes lesions in the shoulder girdle (e.g. posterior sternoclavic ular syndrome, see p. 404), in the upper thoracic area (e.g. discodural interactions, muscular lesions, lesion of a cos tovertebral joint, see p. 405), internal disorders (e.g. in the heart, lungs or diaphragm, see p. 219) and neurological conditions (e.g. long thoracic or spinal accessory neuritis, see p. 543).
extension Examples of partial articular patterns in u n i l ateral cervicoscapular pain (colour indicates pain).
Figure 9.7
on certain movements and postures and it may also shift from one side to the other. The second indicator is the fact that the pain is of the multisegmental type, spreads over several dermatomes and is influenced by neck movements. The asymmetrical pattern of painful movements shows the partial articular pattern, which means that the intervertebral joint is partially blocked by an intra articular displacement of disc substance, usually annular. It is not easy to determine the level at which the pro trusion lies, because any disc at any level gives rise to the same symptoms (multisegmental pain) and signs (partial articular pattern). Oscillatory techniques on a sitting or prone lying patient or anteroposterior gliding move ments with the patient lying supine may sometimes provoke the pain and give an idea as to the level but this cannot always be relied upon.
Natura l h i story. In patients under 50, there is a tendency to spontaneous cure in a few weeks. Nevertheless a number of patients do not become completely cured and are left with a minor ache. Treatme nt. Unilateral pain in the cervicoscapular area is very suitable for manipulation. Usually a few sessions suffice to restore a full painless range of movement. The patient must be informed that the disc can move again, however, and that recurrences are not uncommon. Every new attack confirmed as having the same cause should be treated in a similar way. Continuous traction can be con sidered as an alternative. When there is a tendency to recurrence, prophylactic measures should be taken (i.e. position at work, sleeping position, collar, exercises (see Ch. 13). See Box 9.7 for a summary of unilateral pain in the neck, trapezius or scapular area.
Unilateral root pain
Root pain as the result of a disc protrusion pressing on the dural investment of a cervical nerve root is quite common between the ages of 35 and 60,53 with the peak age being
186 SECTION TWO - THE CERVICAL SPINE
Box 9.8 Cause of root pain accord ing to age
Age (years) � Neuroma Cause
35
�
Disc
60
�
Osteophyte Metastases
45-5454 but does not seem to occur in earlier life. Even after a severe injury to the neck it does not appear before the age of 30 (see Box 9.8). In younger patients suffering from root pain other disorders must be excluded, especially benign tumour (e.g. neurofibroma, schwannoma) before a disc lesion is considered. Over the age of 60, discoradicular interactions causing root pain are extremely rare and osteophytic or metastatic compression is more likely. History. Very often the patient has had periods of unilat eral cervicoscapular pain in previous years but is so used to it that it is not mentioned. The initial symptoms are similar, but for some reason have not resolved. On the contrary, one day the scapular pain may have become much worse, after which the pain has shifted to one side and is now felt in the arm (Box 9.9). The scapular pain usually disappears or diminishes to a degree that it is no longer worthy of mention although occasionally it does persist. Arm pain increases for 2 weeks and remains severe for 1-2 months, particularly at night. Sometimes the patient can only achieve rest by bringing the arm above the head - a position that relieves tension on the root55 but also widens the intervertebral foramen and diminishes the pressure.5 6 Beatty et al.57 believe that this sign is highly suggestive of disc herniation, whereas the sign is unlikely to be present in those patients with radiculopathy caused by spondylosis. During the same period there may be pins and needles in some fingers. After a short period, neural involvement may become much clearer, as paraesthesia tends to dis appear and numbness ensues. 6-10 weeks after the onset of the brachial pain the symptoms gradually subside. Inspection. In very acute cases a pain-avoiding posture may be present - the head is held in side flexion, mostly away from the painful side. The severe root pain also very often obliges the patient to keep the arm at the side, well supported by the other hand.
The patient may experience difficulty in lying flat on the couch because of the excruciating pain, and the half-lying position with a cushion under the neck Examination.
is thus preferred. Next, the patient is asked about the precise site of the pain, which will enable the examiner to determine the exact dermatome and to distinguish the level of the compression. An even better pointer to the latter is paraesthesia, and therefore if the patient mentions pins and needles, more details are sought about their localization and behaviour : how far proximally does the paraesthesia spread, which fingers and what parts of them are involved, and when are the pins and needles felt? A typical feature is that the paraesthesia has neither edge nor aspect being felt within the fingers. Stroking the skin may provoke or increase pins and needles but moving the digits has no influence. Paraesthesia comes and goes, day or night, in an erratic fashion, appears without any definite reason and does not actually last more than an hour at a time. In difficult cases, diagnostic traction may help: if the paraesthesia disappears during manual traction at the head and comes back when traction is released, the cause is clearly cervical. On functional testing some articular signs are found. A slight partial articular pattern of internal derangement is seen: as the protrusion lies more outside the joint and the articular movements no longer interfere with it, the artic ular signs are less important than are the root signs. Some active and passive movements provoke or increase pain in the scapular area in exactly the same way as if root pain were not present. The end-feel is crisp. It is possible, although not at all common, for the neck movements to influence the pain down the arm and / or the pins and needles. Resisted movements of the head are negative. At the end of the normal evolution, neck movements are often no longer painful but the arm still hurts consid erably. The diagnostic clue (apart from the history) is then the characteristic pattern of root palsy on examination of the upper limb. The different movements of the upper limb are then tested against resistance in order to detect paresis. Again the combination of weak muscles indicates which nerve root has become compressed. The degree of motor deficit can be very subtle. The examiner should therefore carefully compare the affected side with the other. When gross
weakness is found, this is a warning sign, indicating . that the lesion is very probably non-discogenic. Cutaneous analgesia is sought at the fingers and the reflexes are tested. There are no cord signs. Box 9.10 summarizes the signs of root pain.
Box 9.9 Symptoms of root pain
Scapular pain caused by unilateral compression of the dura mater is replaced by: • Root pain owing to pressure on the dural sleeve of the nerve root • Weakness and tingling from parenchymatous involvement
Box 9.10 Signs of root pa i n -
Articular signs Ascertaining if a cervical movement increases the pain in the arm or brings on the pins and needles in the hand Estimating conduction along the root
CHAPTER 9
- MECHANICAL DISORDERS 187
Diag nosis. The history is very informative because it shows the typical behaviour of a disc displacement: there is a past record of attacks of multisegmental cervico scapular pain, followed by a moment of shifting of the pain, which has now become segmental, towards the upper limb. From then on the symptoms follow a strict
chronology: pain
�
paraesthesia
�
numbness
�
weakness
The examination confirms the diagnosis: a partial articular pattern is found and root signs point to a lesion at a certain level - strict monoradicular root pain and paraesthesia with, eventually, deficit in the structures belonging to the same segment. Partial palsies do occur, although not so often as in the lower limb. Different root syndromes a n d the i r d ifferenti a l d i a g n osis
(Fig. 9.17). The nerve roots most frequently compressed by a disc are, in order of frequency, the roots C7 (56-70%), C6 ( 19-25%), C5 (2-14%) and C8 (4-10%). 58,59 Each nerve root lesion, whatever its cause may be, gives rise to pain felt in the skin area corresponding with the segment to which the nerve root belongs. The pain is the result of involvement of the dural sheath surrounding the nerve fibres. When nerve fibres become affected it may lead to paraesthesia felt distally in the same dermatome; however some nerve roots do not cause this. Pain and paraesthesia are sometimes felt in areas which do not totally corre spond to one specific dermatome. Variations in the der matomes may occur. It has been shown in animals, by experiments on the derma tomes of the upper limbs in subhuman primates.60 Weakness of the !p.uscles belonging to the same segment is often found, as is cutaneous anal gesia in some (mostly the distal) part of the dermatome. Other soft tissue lesions may lead to exactly the same segmental pain. Therefore resisted tests, undertaken to examine nerve root conduction, also serve to test for alternative causes of pain down the limb. C 1 and (2 nerve roots. The absence of discs at the first two cervical levels implies that nerve root compression by discs cannot occur. Reference of pain to the C1 or C2 derma tomes (headache; Fig. 9.8) does not mean that the C1 or C2 nerve roots are involved; it is frequently multi segmental and the result of compression of the lower cervical dura by a posterocentral disc protrusion. True segmental pain may be found in elderly people, as the result of arthrosis at the upper cervical joints involv ing the capsular and ligamentous structures and is then usually bilateral. Rarely, the C1 or C2 nerve root can be compressed by an osteophyte at the CO-C l or C 1-C2 level. This occurs in elderly patients with gross unilateral arthrosis of the atlantoaxial joint and gives rise to unilateral pain. The condition is rare and presents with a marked full articu lar pattern in which rotation is especially limited. The
Figure 9 . 8
The C 1 and C 2 dermatomes.
Figure 9.9
The C3 dermatome.
accompanying tingling in the occipitoparietal region is a localizing symptom. (3 nerve root. Compression of the third cervical nerve root by a posterolateral disc displacement is very rare. Pain occurs at the lateral aspect of the neck. Pins and needles or numbness may be felt at the lower pinna, the posterior part of the cheek, the temporal area and any part of the lateral aspect of the neck, with a forward projection along the chin (Fig. 9.9). Weakness is clinically not detect able. Cutaneous analgesia is uncommon but if it occurs it occupies any part of the lateral aspect of the neck.
188 SECTION TWO - THE CERVICAL SPINE
Figure 9.10
The C4 dermatome.
In the differential diagnosis, it must be remembered that pain in this region may result from pressure on the dura mater at any level and is then multisegmental. Heart disease may also give rise to reference of pain in the C3 dermatome. Another possibility is a lesion of the tri geminal nerve, with paraesthesia in one cheek as the only symptom. (4 nerve root. Discogenic lesions of the fourth cervical nerve root are also very uncommon. Pain is felt unilater ally spreading from the lower half of the neck towards the point of the shoulder (Fig. 9.10) and paraesthesia does not occur at this level. In theory weakness of the trapez ius muscle should be found but in practice muscular weakness is not detectable. A horizontal band of cuta neous analgesia may be found along the spine of the scapula, the mid-deltoid area and the clavicle. In the differential diagnosis, it should be remembered that the upper scapular area is very often the site of multisegmental pain, referred from the dura mater and resulting from a discodural interaction at any level. Upper scapular pain also occurs in: (a) disorders within the shoulder girdle, e.g. posterior sternoclavicular syn drome or a lesion of the first costotransverse joint; (b) some neurological conditions, e.g. mononeuritis of the long thoracic, spinal accessory or suprascapular nerves; and (c) some pulmonary or visceral disorders, e.g. inflammation of the gallbladder. Pain felt at the shoulder on deep breathing is typical in diaphragmatic pleurisy. (5 nerve root. A C5 nerve root involvement is usually not the result of a disc lesion but is often the outcome of either a traction injury or compression by an osteophyte. Osteophytic palsy of the C5 nerve root may be caused by encroachment on the fourth intervertebral foramen and results in gross weakness of the C5 muscles without pain. Traction palsy of the C5 nerve root occurs after an injury that depresses the shoulder girdle and leads to painless weakness of the muscles. If pain is present, it is felt in the C5 dermatome, along the lateral aspect of the arm and forearm as far as the base
Figure 9.1 1
The C5 dermatome.
of the thumb (Fig. 9.11). Pins and needles do not seem to occur in C5 nerve root compression. Weakness of the supraspinatus, infraspinatus, deltoid and brachial biceps muscles may be found. A C5 sensory palsy from a disc is almost unknown. The biceps jerk may be sluggish or absent; the brachioradialis jerk sluggish, absent or inverted. The differential diagnosis includes: •
•
•
•
•
•
•
Axillary nerve palsy after dislocation of the shoulder: this results in painless weakness and atrophy of the deltoid muscle and consequent weakness of abduc tion of the shoulder. Rotation movements remain normal (p. 360 and p. 556). Mononeuritis of the spinal accessory nerve: there is painless weakness of the trapezius muscle which results in slight limitation of active elevation of the arm (p. 323 and p. 543). Mononeuritis of the long thoracic nerve: presents with painless weakness of the serratus anterior muscle. Active elevation of the arm is grossly limited but does not cause any pain (p. 323 and p. 553). Mononeuritis of the suprascapular nerve; painless weakness of the supraspinatus and infraspinatus muscles lead to weak abduction and lateral rotation movements at the shoulder (p. 360 and p. 554). Traumatic palsy of the suprascapular nerve: an injury in which the arm is strongly pulled away from the trunk may affect the suprascapular nerve, with painless weakness of abduction and lateral rotation at the shoulder (p. 554). Shoulder arthritis, supraspinatus tendinitis or infraspinatus tendinitis: pain down the C5 dermatome can be referred from the joint capsule or from a tendon. In severe supraspinatus tendinitis, abduction against resistance is not only painful but may also be slightly weak. Infraspinatus tendinitis affects lateral rotation against resistance (p. 353 and p. 363). Rupture of the supraspinatus muscle: partial rupture leads to painful weakness and complete rupture to
CHAPTER 9
•
•
•
• •
painless weakness of abduction at the shoulder (p. 358). Rupture of the infraspinatus muscle: lateral rotation is painful and weak in partial rupture, and weak only in complete rupture (p. 367). Metastases in the scapula or fracture: p assive mobility of the scapula is limited and the muscles attached to it are weak (p. 367). Neuralgic amyotrophy: involvement of the infraspina tus muscle leads to weakness of lateral rotation at the shoulder (p. 552). Herpes zoster: when the fifth cervical segment is affected, pain may be felt in the C5 dermatome. Myopathy: bilateral wasting of the supraspinatus and infraspinatus muscles is suggestive of myopathy. Arthritis from immobilization of the shoulder is then a painful complication.
The sixth cervical nerve root can become compressed by the C5 disc or by osteophytic outcrops orig inating from the uncovertebral joint or from the facet joint. The pain runs along the anterior aspect of the arm, the volar aspect of the forearm and the radial side of the hand as far as the thumb and index finger (Fig. 9.12). Pins and needles are very common and are felt in the thumb and index finger. There is weakness of the biceps, brachialis, supinator brevis and the extensores carpi r adiales. Sometimes the subscapularis muscle may also be affected. Occasionally a partial weakness of the scapula is perceptible and vol untary elevation of the arm is lacking in only the final 5°. Cutaneous analgesia is sometimes found at the tips of thumb and index finger. The biceps jerk is sluggish or absent. The differential diagnosis has to be made from the following disorders: (6 nerve root.
•
Thoracic outlet syndrome: nocturnal pins and needles in one or both hands are often a conspicuous feature. Searching for the release phenomenon by scapular testing provides the clue (p. 549).
Figure 9.12
The C6 dermatome.
•
-
MECHANICAL DISORDERS 189
Compression of the median nerve in the carpal tunnel: pins and needles are felt in the three and a half radial fingers but par tial syndromes may occur. The history should be indicative (p. 569).
•
•
•
Palsy of the radial nerve from compression at mid humerus: there is complete p aralysis of the extensors of wrist and fingers and also weakness of the supination of the elbow and of the extension of the thumb (p. 558). Tendinitis or partial rupture of the biceps muscle: pain or painful weakness on resisted flexion of the elbow is the primary sign (p. 447). Tennis elbow: tendinitis at the origin of the extensor carpi radialis brevis may be so acute that the patient often winces and lets the hand go when asked to extend it against resistance (p. 456).
(7 nerve root. Compression of the seventh cervical nerve root by the C6 disc is far more common than is compres sion at any other level. The vast majority of the root p alsies caused by a disc are found here. P ai n is felt at the posterior aspect of the arm and the dorsal aspect of the forearm as far as the second, third and fourth fingers (Fig. 9.13). Rarely, pain is experienced at the anterior and upper aspect of the chest and not in the arm . Pins. and needles are mostly felt in the index, middle and ring fingers. The most conspicuous feature is weakness of extension of the elbow (triceps muscle). There is also weakness of flexion of the wrist, caused by a p alsy of the flexor carpi radialis and occasionally of extension of the wrist. In severe cases, wasting of the midportion of the pectoralis major muscle and weakness of adduction of the shoulder (latissimus dorsi) may be noted. In the unusual circum stances of a larger part than usual of the serratus anterior muscle being derived from the C7 segment, winging of the scapula may be seen.61 Cutaneous analgesia must be sought at the dorsal aspect of the index and middle fingers. The triceps jerk is seldom affected, even in quite severe cases.
Figure 9.13
The C7 dermatome.
190 SECTION TWO - THE CERVICAL SPINE
The follo :ving disorders may give rise to similar symp toms and sIgns and must be included in the differential
•
diagnosis: • • •
• • •
Lead poisoning: one of the first signs is often bilateral weakness of extension of the wrist (see also p. 558). Carcinoma of the bronchus: this may also lead to bilateral weakness of extension of the wrist. Tennis elbow: a painful twinge with weakness of extension of the wrist may be found in acute cases (see C6 root). Golfer 's elbow: pain on resisted flexion of the wrist is the primary sign (see p. 466). Tendinitis of the triceps muscle: this results in pain on resisted extension of the elbow (p. 451). Fracture of the olecranon: resisted extension of the elbow is p ainful and weak but this picture is compli cated by articular signs at the elbow joint (p. 453).
The eighth cervical nerve root emerges between the seventh cervical and first thoracic vertebrae and can be compressed by the C7 disc. Pain is felt at the inferior part of the scapular region and t�e u�ar aspect of the hand, over the middle, ring and httle fingers and the ulnar and distal aspect of the forearm (Fig. 9.14). Pins and needles are experienced in the middle ru:g and little fingers. The condition is easily confuse d WIth ulnar nerve problems ('pseudo ulnar palsy').62 Involvement of both extensors of the thumb causes weakness of thumb extension. Other muscles affected are the extensor carpi ulnaris and flexor carpi ulnaris (weak ness of ulnar deviation of the wrist), the adductor pollicis (weakness of adduction of the thumb), the common exten sor of the fingers (weakness of extension of the fingers) and the abductor indicis (the first dorsal interosseus muscle). Occasaionally the triceps muscle is also slightly weak. C�taneo�s a�algesia is found at the little finger. The differentzal dzagnosis includes : (8 nerve root.
•
Thoracic outlet syndrome: this may result in pins and needles in the ulnar fingers and also sometimes in weakness of the intrinsic muscles of the hand (p. 548).
Figure 9.14
The C8 dermatome.
•
•
Metastases in the C7 or T 1 vertebra: involvement of the C7 and C8 nerve roots at the same time is very suggestive of malignant disease. Angina: when the p ain radiates from the neck and the left pectoral area to the upper limb, especially to the ulnar aspect of the hand and forearm, heart disease should be considered.
Traction palsy of the lower trunk of the brachial plexus: this also affects the fibres derived from the C8 nerve root (p. 546).
•
•
Frictional neuritis of the ulnar nerve at the elbow or pressure on the ulnar nerve at the wrist: the result is pins and needles felt in the ulnar half of the ring finger and in the little finger (p. 568). Thrombosis of the subclavian artery: there is claudication p ain in the upper limb and the radial pulse cannot be felt.
T1 n erve root. This segment includes the upper limb . and IS therefore examined with the neck. Compression of the first thoracic nerve root by a T1 disc protrusion is very uncommon and consequently a palsy of the first thoracic nerve root - weakness of the intrinsic hand muscles - is never caused by a discoradicular conflict. � first thoracic p alsy, together with Horner 's syndrome, IS one of the main symptoms in Pancoast's tumour and also vertebral metastases may involve the T1 nerve root. Pain is felt in two distinct sites: the pectoroscapular area and the ulnar aspect of the forearm (Fig. 9.15). The thoracic p ain may be influenced by coughing and neck flexion, as well as forward movement of the scapulae and stretching of T 1 (flexion of the elbow with the arm held in abduction). Pins and needles are felt at the ulnar side of the hand. In T1 disc lesions there is no weakness of the hand. Cutaneous analgesia is also always the result of a non discal condition. Reduction by manipulation is not easy. If it fails, spontaneous cure has to be awaited, but this may take 6-12 months.
Figure 9.15
The T1 dermatome.
CHAPTER 9
-
MECHANICAL DISORDERS 1 91
T1 problems from a disc protrusion at the T1 / T2 inter vertebral joint are so rare that other possibilities should be considered in the differential diagnosis:
tion is the C8 root, which may easily take 6 months and occasionally the patient is left with a permanently weak thumb. The sensory disturbance recovers very gradually.
Cervical rib: this may compress the lower trunk of the brachial plexus, partly derived from the T 1 nerve root (see p. 548). Compression of the median nerve: in some cases of carpal tunnel syndrome, pain may be experienced in the forearm. Most of the muscles in the hand supplied by the median nerve are also p artly derived from the T1 nerve root (see p. 569). Compression of the ulnar nerve: may also give rise to pins and needles in the ulnar border of the hand. All the small muscles of the hand innervated by the ulnar nerve are also partly derived from the Tl nerve root (see p. 562). Amyotrophic lateral sclerosis: weakness and atrophy of the small intrinsic muscles of the hand is often one of the first signs of amyotrophic lateral sclerosis (see also p. 536).
There are a number of approaches to treat ment of nerve root problems.
•
•
•
•
T2 nerve root. The second thoracic nerve root is exam ined with the neck because it gives rise to symptoms felt in the upper limb. A disc lesion at this level is extremely rare. If it occurs, it gives rise to pectoroscapular pain radiating down the inner aspect of the arm as far as the elbow (Fig. 9.16). The pain is influenced by neck flexion, approximation of the scapulae and sometimes stretching of T 1. Paraesthesia, motor or sensory deficit have never been reported as the result of discoradicular interactions.
Trea tment.
Prophylaxis. Root pain could be avoided when the early stage of the disc protrusion with cervicoscapular pain is recognized and immediately followed by manipulative reduction. Manipulation. This can be tried in patients without neurological deficit and with favourable articular signs (neck movements hurt in the scapular area). Reduction in a few sessions is almost certainly possible in the first 2 months after the onset of the brachial pain. Af ter this period, the results are poor. Manipulation is also always difficult and often impossible in patients with unfavour able signs (the neck movements hurt down the arm or provoke pins and needles in the hand). When the root pain has been present for some time or neurological deficit has taken place, it is better to explain the mechanism to the patient and to w ait for spontaneous cure. During this period, the p atient should be kept under review. Unilateral scapular p ain and root pain of more than 6 months' standing can often be helped with two or three manipulation sessions. The scapular pain ceases and the mechanism of spontaneous cures is re-started. In filtra tion. Alternatively, in these patients where manip ulation fails or is no longer indicated one to six infiltra tions with 2 ml of a steroid solution at the nerve root may
Natural history. In discoradicular interactions, sponta neous cure is the rule for both pain and neurological deficit. Patients with neurological deficit usually recover in about 3 months, those without in 4 months, reckoned from the onset of the pain down the arm. The more marked the palsy, the more quickly the pain abates. Muscle strength will almost certainly have returned to normal 3-6 months after the pain ceased. The only excep-
Manipulation
Unfavourable articular signs Neurological deficit More than 2 months' duration
L Figure 9.16
The T2 dermatome.
Figure 9.17
Sinuvertebral block (with steroid solution) or Daily traction
Recurrences Too much pain No spontaneous cure
Treatment of cervical nerve root involvement. .
192 SECTION TWO - THE CERVICAL SPINE
afford considerable relief. Pain and inflammation are diminished during the period of spontaneous healing. Daily mechanical traction and sometimes a collar for 2-3 weeks may also help to make the pain tolerable. Surgery. This is seldom necessary because the long-term results are no better than when spontaneous cure has been awaited. Operation is considered when the condi tion recurs, when pain is intolerable or when sponta neous cure fails to occur. Recurrences. These are rare after spontaneous recovery from root pain with neurological deficit but are otherwise not infrequent.
Summary
The three previous clinical syndromes are most common (see Box 9.11 ) and can be compared to three pictures found at the lumbar spine (see p. 746-774).
LESS COMMON SYNDROMES According to Cyriax13, the syndromes described in this section are also based on a disc lesion and are typical of the cervical spine. In contrast to the lumbar spine, some cervical disc lesions may imperil the spinal cord. Cyriax held a belief that posterocentral disc protrusions form the first step in evolution towards spinal stenosis or postero central osteophytosis. An unreduced disc exerts continu ous pressure on the posterior longitudinal ligament. After some time, the ligamentous pull draws the perios teum away from the vertebral bone. Bone grows towards the periosteum and osteophytes form that diminish the anteroposterior diameter of the spinal canal and affect the cord. Spinal stenosis syndrome develops (p. 200). In the first stage of development clinical pictures may appear that are still reversible. Acute torticollis: central pain with symmetrical picture History. In young and middle-aged people a torticollis like history with central neckache may come on spontaBox 9. 1 1 The most common cervical spine problems Discod u ral interactions: Acute torticollis resembles acute lumbago: a large posterocentral or slightly posterolateral displace ment compressing the dura mater Cervicoscapular pain is similar to backache: a smaller central or unilateral disc with pressure on the dura mater Discoradicular interaction: Cervical root pain may be compared to sciatica:
a posterolateral disc protrusion compresses the dural sleeve of the nerve root
neously or as the result of severe trauma, usually a whiplash injury, causing a posterocentral disc protrusion. The patient develops a central severe pain in the neck, which may fix the head in flexion. Shortly afterwards both upper limbs may become painful with a feeling of weakness. Paraesthesia appears distally in both arms or in all four limbs. In acute cases, the neck is usually fixed in flexion and synunetrically limited in movement. The devi ation in flexion may, rarely, be so extreme that the chin touches the sternum, extension being totally impossible. The articular pattern is symmetrical. Apart from the gross limitation of extension, both rotations and both lateral flexions are equally limited. Arm movements (active elevation) may be bilaterally painful and possibly limited. There are no root signs. Cord signs are usually absent, except in extreme cases where pyramidal tract signs may be found. Examination.
Diagnosis. Diagnosis rests on the history (sudden onset) and on the clinical examination, showing an extreme limitation in one direction which indicates locking of the intervertebral joint as the result of a block at the posterior aspect. Differential diagnosis. Differential diagnosis includes conditions that present with a full articular pattern, for example fracture of a vertebral body and other bony disorders. The gross limitation of extension is the differ ential diagnostic feature. This is the opposite picture from meningitis in which the head becomes fixed in extension. Natural history. This type of torticollis tends to recover spontaneously, although very slowly. Treatment. Treatment is started when enough elements are present to accept the diagnosis of a discodural inter action. Manipulative reduction is the treatment of choice but rotation manoeuvres are avoided because the disc displacement is posterocentral. Quick thrust manipula tions are used to reduce annular protrusions and slow progressive sustained positioning towards extension is indicated when the displacement is nuclear. These tech niques are done with great care to avoid further retropul sion towards the spinal cord or stretching of the posterior longitudinal ligament.
Central or bilateral pain in the neck, trapezius or scapular area
In middle-aged or elderly people, posterocentral disc displacements tend to be spontaneous. The condition causes pain felt centrally in the neck with or without bilateral radiation to the occiput, to both
ROOT SYN DROMES IN N ECK AND U P P E R L I M B ROOT
Pain
C2 (not a disc)
C3
N E RVE F I B R ES
SH EATH
l c _./
Paraesthesia
Motor deficit
D I FF E RENTIAL DIAGNOSIS
Sensory deficit
l
/
c
Dural reference Osteophyte at the atlanto-axial joint
0J
!
None
tJ
Dural reference
(") I » '1J -i m :;0
\0 I
None
C4
None (trapezius muscle?)
Dural reference
s::
m (")
I » z
(")
»
r
Figure 9.18
Root syndromes in neck and upper limb.
o VI o :;0 o m :;0 VI ..... \0 \AI
..... '" �
VI m
ROOT SYN DROMES IN N E C K AND U P P E R L I M B
Q
o ROOT
N E RVE F I BRES
S H EATH
Paraesthesia
Pain
None
C5
f\ , C6
Supraspinatus Infraspinatus Deltoid Biceps Jerks: biceps, brachioradialis
Biceps Brachialis Supinator Extensor carpi radialis (Su bscapularis) Wasting: Brachioradialis muscle Jerks: biceps
Triceps Flexor carpi radialis (Extensores carpi radiales) (Latissimus dorsi) (Serratus anterior) Wasting : pectoralis major
C7
Figure 9.1 8
Motor deficit
Continued.
D I F F E R ENTIAL DIAGNOSIS
Sensory deficit
None
Combination of a ceNical disc lesion + shoulder lesion C5 root traction palsy Axillary neNe palsy after dislocation Mononeuritis spinal accessory, long thoracic, suprascapular neNe Traumatic suprascapular neNe palsy Herpes zoster Myopathy (deltoid, supra-, infraspinatus muscles) + pain from the capsule of the shoulder joint Rupture of the supra- or infraspinatus tendon Metastases in the scapula Diaphragmatic pleurisy
Pressure on the median neNe i n the carpal tunnel Pressure on the brachial plexus by first rib or a ceNical rib Tendinitis or partial rupture of the biceps muscle Pressure on the radial neNe at mid-humerus Rheumatoid perineuritis (complication of a monarticular rheumatoid arthritis of the shoulder) Tennis elbow
Lead poisoning (bilateral) Carcinoma of the bronchus Tennis elbow, golfer's elbow Tendinitis of the triceps muscle Fracture of the olecranon
z
� o
I -l I m n m
�
n � r VI 3! z m
ROOT SYNDROMES I N N ECK AND U P P E R LIMB
ROOT
SH EATH
N ERVE F I BRES
Pain
C8
Paraesthesia
vrVif;
--..
\
/- T1
�� �
�
Motor deficit
Extensor and flexor carpi u lnares Extensors and adductores pollicis Extensor digitorum communis (Triceps)
Sensory deficit
JV11, \
I
�
D I F F E R ENTIAL DIAGNOSIS
Palsy
=
not a disc
Palsy
=
not a disc
Pressure on the brachial plexus by a cervical rib pressure on the brachial plexus by the first rib C7 or T1 neoplasm Pancoast's tumour (apex of the lung) Angina Traction on the inferior trunks of the brachial plexus with neurological deficit Frictional neuritis of the ulnar nerve at the elbow Pressure on the ulnar nerve at the wrist Thrombosis of the subclavian artery
Cervical rib Pulmonary sulcus tumour Vertebral metastases Pressure on the median or ulnar nerve
Ii J: l>
� 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.
5. Tapiovarra J, Heinivaara O. Correlation of cervico-brachialis and roentgenographic findings. A n n Chir Gynaecol 1954;
43(suppl ):436. 6. Hitselberger WE, Witten R. Abnormal myelograms in asymp tomatic patients. J Neu rosu rg 1968;28:204. 7. Hayashi H, Okada K, Hamada M, Tada K, Veno R. Etiologic factors of myelopathy: a radiographic evaluation of the aging changes in the cervical spine. Clin Orthop Rei Res 1987;214:200.
206 SECTION TWO - THE CERVICAL SPINE
8. Parke WW, Sherk H H . Normal adult anatomy. In: The
9. 10.
11. 1 2.
1 3.
14. 15.
Cervical Spine Research Society, Sherk HH et al. (eds) The Cervical Spille, 2nd edn. Lippincott, Philadelphia, 1989:14-15. Bogduk N, Marsland A. The cervical zygapophysial joints as a source of neck pain. Spine 1 988;13:610-617. Penning L. Plain radiographic evaluation of cervical spine injury. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:250. Friedenberg ZB, Broder HA, Edeiken JE, Spencer H N . Degenerative disk disease of cervical spine. JAMA; 1960;174:374. Gore DR. Radiological evaluation of the degenerative cervical spine. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:765-778. Cyriax JH. Textbook of Orthopaedic Medicille, vol I. Diagnosis of Soft Tissue Lesiolls, 8 th edn. Bailliere Tindall, London, 1982. Kondo K, Molgaard CA, Kurland LT, Onofric BM. Protruded intervertebral cervical disc. Milln Med 1 981;64:75 1 . Kelsey J L , Gi thens PB, Walter S D e t al. A n epidemiologic study of acute prolapsed cervical intervertebral disc. j Bone joint Surg 1 984;66A:907.
1 6. Connell MD, Wiesel SW. Natural history and pathogenesis of cervical disc disease. Orthop Clin North Am 1992;23(3) :369-380. 17. Gore DR, Sepic SB, Gardner GM. Roentgenographic findings of
the cervical spine in asymptomatic people. Spine 1986;6:521-524. 1 8. Boden SD, McCowin PR, Davis DO et al. Abnormal magnetic
19. 20.
21.
22.
23.
24. 25.
resonance scans of the cervical spine in asymptomatic sub jects. j BOlle joint Surg 1990;72A: 1 1 78-1184. Sunderland S, Meningeal-neural relations in the intervertebral foramen. j Neuros urg 1974;40:756-763. Elvey RL. Painful restriction of shoulder movement: a clinical observational study. In: Proceedings: Disorders of the Knee, Ankle and. Shoulder. Western Australian Institute of Technology, Perth, 1979. Kenneally M. The upper limb tension test. In: Proceedings of the 4th Biennial Conference, Manipu lative Therapists Association of Australia, Brisbane, 1985. Rubenach H. The upper limb tension test: the effect of the position and movement of the contralateral arm. In: Proceedings of the 4th Biennial Conference, Manipulative Therapists Association of Australia, Brisbane, 1985. Fardy E. The upper limb tension test: an investigation of responses to the upper limb tension test and the effect of passive movement of the head in sagittal and coronal planes in young asymptomatic subjects. Unpublished thesis, South Australian Institute of Technology, Adelaide, 1985. Elvey RL. Treatment of arm pain associated with abnormal brachial plexus tension. Aust J Physiother 1986;32:224-229. Elvey RL, Quintner JL, Thomas AN. A clinical study of RSI. Aust Fam Physician 1986;15:1314-1 322.
26. Bell A. The upper limb tension test and straight leg raising. In: Dalziell BA, Snowsill JC (eds) Proceedings of the 5th Biennial Conference, Manipulative Therapists Association of Australia, Melbourne, 1987. 27. Landers J. The upper limb tension test. In: Dalziell BA, Snowsill JC (eds) Proceedings of the 5th Biennial Conference, Manipulative Therapists Association of Australia, Melbourne, 1987. 28. Kelmeally M, Rubenach H, Elvey R. The upper limb tension test: the SLR test of the arm. In: Grant R (ed) Physical Therapy of the Cervical and Thoracic Spine, Clinics in Physical Therapy 17. Churchill Livingstone, Edinburgh, 1988. 29. Ginn K. An investigation of tension development in upper
limb soft tissues during the upper limb tension test. In:
30.
31.
32.
33.
34.
35. 36. 37. 38.
39. 40. 41. 42.
Proceedings of Congress, International Federation of Orthopaedic Manipulative Therapists, Cambridge, 1989. Selvaratnam pJ, Glasgow EF, Matyas T. Differential stain pro duced by the brachial plexus tension test on C5 to Tl nerve root. In: Jones HM, Jones MA, Milde MR (eds) Proceedings of the 6th Biennial Conference, Manipu lative Therapists Association of Australia, Adelaide, 1989. Quintner JL. A study of upper limb pain and paraesthesiae fol lowing neck injury in motor vehicle accidents: assessment of the brachial plexus tension test of Elvey. Br ] Rhetllllatol 1989;28:528-533. Butler DS. Mobilisation of the Nervous Systelll. Churchill Livingstone, Melbourne, 1991: 147-160. McNair JFS. Acute locking of the cervical spine. In: Grieve GP (ed) Modem Manual Therapy of the Vertebral COIIlIllII. Churchill Livingstone, London, 1986:35 1 . Jones ET. Congenital anomalies of the atlas. I n : The Cervical Spine Research Society, Clark CR et al. (eds) Tile Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:325-329. Saltzman CL, Hensinger RN, Blane CE, Philips WA. Familial cervical dysplasia. j Bone joint Surg 1991 ;73A:163-1 71. Hensinger RN. Osseolls anomalies of the craniovertebral junc tion. Spine 1986;11 :323-333. Dubousset J. Torticollis in children caused by congenital anomalies of the atlas. j Bone joillt Surg 1986;68A:178. Wirth q, Hagena FW, Wuelker N, Siebert WE. Biterminal tenotomy for the treatment of congenital muscular torticollis: long-term results. j BOlle Joillt Surg 1992;74A(3):427-434. Kahn ML, Davidson R, Drummond OS. Acquired torticollis in children. Orthop Rev 1991 ;20(8) :667-674. Bratt HD, Menelaus MB. Benign paroxysmal torticollis of inJancy. ] Bone Joillt Surg 1992;74B(3):449-457. Wortzman G, Dewar FP. Rotary fixation of the atlantoaxial joint. Radiologlj 1968;90:479. Tom LW, Rossiter JL, Sutton LN, Davidson RS, Potsic WP. Torticollis in children. Otolaryngol Head Neck Surg
1991;105(1): 1-5. 43. Phillips WA, Hensinger RN. The management of rotatory atlanto-axial subluxation in children. ] Bone lG illt Surg 1989;71A(5):664. 44. Wilson BC, Jarvis BL, Haydon RC. Nontraumatic subluxation of the atlantoaxial joint: Grisel's syndrome. Alln Otol Rhinol LaryngoI I987;96:705.
45. Currier BL, Heller JG, Eismont FJ. Cervical spine infections. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:678.
46. Brudny J, Korein J, Levidow L. Sensory feedback therapy as a modality of treatment in central nervous system disorders of voluntary movement. Neu rology 1974;24:925-932. 47. Grandas F, Elston N, Quinn N et al. Blepharospasm: a review of 264 patients. J Neurol Neu ros u rg Psych iatry 1988;51 :767-772. 48. Shtange LA, Roshchina NA. Clinical aspects, pathogenesis
and treatment of neurovascular spastic torticollis. Z Nevropatol Psikhiatr 1992;92(1) :46-48.
49. Zuo YZ. Clinical classification and the treatment of spastic torticollis. Chu ng-Hua Cheng Hsing Shao Shang Wai Ko Tsa Chih 1991;7(4) :262-263.
50. Mumenthaler M. Diseases affecting mainly the brain and its coverings: the parkinsonian syndrome. In: Mumenthaler M (ed) Neu rology, 3rd edn. Thieme, New York, 1990: 100-114. 51. Hensinger RN, Lang JR, MacEwen GD. Klippel-Feil syn drome: a constellation of associated anomalies. ] BOlle joint Surg 1 974;56A: 1246.
CHAPTER 9 - MECHANICAL DISORDERS 207
52. Pizzutillo PD. Klippel-Feil syndrome. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:339-348. 53. Simeone FA. Cervical disc disease with radiculopathy. In: Rothman RH, Simeone IA (eds) The Spine, 3rd edn. Saunders, Philadelphia, 1992:553-559. 54. Radhakrishnan K, Litchy WI, O'Fallon WM, Kurland LT. Epidemiology of cervical radiculopathy: a population-based study from Rochester, Minnesota, 1976 through 1990. Brain 1994;117:325-335. 55. Davidson RI, Dunn EJ, Metzmaker IN. The shoulder abduction test in the diagnosis of radicular pain in cervical extradural com pressive monoradiculopathies. Spine 1981;6:441-446. 56. Farmer JC, Wisneski RJ. Cervical spine nerve root compres sion: an analysis of neuroforaminal pressures with varying head and arm positions. Spine 1994;19:1850-1855. 57. Beatty RM, Fowler FD, Hanson EJ. The abducted arm as a sign of ruptured cervical disc. Neurosu rgery 1987;21:731-732. 58. Henderson CM, Helmessy RG, Shuey HMJ, Shackelford EG. Posterior-lateral foraminotomy as an exclusive operative tech nique for cervical radiculopathy: a review of 846 consecutively operated cases. Neu ros urgery 1983;13:504-512. 59. Levin KH, Maggiano HJ, Wilbourne AJ. Cervical radiculo pathies: comparison of surgical and EMG localization of single-root lesions. NeurologJj 1996;46:1022-1025. 60. Dykes RW, Terzis JK. Spinal nerve distributions in the upper limb: the organization of the dermatome and afferent myotome. Phi/os Trans R Soc Lond 1981;293:509-554. 61. Makin GJ, Brown WF, Ebers Gc. C7 radiculopathy: impor tance of scapular winging in clinical diagnosis. J Neurol Neurosu rg Psychiatry 1986;49(6):640-644. 62. Wallace D. Disc compression of the eighth cervical nerve: pseudo ulnar palsy. Surg Neurol 1982;18:295. 63. Yoshida M, Tamaki 1, Kawakami M, Hayashi N, Ando M. Indication and clinical results of larninoplasty for cervical myelopathy caused by disc herniation with developmental canal stenosis. Spine 1998;23:2391-2397. 64. Hamel E et al. Cervical myelopathy. Neurosurg Rev 1978;1:101-110. 65. Horwitz T. Degenerative lesions in the cervical portion of the spine. Arch Intern Med 1940;55:1178. 66. Kellgren JH, Lawrence JS. Rheumatism in miners, part II: X-ray study. Br J lndust Med 1952;9:197. 67. Pallis C, Jones A, Spillane J. Cervical spondylosis. Incidence and implications. Brain 1954;77:274. 68. Dommisse GF. The blood supply of the spinal cord. In: Grieve GP (ed) Modern Manual Therapy of the Vertebral Column. Churchill Livingstone, London, 1986:47. 69. McCormack BM, Weinstein PR. Cervical spondylosis. An update. West J Med 1996;165(1-2):43-51 . 70. Zeidman SM, Moses H , Shiu-Feng Ling G , Ducker TB. Differential d iagnosis of cervical myelopa thy. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:163-178. 71. Brain WR, Northfield 0, Wilkinson M. The neurological manifestations of cervical spondylosis. Brain 1952;75:13. 72. Tapiovarra J, Heinivaara O. Correlation of cervi co-branchialis and roentgenographic findings. Ann Chir Gynaecal 1954; 43(suppl):436. 73. Friedenberg ZB, Miller WT. Degenerative disc disease of the cervical spine. J Bone Joint Surg 1963;45A:1171. 74. Gore DR, Sepic SB, Gardner GM. Roentgenographic findings of the cervical spine in asymptomatic people. Spine 1986; 11(6):521.
75. Heller JG. The syndromes of degenerative cervical disease. Orthop Clin North Am 1992;23(3):381-394. 76. Friedenberg ZB, Broder HA, Edeiken J E, Spencer H N . Degenerative disk disease of cervical spine. JAMA 1960; 174:374. 77. Gore DR. Radiological evaluation of the degenerative cervical spine. In: The Cervical Spine Research Society, Clark CR et al. (eds). The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:765-778. 78. Boden SO, Wiesel SW, Laws ER et al. The Aging Lumbar Spine. Essentials af Pathophysiology, Diagnosis and Treatment. Saunders, Philadelphia, 1991: 1-51. 79. Star MJ, Curd JG, Thorne RP. Atlantoaxial lateral mass osteoarthritis: a frequently overlooked cause of severe occipitocervical pain. Spine 1992;17:S71-S76. 80. Dreyfuss P, Michaelsen M, Fletcher O. Atlanto-occipital and lateral atlanto-axial joint pain patterns. Spine 1994;19: 1125-1131. 8 1 . Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982. 82. Troisier O. Semiologie et Traitement des Algies Discales et Ligamentaires du Rachis. Masson, Paris, 1973:55. 83. Humphreys SC, Hodges SO, Patwardhan A et al. 1998. The natural history of the cervical foramen in symptomatic and asymptomatic individuals aged 20-60 years as measured by magnetic resonance imaging. A descriptive approach. Spine 1973;23(20):2180-2184. 84. Ebraheim NA, Lu I, Biyani A, Brown JA, Yeasting RA. Anatomic considerations for uncovertebral involvement in cervical spondylosis. Clin Orthop Rei Res 1997;334:200-206. 85. Slip man CW, Lipetz JS, Jackson HE, Rogers DP, Vresilovic EJ. Therapeutic selective nerve root block in the nonsurgical treatment of atraumatic cervical spondylotic radicular pain: a retrospective analysis with independent clinical review. Arch Phys Med Rehabil 2000;81(6):741-746. 86. Mumenthaler M. Diseases affecting mainly the spinal cord: myelopathy in cervical spondylosis. In: Mumenthaler M (ed) NeurologJj, 3rd edn. Thieme, New York, 1990:203-204. 87. Brain WR, Northfield OW, Wilkinson M. The neurologic manifestation of cervical spondylosis. Brain 1952;75:187. 88. Simeone FA, Rothman RH. Cervical disc disease. In: Rothman RH, Simeone FA (eds) The Spine. Saw1ders, Philadelphia, 1982:440-476. 89. Edwards We, La Rocca SH. The developmental segmental sagittal diameter in combined cervical and lumbar spondylo sis. Spine 1985;10:42-49. 90. Debois V, Herz R, Berghmans 0 et al. Soft cervical disc herni ation. Influence of cervical spinal canal measurements on development of neurologic symptoms. Spine 1999;24:1996. 91. Edwards WC, La Rocca SH. The developmental segmental sagittal diameter of the cervical spinal canal in patients with cervical spondylosis. Spine 1983;8:20. 92. Batzdorf U. Complex cervical myelopathies. In: Frymoyer JW (ed) The Adult Spine, Principles and Practice. Raven Press, New York, 1991:1207. 93. Mair WGP, Druckman R. The pathology of spinal cord lesions and their relation to the clinical features in protrusion of cervical intervertebral disc. Brain 1953;76:70. 94. Taylor AR. Vascular factors in the myelopathy associated with cervical spondylosis. Neurology 1964;14:62. 95. Simeone FA, Dillin WA. Treatment of cervical disc disease: selection of operative approach. Con temp Neuros urg 1986;8:1-6 96. Cooper PR. Delayed brain injury: secondary insults. In: Becker DP, Povlishock JT (eds) Central Nervous System Trauma Status Report. National Institutes of Health, Bethesda, 1985:217.
208 SECTION TWO - THE CERVICAL SPINE
97. Cates JR, Soriano MM. Cervical spondylotic myelopathy. J Manipul Physiol Ther 1995;18(7) :471-475.
spine. In: The Cervical Spine Research Society, Sherk HH et al. (eds) The Cervical Spine, 2nd edn. Lippincott, Philadelphia,
98. Shindo K, Tsunoda S, Shiozawa Z. Decreased sympathetic
1989:607. 120. Montgomery OM, Brower RS. Cervical spondylotic myelopa
outflow to muscles in patients with cervical spondylosis. Acta Neural Scand 1997;96(4):241-246. 99. Ferguson RJL, Caplan LR. Cervical spondylitic myelopathy. Neurol Clin North Am 1985;3:373-382. 100. Kameyama T, Ando T, Yanagi T, Yasui K, Sobue G. Cervical
spondylotic amyotrophy. Magnetic resonance imaging demon stration of intrinsic cord pathology. Spine 1998;23(4):448-452. 1 0 1 . Abramovitz IN, Srinivasan M. Painless arm weakness without leg symptoms in cervical spondylotic myelopathy. Poster Exhibition at the Annual Meeting of the Congress of Neurological Surgeons, Seattle, Washington 24-29 Sept 1988. 102. Ohwada T, Mii K, Tachibana S, Yada K. The overstretch syndrome: a new cervical myelopathy caused by the stretch mechanism of the spinal cord. Presented at the Annual Meeting of The Cervical Spine Research Society, Key Biscane, Florida, 30 Nov-3 Dec 1988. 103. Bernhardt M, Hynes RA, Blume HW, White AA III. Current concepts review, cervical spondylotic myelopathy. J Bone Joint Surg 1993;75A:119-128.
104. Kessler JT. Congenital narrowing of the cervical spinal canal. I Neural Neurosurg Psychiatry 1975;38: 1 2 1 8-1224.
thy, clinical syndrome and natural history. Orthop Clin North Am 1992;23(3) :487-493.
121. Ono K, Ebara S, Fiji T et al. Myelopathy hand: new clinical signs of cervical cord damage. J Bone loint Surg 1987;69B: 215-219. 122. Ibarra S, Yonenobu K, Fujiwara K et af. Myelopathy hand char acterized by muscle wasting. Spine 1988;13:785-79l. 123. Shimizu T, Shimada H, Shirakura K. Scapulohumeral reflex
(Shimizu): its clinical significance and testing maneuvers. Spine 1993;15:21 82-2190.
124. Nurick S. The pathogenesis of the spinal cord disorder associ ated with cervical spondylosis. Brain 1972;95:87-100. 125. Nurick S. The natural history and the results of surgical treat ment of the spinal cord disorder associated with cervical spondylosis. Brain 1972;95: 101-108. 126. Hirabayashi K, Miyakawa J, Satomi K et al. Operative results and postoperative progression of ossification among patients with ossification of cervical posterior longitudinal ligament. Spine 1981;6:354-364. 127. Hukuda S, Mochizuki T, Ogata M, Shichikawa K, Shimomura
1 06. Bose B, Northrup BE, Osterholm JL, Cotler JM, DiTunno JF.
Y. Operations for cervical spondylotic myelopathy. A compar ison of the results of anterior and posterior procedures. J Bone Joint Surg 1985;67B :609-615.
Reanalysis of central cervical cord injury management.
128. Clark CR. Cervical spondylotic myelopathy: history and
105. Nurick S. Cervical spondylosis and the spinal cord. Br J Hasp Med 1 975;14:668-676.
Neurosu rgery 1984;15:367-372. 107. Epstein NE, Epstein JA. Operative management of cervical
spondylotic myelopathy. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:839-848. 108. Levine ON. Pathogenesis of cervical spondylotic myelopathy. I New'of Neurosu rg Psychiatry 1997;62(4) :334-340. 109. Stoltmalm HF, Blackwood W. The role of the ligamenta flava
in the pathogenesis of myelopathy in cervical spondylosis. Brain 1964;87:45-5 1 . 1 1 0 . MuhJe C , Metzner J , Weinert 0 et al. Classification system
based on kinematic MR imaging in cervical spondylotic myelopathy. Am I Neuroradiof 1998;19(9 ) : 1 763-1 771 . 1 1 1 . Boulos AS, Lovely TJ. Degenerative cervical spondylolisthesis: diagnOSiS and management in five cases. J Spinal Disord 1996;9(3) :241-245. 112. Teresi LM, Lufkin RB, Reicher MA et al. Asymptomatic degen
1 13. 114. 115.
116. 117.
erative disk disease and spondylosiS of the cervical spine: MR imaging. Radiology 1987;164:83. Good 0, Couch J, Wascaster L. "Numb clumsy hands" and high cervical spondylosiS. Surg NeuroI 1984;22:285-291 . Lestini WF, Wiesel SW. The pathogenesis o f cervical spondyl osis. Clin Orthop Ref Res 1989;239:69. An HS. Clinical presentation of discogenic neck pain, radicu lopathy, and myelopathy. In: The Cervical Spine Research Society, Clark CR et al (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:755-764. Stewart JD. Focal Peripheral Neu ropathies, 3rd edn. Lippincott Williams & Wilkins, Philadelphia, 2000:103. Crandall PH, Gregorius FK. Long-term follow-up of surgical treatment of cervical spondylotic myelopathy. Spine 1977;2:139-146.
118. Epstein
JA. Management of cervical spine stenosis, spondylosiS, and myeloradiculopathy. In: Tindall GT (ed) Con temporary Neuros u rgery, vol 2. Williams & Wilkins, Baltimore, 1985:1-6. 119. Cusick JF. Differential diagnosis of neck and arm pain relative to symptoms caused by degenerative disorders of the cervical
physical findings. Spine 1988;13(7):847-849. 129. Wada E, Ohmura M, Yonenobu K. Intramedullary changes of the spinal cord in cervical spondylotic myelopathy. Spine 1 995;20(20) :2226-2232. 130. Ito T, Oyanagi K, Takahashi H, Takallashi HE, Ikuta F. Cervical
spondylotic myelopathy. Clinicopathologic study on the pro gression pattern and thin myelinated fibers of the lesions of seven patients examined during complete autopsy. Spine 1996;21(7):827-833. 1 3 1 . Fehlings MG, Skaf G. A review of the pathophysiology of cer
vical spondylotic meylopathy with insights for potential novel mechanisms drawn from traumatic spinal cord injury. Spine 1998;23(24):2730-2737. 132. Brugger A. Die Erkriinku ngen des Bewegungsapparates und seines Nervensystems, V. Syndrome des Zen tralnervensystems. Fischer, Stuttgart, 1980:921-968. 133. Fager CA. Results of adequate posterior decompression in the relief of spondylotic cervical myelopathy. J Neurosurg 1973;38:684-692. 134. Grob D. Surgery in the degenerative cervical spine. Spine 1998;23(24):2674-2683. 135. Matsuda Y, Shibata T, Oki S et al. Outcomes of surgical treat
ment for cervical myelopathy in patients more than 75 years of age. Spine 1 999;24:529-534. 136. Yonenobu K. Cervical radiculopathy and myelopathy: when and what can surgery contribute to treatment? Eur Spine / 2000;9(1) :1-7. 137. Ishida Y, Ohmori K, Suzuki K, Inoue H. Analysis of dural
configuration for evaluation of posterior decompression in cervical myelopathy. Neurosurgery 1 999;44(1):91-95; discus sion 95-96. 138. Soo MY, Tran-Dinh HD, Dorsch NW et al. Cervical spine degenerative diseases: an evaluation of clinical and imaging features in surgical decisions. Australas Radial 1997;41(4): 351-356. 139. Hidai Y, Ebara S, Kamimura M et at. Treatment of cervical
compressive myelopathy with a new dorsolateral decompres sive procedure. J Neurosu rg 1 999;90(4) (suppl):1 78-185.
CHAPT ER 9 - MECHANICAL DISORDERS 209
140. Kumar VG, Rea GL, Mervis LJ, McGregor JM. Cervical spondylotic myelopathy: functional and radiographic long-term outcome a fter laminectomy and posterior fusion. Neuros u rgery 1 999; 44 ( 4 ) :77 1 -777; di scussion 777-778. 141. Sampath F, Bendebba M, Davis JD, Ducker TB. Outcome of patients treated for cervical myelopathy. A prospective multi center study with independent clinical review. Spine 2000;25:670-676. 142. Chiles BW 3rd, Leonard MA, Choudhri H F, Cooper PR. Cervical spondylotic myelopathy: patterns of neuro logical deficit and recovery after anterior cervical decom pression. Neuros u rgery 1 999 ;44 ( 4 ) :762-76 9; discussion 769-770. 143. Wang YL, Tsau Je, Huang MH. The prognosis of patients with cervical spondylotic myelopathy. Kao-Hsiung I Hsueh Ko Hsueh Tsa C/till 1997;13(7):425-431 (abstract).
144. Kuhtz-Buschbeck JF, Johnk K, Mader S, Stolze H, Mehdorn M. Analysis of gait in cervical myelopathy. Gait Pos t u re 1999;9(3) : 1 84-199.
145. Emery SE, Bohlman HH, Bolesta MJ, Jones PK. Anterior cervi cal decompression and arthrodesis for the treatment of cervi cal spondylotic myelopathy. Two to seventeen-year follow-up. J Bone Joint Surg 1998;80A(7):941-951 .
146. Naderi S, Ozgen S, Pamir MN, Ozek MM, Erzen C . Cervical spondylotic myelopathy: surgical results and factors affecting prognosis. Neurosu rgery 1998;43(1):43-49; discussion 49-50. 147. Fahlgren H, Jansa S, Lofstedt S. Retrofaryngeal tendinit. Lakiirtigning 1966;63:3779. 148. Resnick D, Niwayama MA. Diagnosis of Bone and Joint Disorders, 2nd edn. Saunders, London, 1988.
THIS PAGE INTENTIONALLY LEFT BLANK
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
8. 9. 10. 11.
12.
13.
14. 15.
center study. Presented at the 35th Annual Meeting of Congress of Neurological Surgeons, Honolulu, Hawaii, September 1985. An H. Cervical spine trawna. Spine 1998;23(24):2713-2729. Anderson LD, 0' Alonzo RT. Fractures of the odontoid process of the axis. I Bone Joint Surg1974;56A:1663-1674. Hadley MN, Browner C, Sonntag VKH. Miscellaneous fractures of the second cervical vertebra. Barrow Neurol lnst Q 1985;1:34. Bohlman HH. Acute fractures and dislocations of the cervical spine: an analysis of three hundred hospitalized patients and review of the literature. J Bone Joint Surg1979;61B:1119. Garfin SR, Rothman RH. Traumatic spondylolisthesis of the axis (hangman's fracture). In: The Cervical Spine Research Society, Sherk HH et a.L (eds) The Cervical Spine, 2nd edn. Lippincott, Philadelphia, 1983:223. Allen BL, Ferguson RI, Lehman TR, O'Brien RP. A mechanistic classi fication of closed, indirect fractures and dislocations of the lower cervical spine. Spine1982;7:1-27. Sonntag VKH. Management of bilateral locked facets of the cervical spine. Neurosurgery1981;150:150. Sonntag VKH. The early management of cervical spine injuries. Arizona Med1982;10:644.
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
the spine. J Bone Joint Surg1986;68A:354-361. 29. Raskas OS, Graziano GP, Herzenberg JE, Heidelberger KP,
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
56.
57.
58. 59 .
60 .
61.
62.
63.
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
-
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
-
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
REFERENCES 1 . Goadsby PJ. Bench to bedside: what have we learnt recently
about headache? Curr Opin NeuroI 1 997;10(3):215-220.
increased body heat. Lancet 1999;354(9183) : 1 001-1002.
2. Silberstein SD, Lipton RB . Chronic daily headache. CUTY Opin Neurol 2000;13(3) :277-283.
J Assoc Physicians India 1 999;47(11 ) : 1 072-1075.
headache. Cephalalgia 1999;19(suppl 25):20-23. 1999;1(6):21-32. Clin
Cornerstone
1 999;
0,
Fredriksen
TA,
Pfaffenrath
V.
Cervicogenic
32. Sjaastad 0, Bovin G. Cervicogenic headache. The differentiation Functional Neurol
1991;6(2):93-100. 33. Sjaastad 0. Cervicogenic headache: the controversial headache.
1(6): 11-20.
demiology of headache. Clin Cornerstone 1999;1(6):1-10.
J Pain
Symptom Management 1993;8(2):87-97.
Headache
and
face
pain.
Med
J
Aust
Clin Neurol Neurosu rg 1992;94(suppl):S1 47-S149. 34. Sjaastad 0, Frederiksen TA. Chronic daily headache: is ' cervico
8. Lipton RB, Pfeffer D, Newman LC, Solomon S. Headaches in 9. Lance JW.
3 1 . Sjaastad
from common migraine. An overview. diagnosis.
7. Lipton RB, Goadsby P, Silberstein SD. Classification and epi
the elderly.
30. Sjaastad 0. The headache of challenge in our time: cervicogenic
headache: diagnostic criteria. Headache 1990;30(11 ) : 725-726.
5. Cady RK. Diagnosis and treatment of migraine. Clin Cornerstone
Headache
Roy Soc Med
headache. Functional NeuroI 1990;5(2):1 55-158.
4. Rasmussen BK. Epidemiology and socio-economic impact of
6. Ryan RE Jr.
J
29. Peatfield RC. Lithium in cluster headache. 1981;74:432.
3. Shah PA, Nafee A. Clinical profile of headache and cranial
neuralgias.
28. Blau IN, Engel HO. A new cluster headache precipitant:
genic headache' one subgroup? Cephalalgia 1 998;18(suppl 21):37-40.
2000;
172(9) :450-455.
35. Vincent MB, Luna RA. Cervicogenic headache: a comparison
with
10. Rasmussen BK, Jensen R, Schroll M, Olesen J. Interrelations
between migraine and tension-type headache in the general population. Arch NeuroI 1992;49(9):914-918.
migraine
and
tension-type
headache.
Cephalalgia
1999;19(suppI 25) : 11-16. 36. Pfaffenrath V, Kaube H. Diagnostics of cervicogenic headache. Functional NeUl·0/ 1990;5:159-164.
11. Rasmussen BK, Jensen R, Schroll M, Olesen J. Epidemiology of
37. Kranzlin P, Walchli B. The concept of cervicogenic headache.
headache in a general population - a prevalence study. f Clin
Annual postgraduate course of the Association of Swiss
EpidemioI 1991;44:11 47-1157.
Chiropractors. Interlaken, Switzerland, 1993:13.
12. Jensen R. Pathophysiological mechanisms of tension-type
38. N ilsson N. The prevalence of cervicogenic headache in a
headache: a review of epidemiological and experimental
random
studies. Cephalalgia 1999;19(6): 602-621 .
1995;20(17) : 1 884-1888.
13. Diamond
S.
Tension-type
headache.
Clin
Cornerstone
1999;1(6):33-44.
headaches.
Med
Clin
North
Am
1991;
75(3):595-603. 15. Russell
of
20-59
year
olds.
Spine
Pressure-pain
threshold
measurements.
Pain
1992;51(2) : 1 69-173. 40. Sjaastad 0, Fredriksen T, Pareja JA, Stolt-Nielsen A, Vincent M.
Coexistence of cervicogenic headache and migraine without
MB, Ostergaard S, Bendtsen L, Olesen J. Familial
occurrence of chronic tension-type headache.
Cephalalgia
1999;19(4}:207-21O.
anisms and treatment. Curr Opin Neurol 2000;13(3):285-289. 17. Launer LJ, Terwindt GM, Ferrari MD. The prevalence and char
acteristics of migraine in a population-based cohort: the GEM study. Neurology 1999;53(3):537-542. 18. Harrigan JA, Kues JR, Ricks DF, Smith R. Moods that predict
coming migraine headaches. Pain 1 984;20:385-396. 19. Hargreaves RJ, Shepheard SL. Pathophysiology of migraine -
new insights. Can
J Neurol
aura. Functional NeuroI 1999;14(4):209-218. 4 1 . Sjaastad 0, Frederiksen TA. Cervicogenic headache: criteria,
classification and epidemiology. Clin Exp Rheumatol 2000;18(2
16. Jensen R, Olesen J . Tension-type headache: an update on mech
Sci 1 999;26(suppl 3) :S12-S19.
20. Aurora SK, Welch KM. Migraine: imaging the aura. Curr Opin Neurol. 2000;13(3):273-276. 21. Frishberg BM. Neuroimaging in presumed primary headache
disorders. Sem NeuroI 1997;17(4):373-382. 22. Diener HC, Limmroth V. Acute management of migraine: trip
tans and beyond. Curr Opin Neu roI 1999;12(3) :261-267. 23. Weitzel KW, Thomas ML, Small RE, Goode JV. Migraine: a com
prehensive review of new treatment options. Pharmacotherapy 1999;19(8) :957-973. 24. Bartleson JD. Treatment of migraine headaches. Mayo Clin Proc 1999;74(7):702-708. 25. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:75. 26. Tuchin PI, Pollard H, Bonello R. A randomized controlled trial
of chiropractic spinal manipulative therapy for migraine.
J Manip Physiol
sample
39. Bovim G. Cervicogenic headache, migraine, and tension-type
headache.
14. Kunkel RS. Diagnosis and treatment of muscle contraction
(tension-type)
population
Ther 2000;23(2):91-95.
27. Silberstein SD, Niknam R, Rozen TD, Young WB. Cluster
headache with aura. Neu rology 2000;54(1) :219-221 .
suppI 19):S3-S6. 42. Mark BM. Cervicogenic headache, differential diagnosis and
clinical management: literature review. Cran iology 1990;8(4): 332-338. 43. PollmalUl W, Keidel M, Pfaffenrath V. Headache and the cervi
cal spine: a critical review. Cephalalgia 1997;17(8):801-816. 44. van Suijlekom JA, de Vet HC, van den Berg SG, Weber WE.
lnterobserver reliability of diagnostic criteria for cervicogenic headache. Cephalalgia 1999;19(9) : 8 1 7-823. 45. Leone M, D' Amico D, Grazzi L, Attanasio A, Bussone G.
Cervicogenic headache: a critical review of the current diagnos tic criteri a. Pain 1998;78(1): 1-5. 46. Leone M, D'Amico D, Moschiano F et al. Possible identification
of cervicogenic headache among patients with migraine: an analysis of 374 headaches. Headache 1995;35(8):461-464. 47. Zwart JA. Neck mobility in
different headache disorders.
Headache 1997;37(1):6-11. 48. Bono G, Antonaci F, Dario A et al. Unilateral headaches and
their relationship with
cervicogenic headache.
Clin
Exp
Rheumatol 2000;18(2 suppI 19):S11-S15. 49. Marcus DA. Migraine and tension-type headaches: the ques
tionable validity of current classification systems. Clin
J
Pain
1992;8(1) :28-36; discussion 37-38. 50. Pryse-Phillips W, Findlay H, Tugwell P et al. A Canadian popu
lation survey on the clinical, epidemiologic and societal impact of migraine and tension-type headache. Can 1992;19(3) :333-339.
J
Neurol Sci
238 S E CTI O N TWO - TH E C E RV I CAL SPI N E
5 1 . Olesen J . (ed) Classification and Diagnostic Criteria for Headache
of the 5th International Conference, International Federation of
Disorders, Cranial Neuralgias and Facial Pain, 1st edn. The
Orthopaedic Manipulative Therapists, June 1-5, Vail, Colorado,
International Headache Society, Copenhagen, 1990. 52. Star MJ,
1992.
Curd JG, Thorne RP. Atlantoaxial lateral mass
70. Moffat DA, Harries ML, Baguley DM, Hardy DG. Unterberger's
osteoarthritis: a frequently overlooked cause of severe occipito
stepping test in acoustic neuroma.
cervical pain. Spine 1992;17:S71-S76.
103(9):839-841 .
J
Laryngol Otol 1 989;
53. Dreyfuss F, Michaelsen M, Fletcher D. Atlanto-occipital and
7 1 . Kuipers-Upmeijer J, Oosterhuis HJ. Unterberger's test not
lateral atlanto-axial joint pain patterns. Spine 1994;19:11 25-1 1 3 1 .
useful in testing of vestibular function. Ned Tijdschr GeHees
54. Argenson e , Francke JF, Sylla S et a l . The vertebral arteries
(segments VI and V2). Allat c/in 1 980;2:24-4 1 . 55. Francke JF, Di Marino V, PalUlier M , Argenson e , Libersa C . The
vertebral arteries: the V3 atlanto-axoidal and V4 intracranial segments - collaterals. Anat c/in 1981;2:229-242. LHA, Meldrum HA. Neurologie en manuele therapie. De vertebrobasilaire insufficientie. Ned Tijdschr Manuele Ther 1985;85/4(2):33. 57. Gutmann G, BiedermalUl H . Funktiollelle Pathologie und Klil1ik del' Wirbelsiiule, Band I, Die Halswirbelsiiule (Teil 2). Fischer,
Stuttga rt, 1984. possible correlation between vertebral artery insu fficiency and degenerative changes in the cervical spine.
Eur Arch
OtorhinolarYllgoI 1998;255(9) :437-440.
(ed) Modern Mal1ual Therapy of the Vertebral Column, Churchill Livi ngstone, New York, 1986:304.
1990;104(8) :599-602.
common causes of vertigo using a structured clinical history. Acta Otorhinolaringol Espallim 2000;51(1):25-30. 74. Bakr MS, Saleh EM. Electronystagmography: how helpful is it?
J Laryllgol Otol 2000;114(3):1 78-183.
75. Ojala M, Palo J. The aetiology of dizziness and how to examine
a dizzy patient. Ann Med 1991 ;23(3) :225-230. insu fficiency following cervical spine i nj ury.
Spine
1 985;
10(1):1 08-110. 77. Karlberg M, Persson L, Magnusson M. Impaired postural Laryngologica 1995;Suppl 520 Pt 2:440-442. 78. Ishiyama A, Jacobson KM, Baloh RW. Migraine and benign
positional vertigo. A n n
60. Guerrier Y, Basseres F. Le Vertige et Ie Vertigilleux. Duphar & Cie,
Brussels, 20-22.
Otol
Rhinol
Laryngol
2000;109(4):
377-380. 79. Oghalai JS, Manolidis S, Barth JL, Stewart MG, Jenkins HA.
61 . Ruckenstein MJ. Vertigo and dysequilibrium with associated
hearing loss. Otolaryngol c/in North Am 2000;33(3) :535-562. 62. EI-Kashlan HK, Telian SA. Diagnosis and i nitiating treatment
for peripheral system disorders: imbalance and dizziness with normal hearing. Otolaryngol c/in North Am 2000;33(3):563-578. treating causes of central
vertigo. Otolaryngol c/in North Am 2000;33(3):579-602. 64. Anon. Protocol for pre-manipulative testing of the cervical
J Physiother 1988;34:97-100.
65. Anon. Protocol for pre-manipulative testing of the cervical
spine. Physiotherapy 1991;41 : 1 5-17.
Unrecognized benign paroxysmal positional vertigo in elderly patients. OtolarYl1gol Head Neck Surg 2000;122(5):630-634. 80. Galm R, Rittmeister M, Schmitt E. Vertigo in patients with
cervical spine dysfunction. Eur Spine J 1998;7(1):55-58.
8 1 . Norre ME. Cervical vertigo.
Diagnostic and semiological
problem with special emphasis upon 'cervical nystagmus'. Acta Otorhil1olarYl1gol Belg 1987;41(3) :436-452. 82. Brandt T. Cervical vertigo - reality or fiction? A udiol Neuro-Otol 1996;1 (4):1 87-196. 83. Karlberg M, Johansson
R, Magnusson M,
Fransson
PA.
Dizziness of suspected cervical origin distinguished by postur
66. Aspinall W. Clin.ical testing for cervical mechanical disorders
which produce ischemic vertigo.
J Laryngol OtoI
control in patients with cervico-brach ial pain. Acta Oto
59. Coman WB. Dizziness related to ENT conditions. In: Grieve GP
spine. A ust
vestibular dysfunction?
76. Bose B, Northrup BE, Osterholm JL. Delayed vertebro-basilar
58. Strek P, Reron E, Maga F, Mod rzejewski M, Szybist N. A
D. Distinguisning and
Unterberger stepping test: a useful indicator of peripheral 73. Lopez-Escamez J, Lopez-Nevot A, Gamiz M et al. Diagnosis of
56. Oostendorp RAB, Bernards ATM, Querido e, Hagenaars
63. Solomon
1994;138(3) : 1 36-139. 72. Hickey SA, Ford GR, Buckley JG, Fitzgerald O'Connor AF.
J
Orthop Sports Phys Ther
1 989;11 : 1 1 76-1 1 82. 67. Michaeli A. Dizziness testing of the cervical spine: can compli
cations of manipulations be prevented? Physiother Theory Pract 1991 ;7:243-250. 68. Hutchison MS. An investigation of pre-manipulative dizziness
ographic assessment of human postu ral dynamics.
J
Vestib
Res 1996;6(1) :37-47. 84. Goebel JA. Management options for acute versus chronic
vertigo. Otolaryngol c/in North Am 2000;33(3):483-494. 85. Kessinger RC, Boneva DV. Vertigo, tilmitus, and hearing loss in
the geriatric patient.
J
Manip Physiol Ther 2000;23(5) :352-362.
86. Garrido Me, Rodrigo FJ, Garcia AJ et al. Benign positional
testing. In: Jones HM et al. (eds) Proceedings of the 6th Bielmial
paroxysmal vertigo in the general ear, nose, and throat clinic.
Conference, Manipulative Therapists Association of Australia,
Acta Otorhinolaryngol Espallim 2000;51(1): 14-18.
Adelaide, 1989. 69. Oostendorp RAB, Hagenaars LHA, Fischer AJEM et al. Dutch
standard 'cervicogenic dizziness'. In: Paris SV (ed) Proceedings
87. De la Meilleure G, Dehaene I, Depondt M et al. Benign paroxys
mal positional vertigo of the horizontal canal. J Neural Neurasurg Psychiatry 1996;60(1):68-7 1 .
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.
THIS PAGE INTENTIONALLY LEFT BLANK
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.
REFERENCES 1. Murphy MJ, Lieponis Jv. Nonoperative treatment of cervical spine pain. In: The Cervical Spine Research Society, Sherk H H et al. (eds) The Cervical Spine, 2nd edn. Lippincott, Philadelphia, 1989:674. 2. Di Fabio RP. Manipulation of the cervical spine: risks and benefits. Phys Ther 1999;79(1):50-65. 3. Miller RG, Burton R. Stroke following chiropractic manipula tion of the spine. lAMA 1974;229: 189. 4. Okawara S, Nibbelink D. Vertebral artery occlusion following hyperextension and rotation of the head. Stroke 1974;5:640. 5. Davidson KC, Weinford EC, Dixon GD. Traumatic vertebral artery pseudoaneurysm following chiropractic manipulation.
Radiology 1975;115:651. 6. Parklin pJ, Wallis WE, Wilson J L . Vertebral artery occlusion following manipulation of the neck. N Z Med 1 1978;88:441. 7. Krueger BR, Okazaki H. Vertebro-basilar distribution infarction following chiropractic cervical manipulation. Mayo Clin Proc 1980;55:322.
8. Kewalramani LS, Kewalramani DL, Krebs M, Saleem A. Myelopathy following cervical spine manjpulation. Phys Med 1982;61: 165. 9. Schmidley JW, Koch T. The noncerebrovascular complications of chiropractic manipulations. Neurology 1984;34:684. 10. Martienssen J, Nilsson N. Cerebrovascular accidents following upper cervical manipulation: the importance of age, gender, and technique. Am I Chiropract Med 1989;2:160-163. 11. Murphy MJ, Lieponis }Y. Nonoperative treatment of cervical spine pain. In: The Cervical Spine Research Society, Sherk H H et al. (eds.) The Cervical Spine, 2nd edn. Lippincott, Philadelphia,
1989:674. 12. Assendelft WJJ, Bouter LM, Knipschild PG. Complications of spinal manipulation: a comprehensive review of the literature. ] Fam Pract 1996;42:475-480. 13. Krueger BR, Okazaki H. Vertebrobasilar distribution infarction following chiropractic cervical manipulation. Mayo Clin Proc 1980;55:322-332.
272 T H E CERVICAL S P I N E
1 4 . Terrett AGJ. Vascular accidents from cervical spine manipula tion: report on 1 07 cases. f A ust Chiropract Assoc 1987;17:15-24. 15. Henderson DJ. Vertebral artery syndrome. In: Vear HJ (ed) Chiropractic Standards of Practice and Quality of Care. Aspen, Gaithersburg, 1992:115-143. 16. Klougart N, Leboeuf-Y de C, Rasmussen LR. Safety in chiro practic practice. Part I: The occurrence of cerebrovascular accidents after manipulation to the neck in Denmark from
1978-1988. J Manip PhysioL Ther 1996;19(6):371-377. 17. Dabbs V, Lauretti WJ. A risk assessment of cervical manipula tion vs. NSAIDs for the treatment of neck pain. J Manip Physiol Ther 1995;18:530-536. 18. Powell FC, Hanigan WC, Olivero We. A risk/benefit analysis of spinal manipulation therapy for relief of lumbar or cervical pain. Neurosurgery 1993;33:73-79. 19. Wolff H D . Komplikationen bei manueller Therapie der Halswirbelsaule. Z Manuelle Med 1978;16:77-81. 20. Hosek RS, Schram SB, Silverman H, Myres J, Williams SE. Cervical manipulation (letter to the editor). lAMA 1981; 245:922. 21 . Haynes MJ. Stroke following cervical manipulation in Perth.
Chiropract f Aust 1994;24:42-46. 22. Gutmann G. Injuries to the vertebral artery caused by manual therapy. Z ManueILe Med 1983;21:2-14. 23. Dvorak J, Orelli F. How dangerous is manipulation to the cervi cal spine? J ManuaL Med 1985;2:1-4. 24. K10ugart N, Leboeuf-Yde C, Rasmussen LR. Safety in chiro practic practice. Part II: Treatment to the upper neck and the rate of cerebrovascular incidents. I Manip PhysioL Ther
1996;19(9):563-569. 25. Jaskoviak P. Complications arising from manipulation of the cervical spine. J Manip Physiol Ther 1980;3:213-219. 26. Henderson DJ. CaSSidy JD. Vertebral artery syndrome. In: Vernon H (ed) Upper Cervical Syndrome: Chiropractic Diagnosis and Treatment. Williams & Wilkins, Baltimore, 1988:195-222. 27. Eder M, Tilscher H. Chiropractic Therapy: Diagnosis and n·eatment. Aspen, Rockville, 1980:61. 28. Haldeman S, Chapman-Smith D, Peterson DM. Guidelines for Chiropractic Qualihj Assurance and Practice Parameters. Aspen, Gaithersburg, 1993;170-172. 29. Patijn J. Complications in manual medicine: a review of the literature. I Manual Med 1991;6:89-92. 30. Lee KP, Carlini WG, McCormick GF, Albers Gw. Neurologic complications following chiropractic manipulation: a survey of California neurologists. Neurology 1 995;45:1213-1215. 31. Carey PF. A report on the occurrence of cerebral vascular accidents in chiropractic practice. I Can Chiropract Assoc
1993;37: 104-106. 32. Leboeuf-Yde C, Rasmussen LR, K10ugart N. The risk of over reporting spinal manipulative therapy-induced injuries: a description of some cases that failed to burden the statistics.
J Manip Physiol Ther 1996;19(8):536-538. 33. Hurwitz EL, Ak€r PD, Adams AH et af. Manipulation and
mobilization of the cervical spine: a systematic review of the literature. Spine 1996;21: 1 746-1759. 34. Michaeli A. Dizziness testing of the cervical spine: can compli cations of manipulation be prevented? Physiother Theory Pract
1991;7:243-250. 35. Michaeli A. Reported occurrence and nature of complications following manipulative physiotherapy in South Africa. Aust J Physiother 1993;39(4):309-315. 36. Middleditch A. The cervical spine - safe in our hands? Proceedings of the World Confederation of Physical Therapy 1 1 th International Congress, London, 1991 : 1 799-1781 . 37. Parkin pJ, Wallis WE, Wilson JL. Vertebral artery occlusion fol lowing manipulation of the neck. N Z Med J 1978;88:44 1 .
38. Fritz VU, Maloon A, Tuch P. Neck manipulation causing stroke. S Afr Med J 1984;66:844. 39. Grant R. Vertebral artery insufficiency: a clinical protocol for premanipulative testing of the cervical spine. In: Boyling ]0, Palastanga N (eds) Grieve's Modern Manual Therapy, 2nd edn. Churchill Livingstone, Edinburgh, 1994:371-380. 40. Terret AGJ, Webb MN. Vertebrobasilar accidents following cervical spine adjustment/ manipulation. J Aust Chiropract Assoc 1982;12:24-27. 41. Oostendorp RA. Vertebrobasilar insufficiency. Proceedings of the International Federation of Orthopaedic Manipulative Therapists Congress, Cambridge, 1988:42-44. 42. Terrett AGJ. Vascular accidents from cervical spine manipula tion: the mechanisms. J Aust Chiropract Assoc 1988;22(5):59-74. 43. Aspinall W. Clinical testing for cervical mechanical disorders which produce ischemic vertigo. J Orthop Sports Phys Ther
1989;11:1 76-182. 44. Carey PF. A suggested protocol for the examination and treat ment of the cervical spine: managing the risk. J Can Chiropract Assoc 1995;39:35-39. 45. De Kleyn A, Nieuwenlwyse P. Schwindelanfalle und Nystagmus bei einer bestimmten Stellung des Kopfes. Acta OtolaryngoI 1927;11:155-157. 46. Brown BSJ, Tatlow WFT. Radiographic studies of the vertebral arteries in cadavers. Radiology 1953;81:80-88. 47. Toole JF, Tucker SH. Influence of head position upon cervical circulation. Studies on blood flow in cadavers. Arch NeUl·ol 1960;2:616-623. 48. Grant R. Clinical testing before cervical manipulation - can we recognise the patient at risk? Proceedings of Tenth International Congress of the World Confederation of Physical Therapy, Sydney, 1987:192-197. 49. Grant R. Dizziness testing and manipulation of the cervical spine. In: Grant R (ed) Physical Therapy of the Cervical and Thoracic Spine. Churchill Livingstone, New York, 1988:111-124. 50. Anon. Protocol for premanipulative testing of the cervical spine. Aust J Physiother 1988;34:97-1 00. 51. Grant R. Vertebral artery concerns: premanipulative testing of the cervical spine. In: Grant R (ed) Physical therapy of the Cervical and Thoracic Spine, 2nd edn. Churchill Livingstone, New York,
1994:145-166. 52. Grant R. Vertebral artery testing - the Australian Physiotherapy Association protocol after 6 years. Manual Therapy 1996;1: 149-153. 53. Rivett DA. Neurovascu lar compromise complicating cervical spine manipulation: what is the risk? J Man Manip Ther
1995;3(4):144-151. 54. Rivett DA, Milburn P. A prospective study o f complications of cervical spine manipulation. J Manual Manip Ther 1996;4(4): 166-170. 55. Combs SB, Triano JJ. Symptoms of neck artery compromise: case presentations of risk estimate for treatment. J Manip Physiol Ther 1997;20(4):274-278. 56. Hutchison MS. An investigation of premanipulative dizziness testing. Proceedings of the Sixth Biennial Conference of Manipulative Physiotherapists of Australia, Adelaide,
1989:104-112. 57. Rivett DA, Sharples KJ, Milburn PD. Effect of premanipulative tests on vertebral artery and internal carotid artery blood flow: a pilot study. J Manip Physiol Ther 1999;22(6):368-375. 58. Cote P, Kreitz BG, Cassidy ]0, Thiel H. The validity of the extension-rotation test as a clinical screening procedure before neck manipulation: a secondary analysis. J Mnnip Physiol
Ther 1996;19(3):159-164. 59. Stevens AJ. Doppler sonography and neck rotation. I Mallual Med 1984;1:49-53.
C H A PT E R 1 3 - TREAT M E NT 273
60. Danek V. Haemodynamic disorders within the vertebrobasilar arterial system following extreme positions of the head.
J Manual Med 1989;4:127-129. 61 . Stevens AJ. Functional Doppler sonography of the vertebral artery and some considerations about manual techniques.
J Manual Med 1991;6:102-105. 62 Refshauge KM. Rotation: a valid premanipulative dizziness test? Does it predict safe manipulation? ] Manip Physiol Ther 1994;17:15-19. 63. Thiel H, Wallace K, Donat J, Yong-Hing K. Effect of various head and neck positions on vertebral artery blood flow. Ciin Biomecb 1994;9:105-110. 64. Kwmasmaa KT, Thiel HW. Vertebral artery syndrome: a review of the literature. ] Orthop Med 1994;16:17-20. 65. Weingart JR, Bischoff HP. Doppler sonography of the vertebral artery with regard to head positions appropriate to manual medicine. ] Manual Med 1992;6:62-65. 66. Powell VJ. An investigation of testing procedures for verte brobasilar insufficiency. Aust J Physiother 1990;36:31. 67. Kleynhans AM, Terrett AGJ. The prevention o f complications from spinal manipulative therapy. In: Glasgow EF (ed) Aspects of Manipulative Therapy, 2nd edn. Churchill Livingstone, Edinburgh, 1985:163-175. 68. Bolton PS, Stick PE, Lord RSA. Failure of clinical tests to predict cerebral ischemia before neck manipulation. ] Manip Physiol
persistent back and neck complaints: results of one year follow up. BM] 1992;304:601--605. 84. Koes BW, Bouter LM, van Marmeren H, Essers AHM. The effectiveness of manual therapy, physiotherapy and treat ment by the general practitioner for nonspecific back and neck complaints: a randomized clinical trial. Spine 1992;
17:28-35. 85. Koes BW, Bouter LM, van Marmeren H et al. A randomized clinical trial of manual therapy and physiotherapy for persist ent back and neck complaints: subgroup analysis and relation ship between outcome measures. ] Manip Physiol Ther
1993;16:211-219. 86. Shekelle PG. Spine update. Spinal manipulation. Spine 1994;19(7):858-861 . 87. Stevens JC, Cartlidge NE, Saunders M e t al. Atlanto-axial subluxation and cervical myelopathy in rheumatoid arthritis. Q ] Med 1971;40:391. 88. Eulderink F, Meijers KAE. Pathology o f the cervical spine in rheumatoid arthritis. A controlled study of 445 spines. ] Pat/wi
1976;120:91. 89. Parke WW, Watanabe R. The intrinsic vasculature of the lumbo-sacral spinal nerve roots. Spine 1985;10:508-515. 90. Takata K, Inoue S, Takahashi K, Ohtsuka Y. Swelling of the
Ther 1989;12:304-307. 69. Manipulative Therapists' Group of the South African Society of
91.
Physiotherapy. Protocol for pre-manipulative testing of the cervical spine. Physiotherapy 1991;41(1):15-1 7. 70. Khurana RK, Genut AA, Yannakakis GD. Locked-in syndrome with recovery. Ann Neuro/ 1980;8:439-441 . 71. Crawford JF, Hwang BY, Asselbergs PI, Hickson GS. Vascular iscllemia of the cervical spine: a review of relationship to thera peutic manipulation. ] Manip Physiol Ther 1984;7:149-155. 72. Mas JL, Bousser MG, Hasboun D, Laplane D. Extracranial vertebral artery dissections: a review of 13 cases. Stroke
92.
1987;18:1037-1047. 73. Rothrock JF, Hesselink JR, Teacher TM. Vertebral artery occlu sion and stroke from cervical self-manipulation. Neurology 1991;41:1 696-1697. 74. Cook JW 4th, Sanstead JK. Wallenberg's syndrome following self-induced manipulation. Neurology 1991;41:1695-1696. 75. Katirji MB, Reinmuth OM, Latchaw RE. Stroke due to vertebral artery injury. Arch NeuroI 1985;42:242-248. 76. Hanus SH, Homer TD, Harter DH. Vertebral artery occlusion complicating yoga exercises. Arch NeuroI 1977;34:574-575. 77. Terrett AGJ. It is more important to know when not to adjust. Chiropract Tech 1990;2(1):1-9. 78. Assendelft WJJ. Chiropractic in the Netherlands: Diagnosis and Effects of Treatment. Akademisch Proefschrift, VU Amsterdam, 1996:105-120. 79. Assendelft WJJ. Chiropractic in the Netherlands: Diagnosis and Effect of Treatment. Akademisch Proefschrift, VU Amsterdam, 1996:163-1 71 . 80. Leboeuf-Y de C, Hennius B, Rudberg E, Leufvenmark P, Thunman M. Side effects of chiropractic treatment: a prospec tive study. J Manip Physiol Ther 1997;20(8):511-513. 81. De Bock S. Medical Complications after Manipulation of the Spine. G.G.5. Manual Therapy, VU Brussels, 1993. 82. Koes BW, Bouter LM, van Marmeren H et al. A blinded ran domized clinical trial of manual therapy and physiotherapy for chronic back and neck complaints: physical outcome measures. J Manip Physiol Ther 1992;15:16-23. 83. Koes BW, Bouter LM, van Marmeren H et al. Randomized clinical trial of manipulative therapy and physiotherapy for
93.
94. 95.
96. 97.
cauda equina in patients who have herniation of a lumbar disc. ] Bone Joint Surg 1988;70A:361-368. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982. Cyriax JH. Textbook of Orthopaedic Medicine, vol II, Treatment by Manipulation, Massage and Injection, 1 1 th edn. Bailliere Tindall, London, 1984:83. Bush K, Hillier S. Outcome of cervical radiculopathy treated with periradicular / epidural corticosteroid injections: a prospective study with independent clinical review. Eur Spine ] 1996;5(5):320-325. Cousins MJ. Epidural neuronal blockade. In: Cousins MJ, Bridenbaugh PO (eds) Neuronal Blockade in Clinical Anesthesia and Pain Management. Lippincott, Philadelphia, 1980:183. Michael J, Murphy J, Lieponis V. Nonoperative treatment of cervical spine pain. In: The Cervical Spine Research Society, Sherk H H et al (eds) The Cervical Spine, 2nd edn. Lippincott, Philadelphia, 1989:673. Shulman M, Nimmagadda U, Valente A. Cervical epidural steroid injection for pain of cervical spine region. Anesthesiology 1984;61:A223. Cathlove RFH, Braha R. The use of cervical epidural nerve blocks in the management of chronic head and neck pain. Can
Anaesth Soc ] 1984;31: 188-191 . 98. Cronen MC, Walderman SD. Cervical steroid epidural nerve blocks in the palliation of pain secondary to intractable tension-type headaches. ] Pain Symptom Management
1990;5:379. 99. Rowlingson JC, Kirschenbaum L. Epidural analgeSic tech niques in the management of cervical pain. Anesth Analg 1 986;65:938-942. 100. Shulman M. Treatment of neck pain with cervical epidural steroid injection. Reg Anesth 1986;11:92. 101. Warfield CA, Biber MP, Crews DA, Dwarakanath GK. Epidural steroid injection as a treatment for cervical radiculitis. Ciin J Pain 1988;4:201. 102. Mooney V. Injection studies: role in pain definition. In: Frymoyer JW (ed) The Adult Spine. Principles and Practice. Raven Press, New York, 1991 :530. 103. Ferrante FM, Wilson SF, Jacobo C et al. Clinical classification as a predictor of therapeutic outcome after cervical epidural steroid injection. Spine 1993;18:730.
274 T H E CERV I CAL S P I N E
104. McGuire RA, Degnan G , Amundson G M . Evaluation o f
105. 106.
107. 108.
current extrication orthroses i n immobilization of the u nstable cervical spine. Spine 1990;15:1064. Hartman JT, Palumbo F, Hill BJ. Cineradiography of the braced normal spine. Clin Orthop Rel Res 1975;109:97. Johnson RM, Hart DL, Owen JR et al. The Yale cervical ortho sis: an evaluation of its effectiveness in restricting cervical motion in normal subjects and a comparison with other cervi cal orthoses. Phys Ther 1978;58:865. Teale C, Mulley GP. Support collars: a preliminary survey of their benefits and problems. Clin Rehab 1990;4:33. Johnson RM, Owen JR, Hart DL, Callahan RA. Cervical orthroses - a guide to their selection and use. Clin Orthop Rel
Res 1981;154:34. 109. Kaufman WA, Lunsford TR, Lance LL. Comparison of three prefabricated cervical collars. Orthop Prosthetics 1986;39:21.
110. Lavernia CJ, Botte MJ, Garfin SR. The spine. In: Rothman RH, Simeone FA (eds) Spinal Orthoses for Traumatic and Degenerative Disease, 3rd edn. WB Saunders, Philadelphia, 1992:1197. 111. Vaccaro AR, Botte MJ, Lind 81, Gardin SR. Cervical orthotics
112. 113.
114. 115.
including traction and halo devices. In: The Cervical Spine Research Society, Clark CR et al. (eds) The Cervical Spine, 3rd edn. Lippincott-Raven, Philadelphia, 1998:113-140. Gore DR, Sepic SB, Gardner GM et al. Neck pain: a long-term follow-up of 205 patients. Spine 1987;12:1-5. Cuatico W. Anterior cervical discectomy without interbody fusion: an analysis of 81 cases. Acta Neurochir 1981;57:269. Bollati A, Galli G, Gandolfini M, Marini G, Gatta G. Microsurgical anterior cervical disc removal without interbody fusion. Surg Neural 1983;19:329. Troisier O. Les Algies Discales et Ligamentaires du Rachis. Masson, Paris, 1953.
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
-
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
REFERENCES 1 . Cyriax )B. Textbook of Orthopaedic Medicine, vol I, Diagnosis and Treatment of Soft Tissue Lesions, 8th edn, Bailliere Tindall, London, 1982:134. 2. Fritz JM, Delitto A. Erhard RE, Roman M. An examination of the selective tissue tension scheme, with evidence for the concept of a capsular pattern of the knee. Phys Ther 1998;78:1046-1061 . 3. Kozin F. Painful shoulder and the reflex sympathetic dystro phy syndrome. In: Arthritis and Allied Conditions, 9th edn. Lea & Febiger, Philadelphia, 1979:1091-1120. 4. Neviaser T. Adhesive capsulitis. Orthop Clin North Am 1 987;18(3): 439-443. 5. Kaltsas O. Comparative study of the properties of the shoulder joint capsule with those of other joint capsules. Clin Orthop Rei Res 1 983;173:20-26. 6. Reeves B. Arthrographic changes in frozen and post-traumatic stiff shoulders. Proc Roy Soc Med 1976;827-830. 7. Neviaser R, Neviaser T. The frozen shoulder: diagnosis and management. Clin Orthop Rei Res 1 987;223:59-64. 8. Murnaghan JP. Adhesive capsulitis of the shoulder: current concepts and treatment. Orthopaedics 1988;11: 153-158. 9. Cod man EA. The Shoulder. Todd, Boston, 1934:216-224. 10. Withers RJW. The painful shoulder: review of one hundred personal cases with remarks on the pathology. J Bone joillt Surg 1 949;31:414-417. 1 1 . Neviaser JS. Arthrography of the Shoulder. Thomas, Springfield, 1975:60-66. 12. Kay NR. The clinical diagnosis and treatment of frozen shoulders. Practitioner 1 981;225(1352): 164-167. 13. Matsen III FA, Lippitt SB, Sidles JA, Harryman OT II. Practical EVllluation of Management of the Shoulder. Saunders, Philadelphia, 1 994:19-109. 14. Obremskey WT. Follow-up of the inferior capsular shift proce dure for atraumatic multidirectional instability. Univ Wash Res Rep 1994;4:45. 15. Hazleman BL. Frozen shoulder. In: Watson MS (ed.) Surgical Disorders of the Shoulder. Churchill Livingstone, New York, 1991 : 1 67-179. 1 6. Sany J, Cillens JP, Rousseau JR. Evolution lointaine de la retrac tion capsulaire de l'epaule. Revue Rhum 1982;49:815-819. 1 7. Clarke GR, Willis LA, Fish BWW, Nichols PJ. Preliminary studies in measuring range of motion in normal and painful stiff shoulders. Rheumatol Rehabi/ 1975;14:39-46. 18. Shaffer B, Tibone JE, Kerlan RK. Frozen shoulder: a long-term follow-up. I Balle loint Surg 1992;74A:738-746.
19. Miller MO, Wirth MA, Rockwood CA Jr. Thawing the frozen shoulder: the 'patient' patient. Orthopedics 1996;19(10):849-853. 20. Mao CY, Jaw WC, Cheng HC Frozen shoulder: correlation between the response to physical therapy and follow-up shoulder arthrography. Arch Phys Med Rehllbil 1997;78(8):857-859. 21. Pearsall AW, Speer KP. Frozen shoulder syndrome: diagnostic and treatment strategies in the primary care setting. Med Sci Sports Exerc 1998;30(4 Suppl):533-539. 22. Nicholson GG. The effects of passive joint mobilisation on pain and hypomobility associated with adhesive capsulitis of the shoulder. Orthop Sports Phys Ther 1985;6:238-246. 23. Watson-Jones R. Simple treahnent of still shoulders. J Bone Joill t Surg 1963;45B:207. 24. O'Kane JW, Jackins S, Sidles JA, Smith KL, Matsen FA 3rd. Simple home program for frozen shoulder to improve patients' assessment of shoulder function and health status. j Am BOllrd Pain Pract 1999;12(4):270-277. 25. Gain AN, Schydlowsky P, Rossel 1, Remvig L, Jf'nsen EM. Treatment of ' frozen shoulder' with distension and glu corticoid compared with glucocorticoid alone. A randomised controlled trial. Scand I Rheumato/ 1998;27(6):425-430. 26. Ritzk TE, Cristopher RP, Pinals RS et al. Adhesive capsulitis, a new approach to its management. Arch Phys Med Rehabil 1 983;64:29-33 27. Hazleman BL. The painful stiff shoulder. RheulIl Phys Med 1972;11:413-421 . 28. Ter Veer H. Distraktie van het schoudergewricht. Cyriax-Info 1989;2 June. 29. Reichrnister JP, Friedman SL. Long-term functional results after manipulation of the frozen shoulder. Md Med I 1999;48(1):7-11 . 30. Andersen NH, Sojbjerg JO, Johannsen HV, Sneppen O. Frozen shoulder: arthroscopy and manipulation under general anesthesia and early passive motion. J Shoulder Elbow Surg 1998;7(3):218-222. 31. Post M. The Shoulder. Lea & Febiger, Philadelphia, 1978:281-284. 32. Reeves B. Arthrographic changes in frozen and post-traumatic stiff shoulders. Proc Roy Soc Med 1976:827-830. 33. Quigley TB. Indications for manipulation and corticosteroids in the treatment of stiff shoulders. Surg Clin North Am 1969;43: 1715-1720. 34. Fareed 0, Gallivan W. Office management of frozen shoulder syndrome. Treatment with hydraulic distension under local anaesthesia. Clin Orthop Rei Res 1989;242:1 77-183.
•
CHAPTER 1 7 - DISORDERS OF THE I N ERT STRUCTU RES 345
35. Melzer C, WaJIny T, Wirth CJ, Hoffmann S. Frozen shoulder treatment and results. Arch Orthop Traull1a Surg 1 995;114:87-9 1 . 36. Hollingworth GR, Ellis RM, Hattersley TS. Comparison of injection techniques for shoulder pain: results of a double blind randomised study. BM] 1983;287(6402):1339-134 1 . 37. Thomas D, Williams RA, Smith DS. The frozen shoulder: a review of manipulative treatment. Rheul11atol Rehabil 1980;19: 1 73-179. 38. de Jong BA, Dahmen R, Hogeweg JA, Marti RK. Intra-articular triamcinolone acetonide injection in patients with capsulitis of the shoulder: a comparative study of two dose regimens. Ciin RehabiI 1998;12(3):211-215. 39. Quinn CEo Frozen shoulder: evaluation of treatment with hydrocortisone injections and exercises. Ann Phys Med 1965;8:22-29. 40. Cyriax J, Troisier O. Hydrocortisone and soft tissue lesions. BM] 1953;2:966-968. 41 . Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis and Treatment of Soft Tissue Lesiolls, 8th edn, Bailliere Tindall, London, 1982:162. 42. Detrisac D, Johnson L. Arthroscopy Shoulder Anatomy: Pathology I7Ild Surgicnl lmplicntiolls. Slack, New Jersey, 1986. 43. Nottage W. Arthroscopic portals: anatomy at risk. Orthop Ciin North Ani 1993;24(1):19-26. 44. Hash:moto T, Suzuhl K, Nobuhara K. Dynamic analysis of intraarticular pressure in the glenohumeral joint. J Shoulder Elbow Surg 1995;4:209-218. 45. Ritzk TE, Gavant MI, Pinals RS et al. Treatment of adhesive capsulitis (frozen shoulder) with arthrograph.ic capsula r d is tension and rupture. Arch Phys Med RehabiI 1994;75:803-807. 46. Sharma RK, Bajekal RA, Bhan S. Frozen shoulder syndrome a comparison of hydraulic distension and manipulation. Int Orthop 1993;17:275-278. 47. van Royen BJ, Pavlov PW. Treahnent of frozen shou Ider by dis tension and manipulation under local anaesthesia. Int Orthop 1996;20(4):207-210. 48. Corbeil V, Dussault RG, Leduc BE, Fleury J. Adhesive capsuli tis of the shoulder: a comparative study of arthrography with intra-articular corticotherapy and with and without capsular distension. Can Assoc Radial ] 1992;43: 1 27-130. 49. Gam AN, Schydlowsky P, Rossel I, Remvig L, Jensen EM. Treatment of 'frozen shoulder' with distension and glucorti coid compared with glucorticoid alone. A randomised con trolled trial. Scnnd ] RheumatoI 1998;27(6):425-430. 50. Pearsall AW 4th, Osbahr De, Speer K. An arthroscopic tech nique for treating patients with frozen shoulder. Arthroscopy 1999;15(1):2-11 . 5 1 . Watson L, Dalziel R, Story 1 . Frozen shoulder: a 12-month clinical outcome trial. ] Shoulder Elbow Surg 2000;9(1):16-22. 52. Segmuller HE, Taylor DE, Hogan CS et al. Arhroscopic treatment of adhesive capsulitis. ] Shoulder Elbow Surg 1995;4:403-408. 53. Poulin de Courval L, Barsauskas A, Berenbaum B et al. Painful shoulder in the hemiplegic and unilateral neglect. Arch Phys Med RehabiI 1990;71(9):673-676. 54. Lysens R, De Weerdt W. De pijnljke schouder na een cerebro vasculair accident. Tijdschr Geneeskd 1992;48(21): 1545-1552. 55. Bruckner FE, Nye CJ. A prospective study of adhesive capsuli tis of the shoulder ('frozen shoulder' ) in a high risk popula tion. Q ] Med 1981;50(198):191-204. 56. Riley D, Lang AE, Blair RD et al. Frozen shoulder and other shoulder disturbances in Parkinson's disease. ] Neurol Neurosurg Psychiat 1989;53:63-66. 57. Bruckner FE, Nye CJ. A prospective study of adhesive capsuli tis of the shoulder ('frozen shoulder') in a high risk popula tion. Q ] Med 1981;50(198): 191-204.
58. Wright V, Haq AM. Periarthritis of the shoulder 1 . Aetiological considerations with particular reference to personality factors. Ann Rheum Dis 1976;35:213-219. 59. Neviaser JS. Adhesive capsulitis of the shoulder. ] Bone Joint Surg 1945;27:211-222. 60. Cyriax JH. Hydrocortisone in Orthopaedic Medicine. Cassell, London, 1956. 61. Rodeo SA, Hannafin J A, Tom J et al. Immunolocalisation of cytokines in adhesive capsulitis. Twelfth Open Meeting of the American Shoulder and Elbow Surgeons, 1995. 62. Muller LP, Rittmeister M, John J, Happ J, Kerschbaumer F. Frozen shoulder - an algoneurodystrophic process? Acta Orthop Belg 1 998;64(4):434-440. 63. Muller LP, Muller LA, Happ J, Kerschbaumer F. Frozen shoulder: a sympathetic dystrophy? Arch Orthop Trauma Surg 2000;129(1-2):84-87. 64. Hutchinson JW, Tierney GM, Parsons SL, Davis TR. Dupuytren's disease and frozen shoulder induced by treat ment with a matrix metalloproteinase inhibitor. ] Bone Joint Surg 1998;80B(5):907-908. 65. Zabraniecki L, Doub A, Mularczyk M et al. Frozen shoulder: a new delayed complication of protease inhibitor therapy? Rev Rhum Engl Ed 1998;65(1):72-74. 66. Steinbrocker 0, Argyros T. Frozen shoulder: treatment by local injections of depot corticosteroids. Arch Phys Med Rehabil 1974;55:209-213. 67. Hannafin JA, DiCarlo ED, Wickiewicz TL, Warren RF. Adhesive capsulitis: capsular fibroplasia of the glenohumeral joint. ] Shoulder Elbow Surg 1994;3(8):5. 68. Nobuhara K, Sugiyama D, Ikeda H, Makiura M. Contracture of the shoulder. Ciin Orthop Rel Res 1 990;254:105-110. 69. Bridgman JF. Periarthritis of the shoulder and diabetes melli tus. Ann Rheum Dis 1972;31:69. 70. Pal B, Anderson J, Dick We, Griffith !D. Limitation of joint mobility and shoulder capsulitis in insulin and non insulin dependent diabetes mellitus. Br J Rheumatol 1 986;25:147-15 1 . 71 . Bowman e, Jeffcoate W, Pattrick M , Doherty M. Bilateral adhesive capsulitis, oligoarthritis and proximal myopathy as presentation of hypothyroidism. Br ] RheumaoI 1988;27:62-64. 72. Reeves B. The natural history of the frozen shoulder syn drome. Scand ] RheumatoI 1975;4(4):193-196. 73. Shaffer B, Tibone JE, Kerlan RK. Frozen shoulder. A long-term follow-up. ] Bone Joint Surg 1 992;74A(5):738-746. 74. Binder AI, B ulgen DY, Hazleman BL, Roberts S. Frozen shoulder: a long-term prospective study. Ann Rheum Dis 1984;43(3):361-364. 75. Hannafin JA, Chiaia TA. Adhesive capsulitis. A treatment approach. Clin Orthop 2000;372:95-109. 76. Siegel LB, Cohen NJ, Gall EP. Adhesive capsulitis: a sticky issue. Am Fam Physician 1999;59(7): 1843-1852. 77. Van de Velde T. Steroidgevoelige artritis van de schou€ler. Resultaten van de behandeling met triamcinolone-acetonide. Cyriax-Il1fo 1990;4:15-23. 78. De Bidcourt J. Inleiding tot de reumatologie. Stafleu 's weten schappelijke uitgeverij, Leiden, 1967. 79. Muller LP, Muller LA, Happ J, Kerschbaumer F. Frozen shoulder: a sympathetic dystrophy? Arch Orthop Trauma Surg 2000;120(1-2):84-87. 80. Kessel L. Clinical Disorders of the Shoulder, 2nd edn. Churchill Livingstone, Edinburgh, 1986. 8 1 . Lehtinen JT, Kaarela K, Belt EA, Kautiainen HJ, Kauppi MJ, Lehto MU. Incidence of glenohumeral joint involvement in seropositive rheumatoid arthritis. A 15 year endpoint study. ] Rheumatol 2000;27(2):347-350.
346 SECTION THREE - T H E S H O U L D E R
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 30% 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 <40 years
Sakurai et al (1998)35
61.5 (partial) 11.5 (massive rotator cuff tears)
Average age
76.3 years
352 SECTION THREE - THE SHOULDER
Table 18.2 Incidence of rotator cuff tears in asymptomatic patients Authors Petterson
(1942)36
Milgrom et al
(1995)37
Incidence (%)
Remarks
20 (partial and full)
50% in subjects between 55 and
50 (tears after age 50)
Rotator cuff lesions are a normal correlate of
85
age; they often present without clinical symptoms Sher et al (1995)38
15 (full) 20 (partial)
Significant increase of tears with age; defects are compatible with normal, painless, functional activity
D IAG NO S I S AND TR EATM E NT
Given the high prevalence rate of asymptomatic macro scopic rotator cuff lesions it is unwise to rely solely on imaging techniques (sonography, CT, MRI) for a diag nosis. The examiner should beware the common belief that what is found on technical investigation is always relevant to the cause of the patient's pain.39 Diagnosis should first of all be functional; paraclinical and tech nical investigations have only a secondary function. During resisted movements, pain and weakness, sepa rately or in combination with each other, are sought. If pain only is found, this points to an uncomplicated ten dinitis or to a partial thickness lesion. A combination of pain and weakness brings a partial (full thickness) tendinous rupture to mind. Painless weakness is usually the outcome of a massive tear of a rotator cuff tendon or of a neurological problem. It is worth emphasizing once again that, when performing resisted movements at the shoulder, it is very important to use the correct tech nique, as has been explained earlier (see p. 298). If this is neglected, misdiagnosis can easily result.40 Treatment options are also determined only by the out come of the clinical examination and not by the exten siveness of the (anatomical) lesion. Asymptomatic cuff lesions for instance, in which the shoulder does not bother the patient but imaging studies document a partial or even a full thickness lesion in the cuff tendon, should not receive treatment. However, if the rotator cuff lesion is symptomatic, it will usually not heal of itself because rotator cuff tendinitis is not self-limiting.41 Initial treatment for a symptomatic cuff lesion should always be conservative, no matter what the result is of the imaging examinations. Non-operative treatment consists of either deep friction transversely to the affected tendon fibres or local infiltration with small amounts of triam cinolone at the tenoperiosteal junction of the affected tendon. In recurrent cases it is wise to add functional exer cises for strength and propriocepsis (see p. 342).42
The use of steroids for rotator cuff disease remains the subject of debate because there exists much controversy regarding both effectiveness and safety. Repeated injec tions with steroids are believed to produce tendon atrophy or to reduce the ability of damaged tendon to repair itself. Such changes have been documented in other tendons (Achilles and patellar) and are extrapo lated to the shoulder. Other studies, however, failed to find a deleterious long-term effect of corticosteroid injec tions in animal tendons.43,44 Although rotator cuff dis orders are generally believed to benefit from steroid injections, evidence for the efficacy of the injections is difficult to demonstrate. The methods of assessment used in most studies are poor because they use very heteroge nous populations.45 In several studies that used a better anatomical classification, treatment with local triam cinolone infiltrations was shown to be superior to placeb046--48 and to methylprednisolone49 in reducing pain, improving active abduction and reducing func tional limitation. The success rate of the infiltrations is further increased if precise diagnostic and infiltration techniques are used.50 In a randomly allocated double blind study, Hollingworth et al compared two different methods of corticosteroid injection. The method of anatomical injection after diagnosis by the technique of selective tissue tension gave 60% success compared with the method using tender or trigger point localization, which gave only 20% success.51 We strongly believe in the beneficial effect of small dose (10 mg) and targeted infiltrations of triamcinolone in the treatment of rotator cuff disorder. Potential hazards are minimal if a few necessary precautions are taken: • • •
the infiltration is always on the tenoperiosteal junction, never in the body of the tendon the arm should be rested for 2 weeks following the infiltration no more than three consecutive infiltrations should be given.
The operative treatment of rotator cuff lesions without rupture is acromioplasty: a wedge-shaped piece of bone is resected from the anterior surface of the acromion, along with the entire attachment of the coracoacromial ligament. The operative treatment of rotator cuff tear is cuff repair. Calcifying tendinitis
Calcium deposits may form in the tendons of the rotator cuff. The aetiology is still a matter of speculation but it is generally accepted that degeneration precedes calci fication. The incidence of calcification ranges from 3 to 20%52 and in most instances the lesion is completely asymptomatic.53 Calcifying has a spontaneous evolution
CHAPTER 18
- DISORDERS OF
THE CONTRACTILE STRUCTURES 353
in that the highest incidence occurs in those aged between 31 and 50,54,55 and calcification is not found in elderly patients. If the lesion causes symptoms, they are treated in the same way as uncomplicated tendinitis of the rotator cuff. The treatment of choice is infiltration with triamcinolone, because deep transverse frictions are contraindicated in calcifying tendinitis. If the pain reap pears after initially successful treatment, the calcium deposits can be dissolved with weekly infiltrations of procaine 0.5%. Surgical intervention is seldom necessary but if it is indicated most calcifications can easily be removed by arthroscopic procedures.
RESISTED ABDUCTION
PAI N
Pain on resisted abduction is the consequence of a lesion of either the deltoid or the supraspinatus muscle. Deltoid muscle
The deltoid is very seldom at fault, although a lesion can sometimes occur as a result of a direct injury. The lesion usually lies in the muscle belly. Disorders of the deltoid cannot provoke a painful arc, because no part of it can he trapped between two osseous structures. Therefore the presence of a painful arc excludes a deltoid lesion. If any doubt exists, two accessory tests are used: •
•
Figure 1 8.4
Resisted horizontal adduction.
Figure 1 8.5
Resisted horizontal extension.
Resisted horizontal adduction (Fig. 18.4): the examiner stands at the painful side and stabilizes this shoulder with one hand. With the other hand he grasps the patient's arm just above the elbow and brings it into horizontal abduction. The patient is now asked to push the arm forwards against the examiner's hand. This tests the anterior portion of the deltoid . Resisted horizontal extension (Fig. 18.5): this is the very opposite of the previous test. The patient is asked to push backwards, the examiner applying counterpres sure in an anterior direction. The posterior fibres of the deltoid are tested in this movement.
Treatment. A lesion in the muscle belly of the deltoid responds equally well to deep transverse friction or to infiltration with 20-30 ml of procaine 0.5% once a week, for about 3 weeks. Friction is given on alternate days until full cure. Supraspinatus
Clinical experience shows that the for pain on resisted abduction supraspinatus muscle, which is by tendinous lesion at the shoulder.
most frequent reason is tendinitis of the far the most common The tendon may be
354 SECTION THREE - THE SHOULDER
affected at four different sites; these each give rise to a slightly different clinical picture but they are all charac terized by a common major finding, which is pain on resisted abduction. Most of the lesions occur at the tenoperiosteal insertion into the greater tuberosity. Inflammation and partial tears may develop within the substance of the tendon on the acromial surface (bursal side) or the deep surface (articu lar side of the tendon).56 If situated on the deep part, pain on full passive elevation is also present. This is believed to be caused by the abutment of the deep surface of cuff insertion against the glenoid rim at the extremes of motion (see Fig. 18.6).57 If situated on the bursal part of the tendon, a painful arc is found. Cyriax regarded this as the most common cause of a painful arc on shoulder ele vation.58 A third possibility is a lesion that involves both superficial and deep aspects tenioperiosteally. In this case, pain on full passive elevation is present, together with a painful arc (Fig. 18.7). The lesion sometimes lies at the musculotendinous junction, just beneath the acromion. In this case, the only sign is pain on resisted abduction. Because this type of lesion is rare, its presence should always be confirmed by a diagnostic infiltration with local anaesthetic. Figure 18.8 summarizes the differential diagnosis of painful resisted abduction. Treatment of tenoperiosteal lesions. The lesions situated at the tenoperiosteal insertion can be treated either by deep friction or by infiltration with steroid. Friction takes longer but has a more definite effect; steroids work quicker but there may be a tendency for recurrence. Localization by palpation. The main problem in treat ment is finding the structure involved. Although the tendon lies rather superficially, many have difficulty in the localization. It cannot be easily localized with the arm in neutral position at the side. Although the greater tuberosity points laterally in this position, part of the
2
." .
Supraspinatus
On full passive elevation the undersurface of the supraspinatus tendon may become squeezed against the upper labral rim.
Figure 1 8.6
insertion can be covered by the outer rim of the acromion. Moreover, all structures here feel the same on palpation. Therefore, it is better to bring the upper arm into full medial rotation by asking the patient to put the lower arm behind the back, the elbow bent to 900 (Fig. 18.9). In this position the tenoperiosteal insertion lies anterior to the acromion.59,6o The fibres at the insertion are now situ ated in a sagittal plane because the tendon curves around the basis of the coracoid process as a result of the medial rotation. First, bony landmarks are defined. Starting at the pos terior acromial angle, the lateral rim of the acromion is
3
Accessory signs indicate the exact localization of the supraspinatus lesion: 1, pain at the end of passive elevation; 2, painful arc; 3, painful arc and pain on full passive elevation; 4, no localizing sign.
Figure 18.7
CHAPTER 18
-
DISORDERS OF THE CONTRACTILE STRUCTURES 355
Resisted horizontal adduction painful Resisted horizontal extension painful
Resisted abduction painful
Figure 1 B.B
Painful arc
Tenoperiosteal: superficial aspect
Passive elevation painful
Tenoperiosteal: deep aspect
Painful arc and passive elevation painful
Tenoperiosteal: both superior and deep aspects
No localizing signs
Musculotendinous junction
Differential diagnosis of painful resisted abduction.
localized. The finger then moves over to the anterior acro mial border, until the acromioclavicular joint is met. The supraspinatus insertion lies lateral to this joint line, just anteriorly to the acromion. Next, the infraclavicular fossa is palpated. This is best started medially, at the level of the coracoid process. The finger is moved laterally, retaining close contact with the anterior border of the clavicle and acromion. Initially, the finger digs smoothly into the deltoid muscle, and remains so until the tenoperiosteal insertion of the supraspinatus is reached. Then a much tougher resist ance is felt under the finger, which does not sink in deeply. The supraspinatus insertion has a width of about 1.0-1.5 cm. It is important to accurately define the medial edge of this insertion, since it permits the localization of the rest of it. The lateral edge is more difficult to palpate because the fibres merge with the anterior of the infra spinatus tendon.
Figure 1B.9
supraspinatus.
Position for localization of a tenoperiosteal lesion of the
Technique: infiltration of the supraspinatus. A tuber culin syringe, filled with 1 ml of triamcinolone, is fitted to a 2.5 cm needle. The patient sits in the same pOSition as for palpation, the arm behind the back. After having pre cisely located the insertion, the needle is thrust in verti cally downwards at its centre (Fig. 18.10). The needle glides in smoothly initially, until it encounters the tenoperiosteal junction, at which point the typical tendi nous resistance is felt. When the needle is thrust in a little further it is arrested against the bone. Then 1 ml of tri amcinolone is infiltrated at five to ten different places over an area of 1 cm2, in close bony contact. During the whole infiltration, a typical counterpressure is felt. After-pain is seldom severe and wears off sponta neously. The arm should be rested for about 2 weeks, and
356 SECTION THREE - THE SHOULDER
recurs a few months later. The patient should then be sent for a standard radiography of the shoulder. If some intratendinous calcification is confirmed, four to five weekly infiltrations with 5 ml of procaine 2% are admin istered. In most cases this is sufficient to dissolve the calcium deposits and to alleviate the pain. If no calcification is visible, the patient must be referred to the therapist for deep transverse friction because it is unwise to infiltrate the tendon repeatedly, even with small doses such as 10 mg of triamcinolone. In cases of recurrent tendinitis it is also good practice to look for an underly ing cause. This may be a small multidirectional or supe rior instability or an anatomical divergence in the acromial roof that causes recurrent impingement. The diagnosis and the treatment of the former have been dis cussed earlier (see p. 337). The diagnosis of the latter is through a lateral X-ray that visualizes the so-called 'supraspinatus outlet' - the space between the cora coacromial roof and head of the humerus (Fig. 18.11). If there is an anatomical divergence in the supraspinatus outlet, and the tendinitis tends to recur despite proper treatment, surgical decompression (deletion of anterior and inferior parts of the roof) is highly recommended.6l Treatment of supraspinatus tendinitis is summarized in Figure 18.12. Technique: deep friction to the supraspinatus. Patients who elect the longer but more certain way are best treated by friction. The same goes for athletes and in recurrence after previous infiltrations with steroids. Friction works better on the superficial part rather than on deeper lesions. The patient adopts the same position as for infiltra tion: seated with the back against the couch, the arm behind the back. The therapist stands laterally on the patient's painful side. The index finger of the ipsilateral hand, reinforced by the middle finger, is placed at the medial edge of the insertion. The hand is meanwhile
Figure 1 B.1 0
Infiltration of a tenoperiosteal lesion of the supraspinatus. .'
reassessment follows after 2 weeks. If the clinical exami nation is still positive, a second infiltration is given. One to three infiltrations are usually curative. Treatment that leads to good but temporary results is a common experience in supraspinatus tendinitis. After one or two infiltrations the pain has disappeared but
A
Figure 1B.1 1
B
Supraspinatus outlet: A: normal acromion B: hooked acromion.
CHAPTER 18 - DISORDERS OF THE CONTRACTILE STRUCTURES 35 7
Treatment of m usculotendi nous lesions. The only effec tive treatment is deep transverse friction, but before this is undertaken the diagnosis must always be confirmed by an infiltration of local anaesthetic. Technique: deep friction to musculotendinous lesions.
Calcium deposits?
'--
�
Weekly procaine infiltrations
Minor instability?
I-
�
Stability training
Anatomical changes in supraspinatus outlet? Figure 1 8.12
I""
__
__
Surgery �--� '-------'
Treatment of supraspinatus tendinitis.
stabilized by the thumb placed against the lateral aspect of the upper arm, almost vertically under the index (Fig. 18.13). W hen the index finger is pulled outwards over the tendon pressure is applied. This is the active phase of the friction. The pressure is directed caudally, not towards the clavicle - easily obtained if the stabiliz ing thumb is put rather low on the upper arm, the nail of the finger that applies friction thus pointing upwards. Friction is given three times a week for about 20 minutes each time. Normally, 10 sessions suffice. The patient should rest the arm during the whole course of treatment. Improvement is to be expected after about five sessions.
The patient sits on a chair with the arm abducted side ways to the horizontal, the elbow and forearm resting on a couch. In this position the musculotendinous junc tion lies in the supraspinous fossa at the angle between the scapular spine and the acromion, just posterior to the clavicle. The therapist stands at the pain-free side facing the shoulder. The ipsilateral middle finger reinforced by the index finger is placed deeply into the scapuloacromial angle, holding the slightly bent finger parallel to the muscle (Fig. 18. 14). Friction is given by pronation-supination movements of the lower arm, the active moment being in supination. Friction is applied for about 15 minutes. Cure is expected after about 10 sessions. PAI N F U L WEAKN ESS
If resisted abduction is found to be both weak and painful, a partial rupture of the supraspinahls tendon is most ikely.62 It is usually affects middle-aged and elderly . people (see p. 351 ). Ruptures of the rotator cuff occur most frequently at the supraspinatus tendon. A full-thickness defect usually starts at the critical zone (articular side of the anterior part near to the bicipital grove) and may propagate either in the direction of the iniraspinatus or towards the sub scapularis tendons.63,64
Figure 1 8.13: Treatment of tenoperiosteal lesion of the supraspinatus: deep
friction.
358 SECTION THREE - THE SHOULDER
The pain felt in a partial rupture of the supraspinatus is the same as in uncomplicated tendinitis. The patient usually does not mention any weakness, this is found only during clinical examination on resisted abduction, which is also painful. To rule out weakness caused merely by pain, resisted abduction is tested again after infiltration of local anaesthetic. The only differential diag nosis is metastatic infiltration of the acromion - a very rare disorder. Here the pain is localized. On clinical exam ination a painful arc is found together with pain and gross weakness on resisted abduction. Imaging tech niques confirm the diagnosis.
movement.67 However, studies in which the supra scapular nerve and the axillary nerve were blocked have shown that both the supraspinatus and the deltoid muscles are capable of initiating elevation of the arm, in both sagittal and coronal planes.68-7o This is not
Treatment
Conservative treatment is reasonable for most partial ruptures of the supraspinatus tendon.65 Treatment is relief of pain, achieved by an infiltration of 1 ml of triam cinolone at the tenoperiosteal insertion and into the most distal part of the tendon. The same position and tech nique are used as for an uncomplicated tendinitis. An infiltration of a partially ruptured tendon is not without danger. Disappearance of inflammation and pain usually removes the natural reserve towards move ment and load . A weakened tendon in combination with increased load must inevitably lead to further ruptures and disaster. Before any decision to infiltrate is made, the patient must be warned against the dangers. Furthermore, if complete rest cannot be fully guaran teed, the therapist must give up infiltrations and must refer the patient for deep transverse frictions. If the treatment leads to good but only temporary results, the same measures should be taken as in uncomplicated but recurrent supraspinatus tendinitis.
(a)
PAI N LESS WEAK N E S S
A painless inability to actively abduct the shoulder can be caused by either a complete rupture of the supraspinatus tendon or a neurological lesion. Total rupture of the supraspinatus tendon
The supraspinatus muscle initiates active elevation of the arm and is active during the entire arc of abduction. It is responsible for about 50% of the torque and it can abduct the joint without action of the deltoid.66 Therefore a total rupture of the supraspinatus tendon presents as painless weakness on resisted abduction. In massive tears of the supraspinatus the patient is unable to actively abduct the arm. This is not only caused by loss of muscular power but also by loss of the passive stabilizing effect of the tendon. Previously it was believed that the arm could not be abducted actively by the deltoid muscle alone if some contraction of the supraspinatus did not initiate the
(b) Figure 18.14 (a) Deep friction to a musculotendinous lesion of the supraspinatus. (b) Anatomy: 1, supraspinatus muscle; 2, acromioclavicular joint; 3, clavicle (transparent); 4, coracoacromial ligament.
CHAPTER 18
in accord with what is found clinically. W hen the supraspinatus tendon is massively ruptured, the patient is unable to initiate active scapulohumeral abduction. Starting from a position of 0° (the arm hanging by the side) the deltoid muscle only pulls the humerus upwards. Elevation is then only produced by rotation of the scapula in relation to the thorax and not by any movement between scapula and humerus. This is explained by the superior displacement of the humerus that occurs during active contraction of the deltoid in the absence of an intact supraspinatus tendon.71 In a normal situation the rotator cuff muscles form a supple mentary musculotendinous glenoid which, in conjunc tion with the osseous glenoid, holds the humeral head stable. Experimental sections of the supraspinatus tendon also show the humeral head to move in a cranial direction until the superior humeral load is applied directly to the acromion (see Fig. 18.15). 72 This phenom enon has been referred to as 'the spacer effect'73 and is one of the most significant plain radiographic signs of massive cuff deficiency.74 Symptoms and signs. The lesion usually affects middle aged and elderly people. In patients under 40 years of age a rupture is usually acute and results from an indi rect trauma, such as a fall on the outstretched hand?5,76 In most cases the rupture is due to a chronic failure of the tendon: repeated failure of small groups of fibres leads to progressive weakness of the supraspinatus making it increasingly susceptible to damage from lesser loads.77,78 The observation that major cuff defects
-
DISORDERS OF THE CONTRACTILE STRUCTURES 359
may occur without recognized injury has led to the concept of ' creeping tendon failure'?9 An acute trauma is usually accompanied by a sharp pain and followed by complete inability to raise the arm actively. The pain remains severe for the first few days and diminishes progressively, later becoming bearable without drugs but still sufficient to interfere with normal activities. On clinical examination active elevation is limited to about 30° which is completely on account of scapular rotation: no active humeroscapular movement is noted. A very pronounced painful arc is present when the eleva tion is performed passively. On muscular testing there is a complete but painless weakness of resisted abduction. After a few weeks the supraspinatus becomes atrophiC; the deltoid maintains its normal size and strength. Although the patient cannot actively elevate the arm from 0°, active elevation becomes possible if the arm is passively moved through the first 30°. Frequently, because the patient is unable to move the arm actively, an immobilizational arthritis will set in after a few months and a capsular pattern emerges (see p. 312). Treatment. Because most total ruptures occur insidi ously in the elderly, surgical correction to restore normal function will not be the first option.8o Some defects cannot be repaired simply because they only offer 'rotten cloth to sew' (McLaughlin).81 Many defects do not need to be repaired because they exist without causing much in the way of clinical symptoms.82 However, surgery should always be considered in a younger patient with a
(a) (a) The glenoid: 1, tendinous; 2, osseous. (b) Spacer effect: massive rupture of the supraspinatus leads to a cranial subluxation of the humeral head during deltoid contraction.
Figure 18.15
360 SECTION THREE - THE SHOULDER
significant acute tear in a previously normal shoulder83,84 and in the patient with a chronic tear associated with significant symptoms and not responding to conservative treatment. Reported results are fair but it should always be kept in mind that repair does not restore the quality of the tendinous tissue and the supraspinatus will remain vulnerable to large or sudden loads.85 Long-term results of repair are better in younger patients with acute tears.86 For most supraspinatus ruptures the treatment of choice is conservative. The first aim is to get rid of the pain. To that purpose an infiltration with 10 mg of tri amcinolone should be given at the remnants of the insertion into the humeral tuberosity to abolish the painful arc, following the same procedure as for uncom plicated supraspinatus tendinitis. The therapist should try to reach the inflamed tissue because infiltrating the gap is useless. Therefore the typical counterpressure on syringe and needle should be felt during the entire procedure. Once the painful arc has gone, the patient should be encouraged to use the arm normally. To lift the arm up he should initiate the elevation by a swing ing movement of the trunk so that the arm is thrown lat erally until it reaches the point where the deltoid muscle becomes effective. It is also wise to prescribe functional exercises for the antagonists of the deltoid and the remaining rotator cuff muscles. In spite of the slight dis ability, the function of the joint is usually good and the patient should be capable of doing a light job.87-89 W hen an immobilizational arthritis has set in it should be treated as such (see p. 313). Neurological lesions
Several neurological disorders may provoke painless weakness on resisted abduction. Axi llary nerve palsy, This may follow a subluxation of the humeral head. The axillary nerve innervates the deltoid muscle. Differential diagnosis is based on testing the strength of both the deltoid and infraspinatus muscles. Isolated painless weakness of abduction is found. A painful arc is not present which differentiates this disorder from a supraspinatus rupture. Active eleva tion is difficult but possible (see p. 556). Suprascapular nerve palsy. This is most often the result of idiopathic neuritis, seldom of an injury. The supra scapular nerve innervates both supra- and infraspinatus muscles. Weakness of abduction and lateral rotation is present. This disorder can be differentiated from a com bined supra- and infraspinatus rupture by the absence of a painful arc (see p. 554). Fifth cervical root palsy. The C5 root innervates both spinatus muscles, the deltoid and the biceps brachii. Weakness on abduction and lateral rotation of the arm
and on flexion of the elbow is present (see p. 188). (See Fig. 18.16 for a summary of resisted abduction.)
RES ISTED ADDUCTION
PAI N
A painful but strong resisted adduction movement of the arm may be caused by a lesion of one of the adductor muscles, a sprain of the acromioclavicular joint or a tendinitis of the long head of the biceps. It may happen that isometric movements indirectly provoke pain in structures other than the ones that are supposed to be tested. Cyriax called this phenomenon 'transmitted stress'. During strong resisted adduction with the arm hanging along the body, the strong actions of latissimus dorsi and pectoralis major pull indirectly on the acromioclavicular joint. Resisted adduction may therefore also provoke local shoulder pain in a chronic strain of the acromioclavicular joint. The pain will then be localized within the C4 dermatome and other passive tests will point in the direction of the acromioclavicular joint (see p. 327). Pain on resisted adduction of the arm may rarely be caused by a tendinitis of the long head of the biceps at the glenoid origin. Cyriax arrived at this conclusion after finding that resisted adduction proved to be painful with the elbow in extension but not if it was kept in flexion. As a consequence, the structure at fault must overlie both shoulder and elbow (see p. 371). The pain is mainly felt under the acromioclavicular joint. More often, however, a positive test will point in the direction of a lesion of one of the adductors: pectoralis major, latissimus dorsi, teres major and teres minor. An important element in distinguishing between them is the localization of the pain. Pain in the thorax anteriorly sug gests the pectoralis major and posterolaterally the other three muscles. Axillary pain may be the result of a problem in the pectoralis major, teres major or latissimus dorsi. The four adductors can be more accurately differenti ated by additional tests. Because the pectoralis major, latissimus dorsi and teres major are medial rotators and the teres minor a lateral rotator, resisted medial and lateral rotation of the arm is the next test to perform in order to arrive at an exact diagnosis. The pectoralis major muscle can be tested on its own by resisted horizontal adduction with the arm forwards (Fig. 18.17a). The examiner stands on the painful side One hand is placed on the patient's shoulder. With the other hand the patient's arm is grasped just above the elbow and brought anteriorly to the horizontal. The patient is now asked to exert further medial force against the examiner's hand. The same can be achieved, but with
CHAPTER 18
-
DISORDERS OF THE CONTRACTILE STRUCTURES 361
5th cervical root
Bursal side _ painful arc Articular side _ pain at end elevation In the tendon - painful arc + pain at end elevation Musculotendinous Figure 1 8.1 6
no localizing signs
Resisted abduction positive.
loss of assessment of muscle strength, when the patient pushes both hands against each other holding both arms horizontally in front of the body. Further differentiation is done by a resisted extension movement (Fig. 18.17b) which involves the latissimus dorsi, teres major and teres minor muscles. The patient tries to move the arm backwards with the arm hanging down and the examiner applying anteriorly directed counterpressure. The only further differentiation required is between a lesion of the latissimus dorsi and the teres major. Because the latissimus dorsi also causes side flexion of the trunk and depression of the scapula, while the teres major does not, testing resisted side flexion towards the painful side and resisted scapular depression may be helpful. Because lesions of the teres minor and teres major are extremely rare, these structures are not discussed in detail. Pectoralis major
Lesions of the pectoralis major may be the result of overuse or of direct injury. The lesion usually lies in the muscle belly, either in its lateral lower portion or in the fibres just below the outer portion of the clavicle (Cyriax:58 p. 145). In rare instances, the pain is felt at the shoulder and radiates down the inner aspect of the arm. The problem must then be sought at the insertion at the crest of the greater tubercle. It should be noted that in severe lesions of the pec toralis major, full passive elevation of the arm and resis ted adduction and medial rotation are positive. In minor lesions, resisted medial rotation is sometimes negative.
The functional tests are followed by palpation, best performed with the patient's arm slightly abducted and the hand resting on the iliac crest. Differential diagnosis is with a rib fracture. In fracture in the anterior thorax, the same tests as in pectoralis major strain are painful. Additionally, all movements of the thoracic spine influencing the site of fracture are painful as well, as is deep inspiration. Treatment. Infiltration of the muscle belly with pro caine usually has a good therapeutic effect. Two or three infiltrations suffice. If not, or if the lesion lies at the insertion, infiltration can be replaced by deep transverse friction. Technique: infiltration of the pectoralis major. The patient adopts the half-lying position and puts the hand on the affected side on the iliac crest. A 4 cm needle is fitted to a syringe filled with 10-20 ml of procaine 0.5%. After accurate palpation, the lesion is held between thumb and index finger and the needle is introduced between them obliquely and to its full length. The finger and thumb are kept in this position during the infiltra tion, to feel whether the product is deposited at exactly the right place (Fig. 18.18). The injection is given while withdrawing the needle. The syringe is emptied gradu ally, over about five withdrawals and reinsertions. Technique: deep transverse friction to the pectoralis
Palpation will demonstrate whether the lesion lies in the belly or the insertion of the muscle and so deter mine the friction method. major.
362 SECTION THREE - THE SHOULDER
(a) Figure 18.17
•
•
(b) Resisted horizontal adduction with the arm forward (a) and resisted extension (b),
To the muscle belly: massage is best given with the patient in the half-lying position and the hand resting on the iliac crest, so that the upper arm is somewhat abducted. This brings the pectoralis major more into prominence. The therapist sits facing the patient at the painful side. With the ipsilateral hand, the painful spot is taken between fingers and thumb and pulled later ally while pressure is applied (Fig. 18.19). This is the active moment of the friction. Massage is given for 20 minutes. Cure is normally obtained after 1 0 sessions. To the insertion: if palpation shows the lesion to lie at the insertion, deep friction is the only treatment. First the bicipital groove is localized, which is best done by putting the finger proximally between the minor and major humeral tubercles and in the long axis of the arm. By rotating the arm alternately medially and lat erally the groove can be identified. The therapist sits facing the patient at the painful side and places the contralateral thumb between the fibres of the deltoid muscle at the outer aspect of the bicipital groove. Counterpressure is applied over the dorsal aspect of the arm by the other fingers. Friction is given by pronation-supination movements.
L atissimus dorsi
Lesions of the latissimus dorsi are sometimes met with in gymnasts and water-skiers but are rare. They are usually found laterally at the uppermost part of the muscle belly. On clinical examination, full passive elevation of the arm and resisted adduction and medial rotation are painful. Treatment. The responses to infiltrations with procaine and deep friction are equally good. The infiltration tech nique is the same as for the pectoralis Technique: deep transverse friction to the latissimus
The patient lies prone, the hand on the iliac crest. The therapist faces the patient's painful side. The tender area is taken between thumb and fingers of the ipsilateral hand, and friction is performed by pulling the hand laterally (Fig. 18.20).
dorsi.
PAI N F U L WEAKN ESS
Ruptures of the pectoralis major follow extreme muscle tension or direct trauma or a combination of both. They have been reported in gymnastics or after a fall.90,91 The
CHAPTER 18 - DISORDERS OF THE CONTRACTILE STRUCTURES 36 3
Figure 18.18
Infiltration of the pectoralis major belly.
lesion is more common in weightlifting and is caused in particular by a bench press.92 The rupture usually occurs at the lateral fibres when the bar is at its lowest (loading of the fibres that are maximally stretched).93 In an acute injury there is sharp and burning pain, sometimes accompanied by significant swelling and ecchymosis. Passive elevation of the arm is very painful and somewhat limited. Resisted adduction and medial rotation of the arm are painful94 and weak. The functional tests are followed by palpation for ten derness and for a gap, best performed with the patient's arm slightly abducted and the hand resting on the iliac crest (see Fig. 18.19). Treatment consists of an infiltration with local anaes thetic followed by deep friction. In athletes, surgical repair may be necessary. PAI N LESS WEAKNESS
A severe C7 root palsy can provoke a painless weakness of adduction (see p. 1 89). Resisted extension of the elbow is also remarkably weak. The triceps reflex is sluggish or absent, together with some weakness on flexion of the wrist, more rarely on extension or on both. Numbness of the second and third fingers is usually present. (See Fig. 18.21 for a summary of resisted adduction.)
Figure 18.19
Deep transverse friction to the pectoralis major belly.
RESISTED LATER A L ROTATION
The main lateral rotators of the shoulder are the infra spinatus and teres minor. The former is by far the stronger of the two. The teres minor also adducts, so that resisted adduction offers the key to differential diagnosis. PAI N
If both resisted lateral rotation and resisted adduction are painful, the teres minor is at fault, although this is extremely uncommon. In contrast, when resisted lateral rotation is painful but other resisted movements are normal, the lesion lies in the infraspinatus. Infraspinatus
There are some localizing signs of lesions of the infra spinatus. A painful arc indicates that the lesion lies at the
364 SECTION THREE - THE SHOULDER
the supraspinatus also apply here. The superficial part responds better to friction than does the deep aspect. It takes longer to achieve a cure by friction than by steroid infiltration but recurrence is less frequent. The body of the tendon is only treatable by deep friction. The patient lies prone resting on the elbows, the shoulders vertically above them. The elbows are flexed to 90°. The upper arm of the affected side is brought into slight lateral rotation by asking the patient to hold the edge of the couch. In this position the whole infraspinatus structure is within the reach of the finger. In order to tighten the tendon and to bring it further later ally from underneath the acromion, the patient moves the shoulder slightly over towards the painful side. First the spine of the scapula is palpated, then the posterior angle of the acromion and the lateral acromial edge. In the infraspinal fossa, the muscle belly of the infraspinatus is located and, when the fingers are moved further towards the greater tuberosity, the musculotendi nous junction, the tendon and finally the tenoperiosteal insertion are located. The latter is about 2 cm wide and lies partly lateral to the outer rim of the acromion and partly lateral behind the acromial angle.
Palpation.
Figure 1 8.20
Deep transverse friction to the latissimus dorsi.
superficial part of the tenoperiosteal insertion. If full passive elevation causes pain, the deep part of the tenoperiosteal insertion is affected (Fig. 1 8.22). If, apart from resisted lateral rotation, no other tests are painful, the lesion is in the body of the tendon. Since these lesions may be located more cranially or more distally at the tenoperiosteal junction or in the tendon, the functional examination should be followed by palpation to define the exact site. Treatment. A lesion at the tenoperiosteal insertion of the infraspinatus can be treated either by deep friction or by infiltration with steroid. The general remarks made for
Figure 1 8.21
Resisted adduction positive.
Technique: infiltration of the infraspinatus tenoperi
A 1 ml syringe is filled with 10 mg of triamci nolone and fitted to a 3 cm long needle. After having located the landmarks, the needle is introduced in an ante rocaudal direction aiming at the tenoperiosteal insertion, which is reached after passing through soft tissue for about 2 cm (Fig. 18.23). Just before arriving at the bone the tough tendinous resistance of the insertion is felt. The total amount is now injected in five to ten slightly different sites. At each partial injection, strong counterpressure is felt. osteally.
CHAPTER 18
-
DISORDERS OF THE CONTRACTILE STRUCTURES 365
3
Figure 1 8.22 Lesions of the infraspinatus; 1, superficial aspect tenoperiosteal insertion; 2, deep aspect tenoperiosteal insertion; 3, body of tendon.
The patient should rest the arm for about 2 weeks and is then re-examined. If pain remains, a second infiltration is given. Two infiltrations normally suffice. Technique: deep friction to the infraspinatus. Deep fric tion is indicated in athletes, if infiltration has been unsuc cessful or when the body of the tendon is affected. The patient lies in the same position as for the infiltra tion. The therapist stands at the painful side. The thumb of the ipsilateral hand is placed on the lesion, while counter pressure is applied with the other fingers at the front of the shoulder (Fig. 18.24). The body of the tendon feels like a cord, whereas the tenoperiosteal insertion feels more like a flat resistance just covering the underlying bone. Friction is undertaken in a caudocranial direction by pronation-supination movements of the arm. The active moment is on supination. To avoid blisters, a piece of cotton wool between thumb and skin can be used: indeed, it may be necessary because in this position the skin is stretched, which allows the finger to glide over it too easily. Firm skin contact must be maintained. Friction is given for 20 minutes, three times a week and is usually curative after 10-15 sessions. It may be difficult for the patient to hold this position for 20 minutes, so a break in treatment, sitting up for a few minutes, should be allowed.
A specific case: abduction and lateral rotation against resistance are both painful
Both resisted abduction and lateral rotation are fre quently painful on clinical examination and often there is a painful arc. This clinical pattern usually causes differ-
Figure 1 8.23
Infiltration of the infraspinatus.
ential diagnostic difficulties that are not always easy to solve (see Fig. 1 8.25). No painful arc. If a painful arc is not present and both resisted abduction and lateral rotation are equally painful, the question is whether a supraspinatus or an
366 SECTION THREE - THE SHOULDER
test correctly, a sheet of paper should be placed between the elbow and the body during the test. If both tests are still painful when correctly per formed, they should be repeated in a supine position, which fully relaxes all the shoulder structures not intended to be tested. If one test becomes painless, the other one remaining painful, full value is given to the latter. For example, if resisted lateral rotation remains painful and resisted abduction becomes negative, the infraspinatus is at fault. If on testing in the supine posi tion both tests remain painful, it is more likely the supraspinatus is at fault, because this structure is more frequently affected. To obtain diagnostic certainty an infiltration with local anaesthetic is necessary and is the only way to determine whether the supraspinatus, infraspinatus or both together are affected. Painful arc. If a painful arc is also found, then the fol lowing lesions may be present: • • • ----�
•
Chronic subdeltoid bursitis Supraspinatus tendonitis Infraspinatus tendonitis Tendinitis of both supraspinatus and infraspinatus.
If a painful arc is present, the tests should be repeated standing and lying. Presence of these signs makes it more likely that chronic bursitis is present:
Signs in favour of chronic bursitis.
• •
Very pronounced painful arc All passive movements painful at full range
I
Both resisted abduction and lateral rotation painful
I
..
I
Deep friction to the infraspinatus.
infraspinatus tendinitis is present or whether both struc tures are inflamed. The test of resisted lateral rotation is first repeated, asking the patient to pay special attention to holding the elbow against the body when pushing the forearm sideways. Abducting the arm at the same time as resisted lateral rotation is performed could render the latter falsely painful when supraspinatus tendinitis is present. If the patient has difficulty in performing the
I
•
I
I
1
I
I
Test correctly performed? Retest in supine position
Only one painful: Which one?
Painful arc
Chronic subdeltoid bursitis Supraspinatus tendinitis Infraspinatus tendinitis Supra- and infraspinatus tendinitis
Supraspinatus tendinitis Infraspinatus tendinitis Supra- and infraspinatus tendinitis Figure 1 8.24
..
I
I No painful arc I 1
I
I
I
J
: Both still painful? Signs in favour of bursitis? Diagnostic local anaesthetic
I
Figure 1 8.25 Differentiation between subdeltoid bursitis and infra- and supraspinatus tendinitis.
CHAPTER 18 - DISORDERS OF THE CONTRACTILE STRUCTURES 36 7
• •
• •
Tests are less painful in a supine position Resisted movements become less painful with axial traction, which prevents the humeral head approach ing the coracoacromial roof Tenderness of the superficial part of the subdeltoid bursa on palpation Infiltration of the deep part of the bursa with local anaesthetic abolishes the pain.
Signs in favour of supraspinatus and infraspinatus lesions. Presence of these signs makes it more likely that tendinitis is the problem: • • • • •
Less pronounced painful arc Testing standing and lying are similarly painful Testing resisted abduction under axial traction is equally painiul In infraspinatus involvement: painiul area in the tendon or tenoperiosteally Infiltration of the suspected tendon with a local anaesthetic diminishes the pain.
PAI N F U L WEAKN ESS
Painiul weakness on resisted lateral rotation is caused by a partial rupture of the infraspinatus tendon. The treat ment is the same as for uncomplicated tendonitis at the insertion. The same remarks as for the treatment of a partial rupture of the supraspinatus also apply here: infiltrations are not given in athletes but rather only if the patient can guarantee complete rest. PAI N LESS WEAKNESS
If resisted lateral rotation is painlessly weak, differential diagnosis between the following lesions must be made. Muscular disorder: total rupture of the infraspinatus tendon
This usually happens in patients over 50 years old who have suffered from overstrain or trauma, very often a fall. Iniraspinatus tears may present in isolation or in com bination with a partial or total rupture of the supraspina tus tendon. The infraspinatus defect then propagates in a posterior direction from an established full thickness tear in the supraspinatus.95 As in supraspinatus tears the lesion usually develops in patients over 50 years of age and is often asymptomatic (see p. 351). The lesion results from a combination of wear and tear and repetitive minitrauma. Sometimes the tear occurs suddenly during an acute overload or a fall. Acute symptoms will be a painful arc on active and passive elevation and pain on full lateral rotation. Resisted lateral rotation is extremely weak but painless. The painful
arc is caused by impingement of the tendon renmants between the greater tuberosity and the coracoacromial roof; the pain at the end of lateral rotation is caused by squeezing against the bulging posterior labrum. After some time (often many months), the inilammation decreases and the pain disappears. Resisted lateral rota tion remains weak. Chronic tears are characterized by marked and visible atrophy in the iniraspinatus fossa. Secondary to the per manent loss of the iniraspinatus, the patient can no longer bring the arm into full lateral rotation. This reduces the elasticity of the anterior capsule of the shoulder and results in a permanent isolated limitation of external rota tion. The impaired external rotation leads to the typical 'hornblower's sign': bringing the hand to the mouth is only possible in internal rotation of the arm with accom panying excessive elevation of the elbow. Hornblower's sign has a 1 00% sensitivity and 93% specificity for irreparable degeneration of the iniraspinatus.85 Treatment. When a painful arc is present an infiltration is given in the tendinous renmants. For this, 1 ml of triam cinolone is infiltrated at the tenoperiosteal insertion, using the same technique as for uncomplicated tendinitis. It is repeated after about 2 weeks if the painful arc has not fully disappeared. Abolishing the pain is only half the treatment. To prevent later limitation of lateral rotation, older patients are instructed to move the arm regularly into full lateral rotation with the help of the other arm or by twisting the trunk to the contralateral side while the forearm is stabi lized against a fixed object. Surgical treatment should be considered in younger patients with acute traumatic ruptures. Neurological disorders
C5 root palsy. Resisted abduction of the arm and flexion of the elbow are also weak (see p. 1 88).
Suprascapular nerve palsy (see p. 551 ). Suprascapular nerve entrapment is usually an acquired neuropathy sec ondary to compression of the nerve in the bony supra scapular notch. Chronic mechanical irritation may be caused by overhead activities such as racket sports, lifting and volleyball. Direct trauma, compression (e.g. backpacking) or a fracture of the scapula may also cause the lesion.97 Sometimes it is idiopathic. During the last decade, there have been several reports on isolated infraspinatus muscle paralysis in volleyball players, caused by a localized neuropathy of the lower branch of the nerve, presumably as a result of repetitive cocking of the arm.98 One German neurophysiological study revealed a compression neuropathy of the supra scapular nerve in 45% of high-level volleyball players,99 another in 33%.1 00
368 SECTION THREE - THE SHOULDER
Symptoms are constant pain in the trapezius and scapu lar area for about 3 weeks followed by functional distur bances in the arm (difficulties in performing overhead activities of the arm). Clinical examination reveals normal movement of neck, scapula and shoulder. Resisted move ments show some painless weakness of abduction (although the supraspinatus is paralysed, the deltoid remains fully active) and gross but painless weakness of lateral rotation (the infraspinatus is completely paralysed). Spontaneous cure is the rule in an idiopathic 'neuritis'. The pain disappears within 3 weeks, weakness within 6-12 months.1 01 Neuralgic a myotro p hy. This usually affects young males and starts with central neck pain, later spreading towards both shoulders and arms. Finally it leaves one ann and remains only in the other one. The pain is very severe and may last for about 6 months. Right from the onset muscular involvement is visible. Often wasting is present together with a total palsy, not just weakness. It affects muscles of both sides, irrespective of segmental origin. A common pattern is paralysis of the infraspina tus and the triceps, extensors of the fingers or extensors of the thumb (Cyriax:58 p. 90) (see p. 552). Myopathy. Bilateral painless weakness of the upper limbs can be the result of myopathy affecting serratus anterior, deltoid and both spinatus muscles. If this is the case, then pronounced weakness and wasting of both spinatus muscles and of the serratus anterior muscle is present. Because of the muscular weakness there is sometimes some degree of immobilizational arthritis. (See Fig. 18.26 for a summary of resisted lateral rotation.)
RES ISTED MED I A L ROTATION
PAI N
Four different structures are tested on resisted medial rotation: subscapularis, pectoralis major, latissimus dorsi and teres major. The latter three are adductors as well and have been discussed previously (see above). If resisted adduction is painless, the lesion must lie in the subscapularis, the insertion of which is large and flat. Subscapularis
The upper portion of the subscapularis inserts through a collagen-rich tendon into the lesser tuberosity. The rest (about 40%) of the tendon inserts into the humerus below the lesser tubercle and medial to the bicipital groove. Here the insertion is directly from muscle to bone. 102 Tendinitis of the subscapularis can be localized tenoperiosteally in the cranial or caudal part of the tendon. Lesions in the muscle belly or in the tendon itself do not seem to occur. A lesion in the cranial part causes a painful arc because of impingement under the coracoacromial arch. If the caudal portion is affected, the accessory test of passive horizontal adduction is painful as a result of pinching of the lesion between the lesser tuberosity and the coracoid process. Full active and passive elevation and full lateral rotation may be painful as well, because they stretch the subscapularis. Passive lateral rotation can even be so painful that it seems limited. To exclude arthritis, the examiner must gently try to bring the arm to full range, so as to confirm that imitation does not exist.
localizing sign
C5 root
localizing sign
Suprascapular nerve Neuralgic amyotrophy Myopathy
Figure 1 8.26
Resisted lateral rotation.
CHAPTER 18
Treatment. Tendonitis of the subscapularis can be treated by friction or infil tration. Friction is a rather painful and difficult technique and so preference is often given to infiltration. Technique: anatomical localization by palpation. The patient sits on the couch, the hand of the affected side resting on the thigh and with the arm slightly laterally rotated. The bicipital groove is now located at the antero lateral aspect of the arm. This is best done at the proximal part, between the two tuberosities. In this position the lesser tuberosity points anteriorly, the greater tuberosity laterally. The examiner places one thumb longitudinally between the tuberosities. Using the other hand, the patient's arm is moved into lateral and medial rotation. On lateral rotation the lesser tuberosity contacts the thumb in the groove, on medial rotation it is the greater hlberosity which comes in contact with it. Once the lesser tuberosity has been identified, the finger is placed at the anteromedial aspect of it and, further dis tally, to the lesser tubercular crest. This is where the inser tion of the subscapularis is found: partly on the lesser tuberosi ty, partly on its crest. The total width is about 3 cm. The insertion does not offer any particular sensation to the palpating fin ger: it feels as hard as bone. Depending on the localizing sign (painful arc or passive horizontal adduction positive), the proximal or the distal half of the structure must be dealt with. Before any treatment is started, the affected part is carefully palpated to localize the most painful region. Palpation vaguely around the insertion must be avoided because this area is always tender.
-
DISORDERS OF THE CONTRACTILE STRUCTURES 3 69
The patient is brought into the half-lying position, the arm in slight lateral rotation. Palpation is done in the same way as for infiltration. The therapist stands at the affected side and faces the patient. The contralateral hand is used. Beginning at the coracoid process, the thumb is brought just underneath it and the other fingers curved laterally around the arm, onto the back of the shoulder. The thumb is now pulled laterally while pressure is applied in a posterior direc tion. During this movement two tendinous structures are momentarily felt slipping under the thumb; these are the coracobrachialis muscle and the short head of the biceps. By moving the thumb yet further laterally, still maintain ing some dorsal pressure, the anteromedial edge of the deltoid is reached and is pulled to the side. Finally the lesser tuberosity is contacted (Fig. 18.28a). The hand is now turned into a vertical position (Fig. 18.28b), still keeping the deltoid to the side. Friction is given by a flexion-extension movement at the wrist, the active moment being when the thumb moves upwards. During the whole procedure the deltoid is kept to the side. This is a painful, difficult and, for the therapist, tiring technique. Progress towards cure tends to be slow and it may take about 1 month's friction before the patien t starts to get better. Only two-thirds of the patients can be fully cured in this way and, if no improvement has occurred after 1 month of friction, it is useless to continue and an infiltration should be given. PAI N LESS WEAK N E S S
A 3 cm needle fitted to a syringe filled with 1 ml of triamci nolone is inserted at the subscapularis insertion in the middle of the most painful part, and directed towards the bone (Fig. 18.27). Just before the humerus is reached, tendinous resistance is felt. As always, the infiltration is given in droplets. This time the needle is moved along a line in a craniocaudal direction over about 1.5 cm so as to include the whole lesion. Counterpressure is experi enced during the infiltration. Care must be taken not to move the needle too far laterally, so as to avoid infiltrat ing the tendon of the long head of biceps, which could lead to its early degeneration. The patient is told to avoid using the arm for about 2 weeks and then reassessed. If full cure is not attained the infiltration is repeated. Results are usually very good as long as the right point has been dealt with. Recurrences are less frequent than in supra- or infra spinatus tendinitis.
Tears of the subscapularis tendon occur either in isola tion or as a propagation of a supraspinatus tear. 103 The former is usually the result of a hyperextension-external rotation trauma or follows an anterior dislocation of the shoulder. lo4 The lower part of the muscle is mostly affected, where the insertion is more or less directly from muscle to bone. In the latter, the lesion is more proximal at the lesser tubercle, the distal part of the tendon remaining unaffected.1 05,106 In traumatic ruphl re there may also be an excessive range of passive lateral rotation. Weakness of internal rotation can also be demonstrated by the 'lift-off' signs described by Gerber and Krushell: the patient places the arm in internal rotation with the dorsum of the hand on the sacroiliac joint. If the patient is unable to internally rotate the arm any further and lift the hand off the pelvis, incompetence of the subscapu laris is suspected. 1 07
Technique: deep friction to the subscapularis. This form of treatment is mainly used in recurrences or in patients who refuse steroids.
Treatment. If shoulder pain is present, an infiltration with corticosteroid into the remnants at the tenoperi osteal insertion can be helpful.
Technique: infiltration of the subscapularis.
Rupture o f the subscapularis tendon
3 70 SECTION THREE - THE SHOULDER
Figure 1 8.27
(a) Figure 1 8.28
Infiltration of the subscapularis.
(b) Deep friction to the subscapularis. (a) Preparative position of the hand. (b) Frictioning position of the hand.
Neurological lesion
Internal rotation is controlled by (5 and (6. In a painless
weakness of internal rotation, a lesion of these nerve roots should be ruled out. (See Fig. 18.29 for a summary of resisted internal relation.)
RESISTED E LBOW FLEXION
An examination of the shoulder is incomplete until the biceps has been tested. The muscle mainly moves the elbow, but in that it crosses the shoulder joint it can be
CHAPTER 18
the cause of pain around the shoulder as well. For this reason, resisted flexion of the elbow must always be included when the shoulder is assessed. PAI N
A positive answer implicates the biceps. I f pain i s felt in the shoulder area, it is unlikely that the brachialis muscle is at fault, because a lesion in this muscle is more likely to cause pain around the elbow. The diagnosis can be confirmed by testing resisted supination of the forearm with the elbow flexed. If this is positive, the brachialis muscle is excluded. The classification of biceps lesions can be divided into tendinitis of the biceps and biceps instability. The former may be an impingement lesion or occurs in isolation as primary lesion of the biceps tendon.lOB Lesions of the biceps can lie at different levels. Only those that can provoke pain at the shoulder are discussed here. These are tendinitis of the long tendon at the glenoid insertion, in its intra-articular course and at the bicipital sulcus (Fig. 1 8.30). Lesions of the muscle belly and further down are discussed in Section 5. Lesion of the long bicipital tendon at the glenoid origin
Strain on the glenoid from the working biceps is greatest when the arm is in overhead abduction and lesions are usually caused by traction injuries in throwing athletes.1 09,110 The pain is usually felt underneath the acromioclavicular joint but may radiate in the C5 der matome. Besides pain on resisted flexion and supination of the elbow, resisted adduction of the arm will also show positive. When the resisted adduction is tested again, this
Subscapularis tendinitis Proximal part Distal part Figure 1 8.29
Resisted internal rotation positive.
-
DISORDERS OF THE CONTRACTILE STRUCTURES 371
time with the elbow flexed, it becomes painless. This phe nomenon is explained by the constant-length phenome non on a structure spanning two joints (see p. 86): the degree of stress on the painful tissue in one joint depends on the position in which the adjacent joint is held. Treatment. The condition can usually be treated successfully with one or two infiltrations of 20 mg of
triamcinolone. Technique: infiltration of the long bicipital tendon. The condition can be treated only by an infiltration. The patient lies supine, the arm in 90° elevation, the elbow flexed to a right angle. An assistant now turns the arm into 45° lateral rotation. In this position, the bicipital groove lies on a line extended from the anterior margin of the acromion. A 2 ml syringe is filled with 20 mg of triamcinolone and a 4 cm needle fitted to it. One thumb is placed just beyond the acromion at the groove. The needle is inserted just distally to the thumb parallel to the bicipital sulcus and aiming at the glenoid (Fig. 18.3 1 ). It is then moved further in between the humeral tuberosities until it strikes the glenoid. A tough resistance is felt just before touching the bone. The steroid is infiltrated here in drops so that the whole insertion is treated. During the infiltra tion some counterpressure is felt. The patient is re-examined after 2 weeks and, if neces sary, the infiltration is repeated.
Intra-articular lesion of the long head of the biceps
Pain on resisted flexion and supination of the elbow is found, together with a painful arc, which shows the lesion to lie at the intra-articular part of the tendon. As this part of the tendon lies intra-articularly, an intra articular injection with 2 ml of steroid is required.
C5 root lesion
painful arc passive horizontal adduction
3 72 SECTION THREE - THE SHOULDER
2
3
4
Figure 1 8.30 Lesions of the biceps at shoulder: 1, at the glenoid insertion; 2, at the intra-articular course of tendon; 3, at the tendon in the sulcus; 4, subscapularis muscle.
Lesion in the sulcus of the long head of biceps
The only positive sign is pain on resisted flexion and supination felt at the upper part of the arm. There is a full range of movement and a painful arc is absent. Palpation localizes the lesion in the sulcus. Technique: deep friction to the long head. This lesion responds well to deep friction. The patient adopts the
Figure 1 8.31
half-lying position, the palm of the hand on the thigh, the elbow at the side. The greater tuberosity then points lat erally, the lesser tuberosity anteriorly. The sulcus lies in between the tubercles. In order to precisely locate the groove, the first part of the procedure for palpation for subscapularis tendinitis is performed (see above). The therapist sits at the side, facing the patient. The patient's arm is put into a degree of lateral rotation. The thumb of the contralateral hand is put flat in the sulcus, the tip pointing cranially and the radial side in contact with the medial aspect of the sulcus. In this position the thumb lies on the medial aspect of the tendon. The other fingers give counterpressure at the back of the arm. Pressure towards the bone is applied with the thumb. With the other hand the therapist grasps the patient's lower arm, the elbow bent to 90° and brings the arm into medial rotation until the radial side of the frictioning thumb comes in contact with the outer edge of the sulcus (Fig. 18.32). During this movement the tendon glides under the thumb and friction is achieved. The arm is now brought back into lateral rotation while releasing the pressure on the tendon (passive moment). Treatment is carried out for 20 minutes, three times a week. Two to four sessions should be sufficient. Instead of rotating the patient's arm, pronation-supination movements of the thera-
Alternative technique.
Infiltration of the long bicipital tendon at the glenoid.
CHAPTER 18
pist's contralateral arm have the same effect. The active movement is on supination. Snapping long head of the biceps
Biceps instability is seen most commonly in throwing athletes. Motion is often accompanied by a palpable snap or pop at a certain position in the arc of rotation.1ll According to SHitis and Aalto, a rupture of the inter tubercular transverse ligament allows for no appreciable medial or lateral movement of the tendon.IOB The key structure which guides the tendon in its groove is the medial portion of the coracohumeral ligament, which inserts at the lesser tubercle. It fills the space between the upper margin of the subscapularis and the anterior border of the supraspinatus. If it is transected, the long tendon of the biceps can easily be displaced medially. Instability test. Dislocation of the biceps is tested with the biceps instability test of Abbott and Saunders.112 The arm, abducted to 90° and fully externally rotated, is slowly brought to the side and slightly internally rotated. A palpable and even audible and sometimes painful click is noted as the biceps tendon, now forced against the lesser tuberosity, becomes subluxated or dislocated from the groove.
-
DISORDERS OF THE CONTRACTILE STRUCTURES 3 7 3
Rupture of the biceps tendon
Classically, the rupture takes place at the proximal part of the long head of the tendon. It is usually the result of degeneration and occurs spontaneously, provoking almost no discomfort. Distal ruptures are infrequent and are more often encountered in younger patients, usu ally as a result of a local trauma, such as a direct blow. The victims are usually male and over 50 years of age. Sometimes a loud crack is heard at the moment of rupture, with some transient pain in the upper arm. The most significant sign is the prominence that persists from the distal displacement of the muscle belly and which is best visible on contraction. On testing, no appreciable loss of muscle power is found. Usually treatment is not required, although, in cases of less than 6 weeks' standing surgical correction may be succcessful. ll3 PAI N LESS WEAKN ESS Fifth cervical root palsy
Painless weakness is found on resisted abduction and lateral rotation of the arm and on resisted flexion of the elbow. Sixth cervical root palsy
Weakness is found on resisted flexion of the elbow (biceps and brachialis), resisted supination (supinator brevis), resisted extension and radial deviation of the wrist (extensor carpi radialis longus and brevis).
RES ISTED E LBOW EXTENSION
PAI N
If this movement causes pain a t the shoulder it i s logical to think of a lesion of the triceps although this is very uncommon. On contraction of the triceps the head of the humerus moves towards the acromion. If a lesion lies between one of the tuberosities and the coracoacromial roof it can he pinched. Therefore pain on resisted exten sion of the elbow has usually the same meaning as a painful arc. To exclude with certainty a lesion of the triceps, palpation of the muscle can be used. If it is posi tive it should always be followed by a diagnostic infiltra tion with local anaesthetic, because local tenderness is often present even in normal circumstances. PAI N LESS WEAKN ESS
Figure 18.32
Deep friction to the long head of the biceps.
Weakness on extension of the elbow is mainly the result of C7 root palsy caused by a C6 cervical disc lesion. Spontaneous pain is felt at the dorsal aspect of the ann
3 74 SECTION THREE - THE SHOULDER
and is increased by movements of the neck. Resisted extension of the elbow is painless. The latissimus dorsi (adduction of the arm) and the radial flexor, seldom the extensors, of the wrist may also be reduced in power. Theoretically the triceps reflex should be impaired, but in practice it seldom is.
RES ISTED FLEXION OF THE ARM
The patient is asked to push the arm forwards against the examiner 's hand, the latter giving counterpressure in the opposite direction (Fig. 1 8.33). Pain on this movement alone is the outcome of a lesion of the coracobrachialis muscle, which is rare. Although resisted adduction should also be painful, in practice it is not. The lesion normally lies at the upper part of the cora cobrachialis. Thus it can give rise to pain felt in the upper outer chest, radiating towards the inner side of the arm. It is treated by deep transverse friction.
Figure 1 8.33
Resisted fiexion.
R E F E R E N CES 1 . Bjelle A. Epidemiology o f shoulder problems. Bailliere's Clin
2.
3.
4.
5.
6. 7.
8.
RheumatoI 1989;3:437-451. Clark JM, Sidles JA, Matsen III FA. The relationship of the glenohumeral joint capsule to the rotator cuff. Clin Orthop 1990;254:29-34. Ulthoff HK, Sarkar K, Lohr J. Repair in rotator cuff tendons. In: Post M, Morrey BF, Hawkins RJ (eds) Surgery of the Shoulder. Mosby-Year Book, St Louis, 1990:216-219. Fukuda H, Hamada K, Yamanaka K. Pathology and patho genesis of bursal side rotator cuff tears viewed from en-block histologic sections. Clin Orthop 1990;254:75-80. Ulthoff HK, Sarkar K. The effect of ageing on the soft tissues of the shoulder. In: Matsen FA III, Fu FH, Hawkins RJ (eds) The Shoulder: A Balance of Mobility and Stability. American Academy of Orthopaedic Surgeons, Rosemont, IL, 1993:269-278. Satoshi 0, Uhthoff H. Acromial enthesopathy and rotator cuff tear. Clin Orthov Rei Res 1990;254:39-48. Riley Gp, HarraH RL, Constant CR et al. Tendon degeneration and chronic shoulder pain: changes in the collagen composition of the human rotator cuff tendons in rotator cuff tendinitis. A n n Rheum Dis 1994;35:359-366. Bigliani LU, Morrison DS, April EW. The morphology of the acromion and its relationship to rotator cuff tears. Orthop Trans 1986;10:228.
9. Morrison DS, Bigliam LV. The clinical significance of variations in acromial morphology. Orthop Trans 1987;11:234. 10. Cotton RE, Rideout D. Tears of the humeral rotator cuff: a radiological and pathological necropsy survey. ] Bone Joint Surg 1964;46B:314-328. 11. Aoki M, Ishii S, Usui M. Clinical application for measuring the slope of the acromion. In: Post M, Morrey BF, Hawkins RJ (eds) Surgery of the Shoulder. Mosby-Year Book, St Louis, 1990:200-203. 12. Chung SM, Nissenbaum MM. Congenital and developmental defects of the shoulder. Orthop Clin North Am 1975;6:381-392. 13. Ogata S, Uhthoff HK. Acromial enthesopathy and rotator cuff tear: a radiologic and histologic postmortem investigation of the coracoacromial arch. Clin Orthop 1990;254:39-48. 14. Flatow EL, Soslowsky LJ, Ticker JB et al. Excursions of the rotator cuff under the acromion. Patterns of subacromial contact. Am ] Sports Med 1994;22:779-788. 15. Putz R, Reichelt A. Structural findings of the cora co acromial ligament in rotator rupture, tendinosis calcarea and supraspinatus syndrome. Z Orthop lhre Grenzgeb 1990;128: 46-50. 16. Rothman RH, Parke WW. The vascular anatomy of the rotator cuff. Clin Orthop 1965;41:176-186. 17. Lindblom K. On pathogenesis of ruptures of the tendon aponeurosis of the shoulder joint. Acta RadioI 1939;20:563-577.
CHAPTER 18 - DISORDERS OF THE CONTRACTILE STRUCTURES 3 75
18. Moseley HF, Goldie L. The arterial pattern of the rotator cuff of the shoulder. J Balle Joint Surg 1963;45B:780. 19. Rathbun JB, Macnab L. The microvascular pattern of the rotator cuff. ] Bone Joint Surg 1970;52B:540-553. 20. Fukuda H, Hamada K, Yamanaka K. Pathology and patho genesis of bursal-side rotator cuff tears viewed from en bloc histologic sections. Clin Orthop 1990;254:75-80. 21. Lohr J, Uhthoff H. The microvascular pattern of the supraspina tus tendon. Clin Orthop Res 1990;254:35-38. 22. Worland R. Treatment of rotator cuff impingement. Orthop Rev 1993;22(1):76-79. 23. Neviaser R. Observations on impingement. Clin Orthop Rel Res 1990;254:60-63. 24. Cod man EA. The Shoulder. Rupture of the Supraspinatus Tendon and Other Lesions il1 or about the Subacromial Bursa. Thomas Todd, Boston, 1934. 25. Matsen FA III, Arnitz CT, Lippitt SB. Rotator cuff. In: Rockwood CA, Matsen FA III (eds) The Shoulder, 2nd edn. Saunders, Philadelphia, 1998. 26. Keyes EL. Anatomical observations of rupture of the supraspinatus tendon. Based upon a cadaveric study of 73 cadavers. Ann Surg 1933;97:849-856. 27. Wilson CL. Lesions of the supraspinatus tendon. Degeneration, rupture and calcification. Arch Surg 1943;46:307. 28. Grant JCB, Smith CG. Age incidence of rupture of the supraspinatus tendon, abstract. Anat Rec 1948;100:666. 29. Cotton RE, Rideaout D. Tears of the humeral rotator cuff: a radiological and pathological necropsy survey. J Bone Joint Surg 1963;46B:314-328. 30. Uhtoff J, Loehr J, Sarkar K et al. The pathogenesis of rotator cuff tears. In: Proceedings of the Third International Conference on Surgery of the Shoulder, Fukuora, Japan, 1986. 31. Osaki J, Fujimoto S, Nakagawa Y et al. Tears of the rotator cuff of the shoulder associated with pathologic changes in the acromion: a study in cadavera. I Bone Joint Surg 1988;70A: 1224-1230. 32. Kummer FJ, Zuckerman JD. The incidence of full thickness rotator cuff tears in a large cadaveric population. Bull Hasp It Dis 1995;54:30-3 1 . 33. Jerosch J, Muller T, Castro WHo The incidence o f rotator cuff rupture. An anatomic study. Acta Orthop Belg 1991;57(2): 124-129. 34. Fukada H, Mikasa M, Yamanaka K et al. Incomplete rotator cuff tears diagnosed by subacromial bursography. Clin Orthop 1987;223:51-58. 35. Sakurai G, Ozaki J, Tomita Y, Kondo 1, Tarnai S. Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus tendon: cadaveric and clinical studies. I Shoulder Elbow Surg 1998;7(5):510-515. 36. Petterson G. Rupture of the tendon aponeurosis of the shoulder joint in antero-inferior dislocation. Acta Chirur Scand 1942; 77(suppl):1-187. 37. Milgrom C, Schaffler M, Gilbert S, van Holsbeeck M. Rotator cuff changes in asymptomatic adults. The effect of age, hand dominance and gender. I Bone Joint Surg 1995;77B(2):296-298. 38. Sher JS, Uribe JW, Posada A et al. Abnormal findings on mag netic resonance images of asymptomatic shoulders. I Bone Joint Surg 1995;77:933-936. 39. Ellman H. Diagnosis and treatment of incomplete rotator cuff tears. Clin Orthop Rel Res 1990;254:64-74. 40. Pellecchia GL, Paolino J, Connell J. Intertester reliability of the Cyriax evaluation in assessing patients with shoulder pain. 10SPT 1996;23:34-38.
41. Chard MID, Sattelle LM, Hazleman BL. The long-term outcome of rotator cuff tendinitis - a review study. Br ] Rheumatol 1988;27:385-389. 42. Kamkar A, Irrgan JJ, Whitney SL. N onoperative management of secondary shoulder impingement syndrome. J Orthop Sports Physical Therapy 1993;17:212-224. 43. Matthews LS, Sontesgard DA, Phelps DB. A biomechanical study of rabbit patellar tendon: effects of steroid injection. J Sports Med 1974;2:9. 44. Kennedy Je, Willis RB. The effects of local steroid injections on tendons: a biomechanical and microscopic correlative study. Am J Sports Med 1976;4:11-21 . 45. Van der Heyden GJ, Van der Windt DA, Kleijnen J, Koes B, Bouter LM. Steroid injections for shoulder disorders: a system atic review of randomized clinical trials. Br ] Gen Pract 1996;46:309-316. 46. Adebajo AO, Nash P, Hazleman BL. A prospective double blind dummy placebo controlled study comparing triam cinolone hexacetonide injection with oral diclofenac 50 mg TDS in patients with rotator cuff tendinitis. I Rheumatol 1990; 17(9):1207-1210. 47. Goupille P, Sibi lia J . Local corticosteroid injections in the treatment of rotator cuff tendinitis (except for frozen shoulder and calcific tendinitis). Groupe Rhumatologique Francais de I'Epaule (G.R.E.P.). Clin Exp Rheumatol 1996; 14(5):561-566. 48. Blair B, Rokito AS, Cuomo F, Jarolem K, Zuckerman ]D. Efficacy of injections of corticosteroids for subacromial impingement syndrome. J Bone 10int Surg 1996;78A(11):1685-1689. 49. Valtonen EJ. Subacromial triamcinolone mexacetonide and methylprednisolone injections in treatment of supra spinam tendinitis. A comparative trial. Scand J Rheumatol 1976; 16(suppl):1-13. 50. Symonds G. Accurate diagnosis and treatment in painful shoulder conditions. J Int Med Res 1975;3:261-266. 5 1 . Hollingworth GR, Ellis RM, Hattersley TS. Comparison of injection techniques for shoulder pain: resul ts of a double blind, randomised study. BM] (Ci in Res edn) 1983;287(6402): 1339-1341. 52. Bosworth BM. Calcium deposits in the shoulder and sub acromial bursitis. A survey of 12, 1 22 shoulders. JAMA 1941;116:2427-2428. 53. Ruttiman G. Ueber die Hufigkeit rontgenologischer Veranderungen bei Patienten mit typischer Periarthritis humeroscapularis und Schultergesunden. Inaugural disserta tion. Zurich, 1959. 54. De Palma AF, Kruper JS. Long term study of shoulder joints affected with and treated for calcific tendinitis. Clin Orthop 1961;20:61-72. 55. Welfling J, Kahn MF, Desray M et al. Les calcifications de l'epaule IE La mala die des calcifications tendineuses multiples. Rev Rheum 1965;32:325-334. 56. Neer CS III. Impingement lesions. Clin Orthop 1983;173:70-77 57. Matsen FA III, Lippitt SB, Sidles JA, Harryman DT. Practical evaluation and management of the shoulder. Saunders, Philadelphia, 1994. 58. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis and Treatment of Soft Tissue Lesions, 8th edn, Bailliere Tindall, London, 1982. 59. Vaes P, Annaert JM, Claes Ph, Opdecam P. Anatomische en kine siologische studie van de ratatorcuffpezen. Ned Tijdschr Manuele Ther 1992;11(1):2-1 1 .
3 76 SECTION THREE - THE SHOULDER
60. Mattingley GE, Mackarey PJ. Optimal methods for shoulder tendon palpation. A cadaver study. Phys Ther 1996;76:166-174. 61. Stuart M, Azevedo A, Cofield R. Anterior acromioplasty for treatment of the shoulder. Clin Orthop Rei Res 1990; 260:195-200. 62. Kirschenbaum D, Coyle M, Leddy J, Katsaros P, Tan F, Cody R. Shoulder strength with rotator cuff tears. Clin Orthop Rei Res 1993;288:174-1 78. 63. Codman E, Akerson I. The pathology associated with rupture of the supraspinatus tendon. Ann Surg 1931;93:348. 64. Yamanaka K, Matsumoto T. The joint side tear of the rotator cuff: a followup study by arthrography. Clin Orthop 1994;304: 68-73. 65. Wright SA, Cofield RH. Management of partial-thickness rotator cuff tears. J Shoulder Elbow Surg 1996;5(6):458-466. 66. Markhede G, Monastyrski J, Stener B. Shoulder function after deltoid muscle removal. Acta Orlhop Scand 1985;56:242-244. 67. Post M, Silver R, Singh M. Rotator cuff tear. Clin Orthop Rei Res 1983;173:78-9 1 . 68. Howell SM, Imobergsteg AM, Seger DH et a l . Clarification of the role of the supraspinatus muscle in shoulder function. J Bone joillt Surg 1986;68A:398-404. 69. Colachis S, Strohm B. Effect of suprascapular and axillary nerve blocks on muscle force in upper extremity. Arch Physical Med Rehabi/ 1971;52(1):22-29. 70. Kronberg M, Nemeth G, Brostrom LA. Muscle activity and coordination in the normal shoulder: an electromyographic study. Clin Orthop 1990;257:76-85 71. Ozaki J, Fujimoto K, Nakagawa Y, Masuhara K, Tamai S. Reconstruction of chronic massive rotator cuff tears with synthetic materials. Clin Orthop Rei Res 1986;202:173-183. 72. Lazarus MID, Harryman DT, Yung SW et al. Anteriosuperior humeral displacement: limitation by the cora co-acromial arch. AAOS AlUlual Meeting, Orlando, FL, 1995. 73. Flatow EL, Soslowsky U, Ticker JB el al. Excursions of the rotator cuff under the acromion. Patterns of subacromial contact. Am J Sports Med 1994,22:779-788 74. Kaneko K, DeMoy EH, Brunet ME. Massive rotator cuff tears. Screening by routine radiographs. Clin Imaging 1995;19:8-11 . 75. Itoi E , Tabata S . Rotator cuff tears in the adolescent. Orthop 1 993;16(1):78-81 . 76. SooHoo NF, Rosen P. Diagnosis and treatment o f rotator cuff tears in the emergency department. J Emerg Med 1 996;14(3):309-317. 77. Neviaser R. Ruptures of the rotator cuff. Management of shoul der problems. Orthop Clin North Am 1987;18(3):387-394. 78. Bokor D, Hawkins R, Uckell G el al. Results of non-operative management of full-thickness tears of the rotator cuff. Clin Orthop Rei Res 1993;294:103-110. 79. Petterson G. Rupture of the tendon aponeurosis of the shoulder joint in antero-inferior dislocation. Acta Chir Scand 1942; 77(suppl):1-187. 80. Hattrup SJ. Rotator cuff repair: relevance of patient age. j Shoulder Elbow Surg 1995;4(2):95-100. 8 1 . McLaughlin HL Repair of major cuff ruptures. Surg Clin North Am 1963;43:1535-1540. 82. Harryman DT, Mack LA, Wang KY et al. Repairs of the rotator cuff. J Bone Joint Surg 1991;73A:982-989. 83. Gerber C, Fuchs B, Hodler J. The results of repair of massive tears of the rotator cuff. J Bone Joint Surg 2000;82A(4):505-515. 84. Ma HL, Wu J), Lin CF, Lo WHo Surgical treatment of full thickness rotator cuff tear in patients younger than 40 years. Chu ng Hua l Hsueh Tsa Chih (Taipei) 2000;63(6):452-458. 85. Nobuhara K, Hata Y, Komai M. Surgical procedure and results of repair of massive tears of the rotator cuff. Clin Orthop 1994;394:54-59.
86. Watson M. Major ruptures of the rotator cuff. The results of surgical repair in 89 patients. J Bone Joint Surg 1985;67B(4): 618-624. 87. Wirth MA, Basamania C, Rockwood CA Jr. Nonoperative man agement of full-thickness tears of the rotator cuff. Orthop Clin North Am 1997;28(1):59-67. 88. Mantone JK, Burkhead WZ Jr, Noonan J Jr. Nonoperative treat ment of rotator cuff tears. Orthop Clin North Am 2000;31(2): 295-31 1 . 89. Itoi E , Tabata S. Conservative treatment o f rotator cuff tears. Clin Orthop 1992;275:165-173. 90. Rask M. Pectoralis major muscle rupture: report of five patients. J Neural Orthop Med Surg 1992;13:272-274. 9 1 . Scott B, Wallace W, Barton M. Diagnosis and assessment of pectoralis major rupture by dynamometry. J Bone Joint Slirg 1992;74B:111-114. 92. Zeman SC, Rosenfeld RT, Lipscomb PR. Tears of the pectoralis major muscle. Am J Sports Med 1979;7:343-347. 93. Wolfe SW, Wickiewicz TL, Cavanaugh JT. Ruptures of the pectoralis major muscle. An anatomic and clinical analysis. Am J Sports Med 1992;20:587-593. 94. Kretzler HH Jr, Richardson AB. Rupture of the pectoralis major muscle. Am J Sports Med 1989;17:453-458. 95. Yamanaka K, Matsumoto T. The joint side tear of the rotator cuff: a followup study by arthrography. Clin Orti1op 1994; 304:68-93. 96. Walch G, Boulahia A, Calderone S, Robinson AH. The 'drop ping' and 'hornblower's' signs in evaluation of rotator-cuff tears. J Bone Joint Surg 1998;80B(4):624-628. 97. Berry H, Kong K, Hudson AR, Moulton RJ. Isolated supra scapular nerve palsy: a review of nine cases. Can J Neural Sci 1995;22(4):301-304. 98. Montagna P, Colonna S. Suprascapular neuropathy restricted to the infraspinatus muscle in volleyball players. Acta Neural Scand 1993;87(3):248-250. 99. Eggert S, Holzgraefe M. Compression neuropathy of the suprascapular nerve in high performance volleyball players. Sportverletz Sportschaden 1993;7(3):136-142. 100. Holzgraefe M, Kukowski B, Eggert S. PrevalenCE of latent and manifest suprascapular neuropathy in high-performance volleyball players. Br J Sports Med 1994;28(3):177-179. 101. Black KP, Lombardo JA. Suprascapular nerve injuries with isolated paralysis of the infraspinatus. Am J Sports Med 1990;18(3):225-228. 102. Hinton MA, Parker AW, Drez D, Altchek D. An anatomic study of the subscapularis tendon and the myotendinous junction. J Shoulder Elbow Surg 1994;3:224-229. 103. Sakurai G, Ozaki J, Tomita Y, Kondo T, Tarnai S. Incomplete tears of the subscapularis tendon associated with tears of the supraspinatus tendon: cadaveric and clinical studies. J Shoulder Elbow Surg 1998;7(5):510-515. 104. Deutsch A, Altchek DW, Veltri DM, Potter HG, Warren RF. Traumatic tears of the subscapularis tendon. Clinical diagno sis, magnetic resonance imaging findings, and operative treat ment. Am J Sports Med 1997;25(1):13-22. 105. Li XX, Schweitzer ME, Bifano JA et al. MR evaluation of sub scapularis tears. J Comput Assist Tomogr 1999;23(5):713-717. 106. Nove Josserand L, Levigne C Noel E, Walch G. Isolated lesions of the subscapularis muscle. 11 propos of 21 cases. Rev Chir Orthop Reparatrice Appar Mot 1994;80:595-601 . 107. Gerber C Krushell RJ. Isolated ruptures o f the tendon o f the subscapularis muscle. J Bone Joint Surg 1991;73B(3):389-394. 108. Slatis P, Aalto K. Medial dislocation of the tendon of the long head of the biceps brachii. Acta Orti1op Scand 1979;50:73-77, 97-104.
CHAPTER 18
109. Grauer JD, Paulos LE, Smutz WP. Biceps tendon and superior labral injuries. Arthroscopy 1992;8:488-497. 110. Andrews J, Carson W, McLeod W. Glenoid labrum tears related to the long head of the biceps. Am J Sports Med 1985;13:337-341. 111. Petersson q. Spontaneous medial dislocation of the tendon of the long biceps brachii . CLin Ort/1Op 1986;211:224-227.
-
DISORDERS OF THE CONTRACTILE STRUCTURES 3 7 7
112. Abbott LC, Saunders LB. Acute traumatic dislocations of the tendon of the long head of the biceps brachii; report of 6 cases with operative findings. Surgery 1939;6:817-840. 113. Van Laarhoven C, Van Der Werken C. Bicepspeersrupturen. Ned Tijdschr Geneeskd 1990;134(21):1 048-1053.
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
Disorders associated with a painful arc
Disorders of the inert structures 380 Acute subdeltoid bursitis 380 Chronic subdeltoid bursitis 380
Sprain of the acromioclavicular j oint Acromial metastases
380
380
Disorders of the contractile structures Supraspinatus tendinitis 380 Infraspinatus tendinitis 381 Subscapularis tendinitis 381
380
Tendinitis of the long head of the biceps
Disorders mimicking painful arc Capsular laxity of the shoulder Snapping biceps tendon 382 Cervical disc lesion
382
382 382
381
A painful arc is pain felt at about half range in a move ment, in the absence of pain before and after the mid range (see p. 296).Pain may or may not recur at the end of the movement. An arc results from a momentary impingement of a lesion, lying in such a position that it is caught between the lesser or greater humeral tuberosities and the overlying anterior part of the acromion, the coracoacromial ligament or the acromio clavicular jointl-4 (Fig. 19.1). A painful arc is mainly found on elevation, sometimes on medial rotation of the arm. Irrespective of the precipitating movement, the diagnostic significance remains the same: temporary impingement. An arc on elevation is usually most pronounced during the active movement, and more on the way up than on the way down. This is due to the muscular activ ity, which pulls the numeral head closer to the acromion during active elevation.5 Sometimes the patient tries to avoid the painful moment by changing the direction of the elevation when the pain is felt. Indeed, some patients abduct until they feel the pain start at mid-range and then bring the arm in front of the body to avoid further impingement. Occasionally the patient may experience the pain at mid-range only on the way down, or even on passive medial rotation. This has the same meaning as a painful
Figure 19.1
Site of impingement (red) in painful arc. 379
380 SECTION THREE - THE SHOULDER
arc on the way up. If the examiner has the impression that passive elevation or medial rotation is limited, it is important to insist that the movement is gently contin ued, otherwise the patient may voluntarily stop the movement too early, due to pain. The apparent limita tion may be overcome by persistence, and it may be possible for the patient to then get beyond the painful moment. Thus, what might initially be regarded as a limited movement can be proved to be a painful arc with full range, which has completely different diag nostic implications. Neer introduced the term 'impingement syndrome', now widely recognized and further divided into a 'subacromial' and a 'subcoracoid' impingement syn drome.6-9 Cyriax always considered painful impinge ment as a sign rather than a syndrome: it does not implicate just one lesion but one of severaLlO,lJ Since the exact diagnosis is in the majority of the cases based on other tests - very often on resisted movements a painful arc usually has value as a localizing sign, defining exactly in which particular part of the structure the lesion lies. Movement in the subacromial space is between a convex, cuff-covered proximal humerus and a concave surface consisting of the coracoacromial roof and the infe rior part of the acromioclavicular joint.12 The gliding
surface between these two moving spheres is the bursa. Pathology in one or more of these structures may partly interfere with movement and thus cause the clinical sign, 'painful arc' (Fig. 19.2).
DISORDERS OF THE INERT STRUCTURES ACUTE SUBDELTOID BURSITIS
In acute subdeltoid bursitis an arc is present for the first few hours after the onset. At the ertd of the spontaneous course, say after 4-5 weeks, when the pain has become much less, the arc appears again. In practice, the arc is seldom found because the patient presents 2-3 days after the onset, once the pain has become unbearable. At this stage, the pain is so severe that active and passive elevation beyond the horizontal are not possible (see p.319).
CHRONIC SUBDELTOID BURSITIS
In almost all cases of chronic subdeltoid bursitis a painful arc is present. Here it is not regarded as a local izing sign but as a basic element in the diagnosis. It is
.------ Acromioclavicular joint Subacromial bursa --------,
Infraspinatus
-------..�PPJ��/;}
Supraspinatus -------lifj
,.---����,._.�Rffl'H'---- Biceps
L-----*'r--4JfH.'-..,.-- Subscapularis
Figure 19.2
Structures that may be responsible for the existence of painful arc.
CHAPTER 19
most commonly associated with pain at the end of all passive movements, sometimes as the only sign, some times combined with pain on resisted abduction and lateral rotation. When an arc is very pronounced, the diagnosis is most probably chronic subdeltoid bursitis. Occasionally, the arc is very subtle. It may be absent on lateral eleva tion, but when it is repeated with the arm anteriorly it may show. The same goes for lateral elevation with the arm in medial or lateral rotation. In these cases, eleva tion should be repeated in several different ways (see p.333). SPRAIN OF THE ACROMIOCLAVICULAR JOINT
Pain at the end of all passive movements, together with more pain on passive horizontal adduction is typical of a sprain of the acromioclavicular joint. In some cases, a painful arc is also present. It indicates that the lesion lies where it can impinge, which only happens to the inferior !igament. A sprain of the superficial ligament can never cause a painful arc but palpation elicits local tenderness. Differentiation from a chronic subdeltoid bursitis may be very difficult. A diagnostic infiltration with local anaesthetic may be necessary (see p. 327).
-
PAINFUL ARC 381
SUPRASPINATUS TENDINITIS
This is the most common cause of painful arc. For this reason, many authors consider that a painful arc usually means that the supraspinatus is involved.14,15 This is not so, since the arc should be regarded only as a localizing sign; resisted abduction identifies the structure at fault.If an arc is also present it shows the lesion to lie at the superficial (bursal) aspect of the tenoperiosteal insertion (see p. 353).
INFRASPINATUS TENDINITIS
In this case, pain on resisted lateral rotation is the basic sign. The arc shows the lesion to lie at the superficial aspect of the tenoperiosteal insertion (see p. 364).
SUBSCAPULARIS TENDINITIS
Pain on resisted medial rotation draws attention to the subscapularis muscle. As the insertion of the subscapu laris is about 3 cm long, only the proximal half of it can impinge on elevation. If the lesion lies in the lower half an arc is not found but passive horizontal adduction is painful (see p. 369).
ACROMIAL METASTASES
TENDINITIS OF THE LONG HEAD OF THE BICEPS
This is a rare disorder. Due to the metastases, the acromion becomes so tender that even the slightest pres sure from below or above causes severe local pain, which does not spread in the arm. In consequence, local tender ness on palpation and a painful arc are found. Resisted abduction is usually very painful and extremely weak. These signs, together with localized warmth, call for immediate radiography.
This is a rare lesion which causes pain in the shoulder on resisted flexion and supination of the elbow. The combi nation of these signs with a painful arc means that the lesion must lie where it can impinge. The intra-articular part of the long head of the tendon is the only site.
Warning Local tenderness on palpation and localized warmth over the acromion, together with a painful arc and painful weak resisted abduction, should prompt suspicion of metastases.
DISORDERS OF THE CONTRACTILE STRUCTURES
All the contractile structures mentioned below may give rise to a painful arc in that some part of them can be pinched between humerus and coracoacromial arc.13
DISORDERS MIMICKING PAINFUL ARC CAPSULAR LAXITY OF THE SHOULDER
In some instances of shoulder instability the following is encountered: when the patient lifts the arm up sideways there is a little 'stop' at about midway but once beyond this point, the normal movement continues. At the same time, the patient has the impression that something comes out of place and then slips back. In this event, the stop is caused by a partial dislocation of the humeral head, which slips back when the movement continues. Such momentary subluxation is not usually painful. It has nothing to do with an impingement and therefore is not regarded as a painful arc. Recent investigations have shown that slight instability of the shoulder may be one of the precipitating factors in the development of rotator
382 SECTION THREE - THE SHOULDER
cuff disease. It is therefore highly possible that subluxa tion of the humerus coexists with a lesion of one of the rotator cuff tendons and thus with a painful arc.I6-19 Apprehension tests for shoulder instability must be performed to arrive at the diagnosis. It can also be helpful to palpate the shoulder joint during active elevation (see p.337). SNAPPING BICEPS TENDON
Sometimes the long head of the biceps may slip out of the groove on active elevation, giving rise to a momentary sensation of instability. No pain is present but a sort of popping may be felt. Because no impingement occurs, this sensation can not be regarded as a painful arc. The biceps dislocation test reveals the exact nature of the lesion (see p.373).
ization of the pain is very seldom due to a shoulder problem. The pain at mid-range on elevation is then explained by the muscular tension at the neck becoming greatest around the horizontal. The momentary pain can not be considered as a real painful arc: the sign results from transmitted stress and is not provoked by any kind of impingement. However, it is not always easy to be absolutely sure whether there is only one lesion or whether there are two. It is wise in these doubtful cases to start treating the most proximally located disorder (the neck) until all neck signs become normal: full range, no pain. The shoulder should then be re-examined and, if still painful, a shoulder problem must also be present and is then dealt with. Disorders associated with painful arc are listed in Box 19.1.
CERVICAL DISC LESION
In a cervical discodural interaction, neck and scapulo humeral pain is sometimes provoked or increased at about mid-range during active elevation. Passive tests of the shoulder are fully negative, although some resisted movements may be painful. At the cervical spine, a partial articular pattern is found. The presence of a painful arc in combination with signs and symptoms of a discodural interaction at the neck may confuse the examiner.Two possibilities then emerge: either the painful arc is caused by the neck problem or there is a double lesion - one at the neck and one at the shoulder. In the former, the arc is usually felt in the scapular area, sometimes radiating down the arm. Scapular local-
Box 19.1 Disorders associated with painful arc Inert structures Acute subdeltoid bursitis Chronic subdeltoid bursitis Sprain of the acromioclavicular joint Acromial metastases
Contractile structures Supraspinatus tendinitis Infraspinatus tendinitis Subscapularis tendinitis Tendinitis of long head of biceps Disorders mimicking painful arc Capsular laxity of the shoulder Snapping biceps tendon Cervical disc lesion
REFERENCES 1. Solem-Bertoft E, Thuomas K, Esterberg C. The influence of
9. Ha'eri G, Orth M, Wiley A. Shoulder impingement syndrome
scapular retraction and protraction on the width of the subacro
results of operative release.
mial space. Clin Orthop Rei Res 1993;296:99-103.
128-132.
2. Worland R. Treatment of rotator cuff impingement. Orthop Rev 1993:76-79. 3. Rockwood C, Lyons F. Shoulder impingement syndrome: diag nosis, radiographic evaluation and treatment with a modified Neer acromioplasty. J Bone Joint Surg 1993;75A(3):409-424.
4. Burns W, W hipple T. Anatomic relationships in the shoulder impingement syndrome. Clin Orthop Rei Res 1993;294:96-102.
5. Sigholm G, Styf J, Herberts P. Pressure recording in the sub acromial bursa. J Orthop Res 1988;6:123-128.
6. Neer C. Anterior acromioplasty for the chronic impingement syndrome of the shoulder. J Bone Joint Surg 1972;54A:41.
7. Post M, Cohen J. Impingement syndrome, a review of late stage II and early stage III lesions. Clin Orthop Rei Res 1986;207:126-132.
8. Patte D. The subcoracoid impingement. Clin Orthop Rei Res 1990;254:81-86.
Clin Orti1op Rei Res 1982;168:
10. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:147.
11. Fu F, Harner C, Klein A. Shoulder impingement syndrome. A critical review. Clin Orthop Rei Res 1991;269:162-173.
12. Harryman DT, Sidles JA, Clark JM et al. Translation of the humeral head on the glenoid with passive glenohumeral motion. J Bone Joint Surg 1990;27A:1334-1342.
13. Abrams J. Special shoulder problems in the throwing athlete: pathology, diagnosis, and nonoperative management. Clin Sports Med 1991;10(4):839-861.
14. Hawkins R, Abrams J. Impingement syndrome in the absence of rotator cuff tear (stages I and II). Orthop Clin North Alii
1987;18(3):373-382. 15. Neer C. Impingement lesions. Clin Orthop Rei Res 1983; 173:70-77.
CHAPTER 19 - P AINFUL ARC 383
16. Jobe F, Giangarra C, Kvitne R. Anterior capsulolabral recon
18. Lazarus MD, Harryman DT, Yung SW et 01. Anterosuperior
struction of the shoulder in athletes in overhand sports. Am ]
humeral displacement: limitation by the coracoacromial arch. AAOS Annual Meeting, Orlando, 1995. 19. Poppen LA, Walter KS. Normal and abnormal motion of the shoulder. J Bone Joint Surg 1976;58A:195.
Sports Med 1991;19:428-434.
17. Flatow EL, Soslowsky LJ, Ticker JB et 01. Excursion of the rotator
cuff under the acromion. Patterns of subacromial contact. Am ] Sports Med 1994;22:779-788.
THIS PAGE INTENTIONALLY LEFT BLANK
SECTION FOUR
The shoulder girdle
SECTION CONTENTS 20. Applied anatomy of the shoulder girdle
387
Osteoligamentous structures 387 Muscles and their innervation 390 Mobility of the shoulder girdle 393 21. Clinical examination of the shoulder girdle
395
History 395 Inspection 396 Functional examination Palpation 399
396
22. Interpretation of the clinical examination
401
23. Disorders of the inert structures
403 403 Pain on active elevation combined with pain on passive elevation 406 Pain on active elevation combined with pain on active protraction Pain and limitation of active and passive elevation 407 Limitation of active elevation and weakness of resisted elevation 408 Paraesthesia brought on by active and/or passive elevation 408
Crepitus during scapular elevation 408 Pain on active and passive scapular approximation 24. Disorders of the contractile structures Pain on resisted elevation 411 Pain on resisted protraction 412 Pain on resisted approximation 412 Weakness of scapular approximation Pain on resisted depression 413
411
412
409
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Osteoligamentous structures
387
Acromioclavicular joint 387 Sternoclavicular joint 388 Scapulothoracic gliding mechanism Costovertebral joints 390 Muscles and their innervation
389
390
Anterior aspect of the shoulder girdle Posterior aspect of the shoulder girdle Mobility of the shoulder girdle
Applied anatomy of the shoulder girdle
390 391
393
The shoulder girdle forms the connection between the spine, the thorax and the upper limb. It contains three primary articulations, all directly related to the scapula: the acromioclavicular joint, the sternoclavicular joint and the scapulothoracic gliding surface. The shoulder girdle acts as a unit: it cannot be functionally separated from the secondary articulations, i.e. the lower cervical spine, the cervicothoracic jlmction and the upper thoracic spine, to which it is connected via the costovertebral joints.
OSTEOLIGAMENTOUS STRUCTURES The clavicle articulates at the medial aspect with the sternum - the sternoclavicular joint - and at the lateral aspect with the acromion to form the acromioclavicular joint. In this way it connects the scapula to the trunk (Fig. 20.1).
ACROMIOCLAVICULAR JOINT The rather flat articular surface at the lateral end of the clavicle articulates with the flat articular surface at the medial border of the acromion. The joint has a joint capsule which is reinforced by ligaments: cranially the superior acromioclavicular ligament and caudally the inferior one. The joint often contains an intra-articular disc, which is sometimes incomplete (meniscoid) and is subject to early degeneration. The joint line runs obliquely, from craniolateral to caudomedial (Fig. 20.2). Extra-articular ligaments are important for the stability of the joint and to keep the movements of the lateral end of the clavicle within a certain range. Together they form the roof of the shoulder joint. They are the coracoacromial ligament - between the lateral border of the coracoid
process and the acromion - and the coracoclavicular liga ment. The latter consists of: • The trapezoid ligament which runs from the medial
border of the coracoid process to the trapezoid line at the inferior part of the lateral end of the clavicle. • The conoid ligament which is spanned between the
base of the coracoid process and the conoid tubercle just medial to the trapezoid line. 387
388 SECTION FOUR - THE SHOULDER GIRDLE
Figure 20.1
Bony structures of the shoulder girdle (anterior and posterior view).
Movements in the acromioclavicular joint are directly
ities. The rather loose joint capsule is reinforced by ante
related to those in the sternoclavicular joint and those of
rior and posterior sternoclavicular ligaments. There are
the scapula. This joint is also discussed in Chapter 14.
two extracapsular ligaments: the interclavicular ligament, which interconnects both clavicles and covers the jugular notch, and the costoclavicular ligament, between the
STERNOCLAVICULAR JOINT
sternal end of the first rib and the medial part of the
The sternoclavicular joint is more complex. It is formed
clavicle (Fig. 20.3).
by the articular surface at the medial aspect of the clavi
Close behind the joint lie some vital structures: some
cle and the articular surface at the superolateral corner of
important blood vessels (aorta, brachiocephalic trunk,
the sternal manubrium. The two joint surfaces are dis
brachiocephalic vein, subclavian artery, subclavian vein,
congruent and this is resolved by the presence of an
jugular vein and carotid artery ), the trachea, the oesoph
intra-articular disc, which divides the joint into two cav-
agus, the lung and pleura (Fig. 20.4).
"' ;;::.. - Clavicle --'--"....
Coracoid process -----, Coracoacromial ligament
.:-¥ft"�*,,�$?"'7""-- Trapezoid part, JfIL�;;:i;����"':::::�� :-. �'h"""-"""-""""'- conoid part of coracoclavicular ligament
Supraspinatus tendon (cut) ���""-, Coracohumeral ligament
----,.���
�����������
====1t
Greater tUbercle8 " lesser tubercle of humerus
L-"';:"'h' '-- Coracoid process
Intertubercular synovial sheath ----"Iito-.. (communicates with articular synovial cavity)
'H-:- Openings of subcoracoid ':!!!!!�iiiiirt::� I,;:��---:;H
Biceps brachii tendon ---tl--\f (long head) Subscapularis tendon (cut)
Figure 20.2
The acromioclavicular joint.
,-�-- Superior transverse scapular ligament and scapular notch
-tl-__�-'
-
bursa to shoulder joint
.. of subscapular bursa """....--'-1H--Outiine Capsular ligaments
CHAPTER 20 - APPLIED ANATOMY 389
Clavicle
Interclavicular ligament
Costoclavicular ligament
Figure 20.3
The sternoclavicular joint.
Movements in the sternoclavicular joint are possible
consequences for the joints with which it articulates -
around three axes:
sternoclavicular and acromioclavicular - and indirectly
• Clavicular elevation and depression occur around an
for the glenohumeral joint.
anteroposterior axis • Clavicular protraction - the lateral end of the clavicle
moves forwards, and retraction - the lateral end of the clavicle moves backwards, around a vertical axis • Backwards and forwards rotation of the clavicle
SCAPULOTHORACIC GLIDING MECHANISM The scapulothoracic gliding mechanism is a 'virtual arti culation' indicating that the scapula is mobile in relation
around its longitudinal axis
to the thorax.
Glenohumeral and scapular movements also mobilize
The gliding surfaces are formed by the anterior aspect
the clavicle and thus influence the sternoclavicular joint.
of the scapula and the posterior aspect of the thorax. In
Diminution of the mobility of the clavicle will have direct
between the scapula and the thorax lie the subscapular
R. internal and external carotid arteries -----+-----r--,
r-T-----:-- L. internal and external jugular veins
R. common carotid artery
Oesophagus
Apex of R.lu
Trachea ------,
Aorta
Figure 20.4 Vital structures lying in the rnediastinum behind the sternoclavicular joint.
390 SECTION FOUR - THE SHOULDER GIRDLE
and the serratus anterior muscles (see below). Together
• At the transverse process - the costotransverse joint:
with their fasciae they take part in the gliding mecha
the tubercle of the rib articulates with the articular
nisms that occur during movement.
facet on the transverse process of the vertebra. The
The scapula moves in three directions: • Up and down (elevation and depression, respec
tively) when the lateral end of the clavicle does the same. The medial border of the scapula remains more or less parallel to the spine. • Lateral and medial rotation - the inferior angle
moves laterally and medially. These movements are mainly induced by movements of the arm towards
joint capsule is again reinforced by several ligaments: costotransverse ligament - between the neck of the rib
and the transverse process; lateral costotransverse liga ment
-
between the angle of the rib and the tip of the
transverse process; and the superior costotransverse lig ament - between the crest of the neck of the rib and
the inferior border of the transverse process of the vertebra above (Fig. 20.6).
abduction/ elevation and extension. •
It glides laterally and medially - protraction and retraction or approximation - when the lateral end of the clavicle does the same. The scapula glides away from the spine but its medial border remains parallel to the spine (Fig. 20.5).
MUSCLES AND THEIR INNERVATION Those muscles that create movement at the acromio clavicular joint, the sternoclavicular joint or in the scapulothoracic gliding mechanism, or those muscles that connect the scapula to the trunk, can be considered as
COSTOVERTEBRAL JOINTS The ribs articulate with the thoracic spine at two levels: •
At the vertebral body - the costovertebral joint: the head of the rib articulates with the lateral aspect of one or two vertebral bodies. The joint capsule is rein forced by the radiate ligament of the joint at the head of
'shoulder girdle musculahue'. Many of these muscles also have influence on the secondary articulations: the cervical spine, the shoulder or the thoracic spine and are discussed in Chapters 6, 14 and 38 respectively. In this chapter only those muscles that are not discussed elsewhere are described.
the rib. Intra-articularly the head of the rib is con
ANTERIOR ASPECT OF THE SHOULDER GIRDLE
nected to the intervertebral disc by the intra-articular
The muscles at the anterior aspect of the shoulder girdle
ligament of the joint at the head of the rib.
are outlined in Table 20.1 and Figure 20.7.
2
ifttII-\--- 4
Figure 20.5
The scapulothoracic gliding mechanism.
Figure 20.6 The costovertebral joints. (1) anterior longitudinal ligament; (2) disc; (3) costotransverse ligament; (4) superior costotransverse ligament; (5) radiate ligament.
CHAPTER 20 - APPLIED ANATOMY
Table 20.1
391
Anterior muscles of the shoulder girdle
Muscle
Nerve
Spinal nerve root
Sternocleidomastoid Subclavius Pectoralis minor Pectoralis major Deltoid Pectoral part Biceps brachii Coracobrachialis
Spinal accessory and cervical plexus Nerve to subclavius Pectoral nerves Pectoral nerves Axillary nerve Pectoral rami Musculocutaneous nerve Musculocutaneous nerve
C1-C2 C5-C6 C6-C8 C5-T1 C4-C6 C4-C5 C5-C6 C6-C7
Subclavius muscle The subclavius takes origin at the junction between the bone and the cartilage at the sternal end of the first rib. It inserts at the inferior and lateral aspect of the clavicle. It pulls the clavicle against the sternum and has a stabiliz ing effect on the sternoclavicular joint.
Pectoralis minor muscle The pectoralis minor muscle takes origin anteriorly at the third to fifth ribs and inserts at the inferior and medial border of the coracoid process. Its contraction results in a depression and protraction of the scapula.
Costocoracoid fascia
5
The costocoracoid fascia is a strong aponeurosis that envelops the subclavius, pectoralis minor and partly the coracobrachialis muscles. It runs deeply from the cora coid process and is attached to the anterior costal wall.
4 --f--t--+--+H�
POSTERIOR ASPECT OF THE SHOULDER GIRDLE The muscles at the posterior aspect of the shoulder girdle are outlined in Table 20.2 and Figure 20.S. Table 20.2
Posterior muscles of the shoulder girdle
Muscle
Nerve
Spinal nerve root
Figure 20.7 Anterior muscles of the shoulder girdle. (1) pectoralis major; (2) deltoid; (3) serratus anterior; (4) pectoralis minor; (5) subclavius.
Sternocleidomastoid muscle The sternocleidomastoid muscle originates with two heads, one from the manubrium of the sternum and one from the medial end of the clavicle. It inserts at the mastoid
process
and
the
superior
nuchal
line.
Contraction of the muscle puts stress on to the sterno clavicular joint.
Trapezius Levator scapulae Rhomboids Serratus anterior Latissimus dorsi Teres major Subscapularis Infraspinatus Teres minor Supraspinatus Deltoid Triceps brachii
Spinal accessory nerve Dorsal scapular nerve Dorsal scapular nerve Long thoracic nerve Thoracodorsal nerve Thoracodorsal nerve Subscapular nerve Suprascapular nerve Axillary nerve Suprascapular nerve Axillary nerve Radial nerve
C2-C4 C4-C5 C4-C5 C5-C7 C6-C8 C6-C7 C5-C8 C4-C6 C5-C6 C4-C6 C4-C6 C6-C8
392 SECTION FOUR - THE SHOULDER GIRDLE
Posterior muscles of the shoulder girdle. (1) Rhomboids; (2) Levator scapulae; (3) Trapezius; (4) Deltoid; (5) Latissimus dorsi;
Figure 20.8
c:
0
"""
19 2
Figure 20.9
c:
0
=
19 2
Movements at the shoulder girdle.
Elevation
t
CHAPTER 20 - APPLIED AN ATOMY 393
Levator scapulae muscle
and scapulothoracic gliding mechanism. It can only be
The levator scapulae takes origin at the posterior tuber
maximal when the secondary articulations also function
cles of the transverse processes of the first to fourth
normally.
cervical vertebrae and inserts at the superior angle and
The movements that occur when the shoulder is moved
superior part of the medial border of the scapula. It
and that can be assessed in shoulder girdle examination
elevates and medially rotates the scapula.
are:
Serratus anterior muscle
• Elevation: the shoulder moves upwards in the frontal
The serratus anterior has origin with nine or ten heads at the lateral aspect of the first to eighth or ninth ribs and inserts along the entire medial border of the scapula, from the superior to the inferior angle. Three different parts are recognized: superior, medial and inferior. It fixates the scapula against the thorax and moves the scapula towards protraction and lateral rotation.
plane. The range is approximately 30-45°. • Depression: the shoulder moves downwards in the
frontal plane. The range is about 5°. • Protraction: the shoulder moves forwards in a trans
verse plane with a range of up to 30°. • Retraction: the shoulder m oves backwards in a trans
verse plane. The range is about 30°. This movement is also referred to as 'scapular approximation'.
MOBILITY OF THE SHOULDER GIRDLE
Anterior and posterior rotation of the clavicle cannot be examined separately. It is the result of arm move
Mobility in the shoulder girdle depends on the mobility
ments towards flexion or elevation and extension
of the primary joints - acromioclavicular, sternoclavicular
(Fig. 20.9).
THIS PAGE INTENTIONALLY LEFT BLANK
Clinical examination of the shoulder girdle
CHAPTER CONTENTS History
395
Inspection
396
Functional examination
396
Active movements 396 Passive movements 398 Resisted movements 399
Palpation
399
The shoulder girdle acts as a zone of transition. It is localized between three other regions: the cervical spine, the upper thoracic spine and the shoulder. SYMPTOMS REFERRED TO THE SHOULDER GIRDLE
Pain originating from the cervical spine or from the upper thoracic spine is frequently felt at the shoulder girdle, for example at the base of the neck, in the trapez ius muscle or in the scapular area. It may also radiate towards the subclavicular, pectoral or axillary regions or into the upper limb. This overlaps with possible symptoms from shoulder girdle disorders. Shoulder girdle movements are therefore included in both the cervical (see p. 147) and thoracic (see p. 593) examinations. This preliminary screening may arouse suspicion about the shoulder girdle. SYMPTOMS REFERRED FROM THE SHOULDER GIRDLE
Pain that originates from a disorder in the shoulder girdle is usually experienced at the base of the neck, in the pectoroclavicular area or in the trapezius muscle. It rarely spreads down the arm and thus arm pain may implicate either the spine or the shoulder. Paraesthesia in the arm may result from a condition affecting the brachial plexus in the shoulder girdle.
HISTORY
Symptoms from a disorder in the shoulder girdle are not typical. They mimic those of neck, upper thorax or shoulder. History taking will therefore start in the same way as for the examination of the cervical (see p. 147) or thoracic spine (see p. 593) or of the shoulder (see p. 292). The exam iner will notice elements that may lay blame on the spinal joints (e.g. pain shifting from the centre to one side) or fea tures that point towards a lesion of the shoulder girdle (e.g. increase of symptoms following scapular movements). 395
396 SECTION FOUR - THE SHOULDER GIRDLE
INSPECTION
On inspection, special attention must be given to swelling (i.e. in the supraclavicular fossa), changes in the colour of the skin, muscular atrophy, difference in height of the shoulders and winging of the scapula.
shoulder girdle (e.g. positive scapular tests), these will be examined thoroughly. When the history is unspecific a preliminary examina tion (quick survey) of the upper quadrant is done (see p. 294). This includes tests for: • • •
The neck The shoulder girdle The shoulder The arm: as a neurological examination and to exclude local disorders in the upper limb.
FUNCTIONAL EXAMINATION
•
The functional examination of the shoulder girdle is never done as primary testing but follows evaluation of one of the other regions, which may provide elements that implicate the shoulder girdle.
Functional examination of the shoulder girdle is very simple: three active, three passive and four resisted movements are performed (see Fig. 21.1), summarized in Box 21.1 (p. 397).
Clinical examination of the shoulder girdle is an accessory to general assessment.
If the patient has described symptoms that could orig inate from the spine or from the shoulder, the cervical, thoracic or shoulder examination is performed. When, in this examination, signs are found that point towards the
ACTIVE MOVEMENTS
The active tests cause movement in the three primary articulations. During all active movements (Fig. 21.2), attention is paid to pain, range of motion and abnormal sensations, such as paraesthesia or crepitus. The move ments may stretch inert or contractile structures and make muscles work. A decreased range of movement is
Shoulder girdle examination Figure 21.1
Strategy for the examination of the shoulder girdle.
CHAPTER 21
-
CLINICAL EXAMINATION 397
Box 21.1 Summary of examination of the shoulder girdle Active movements of the shoulders Elevation of both shoulders Protraction of both shoulders Retraction of both shoulders Passive movements of the shoulder Elevation Protraction Retraction Resisted movements of the shoulder Elevation Protraction Retraction Depression Palpation
(a)
usually the result of either a neurological disorder or a problem of an inert structure. Active elevation of both shoulders ('shrugging')
The examiner stands behind the patient and asks for both shoulders to be shrugged. This movement requires full mobility of the scapulae. The normal range is between 30 and 45°. Active protraction of both shoulders
The patient brings both shoulders forwards. The normal range of scapular abduction is about 30°. Active retraction of both shoulders
The patient is asked to pull both shoulders backwards. Normally, about 30° is possible. General considerations concerning active scapular movements
difference in height between the shoulders on shrug ging indicates impaired mobility. This may be the result of disturbance of the scapulothoracic gliding mechanism or of a neurogenic condition leading to weakness of the scapular elevators. Pain found on active elevation may be due to a problem of a contractile or an inert structure. Passive and resisted movements reveal the true nature of the lesion. Crepitus present on active elevation means the posterior thoracic wall has roughened, which often has an unknown cause. Paraesthesia when the shoulders are kept shrugged for a while are pathognomonic of a thoracic outlet syndrome (postural variety). Pathological findings on the other active movements may be due to muscular activity, stretching of an inert structure or a movement in one of the three primary artic ulations (acromioclavicular joint, sternoclavicular joint or scapulothoracic gliding surface).
(b)
A
(c) Figure 21.2
(c) retraction.
Active movements of the shoulders: (a) elevation; (b) protraction;
398 SECTION FOUR - THE SHOULDER GIRDLE
Because active elevation, retraction and protraction of the shoulders pull the dura mater in a cranial direction via the first thoracic nerve root, pain on one of these movements may have a dural origin. This may occur in thoracic discodural interactions. PASSIVE MOVEMENTS
For a clear differential diagnosis between disorders of inert and contractile structures, active tests must be followed by passive and resisted movements. Passive movements (Fig. 21.3) put local inert structures under tension, have some influence on the joints at both ends of the clavicle and may passively stretch some contractile structures. Because the scapula glides on the thorax during these movements, the scapulothoracic gliding surface also must function properly. The problem can be either of the scapulothoracic gliding surface, as in scapular metastases, or of one of the musculoligamentous attachments of the scapula to the trunk, or the outcome of an apical tumour of the lung. Total ankylosis of the acromioclavicular or of the sternoclavicular joint due to ankylosing spondylitis or to arthrosis are other possible causes. For all passive tests, attention is paid to their influence on the pain, the range of movement and the end-feel. The 'normal' range of movement is the same as for ihe active tests; in normal subjects, the end-feel is elastic for all three passive movements, due to combined ligamentous and muscular stretching.
(a)
Passive elevation of the shoulder
The examiner stands behind the patient, places one hand underneath the flexed elbow and brings the shoulder up by an upward directed pressure on the olecranon. The other hand fixates at the contralateral side of the base of the neck (Fig. 21.3a).
(b)
Passive protraction of the shoulder
The patient is supine. The examiner stands at the patient's painful side and asks the patient to bring the shoulder forwards actively. The ipsilateral hand on the sternum is used for fixation, with the contralateral hand on the scapula. The patient is then asked to relax and the examiner continues the movement passively to the end of range where an extra pressure is given to assess end-feel (Fig. 21.3b). Passive retraction of the shoulder
The patient is asked to lie prone with the arm on the back. The examiner, at the patient's painless side, asks the patient to pull the shoulder actively backwards and then places the contralateral hand at the spine and fixes that area. The ipsilateral hand lies at the anterior aspect of the
(c)
�
Figure 21.3
(c) retraction.
Passive movements of the shoulder: (a) elevation; (b) protraction;
CHAPTER 21 - CLINICAL EXAMINATION 399
shoulder. The patient is asked to relax and the examiner continues the movement passively to the end of range where an extra pressure is given for the judgement of the end-feel (Fig. 21.3c). RESISTED MOVEMENTS
During resisted movements (Fig. 21.4) pain and weak ness are assessed. Resisted elevation of the shoulder
This is a test for the pectoralis major, serratus anterior and pectoralis minor muscles. Resisted retraction of the shoulder
The same technique is used as for resisted protraction but one hand is placed on the posterior aspect of the shoulder and one on the sternum (Fig. 21.4c). The following muscles are tested: rhomboids, middle and lower parts of the trapezius and latissimus dorsi. Resisted depression of the shoulder
The examiner stands at the patient's painful side and puts both hands on the shoulder. The patient is asked to shrug the shoulder against the examiner's resistance (Fig. 21.4a). This movement tests the levator scapulae and the upper part of the trapezius, as well as the integrity of the C2-C4 nerve roots.
The patient bends the elbow to a right angle. The exam iner puts both hands under the elbow and asks the patient to press down (Fig. 21.4d). This test examines the pectoralis minor, subclavius or latissimus dorsi muscle.
Resisted protraction of the shoulder
PALPATION
The examiner stands at the patient's side and puts one hand on the anterior aspect of the shoulder, the other one on the posterior thorax between the scapulae. The patient is now asked to press the shoulder forwards (Fig. 21.4b).
The functional tests are sometimes followed by palpa tion, if the structure at fault lies within the reach of the fingers.
Figure 21.4
(a)
(b)
(c)
(d)
Resisted movements of the shoulder: (a) elevation; (b) protraction; (c) retraction; (d) depression.
THIS PAGE INTENTIONALLY LEFT BLANK
Interpretation of the clinical examination of the shoulder girdle Passive elevation is painful
�
I----.- Disorders of sternoclavicular joint Sprain of sternoclavicular joinUligaments Posterior sternoclavicular syndrome Arthrosis Rheumatoid arthritis Septic arthritis Sprain of acromioclavicular joint Disorders of first rib
t
Interpretation of the clinical examination of the shoulder girdle
Sprain of first costotransverse joint Stress fracture of first rib
Traction fracture of spinous process C71T1 Lesion of conoid/trapezoid ligament Beginning of idiopathic contracture of costocoracoid fascia Neural compression
t Active protraction is painful
compression of dura mater
T1-T2 nerve root compression
1----"1'" Lesion of conoid/trapezoid ligament
L-___________---'
Compression ofT1-T2 nerve root Idiopathic contracture of costocoracoid fascia
Active approximation is painful + passive approximation is painful '--'----'--'-------'-----'
1----"1'"
Compression of dura mater Compression of upper thoracic dural sleeve
Active elevation is painful and limited + 1___..... Ankylosis of acromioclavicular joint passive elevation is painful and limited I'" Disorders of sternoclavicular joint
t
�
AnkYIOSiS Traumatic dislocation Hyperostosis
Disorders of costocoracoid fascia Idiopathic contracture Neoplasm Healed apical tuberculosis Postradiation therapy Haematoma between costocoracoid fascia and ribs Scapular metastases Apical tumour of lung Active elevation is limited + resisted elevation is weak
Resisted elevation is painful
Disorder of spinal accessory nerve
L C2 - C4 nerve root lesion f----.- Levator scapulae Trapezius
Contractile structures
Traction fracture of spinous process C7-T1 Stress fracture of first rib Resisted protraction is painful
1----pPectoralis major
L-___________---'
Pectoralis minor Serratus anterior
Resisted approximation is painful
1---..... Rhomboids Trapezius
Resisted approximation is weak
Resisted depression is painful
1----- Disorder of spinal accessory nerve 1---..... Subclavius
L-___________---'
Pectoralis minor Latissimus dorsi
401
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Pain on active elevation combined with pain on passive elevation 403
Disorders of the sternoclavicular joint 403 Sprain of the acromioclavicular joint 405 Disorders of the first rib 405 Traction fracture of the spinous process C7 or T1 406 Lesion of the conoid/trapezoid ligament 406 Idiopathic contracture of the costocoracoid fascia 406 Neural compression 406
Disorders of the inert structures
Pain on active elevation combined with pain on active protraction
406
Lesions of the inert structures are mainly characterized
Pain and limitation of active and passive elevation Ankylosis of the acromioclavicular joint 407
407
ments. Combination with pain on resisted movements
Disorders of the sternoclavicular joint 407 Disorders of the costocoracoid fascia 407 Scapular metastases 408 Apical tumour of the lung 408
draws attention to muscular or tendinous lesions (see Ch.
Paraesthesia brought on by active and/or passive
408
Pain on active and passive scapular approximation
involvement.
PAIN ON ACTIVE ELEVATION COMBINED WITH PAIN ON PASSIVE ELEVATION
408
Crepitus during scapular elevation
24). Combination with weakness when the resisted
movements are performed is suggestive of neurological
limitation of active elevation and weakness of resisted elevation 408
elevation
by pain and / or limitation on active and passive move
409
DISORDERS OF THE STERNOCLAVICULAR JOINT Disorders of this joint are usually the result of an injury; arthrosis, hyperostosis and rheumatoid or septic arthritis are other possibilities.! All conditions give rise to both scapular and shoulder signs and occasionally to signs on movements of the neck. The clinical pattern closely resembles that of an acromioclavicular joint lesion but the localization of pain at the medial end of the clavicle draws attention to the sternoclavicular joint. In posterior sternoclavicular syndrome, the pain is felt posteriorly at the base of the neck. Positive signs are commonly found at three levels: neck or upper thorax, shoulder girdle and shoulder. Neck signs. All active or resisted movements of the neck
that involve the sternocleidomastoid muscles may also provoke some pain: active and resisted rotation towards the painless side and resisted side flexion towards the painful side. Shoulder girdle signs. There is pain on full active and
passive elevation of the shoulder. The other active and passive movements are not or are only slightly painful. Shoulder signs. Pain is also found on active and passive
movements of the arm because almost all arm move ments have some influence on the sternoclavicular joint. Pain is most marked on elevation of the arm. When a disorder of the sternoclavicular joint is sus pected, passive horizontal adduction of the arm should be performed: pain is most pronounced with this test (Fig.
23.1). 403
404
SECTION FOUR - THE SHOULDER GIRDLE
Figure 23.1
Passive horizontal adduction.
Sprain of the sternoclavicularjoint/ligaments
Figure 23.2
Injection of the sternoclavicular joint
This is usually the result of an injury such as a fall on the outstretched hand or on the shoulder. Occasionally, a sprain is the result of overuse, which mainly occurs in arthrotic joints. Pain is felt unilaterally over the lateral manubrial angle and may radiate into the clavicular area. It can be elicited by active and passive elevation of the scapula and by all passive movements of the arm. Resisted movements are negative. Passive horizontal adduction - an accessory test - is the most painful movement. On palpation there is tenderness over the joint line or in the ligaments. Treatment. When the onset is recent, the arm should be
Posterior sternoclavicular syndrome This rare disorder may arise spontaneously in middle aged people and usually causes a misleading clinical picture. Patients complain of unilateral pain at the base of the neck. Surprisingly, the pain is felt more posteriorly and not at the sternoclavicular joint itself, which suggests a lesion of the cervical spine. Nevertheless, clinical exami nation of the neck does not localize the problem: there is usually full range on passive movements and no pain on active and resisted movements. Both active and passive
placed in a sling to diminish the effect of gravity. An
elevation of the arm are painful. Sometimes it is even
intra-articular steroid injection is given at once.
hard to achieve full range. All other movements of the
Technique: injection of the sternoclavicular joint. The patient lies supine. The gap between the medial end of the clavicle and the sternum is palpated. A needle of
2.5 cm is introduced, penetrating the joint to a depth of 1 cm (Fig. 23.2), and 1 ml of triamcinolone acet
about
onide is injected. If excessive resistance is encountered, the needle is in the meniscus; if this occurs, the tip of the
arm are normal, except for passive horizontal adduction which is most painful. Clinical examination of the shoulder girdle is required. Pain is elicited by active and passive elevation of the shoulder. Resisted shoulder elevation is negative, which excludes the trapezius and levator scapulae muscles. No pain is found on palpation of the anterior portion of the sternoclavicular joint.
needle should be partly withdrawn with continuous
Treatment. One or two infiltrations of
pressure on the plunger until the steroid floats in with
cinolone into the posterior sternoclavicular ligament is
little resistance.
helpful and can be done in one of two ways:
20 mg triam
CHAPTER 23 - DISORDERS OF THE INERT STRUCTURES
• By approaching the ligament from above and
405
immune system, with rheumatoid arthritis and diabetes
allowing the needle to progress behind the joint until ligamentous resistance is felt
mellitus, and in drug addicts. 5 -7 The patient usually has fever, chills and sweating, and complains of pain and
• From the front, passing through the joint as for an
swelling in the sternoclavicular area, sometimes at
intra-articular injection.
the base of the neck. In about
In both instances, the steroid must be infiltrated into
erythematous mass is present at the joint because of abscess formation.8-10
the posterior ligament and counterpressure must be present during the whole procedure. Therefore the tip of the needle is partly withdrawn and reinserted several times, over the whole of the posterior ligament, as
A combination of neck signs, shoulder signs and shoulder girdle signs is found on examination: •
the product is injected. Throughout, special care must
sternocleidomastoid and scaleni muscles. •
The patient is reassessed after
2 weeks; if symptoms
are still present a second infiltration is given. Normally two or three infiltrations suffice.
Passive and resisted neck movements are painful as the result of passive and active stretching of the
be taken not to penetrate neighbouring visceral struc tures.
20% a local, warm and
Active and passive elevation of the arm are very limited.
•
Active and passive shoulder girdle movements are painful and limited. There is warmth, swelling and exquisite tenderness over the sternoclavicular joint.
Arthrosis Arthrosis of the sternoclavicular joint is common. It occurs mainly in postmenopausal women. The chief com plaint is cosmetic: there is a visible thickening of the joint. The pain, if any, is minor. Elevation of the arm is limited as the result of the limitation of the shoulder girdle movement.
Movements of the shoulder
girdle are
uncomfortable but not really painful.
There is an elevated erythrocyte sedimentation rate and tomography or CT scan are mostly likely to show bony erosions and destructive changes at the medial end of the clavicle and the clavicular aspect of the sternum. Treatment. Inpatient treatment is required, the joint being
immediately aspirated and antibiotics started. When an
Radiography shows degenerative changes (osteo
abscess is present, surgical drainage is necessary. 11
phytes, bone cysts, hyperostosis and diminution of the joint line), most pronounced at the inferior aspect of the clavicular head. OccaSionally calcification is seen in the ligaments. For the overuse phenomenon in arthrosis an intra articular injection of triamcinolone acetonide is also given but patients must be warned that overuse will always have to be avoided, otherwise pain will recur.
SPRAIN OF THE ACROMIOCLAVICULAR JOINT Pain is usually confined to the area of the acromio clavicular joint. Both active and passive elevation of the scapula may be slightly painful but painless move ment is not uncommon. The diagnosis becomes clear when the shoulder is examined.
Local pain over
the acromioclavicular joint is provoked at the end range
Rheumatoid arthritis Rheumatic conditions may also affect the sternoclavicu lar joint. This often occurs in ankylosing spondylitis.2 It gives rise to the same clinical pattern as in a sprain, but local swelling from synovial thickening is present. A pro gressive ankylosis develops with pronounced limitation of movement in the shoulder girdle. Other sites of rheumatoid arthritis should bring the disorder in mind, although the sternoclavicular joint may be the first joint affected.
of the three passive movements of the shoulder exami nation: passive elevation, lateral rotation and medial rotation (for a detailed description, see Ch. 17, pp.
327-332). DISORDERS OF THE FIRST RIB The first rib can become affected in that it becomes sprained at the level of the articulation with the spine or becomes the site of a stress fracture.
Treatment. Local infiltration of triamcinolone acetonide
may cure the patient.
Sprain of the f irst costotransverse joint The patient complains of unilateral pain at the base of
Septic arthritis Bacterial
agents
the neck elicited by certain movements of the ann and such
as
Staphylococcus
aureus,
shoulder. On examination pain is elicited by active and
Streptococcus group B and Brucella have been isolated
passive side flexion away from the painful side and
in septic arthritis of the sternoclavicular joint.3,4 Septic
resisted flexion towards the painful side. Flexion may
arthritis occurs in elderly patients with a deficient
also be positive.
406
SECTION FOUR - THE SHOULDER GIRDLE
Such a pattern - in fact a contractile tissue pattern draws attention to the scaleni muscles. In this case the lesion does not lie in the scaleni but in the structure to which the muscle is attached. Pain is also present on active and passive elevation of the arm and the scapula, resulting in a mixed pattern of neck, shoulder and shoulder girdle signs (see p.
205).
Shoulder elevation is considered one of the dural signs because it stretches or moves the thoracic dura mater via traction on the intercostal nerves. The same applies to the upper thoracic nerve roots.
Compression of the dura mater Dural mobility may be impaired as the result of com
Stress f racture of the f irst rib Pain occurs spontaneously and is felt unilaterally at the base of the neck and in the scapulopectoroclavicular area. The clinical picture is typical. There are neck, shoulder girdle and shoulder signs. In the neck a 'con tractile tissue pattern' is found: pain on active and passive side flexion towards the painless side, combined with pain on resisted side flexion towards the painful side. All scapular movements are more or less painful and active elevation of the arm is impossible because of the pain: the arm stops at the horizontal. Passive eleva tion is full but painful. Radiography is confirmative (see also p.
NEURAL COMPRESSION
322).
pression from a space-occupying lesion in the spinal canal. In most instances it is a discodural interaction caused by a posterocentral thoracic disc protrusion. It gives rise to multi segmentally referred pain, which may increase on all active and passive scapular movements (see p.
144 and 178).
T1-T2 nerve root compression The mobility of the upper thoracic nerve roots is reduced when a space-occupying lesion in the lateral root recess or in the intervertebral foramen causes compression. Again the disc (a posterolateral protrusion) may be responsible in rare instances but reduction of the forami nal size may also be related to degenerative conditions. The active and passive movements of the shoulder may
TRACTION FRACTURE OF THE SPINOUS
all have an influence on the symptoms: pain and paraes
PROCESS C7 OR T1
thesia at the inner aspect of the upper limb. Motor deficit
Following serious exertion the patient feels a sudden pain at the cervicothoracic junction. Neck signs are subtle but arm signs are pronounced: the patient is hardly able to bring both arms actively above the horizontal. Passive
is uncommon and if it occurs - possibly in the intrinsic muscles of the hand - the sign should be regarded as a warning one. Apical tumour of the lung is most likely (see p.
190-191).
arm elevation is painful but not limited. Active and resis ted shoulder movements are painful. Radiography shows avulsion of the seventh cervical or first thoracic spinous process (see p.
322 and 213).
PAIN ON ACTIVE ELEVATION COMBINED WITH PAIN ON ACTIVE PROTRACTION Pain on active forwards movement of the shoulder does
LESION OF THE CONOID/TRAPEZOID
not occur in isolation. It is usually combined with pain on active elevation. This clinical picture may occur in rather
LIGAMENT
uncommon situations:
Pain is felt in the midclavicular area and is often due to 'smash' movements, such as occur in volleyball, baseball
• Lesion of the conoid and/or trapezoid ligament: this
gives rise to pain located in the infraclavicular fossa,
and serving in tennis. It is increased at the extremes of all
provoked by both arm and shoulder movements
passive movements of the arm but resisted movements remain negative. Forced passive lateral rotation with the arm abducted to 90° is also painful, as are the extremes of all active and passive shoulder movements (see p.
331).
(see p. •
331).
Compression of an upper thoracic nerve root (Tl/T2): a discoradicular interaction at the first or second tho racic level gives rise to a partial articular pattern of the thoracic spine. Dural symptoms and signs should
IDI OPHATIC CONTRACTURE OF THE COST OCORACOID FASCIA In its initial stage, this gives rise to pain in the antero lateral pectoral area, sometimes in the posterior thorax
be sought although they are not necessarily present. Any other space-occupying lesion (e.g. a tumour) is also possible and even more probable (see p.
190).
• Idiopathic contracture of the costocoracoid fascia: the
clinical picture strongly resembles a sprained
around the scapula. Pain is provoked by full elevation of
coracoclavicular ligament. Often arm and shoulder
arm and shoulder (see p.
elevation are slightly limited.
332).
CHAPTER 23 - DISORDERS OF THE INERT STRUCTURES
PAIN AND LIMITATION OF ACTIVE AND PASSIVE ELEVATION ANKYLOSIS OF THE ACROMIOCLAVICULAR JOINT Limitation on active and passive elevation of the scapula may be the outcome of complete ankylosis of the acromioclavicular joint as the result of ankylosing spondylitis, arthrosis or rheumatoid arthritis. The arm cannot
actively
horizontal.
or passively be raised above the
Examination of the glenohumeral joint
reveals normal mobility. Examination of the shoulder girdle shows that scapular elevation is totally limited (see p.
322).
407
Treatment. Luxation of the bone often needs surgical
repair.2o In subluxation it usually suffices to do a passive retropulsion of the shoulder girdle by immobilization,21 for example fixating it with a 'figure-of-eight' bandage. Intra-articular
triamcinolone
may
occasionally
be
added.
Sternoclavicular hyperostosis This is a rare condition, in which progressive ossification develops in the sternoclavicular joint, the joint between the first rib and the sternum and the sternoclavicular and costoclavicular ligaments. In advanced cases the forma tion of a massive osseous block between sternum, clavicle and first rib can be seen. It may be associated with seronegative spondyloarthropathy22 and occasion ally with pustulosis palmaris and plantaris. It is then
DISORDERS OF THE STERNOCLAVICULAR JOINT
Ankylosis of the sternoclavicularjoint Ankylosis of the sternoclavicular joint as a result of ankylosir,g spondylitis, arthrosis or rheumatoid arthritis gives rise to an identical clinical pattern as that of ankylo sis of the acromioclavicular joint. However, pain - if present - is at the medial end of the clavicle (see p.
322).
known as SAPHO syndrome (synovitis-acne--pustulosis
hyperostosis-osteitis). 23-25
There is gross limitation of shoulder girdle movements which may end in complete ankylosis.26 Active and passive elevation of the shoulder girdle is impossible. Elevation of the arm is grossly limited and shows a forward component. The scapula is totally immobile during arm elevation. Overcompensation on
Traumatic dislocation
shoulder
movements may
result in a lesion of the acromioclavicular joint.
Traumatic dislocation of the sternoclavicular joint is not common. The medial portion of the clavicle may be displaced anteriorly or posteriorly. Anterior luxation is by far the more common. It out numbers posterior dislocations by up to 20 to 1.12 This is
Treatment. There is no causative treatment for this con
dition. Steroid infiltration in the ligaments may give some temporary relief. The results after surgery are poor.
because the posterior capsule and ligaments are stiffer than the anterior structures, so that posterior luxation is more difficult.13 Some cranial displacement is associated because of the weight of the arm. Symptoms and signs resemble those of a proximal fracture of the clavicle: the patient supports the painful arm, the shoulder girdle looks 'shortened' and the head is held deviated towards the affected side. The active and
DISORDERS OF THE COSTOCORACOID FASCIA Disorders of the costocoracoid fascia may also limit active and passive shoulder elevation. Several disorders may be responsible for stretching pain or contracture of the costocoracoid fascia: • Idiopathic contracture: an idiopathic contracture of the
passive movements of the shoulder girdle are all
costocoracoid fascia is a very uncommon cause of
extremely painful. The luxation deformity is clearly
limited elevation of the arm.27 It comes on
visible.
spontaneously and initially causes unilateral
Subluxation
is usually
not
inconvenient
to the
pectoroscapular pain on full elevation of the arm and
patient.14 Some people can dislocate the medial portion
on active and passive elevation of the shoulder. At a
of the clavicle voluntarily as a 'party trick'. In this event,
later stage, the pain becomes permanent and a limita
pain is not felt but an audible click is present. Anterior
tion of about
displacement must be distinguished from synovial
arm and shoulder may set in. The limitation of eleva
swelling, which may take place in rheumatoid arthritis.
tion of the arm suggests a psychogenic disorder but
The
history
of
an
injury
suggests
displacement.
10° on active and passive elevation of
the few 'missing' degrees on shoulder elevation
Radiography is of little help.
provide the key to the diagnosis. Forward movement
A posterior dislocation may threaten or damage mediastinal structures.15-18 It may result in venous
range, although backward movement (retraction) is
congestion of arm and head, as well as dyspnoea and
normal. No resisted movements hurt. On examination
swallowing disturbances.19
of the neck, slight pain may be fOlmd on active flexion
of the shoulder (protraction) is painful but of full
408
SECTION FOUR - THE SHOULDER GIRDLE
to the contralateral side and on resisted side flexion
Warning
towards the painful side.
A physician who examines a patient complaining of
• Neoplasm: the previous disorder must be
differentiated from an invasion by a tumour of the costocoracoid fascia which gives rise to the same signs but is more rapid and swifter in its evolution.
pectoroscapular pain should always bear in mind the possibility of an apical lung tumour and look for unusual symptoms and signs.
Other neurological signs (e.g. Horner's syndrome) should be looked for. • Healed apical tuberculosis: this may also limit mobility
and elasticity of the costocoracoid fascia, causing the
LIMITATION OF ACTIVE ELEVATION AND WEAKNESS OF RESISTED ELEVATION
same clinical picture as in idiopathic contracture. • Postradiation therapy: similar clinical features may be
This presentation points towards a lesion of the nerve
encountered after radiation therapy for cancer of the
root
lung or breast.
cause.
• Haematoma between the costocoracoid fascia and the
C2-C4. It appears that disc protrusion is never the
Disorders affecting the spinal accessory nerve may
ribs with subsequent traumatic fasciitis may result
give rise to weakness of the trapezius muscle and thus of
from injury to the anterior chest wall. This again
scapular elevation (see p.
543).
gives rise to a similar clinical picture: pain and limitation of both ac;:tive and passive elevation of the shoulder and arm. The radiograph shows no evidence of rib fracture. The disorder undergoes spontaneous cure over about
Painless weakness on one of the resisted movements is suggestive of a neurological lesion.
3 months. PARAESTHESIA BROUGH T ON BY ACTIVE ANDIOR PASSIVE ELEVATION
SCAPULAR METASTASES Scapular metastases are accompanied by unilateral scapular pain, which is increased by all active and passive movements of the shoulder. As the result of excessive pain, active and passive elevation of the
If pins and needles come on in fingers or hand during active or passive elevation of the scapula, a thoracic outlet syndrome is very likely (see p.
546).
shoulder may become limited.
CREPITUS DURING SCAPULAR ELEVATION Warning The type and localization of the pain, together with - in its later stage - muscular atrophy and weakness, and a poor
Painless crepitus is sometimes heard and felt on moving the scapula actively up and down and means that the scapulothoracic gliding surface is no longer functioning
general condition, must warn the examiner, and a
normally. When the patient abducts the scapula by
radiograph must be taken at once.
moving the shoulders forwards the noise may stop. This can occur unilaterally or bilaterally and implies that the posterior thoracic wall, just beyond the lateral edge of
APICAL TUMOUR OF THE LUNG
the iliocostalis muscle, has become rough.28 It is usually
Pancoast's tumour is not uncommon. It grows from the
painless and does not require treatment. Exceptionally.
upper part of the lung and may involve most structures
scapular pain occurs after exertion or even at rest. It
in that area, such as the brachial plexus, the sympathetic
occurs mainly in professions where thoracic hyper
ganglia at the base of the neck, the ribs and the verte
kyphosis is maintained for a long period of time (e.g. sec
brae. It gives rise to pain felt in the pectoroscapular area
retaries and phYSiotherapists).
which may radiate down the upper limb. It may affect
Other cases, usually associated with pain, are the
the normal functioning of the thoracic spine, the
result
shoulder girdle and the shoulder. In the shoulder girdle
elastofibroma lying between the scapula and the bony
of
local
injury,
an
inflamed
bursa
or
an
the
thorax, or an inflammation of other soft tissues in this
shoulder may be painful and limited. Accompanying
location.29 Bursitis is frequently encountered in baseball
symptoms and signs, such as Horner 's syndrome or
pitchers.3D True scapular 'snapping' is the outcome of an
examination,
active
and
passive
elevation
of
atrophy of the intrinsic muscles of the hand, reveal the
osseous projection on the thorax or the anterior wall of
disorder (see p.
the scapula.31
322).
CHAPTER 23 - DISORDERS OF THE INERT STRUCTURES
Treatment Deep friction. In roughening of the posterior thoracic
wall deep friction can be tried. The affected area is out lined by asking the patient to abduct the scapula pro gressively, meanwhile testing scapular elevation at each degree of abduction. In the position that crepitus ceases, the scapula has been brought so far laterally that it has
409
PAIN ON ACTIVE AND PASSIVE SCAPULAR APPROXIMATION This presentation draws attention to interference with the dura mater or the dural nerve root sleeve by an upper thoracic disc protrusion or a spinal tumour.
lost contact with the roughened thorax. The lesion now lies just medial to the medial scapular border. If local tenderness is not found on palpation, the whole upper area around the medial part of the scapula must be treated.
Technique: deep friction to the posterior thoracic wall. The patient lies prone with the shoulder well abducted and the arm in full medial rotation. The therapist stands at the opposite side and gives massage with all fingers in a mediolateral direction for about
20 minutes (Fig. 23.3);
friction is repeated on alternate days. The crepitus will not disappear but the pain usually does, although
20
sessions may be required. Surgery. If massage fails, the superomedial angle of the
scapula can be removed.32 In some cases the whole vertebral border has been removed.33
Figure 23.3
Deep friction to the posterior thoracic wall.
REFERENCES 1. Veys E, Mielants H, Verbruggen G. Reumatologie. Omega, Ghent, 1985:169. 2. Emery RJ, Ho EK, Leong Je. The shoulder girdle in ankylosing spondylitis. f Bone Joillt Surg 1991;73A(10): 1526-1531. 3. Tabatabai M, Sapico F, Canawat H, Harley H. Sternoclavicular joint infection with group B streptococcus. J Rheumatol 1986;13(2):466. 4. Spearman P, Lakey 0, Jotte S et al. Sternoclavicular joint septic arthritis with small-colony variant Staphylococcus aureus. Diagn Microbiol Infect Dis 1996;26(1):13-15. 5. Gillis S, Friedman B, Caraco Y et al. Septic arthritis of the sternoclavicular joint in healthy adults. I Intern Med 1990;228(3): 275-278. 6. Covelli M, Lapadula G, Pipitone N, Numo R, Pipitone V. Isolated sternoclavicular joint arthritis in heroin addicts and/ or HIV positive patients: three cases. Clin Rheumatol 1993; 12(3):422-425. 7. Guerra C, Spillane LL. Sternoclavicular septic arthritis in a patient with end-stage liver disease. Ann Emerg Med 1996;27(2):264-266. 8. Ibanez R, Ruiz P, Garcia-Chillon A et al. Sternoclavicular brucel losis. J RheumatoI 1987;14:183-185. 9. Wohlgethan JR, Newberg AH, Reed JI. The risk of abscess from sternoclavicular septic arthritis. J RheumatoI1988;15(8):1302-1306. 10. Asnis OS, Dhaliwal GS. Bilateral sternoclavicular joint septic arthritis presenting as cutaneous abscesses. Clin Infect Dis 1994;19(5):964-966. 11. Van Linthoudt 0, Velan F, Ott H, Wohlgethan J. Abscess forma tion in sternoclavicular joint septic arthritis. I RheumatoI 1989;16(3):413-414.
12. Rockwood CA Jr. Disorders of the sternoclavicular joint. In: Rockwood CA Jr, Matsen FA III (eds) The Sholiider. Saunders, Philadelphia, 1990:477-525. 13. Delmis MG, Kummer FJ, Zuckerman JO. Dislocations of the sternoclavicular joint. Bull Hosp It Dis 2000;59(3):153-157. 14. Kessel L. Clinical Disorders of the Sholiider, 2nd edn. Churchill Livingstone, London, 1986. 15. Neer C, Welsh R. The shoulder in sports. Orthop Clin North Am 1977;8(3):583-591. 16. Martin S, Altchek 0, Erlanger S. Atraumatic posterior disloca tion of the sternoclavicular joint. Clin Orthop Rei Res 1993;292:159-164. 17. Jougon JE, Lepront OJ, Oromer CEo Posterior dislocation of the sternoclavicular joint leading to mediastinal compression. Ann Thoracic Surg 1996;61(2):711-713. 18. Ferrera PC, W heeling HM. Sternoclavicular joint injuries. Alii J Emerg Med 2000;18(1):58-61. 19. Martin SO, Altcheck 0, Erlanger S. Atraumatic posterior dislo cation of the sternoclavicular joint: a case report and literature review. Clin Orthop ReIRes 1993;292:159-164. 20. Thomas OP, Williams PR, Hoddinott He. A 'safe' surgical technique for stabilisation of the sternoclavicular joint: a cadaveric and clinical study. Ann Roy Coli Slirg Eng 2000;82(6): 432-435. 21. Yeh GL, Williams GR Jr. Conservative management of sterno clavicular injuries. Orthop Clin North Alii 2000;31(2):189-203. 22. Colhoun EN, Hayward C, Evans KT. Inter-sterno-costo-clavicu lar ossification. Clin RadioI1987;38(1):33-38. 23. Saghafi M, Henderson MJ, Buchanan WW. Sternoclavicular hyperostosis. Sem Arthritis Rhellm 1993;22(4):215-223.
410
SECTION FOUR - THE SHOULDER GIRDLE
24. Davies AM, Marino AJ, Evans N et al. SAPHO syndrome: 20-year follow-up. SkeletaL Radio/1999;28(3):159-162. 25. Orion E, Brenner S. Stress-induced SAPHO syndrome. J Eur Acnd Dermatol Venereo/1999;12(1):43-46. 26. Hallas J, Olesen KP. Sterno-costo-clavicular hyperostosis. A case report with a review of the literature. Acta RadioL 1988;29(5): 577-579. 27. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesiolls, 8th edn. Bailliere Tindall, London, 1982. 28. Reilly J. The chronically inflamed bursae. Ciin Sports Med 1987;6(2):345-370.
29. Haney T. Subscapular elastofibroma in a young pitcher. Am J Sports Med 1990;18(6):642-644. 30. Sisto D, Jobe F. The operative treatment of scapulothoracic bursitis in professional pitchers. Am ] Sports Med 1986; 14:192. 31. Milch H. Snapping scapula. Ciin Orthop Rei Res 1961;20:139. 32. Richards R, McKee M. Treatment of painful scapulothoracic crepitus by resection of the superomedial angle of the scapula. Ciin Orthop Rei Res 1989;247:111-116. 33. Cameron H. 1984 Snapping scapulae: a report of three cases. Eur J Rheumatol Inflamm 1989;7:66.
CHAPTER CONTENTS Pain on resisted elevation 411 Lesion of the levator scapulae muscle Lesion of the trapezius muscle 412
411
Pain on resisted protraction 412 Lesion of the serratus anterior muscle Pain on resisted approximation
Disorders of the contractile structures
412
412
Weakness of scapular approximation Pain oil resisted depression 413 Lesion of the subclavius muscle
412
413
Lesions of the contractile structures
• These are characterized by pain on resisted movements together with a normal range on passive movements
• Usually the corresponding active movement is also painful
PAIN ON RESISTED ELEVATION This, together with pain on active elevation, points to a lesion of one of the elevators of the shoulder - the
scapulae
or the
trapezius muscle.
levator
Disorders of these struc
tures are extremely rare. They usually respond well to two or three infiltrations with procaine. If the pain is centrally located and is provoked by bilat eral elevation of the arm,
process of C7 and/or
traction fracture of the spinous
T1 is most likely. This presents as a
stress fracture of one of the lower cervical spinous processes. The lesion should be suspected when bilateral limitation of about 90° on active elevation of the arm is found. Active elevation of both shoulders is also painful, as is resisted shoulder elevation. Passive elevation is painless. Movements of the neck are only slightly painful (see p. 323). A
stress fracture of the first rib is another possible cause.
It gives rise to unilateral pain at the base of the neck not preceded by trauma. Active elevation of the arm cannot progress beyond the horizontal and is painful but passive elevation is normal. Pain is increased by active and resisted shoulder elevation and by active and passive side flexion of the neck to the opposite side. Resisted side flexion to the painful side is also painful (see p. 322).
LESION OF THE LEVATOR SCAPULAE MUSCLE Pain is felt unilaterally in the upper scapular area, mostly of the dominant shoulder.l It is activity-related: neck movements as well as shoulder girdle or arm movements may be of influence. So are prolonged postures such as sitting with the head in slight flexion as happens during computer work. On examination the pain is elicited during resisted elevation of the shoulder. The neck examination may be 411
412 SECTION FOUR - THE SHOULDER GIRDLE
slightly positive. Palpation shows the lesion to lie at the insertion on the superior angle of the scapula. The lesion responds to deep transverse friction at the tender spot, which may lie at the superior border or at the medial border of the scapula next to the superior angle.
LESION OF THE TRAPEZIUS MUSCLE A muscular lesion in the trapezius is as uncommon as pain in the trapezius is common. Usually pain in that area is referred from the cervical spine: it is the most common localization of cervical pain and is typically multiseg mentally referred (see p. 149). Because the trapezius is often the seat of pain and tenderness, an examination, if based on palpation, will easily result in a diagnosis of 'trapezius syndrome'. Proper functional testing, however, usually turns out to be negative, showing that no focal lesion is present. If a muscular lesion occurs it will give rise to rather localized pain which can be provoked by testing against
Figure 24.1
Resisted horizontal abduction.
resistance: neck extension and / or side flexion will be positive. Resisted elevation of the shoulder is also painful. The lesion responds to local infiltration of a local anaesthetic or to deep friction.
horizontal abduction is now performed in this position and elicits pain (Fig. 24.1). Treatment is by deep transverse friction.
Technique: deep friction to the serratus anterior. The patient lies prone, the ipsilateral arm in full medial rota
PAIN ON RESI STED P ROT R A CT ION
tion, the elbow flexed to 90°, the hand lying on the back. The therapist stands at the side and brings the arm
When the pain is felt anteriorly, this suggests that the
further into medial rotation by using the forearm which
lesion lies in the pectoralis minor or major muscle. Active
lifts the medial edge of the scapula off the thorax. The
protraction usually also elicits pain. When the
pectoralis
thumb is now placed at the anterior aspect of the medial
minor is at fault, resisted scapular depression is painful. If the lesion lies in the pectoralis major, resisted adduction
scapular margin. The other fingers are put on the poste
and medial rotation of the arm is positive. Both lesions can be treated by procaine infiltrations or deep friction (see p. 362). If the pain is located in the scapular area a lesion of the
serratus anterior is
probable.
LESION OF THE SERRATUS ANTERIOR MUSCLE
rior aspect of the scapula and provide counterpressure (Fig. 24.2). Massage is given along the scapular border by adduction-abduction movements of the arm, performed in a craniocaudal direction, for about 20 minutes, three times a week. Full cure is normally achieved in
3-5 weeks.
PAIN ON RESISTED A P P ROXIMATION
On arm movement, the serratus anterior keeps the verte bral border of the scapula firmly attached to the thorax. In a lesion at its scapular insertion, unilateral scapular pain is felt on moving the arm. Because the pain is felt at the inner side of the scapula, the attention of the examiner is drawn to one or other structure in this area.
If resisted approximation is painful but pain is not elicited on passive approximation, the lesion must lie in the
rhomboid
or in the
trapezius.
The response to infiltra
tions with procaine is good.
Therefore it is discussed here, although it is likely to be encountered in the clinical examination of the shoulder. Pain is felt on full active elevation of the arm, whereas
WEAKNESS OF SCAPULAR A P P ROXIMATION
passive elevation remains painless. Resisted abduction of the arm does not hurt. In this event, the patient is asked to bring the arm horizontal in front of the body. Resisted
This is the result of neuritis of the spinal accessory nerve. Unilateral resisted approximation of the scapula is weak,
CHAPTER 24
-
DISORDERS OF THE CONTRACTILE STRUCTURES 413
LESION OF THE SUBCLAVIUS MUSCLE The patient complains of pain around the clavicle or in the upper pectoral area on certain activities or move ments. Examination of the shoulder is negative which excludes the pectoralis major and the structures originat ing at the coracoid process (short head of biceps or coracobrachialis). Shoulder girdle examination shows the 'contractile tissue pattern': active and passive shoulder elevation are positive, as is resisted shoulder depression. On palpation a tender spot is found in the muscle belly of the subclavius. Treatment of the subclavius is by deep transverse fric tion. The lesion usually does not respond to infiltration with procaine.
Technique: deep friction to the subclavius. The patient lies supine, the arm raised with the hand on the head. The therapist stands at the ipsilateral side and puts the middle finger, reinforced by the index, just below and parallel to the clavicle on the painful spot (Fig. 24.3). Friction is given by pronation-supination movements of the arm. This is performed for about 20 minutes on alter nate days. The patient is usually cured in 10 sessions. A summary of shoulder girdle disorders is outlined in Box 24.1.
Figure 24.2
Deep friction to the serratus anterior.
together with a loss of about 5° of active elevation of the arm (see p. 413).
PAIN ON RESISTED DEP RESSION A positive result suggests that there is a problem in the subclavius, the pectoralis minor or the latissimus dorsi and is usually combined with pain on active and passive elevation, which demonstrates that one of the shoulder depressors is involved. A sprain of the
subclavius
is
mostly likely. The patient complains of pain in the ante rior claviculopectoral area. Alternatively, a sprain of the
pectoralis minor
may be responsible. Pain on resisted
forward movement of the shoulder then establishes the diagnosis. When the
latissimus dorsi
is at fault, resisted
adduction and medial rotation of the arm is also painful.
Figure 24.3
Deep friction to the subclavius.
414 SECTION FOUR - THE SHOULDER GIRDLE
Box 24.1 Summary of shoulder girdle disorders
•
Disorders of the inert structures Pain on active elevation Combined with pain on passive elevation Disorders of the sternoclavicular joint: Sprain of the sternoclavicular joint/ligaments Posterior sternoclavicular syndrome Arthrosis Rheumatoid arthritis Septic arthritis Sprain of the acromioclavicular joint Disorders of the first rib: Sprain of the first costotransverse joint Stress fracture of the first rib Traction fracture of the spinous process C7 or T1 Lesion of the conoid/trapezoid ligament Idiopathic contracture of the costocoracoid fascia Neural compression: Compression of the dura mater T1-T2 nerve root compression
Combined with pain on active protraction Lesion of the conoid/trapezoid ligament Compression of T1-T2 nerve root Idiopathic contracture of the costocoracoid fascia
Pain and limitation of active and passive elevation Ankylosis of the acromioclavicular joint Disorders of the sternoclavicular joint: Ankylosis Traumatic dislocation Hyperostosis Disorders of the costocoracoid fascia Idiopathic contracture Neoplasm
Scapular metastases Apical tumour of the lung
Limitation of active elevation and weakness of resisted elevation Lesion of the C2-C4 nerve roots Neuritis of the spinal accessory nerve Paraesthesia brought on by active and/or passive elevation Thoracic outlet syndrome
Crepitus during scapular elevation Disturbance in the scapulothoracic gliding mechanism Pain on active and passive scapular approximation Involvement of upper thoracic dura mater or dural nerve root sleeve
• Disorders of the contractile structures Pain on resisted elevation Lesion of the levator scapulae or trapezius muscle Traction fracture of the spinous process of C7 and/or T1 Stress fracture of the first rib
Pain on resisted protraction Lesion of the pectoralis minor or pectoralis major muscle Lesion of the serratus anterior muscle
Pain on resisted approximation Lesion of the rhomboid muscles Lesion of the trapezius muscle Weakness of scapular approximation Neuritis of the spinal accessory nerve
Pain on resisted depression
Healed apical tuberculosis
Lesion of the subclavius muscle
Postradiation therapy
Lesion of the pectoralis minor muscle
Haematoma
Lesion of the latissimus dorsi muscle
REFERENCE 1. Menamem A, Kaplan 0, Dekel S. Levator scapulae syndrome: an anatomic-clinical study. Bull Hasp Jt Dis 1993;53(1):21-24.
SECTION FIVE
The elbow
SECTION CONTENTS 25. Applied anatomy of the elbow
417
Joints and ligaments 417 Biomechanical aspects 419 Muscles and tendons 420 Nerves 424 Bursae 426 26. Clinical examination of the elbow Referred pain History 427
427
427
Inspection 428 Functional examination Palpation 431 Accessory tests
428
431
27. Interpretation of the clinical examination
435
28. Disorders of the inert structures 437 Limited range of movement 437 The capsular pattern 437 Traumatic arthritis 437 Arthrosis
439
Monoarticular steroid-sensitive arthritis
439
Crystal synovitis 439 Haemarthrosis 439 Rheumatoid-type arthritis 439 Septic arthritis 440 The non-capsular patterns 440 Limitation of flexion or extension in isolation 440 Acute limitation of supination and extension in children Limitation of pronation
443 Full range of movement 443 Pain on full passive supination Ligamentous lesions
443
443
Pain on full passive pronation Bursitis 445
444
29. Disorders of the contractile structures Resisted flexion of the elbow 447 Resisted extension of the elbow 451 Resisted supination 453 Resisted pronation 454 Pain on resisted extension of the wrist
447
454
Weakness on resisted extension of the wrist Resisted flexion of the wrist 466
465
443
THIS PAGE INTENTIONALLY LEFT BLANK
Applied anatomy of the elbow
CHAPTER CONTENTS Joints and ligaments Joints 417 Ligaments 418
417
Biomechanical aspects 419 Flexion-extension 419 Pronation-supination 420 Muscles and tendons 420 Flexor muscles 420 Extensor muscles 421 Supinator muscles 422 Pronator muscles 422 Muscles controlling wrist movement
422
Nerves 424 Ulnar nerve 424 Median nerve 424 Medial cutaneous nerve of the forearm Radial nerve 424 Bursae
426
JOINTS AND LIGAMENTS The elbow joint helps the hand to approach or move away from the body, whatever the arm position resulting
424
from shoulder movement. It consists of three 'joints', which Ije within one joint capsule and together have two separate functions.
JOINTS The three 'joints' are the humeroulnar, the humeroradial and upper radioulnar joint (Figs 25.1-25.3). Their two functions are flexion/ extension, which is performed at the humeroulnar and humeroradial joints,
and
pronation/ supination, which takes place at the upper radioulnar joint in close association with the lower radioulnar joint.
humerus ----IlI---
6
3
radius
Figure 25.1 Humeroulnar and humeroradial joints (anterior view). The dotted line shows the insertion of the joint capsule. On humerus: 1, trochlea; 2, coronoid fossa; 3, medial epicondyl; 4, capitulum; 5, radial fossa; 6, capitulotrochlear sulcus. On ulna: 7, coronoid process; 8, radial notch. On radius: 9, radial head.
417
418 SECTION FIVE - THE ELBOW
3
6
2
2
Figure 25.3 Upper radioulnar joint. On ulna: 1, trochlear notch; 2, coronoid process; 3, olecranon process; 4, radial notch; 5, ulnar tuberosity. On radius: 6, circumference; 7, articular facet; 8, radial tuberosity. Figure 25.2 Humeroulnar and humeroradial joints (posterior view). The dotted line shows the insertion of the jOint capsule. On humerus: 1, olecranon fossa; 2, lateral epicondyle. On ulna: 3, olecranon process.
At the distal end of the humerus lie the two epi condyles, of which the medial one is more developed than the other. They are both extracapsular.
LIGAMENTS The three joints work closely together and make prona tion and supination movements possible whatever the extent of flexion or extension of the elbow. • The humeroulnar joint acts as a hinge. The articular
The capsule is reinforced by strong lateral ligaments (Fig. 25.4). •
surfaces on the humerus are the spool-shaped
humerus towards the annular ligament, a middle part
trochlea with, proximal to it, the coronoid fossa
towards the coronoid process, and a posterior part,
(ventral aspect) and the olecranon fossa (dorsal
directed towards the olecranon. All three parts are
aspect). The other part of the joint is formed by the
reinforced by an oblique band (ligament of Cooper)
olecranon, with its trochlear notch and its olecranon (proximal) and coronoid (distal) processes. • The humeroradial joint - a ball-and-socket
distally on the ulna. •
The lateral collateral ligament connects the lateral epicondyle to the radial annular ligament (anteriorly
joint - consists of (a) the spheroidal capitulum of the
via the radial collateral ligament and posteriorly via
humerus and (b) the proximal surface of the head of
the lateral ulnar collateral ligament which inserts at
the radius. Proximal to the capitulum lies the radial
the supinator crest of the ulna) and is interwoven
fossa and beside it a capitulotrochlear sulcus
with the superficial extensor muscles.
(between capitulum and trochlea). The articular facet of the radius, with which the proximal part of the
The medial collateral ligament has an anterior part, which runs from the medial epicondyle of the
These ligaments help to maintain the articular
humeroradial joint articulates, is at the top of the head
surfaces in contact with each other. They also limit
of the radius. This facet exactly follows the shape of
lateral movements. Other ligamentous structures are:
the humeral capitulum. Because it articulates with the capitulotrochlear sulcus at the ulnar side, it allows
•
pronation-supination movements as well.
radial head to the proximal ulnar extremity so that
• The upper radioulnar joint is a trochoid (cone
they can articulate. It plays an important role in
shaped) joint. The circumference of the head of the radius articulates with the radial notch of the ulna.
pronation-supination. •
The three joints lie within the same lax joint capsule, which is spanned by muscular fibres of the brachialis, triceps and anconeus muscles.
The radial annular ligament, a V-shaped fibrous collar, covered with cartilage at its inner aspect, joins the
The quadrate ligament attaches the radial neck to the distal aspect of the radial notch of the ulna.
•
The oblique cord extends inferolaterally from the lateral border of the tuberosity of the ulna to the radius, just
CHAPTER 25 - APPLIED ANATOMY 419
flEXION-EXTENSION The trochlear surface of the humerus articulates with the trochlear notch of the ulna along an imaginary line A-A: which runs slightly oblique (downwards and out wards) in its posterior course. This obliquity explains the physiological valgus position of the elbow in exten sion (Fig. 25.5). In its anterior course, the axis of move ment is horizontal: therefore, in flexion, the forearm lies exactly in front of the upper arm. There are, of course, individual differences. Extension is mainly limited by the olecranon abutting against the posterior aspect of the humerus in the ole cranon fossa (Fig. 25.6) and by stretching of the anterior part of the joint capsule. The forearm then usually lies in line with the upper arm, except in most women and in some men, in whom the elbow may sometimes over extend. This overextension is the result of the format of the olecranon fossa and process. The end-feel of this movement is hard. Flexion stops when, at the end of the range, the mus cular masses of the upper arm and forearm come into contact with each other. The end-feel is, of course, hard in those cases in which the muscles are very poorly developed, because the movement is then stopped by the other limiting factors: (1) the contact between (a) the coronoid fossa of the humerus and the coronoid process of the ulna and (b) the head of the radius and the radial Figure 25.4 The medial (upper ) and radial (lower ) col iateral l igaments. Upper: 1, an terior part; 2, m iddle part; 3, poster ior part; 4, l igament of Cooper. Lower: 1, annular ligament; 2, rad ial col iateral ligament; 3, lateral ulnar coliateral l igament.
fossa of the humerus, as well as (2) the tension in the posterior capsule.
below its tuberosity. It prevents downwards move ment of the radius. •
The interosseous membrane and the oblique cord join the two bones of the forearm to prevent any longitudinal movement and assist as a fulcrum in pronation-supination (i.e. diagonal rotation). They are both syndesmosis connections.
BIOMECHANICAL ASPECTS The distal extremity of the humerus is a fork, the axis of its articular surfaces running through the humeral capitulum and trochlea. The coronoid fossa, into which the coronoid process of the ulna fits, as is the case for the olecranon fossa and olecranon process, together with the forward projection of both the lower humeral and the upper ulnar extremi ties, allows a considerable range of flexion-extension between forearm and upper arm.
Figure 25.5
The phys iological valgus position. Oblique line is A-A' (see text)
420 SECTION FIVE - THE ELBOW
pronation, the concave anterior side of the radius lies posteriorly. -
MUSCLES AND TENDONS FLEXOR MUSCLES The flexor muscles are the brachialis, the brachioradialis and the brachial biceps (Table 25.1). Their action is maximal when the elbow is flexed at 90°. Brachialis. This runs from the anterior and distal aspect
of the humerus towards the ulnar tuberosity and the joint capsule (Fig. 25.8). It is a monoarticular muscle. Its only function is to bend the elbow, irrespective of the degree of pronation-supination of the forearm. Brachioradialis. This muscle has its origin at the lateral
supracondylar ridge of the humerus and inserts at the Figure 25.6
The range of flexion-extension movement.
radial aspect of the styloid process of the radius. It brings the pronated or supinated forearm back in the neutral position between pronation and supination. In this posi tion it acts as a flexor of the elbow, an action which
PRONATION-SUPINATION
diminishes when the forearm is held in supination.
Pronation-supination takes place mainly in the joint
Biceps. This is the dominant flexor of the elbow. It orig
formed by the radial head and the osteofibrous ring,
inates from the scapula, where it has two heads, the long
which contains the radial notch of the ulna together
head from the supraglenoid tubercle, the short head
with the inner aspect of the annular ligament. However,
from the coracoid process, and it inserts with a strong
there is also movement between (a) the head of the radius and (b) the capitulum of the humerus and the capitulotrochlear sulcus. Pronation-supination is the result of a combined action of the proximal and distal radioulnar joints, which are coaxial. Movement takes place around the longitudi nal axis of the forearm, which rLlns from the facet on the head of the radius to the styloid process of the ulna. Both movements can best be measured with the elbow held at a 90° angle in order to prevent compensa tory rotations of the upper arm. Starting from the inter mediate position with the hand vertical and the thumb pointing upwards, the supination has a range of 90°. In full supination the two bones lie parallel to each other. The limiting factor is purely ligamentous (interosseous membrane, oblique cord and anterior ligament of the distal radioulnar joint) and explains the elastic end-feel. The oblique cord prevents a downwards shift of the radius. During pronation the radius crosses over the ulna (Fig. 25.7). This is possible only because of the direction of the fibres of the interosseous membrane. The radial tuberosity thereby turns towards the ulna. This move ment has an 85° amplitude and is limited by stretching of the interosseous membrane and squeezing of the flexor muscles, again with an elastic end-feel. In full
Figure 25.7
Supination-pronation.
CHAPTER 25 - APPLIED ANATOMY 421
Table 25.2 The extensor muscles
Table 25.1 The flexor muscles
Innervation
Innervation Muscle
Peripheral
Nerve root
Brachialis
N. musculocutaneus
C5-C6
(N. radialis) Brachioradialis
N. radialis
Brachial biceps
N. musculocutaneus
Muscle
Peripheral
Nerve root
Triceps
N. radialis
Anconeus
N. radialis
C7-C8 C7-C8
C5-C6 C5-C6
aspect of the humerus, proximally to that sulcus. The three muscular bodies join in one tendon, that inserts at thick tendon at the radial tuberosity. Part of the tendon
the olecranon and at the posterior aspect of the joint
blends into the aponeurosis of the forearm at the ulnar
capsule (Fig. 25.10).
side (Fig. 25.9). Because the biceps is a biarticular muscle,
Because the triceps is partly biarticular, its extension
it also acts on the shoulder. Its essential function is elbow
action to the elbow joint depends not only on the posi
flexion but its secondary function is supination of the
tion of the elbow but also on the position of the shoul
forearm. Such supination action of the biceps increases
der. The triceps has its maximal force in a movement
the more the elbow is flexed and is maximal at 90°; it
which combines the two: elbow extension and shou IdeI' extension.
diminishes again when the elbow is fully flexed.
Anconeus. Originating at the dorsal aspect of the lateral
EXTENSOR MUSCLES Extension of the elbow is performed by two muscles: the triceps and the anconeus (Table 25.2).
epicondyle of the humerus and at the lateral collateral ligament, this muscle runs towards the posterior and proximal aspect of the ulna and the joint capsule. It may be considered as a continuation of the lateral head of the
The triceps. The triceps originates from three heads as
triceps. It thus helps the triceps in its extensor function
its name implies: the long head from the infraglenoid
and also spans the joint capsule. From the clinical point of
tubercle of the scapula, the medial head from the dorsal
view this muscle may be ignored.
aspect of the humerus, distally to the sulcus for the radial nerve, and the lateral head also from the dorsal
2
3
4
Figure 25.8
Brachialis muscle: 1, ulnar tuberosity.
Figure 25.9 Sites of lesions in the biceps: 1, tendon in biCipital groove; 2, muscle belly; 3, musculotendinous junction; 4, tenoperiosteal junction.
422 SECTION FIVE - THE ELBOW
Table 25.4 The pronator muscles Innervation Muscle
Peripheral
Nerve root
Pronator teres
N. medianus
C6-C7
Pronator quadratus
N. interosseus palmaris
C8-T1
(N. medianus)
PRONATOR MUSCLES Pronation is performed by two muscles: the pronator quadratus and the pronator teres (Table 25.4). Pronator quadratus. This is at the distal aspect of the
forearm. It runs from the distal and anterior part of the ulna to the distal and anterior part of the radius, so encircling the ulna. Its role is dealt with in Section 6. Pronator teres. The pronator teres has a multiple
origin: the humeral head from the medial epicondyle of the humerus (partly from the common flexor tendon) and the ulnar head from the coronoid process of the ulna. Its insertion lies halfway down the radius at the lateral aspect. Because the pronator teres is a biarticular muscle, theoretically it also assists in the flexion of the Figure 25.10 Sites of lesions of the triceps: 1, musculotendinous junction, 2, body of the tendon; 3, tenoperiosteal insertion.
elbow but this action is of course very secondary. The pronator muscles are not as strong as the supinator muscles.
SUPINATOR MUSCLES
MUSCLES CONTROL LING WRIST MOVEMENT
Supination movement is the result of the action of two muscles: the supinator brevis and brachial biceps (Table 25.3).
Two groups of muscles originate at the elbow but control wrist movements: they are the flexors and extensors of the wrist (and fingers).
Supinator brevis. This takes origin at the supinator crest
of the ulna, the lateral epicondyle, the radial collateral ligament and the annular ligament. The muscular fibres encircle the radius and insert via a short tendon at the radius between the radial tuberosity and the insertion of the pronator teres muscle. The muscle supinates the forearm in whatever position there is between flexion and extension of the elbow.
Extensors of the wrist and fingers (Table 25.5) Extensor carpi radialis longus. This takes its origin at the
lateral supracondylar margin of the humerus, just proxi mal to the lateral epicondyle and at the lateral inter muscular septum (Fig. 25. 11). Extensor carpi radialis brevis. The origin is at the ante
Brachial biceps. This is the strongest supinator of the
forearm (see above).
rior aspect of the lateral epicondyle but the muscle also partly originates from the lateral collateral ligament and from the annular ligament of the radius.
Table 25.3 The supinator muscles
Table 25.5 The extensor muscles of the wrist and fingers Innervation
Innervation Muscle
Peripheral
Nerve root
Supinator brevis
N. radialis
C5-C6
Brachial biceps
N. musculocutaneus
C5-C6
Muscle
Peripheral
Nerve root
Extensor carpi radialis longus
N. radialis
C&-C7
Extensor carpi radialis brevis
N. radialis
C7
Extensor carpi ulnaris
N. radialis
C7-C8
Extensor digitorum communis
N. radialis
C6-C8
CHAPTER 25
-
APPLIED ANATOMY 423
11I11i1,.,_- 2
6
4
5
Figure 25.11 Lateral view of the extensors of the elbow: 1, triceps muscle; 2, extensor carpi radialis longus muscle; 3, extensor carpi radialis brevis muscle; 4, supinator muscle; 5, radial nerve; 6, lateral epicondyle.
Both muscles run together towards the wrist. They
---
5
cause extension of the wrist (especially the extensor carpi radialis brevis muscle) as well as radial deviation. Extensor carpi ulnaris. Running from the dorsal and
lateral aspects of the lateral epicondyle, as well as from the radial collateral ligament and the fascia of the forearm towards the wrist, this assists slightly in the extension of the wrist but its main function is ulnar deviation. Extensor
digitorum communis. The origin
(together
with the extensor carpi ulnaris muscle) is just dorsal to the extensor carpi radialis brevis muscle from the lateral epicondyle, the radial collateral ligament, the annular ligament of the radius and the fascia of the forearm; the muscle runs towards the fingers. Its main function is finger extension but it also assists in extension (and ulnar deviation) of the wrist.
Figure 25.1 2 Muscles originating at the medial epicondyle (anterior aspect) 1, pronator teres muscle; 2, common flexor tendon; 3, flexor carpi radialis muscle; 4, palmaris longus muscle; 5, flexor carpi ulnaris muscle.
Flexor carpi radialis. Starting at the anterior aspect of the
medial epicondyl, this muscle runs towards the wrist. Its main function is flexion of the wrist; its radial deviation function is secondary. Flexor carpi ulnaris. Starting with a humeral head at
the medial epicondyle, this also has an ulnar head at the
Flexors of wrist and fingers (Table 25.6) The flexors of the wrist and fingers take their origin at the medial epicondyle of the humerus (Fig. 25. 12), mainly in a common flexor tendon which has a superficial and a deep layer. The superficial layer con sists of the humeral head of the pronator teres muscle, the flexor carpi radialis, the palmaris longus, the
olecranon and the upper part of the posterior margin of the ulna. It flexes the wrist and assists the extensor carpi ulnaris in performing ulnar deviation of the wrist. Palmaris longus.This is not always present. When it is, it
runs towards the hand into the palmar aponeurosis, of which it is a tensor. It also helps in flexion of the wrist.
humero-ulnar head of the superficial flexor digitorum
Superficial flexor digitorum. The origin is threefold: a
and the humeral head of the flexor carpi ulnaris.
humeral head originating from the common flexor tendon at the medial epicondyle of the humerus, an ulnar head from the coronoid process and a radial head from the anterior aspect of the radius. Apart from flexion of the fingers, it also assists in ulnar deviation of
Table 25.6 The flexor muscles of the wrist and fingers Innervation
the wrist.
Muscle
Peripheral
Nerve root
Flexor carpi radialis
N. medianus
C6-C7
Flexor carpi ulnaris
N. ulnaris
C7-C8
Palmaris longus
N. medianus
C7-T1
Superficial flexor digitorum
N. medianus
C7-T1
Flexor pollicis longus
N. medianus
C7-C8
Flexor pollicis longus. This lies in the deeper layer. It
has a humeral head, originating from the medial epi condyle and, more important, a radial head originating from the anterior aspect of the radius, just distal to the supinator muscle and the interosseous membrane. It flexes the thumb and assists in flexion of the wrist.
424 SECTION FIVE - THE ELBOW
NERVES The nervous structures are discussed here because entrap ment may occur in the elbow region. Only the appropriate part of the nerve is described. For a more extensive description, see pp. 557-573.
ULNAR NERVE
2
The ulnar nerve courses under the medial head of the triceps muscle towards the posterior aspect of the medial epicondyle, where it lies superficially in a shallow groove behind this bone (sulcus for the ulnar nerve; Fig. 25.13) and is therefore very vulnerable to direct contusion. It becomes stretched during flexion of the elbow. The nerve runs further distally in between the two heads of the flexor carpi ulnaris muscle, which form an aponeurotic
Figure 25.14 The course of the ulnar nerve through the cubital tunnel: 1, medial epicondyle; 2, medial collateral ligament (posterior part); 3, common flexor tendon; 4, aponeurotic arch; 5, flexor carpi ulnaris muscle.
arch. Together with the medial epicondyle, the olecranon and the medial collateral ligament, this arch forms the 'cubital tUlUlel' (Fig. 25.14).
the upper arm, the nerve courses between the radial and
MEDIAN NERVE
just medially to the bicipital tendon and beneath its
the ulnar nerves. It passes through the antecubital fossa
At the elbow, the median nerve is of lesser clinical significance, because it is seldom affected at this level. In
aponeurosis. It lies between the two heads of the prona tor teres muscle and runs further under a tendinous arch connecting the heads of the superficial flexor digitorum muscle (Fig. 25.15). The median nerve is liable to anomalies consisting of either communications with other nerves or unusual branching. The commonest anomaly is the Martin-Gruber anastomosis: one or more branches from the median nerve pass to the ulnar nerve in the forearm. The practical consequence of this is that a median nerve palsy may involve the intrinsic hand muscles and that ulnar nerve disorders may spare the muscles usually innervated by it.
MEDIA L CUTANEOUS NERVE OF THE FOREARM This nerve becomes superficial at mid-arm as it runs through an opening in the brachial fascia, the basilic hiatus, and supplies the skin from the inner aspect of the elbow as far as the wrist. In the elbow region, it crosses over the median basilic vein and lies in a position where it is subject to injury by extravenous injections.
RADIA L NERVE In the distal part of the upper arm, the radial nerve lies lateral to the median nerve. It courses between the bicipital tendon and the proximal part of the brachio radialis muscle. Level with the head of the radius the nerve then Figure 25.13
The course of the ulnar nerve.
divides into a deep motor branch (the deep radial nerve),
CHAPTER 25 - APPLIED AN ATOMY 425
Figure 25.16 The course of the radial nerve: 1, radial nerve; 2, superfcial radial nerve (sensory); 3, posterior interosseous nerve (motor); 4, arcade of Friihse in the supinator muscle (forming the 'radial tunnel').
Figure 25.15 The course of the median nerve: 1, pronator teres muscle; 2, superficial flexor digitorum muscle; 3, tendinous arch; 4, Martin-Gruber anastomosis with the ulnar nerve.
The posterior interosseous nerve turns around the neck of the radius and comes to lie at the dorsal aspect of the forearm where it passes through an opening in the supina tor muscle: the arcade of Fr6hse, formed by the edge of the
from which the posterior interosseous nerve branches off
upper border of the superficial part of this muscle. At
a bit further down, and a superficial sensory branch (the
this location (the 'radial tunnel') it may sometimes be
superficial radial nerve) (Fig. 25.16).
compressed and cause radial tunnel syndrome (see p. 560).
(a)
(b)
La!. epicondylar B Subtendinous B. ---l--/;t\-t-lAAl<\=-= Radiohumeral B. ----jH/!if-f1\\\-
Bicipital radial B.--Ht-lffilli\W�H
Figure 25.17 (a and b) Bursae of the elbow.
Olecranon B. ----t--llml),.#h+--
426 SECTION FIVE - THE ELBOW
bursa and sub tendinous tricipital bursa); under the
BURSAE
biceps tendon at its attachment to the radial tuberosity;
Bursae are regularly found: in the region of the insertion
superficial epicondylar and radiohumeral bursae occur.
of the triceps into the olecranon (subcutaneous olecranon
(Fig. 25.17).
and at the lateral aspect of the elbow, where both
CHAPTER CONTENTS Referred pain
427
Pain referred to the elbow 427 Pain referred from the elbow 427
History
427
Inspection
428
Functional examination
428
Passive movements 428 Resisted movements at the elbow 428 Resisted tests of the flexors and extensors of the wrist 430
Palpation
Clinical examination of the elbow
REFERRED PAIN
431
Accessory tests
431
One of the rules of referred pain is that the further dis tally the lesion lies, the more accurately the patient can localize it. It is therefore reasonable to start immediately with the clinical examination of the elbow and, only when this seems to be negative, to check the cervical spine, the shoulder girdle and the shoulder. PAIN REFERRED TO THE ELBOW
Pain referred to the elbow from structures that lie higher up in the limb is a possibility. The localization of the pain indicates the segment in which the lesion lies: the lateral aspect of the elbow is formed by the C5 der matome, the anterior aspect by C6, the inner aspect by Tl-T2 and posteriorly by C7. PAIN REFERRED FROM THE ELBOW
Pain referred from the elbow is uncommon. A lesion at the origin of the extensor carpi radialis brevis may give rise to pain radiating down the posterior aspect of the forearm to the hand as far as the third and fourth finger. A lesion at the distal bicipital insertion radiates down the proximal and palmar aspect of the forearm. Proximal reference of elbow pain is very rare.
HISTORY
The history is not very important in elbow problems but some questions should be asked . •
•
Where is the pain? The location of the pain is usually closely related to the site of the lesion. When the patient indicates exactly where his symptoms are felt, all causes that cannot produce pain in that area are automatically excluded. How did it all start? Did the symptoms start spontaneously or has there been any trauma and, if so, what type? If the onset was spontaneous, did it begin suddenly or gradually or as the result of a particular activity? 427
428 SECTION FIVE - THE ELBOW
What was the evolution? Was there any change in the
•
location, intensity or frequency of the painful episodes? Did the pain spread and, if so, where to? This may indicate the dermatome and, in consequence, the segment in which the lesion must be sought.
Is there any junctional loss? Has the elbow ever been swollen? If the swelling came on
• •
•
•
after a trauma, how soon did it appear? Immediate general effusion is probably the result of a haemarthro sis; graduaJIy increasing swelling usually indicates the presence of synovial fluid. Spontaneous swelling may be the result of an impacted loose body or a rheuma toid condition. Localized swelling may occur in bursi tis or in some exceptional cases of tennis elbow. What influences the pain? Is the pain constantly present, or does it come on during or after activity either general or specific? In an arthrotic or arthritic joint the maintenance of a certain posture at the extreme of the possible range may become very painful. Release from this position is usually very uncomfortable. 'Twinges' when picking up objects (e.g. a telephone or a coffee pot) with an outstretched elbow is a well-known symptom in terulis elbow. Are any other joints involved? In rheumatoid-type conditions other joints may be affected.
humerus or in the upper radioulnar joint - or of the non capsular type. Passive flexion. The examiner places the con tralateral hand at the dorsal aspect of the patient's shoulder to prevent the body from trying to move back wards in order to escape from the pain. The ipsilateral hand takes hold of the patient's forearm just proximally to his wrist and moves the joint into as much flexion as possible (Fig. 26.1a). The normal end-feel is one of tissue approximation as the muscles of the forearm come in contact with the brachial muscles at an angle of about 160°. o
Passive extension. With the contralateral hand the examiner takes hold of the patient's upper arm at the level of the olecranon. The ipsilateral hand is put at the distal end of the patient's forearm. Both hands move in opposite directions so as to extend the elbow (Fig. 26.1b). The normal end-feel in passive extension is hard and bony, caused by the olecranon coming into contact with the posterior aspect of the humerus, and by tightening of the anterior capsule of the joint. As the forearm now lies in line with the upper arm, the angle of extension is 0°. In instances of overextension the angle may become 5-10°. o
Passive pronation. The elbow is bent to a right angle. The examiner stands in front of the patient and grasps the distal forearm just proximal to the wrist with both hands. The heel of the contralateral hand is placed at the palmar aspect of the ulna, the fingers of the other hand at the dorsal aspect of the radius. A simulta neous movement of both hands presses the wrist into full pronation (Fig. 26.1c). The extreme of movement is characterized by an elastic, capsular end-feel as the 85° range is approached. Together with passive supination this movement tests the integrity of the upper radioulnar joint. Pain at the end of the range may also be a localizing sign in tendinitis of the insertion of the bicipital tendon onto the radial tuberosity, because of pinching of the tendon between the radial tuberosity and the ulna. o
INSPECTION
Inspection may reveal diffuse or local swelling: arthritis causes a more generalized effusion, whereas other lesions (bursitis and tendinitis) may give rise to more localized swelling. There may also be redness of the skin or muscular atrophy.
FUNCTIONAL EXAMINATION o
The examination consists of 10 tests: four passive movements and six resisted movements.
PASSIVE MOVEMENTS
The passive movements (Fig. 26.1) are used to examine the inert structures: the joint, the capsule, the capsular lig aments and the bursae. It is also clear that by passively testing the elbow, one also indirectly stretches or pinches muscular and tendinous structures. The range of movement is ascertained and the end feel noted. The four passive tests give the examiner an idea of the behaviour of the inert structures around the elbow. The pattern that is formed suggests a lesion either of the cap sular type - arthritis, in the joint between forearm and
Passive supination. The position of the examiner's hands is slightly changed: the heel of the ipsilateral hand applies pressure at the dorsal aspect of the ulna and the fingers of the other hand pull at the palmar aspect of the radius. The forearm is twisted into supination as far as it goes (Fig. 26.1d). Normally the capsular end-feel is noted at about 90°. o
RESISTED MOVEMEN TS AT THE ELBOW
The same four movements are repeated but against isometric resistance to examine the contractile structures (Fig. 26.2).
CHAPTER 26 - CLINICAL EXAMINATION 429
(a)
(b)
(e)
(d)
Figure 26.1
Passive movements: (a) fiexion, (b) extension, (c) pronation, (d) supination.
The patient holds the forearm in supination. The examiner puts the contralateral hand on top of the patient's shoulder to prevent it from moving upwards during the contraction. The other hand is placed on the distal forearm with the examiner 's forearm held vertically, to prevent the patient's forearm from moving as the flexor muscles are contracted (Fig. 26.2a). The muscles thus tested are the brachial biceps, the brachialis and the brachioradialis. The brachialis is strong flexor and the brachioradialis is clinically unimportan t. o
Resisted flexion.
Again the contralateral hand is placed on top of the patient's shoulder. The other one is placed vertically under the patient's forearm and prevents the arm from moving downwards (Fig. 26.2b). If o
Resisted extension.
necessary, in a very strong patient, the examiner 's own elbow may be supported on the thigh. The muscles that are tested with this movement are the triceps and, secondarily, the anconeus muscle. Pain at the shoulder during this movement has the same applications as painful arc (see Ch. 19). Resisted pronation. The patient's forearm is held in the neutral position between pronation and supination. In order to prevent any movement during the resis ted movement, the examiner 's hands should be placed as follows: the ipsilateral hand, held in supination, is placed under the patient's distal forearm; the contralateral hand, held in pronation, is placed on top. The patient is asked to perform a pronation movement and resistance is given with the heels of both hands (Fig. 26.2c). o
430 SECTION FIVE - THE ELBOW
(a)
(b)
(c)
(d) Resisted movements: (a) flexion, (b) extension, (c) pronation, (d) supination.
Figure 26.2
This movement mainly tests the pronator teres muscle but will also be painful in the presence of golfer's elbow. Resisted supination. The hands are placed in a slightly different position from the previous test so that resistance is given against the palmar aspect of the distal ulna and the dorsal aspect of the distal radius (Fig. 26.2d). In this test, the brachial biceps is tested with respect to its secondary function, and also the supinator brevis muscle. o
RESISTED TESTS OF THE FLEXORS A N D EXTEN SORS O F THE WRIST
There are two muscle groups the flexors and extensors of that control the wrist movements but lie at the -
the wrist
-
elbow and therefore can give rise to symptoms about this joint. They should be systematically tested in the elbow examination. The patient's elbow is held in extension, so as to put maximum stress on these structures (Fig. 26.3). Resisted flexion of the wrist. The patient's hand is held palm downwards. The examiner passes the contralateral arm under that of the patient and grasps the forearm just proximally to the wrist in order to fix the upper limb. The upper arm lies under the patient's elbow and holds it in full extension. The hand of the other arm is now brought into the palm of the patient's hand and resists the patient's attempt to flex the wrist (Fig. 26.3a). The following muscles are tested: flexor carpi radialis, flexor carpi ulnaris, flexor digitorum superficialis and flexor digitorum profundus. o
CHAPTER 26 - CLINICAL EXAMINATION 431
(a)
Figure 26.4 Accessory test: resisted extension of the wrist with the fingers actively flexed.
The elbow joint can be palpated either at rest or during movement in order to detect warmth, swelling, synovial thickening (palpation laterally over the head of the radius), crepitus or clicking. The muscle or tendon at fault is palpated to define the exact site of the lesion.
(b) Figure 26.3
ACCESSORY TESTS
Resisted movements: (a) flexion and (b) extension of the wrist. Resisted extension of the wrist with the fingers actively
The patient is asked to actively flex the fingers by pressing the fingertips into the palm of the hand. Resisted extension of the wrist is now executed as already described (Fig. 26.4). flexed.
Resisted extension of the wrist. The patient remains in the same position as in the previous test. The examiner puts the hand on top of the patient's hand to resist an attempt to execute an extension move ment (Fig. 26.3b). The muscles tested are the extensors of wrist and fingers: extensor carpi radialis longus and brevis, exten sor carpi ulnaris, extensor indicis proprius, extensor digitorum communis and extensor digiti minimi. o
PALPATION
After the clinical examination (and only if it is likely to supply more information) the elbow is palpated.
Resisted radial and ulnar deviation. With the elbow in extension and the wrist in the neutral position between flexion and extension, radial and ulnar deviation are tested against resistance (Fig. 26.5). These tests differenti ate between a lesion of the radial extensors or flexors of the wrist or of the ulnar extensors or flexors. Resisted extension and flexion of the fingers. When a lesion of the finger extensors has been diagnosed, the examiner may test resisted extension of each finger in turn (Fig. 26.6a) to find out which tendon is at fault. If a finger flexor is affected, resisted flexion of each finger (Fig. 26.6b) may disclose the exact tendon.
432 SECTION FIVE - THE ELBOW
Resisted supination in extension. In order to differentiate between lesions of the brachial biceps and the supinator brevis muscle, this test should be performed. When the arm is brought into extension, the action of the biceps is dimin ished considerably but the supinator contracts normally.
Percussion to the ulnar nerve in the groove between the olecranon and the medial epicondyle
Tinel's sign.
(a) Figure 26.5
(b) Accessory tests: resisted (a) radial and (b) ulnar deviation.
(a) Figure 26.6
(Fig. 26.7) gives rise to distal paraesthesia in the terri tory of the ulnar nerve - in the forearm and the hand TineI's sign. This test can be used to assess the progress of the regeneration of the sensory fibres of the nerve. The most distal point where the pins and needles are felt indicates the limit of regeneration. The clinical examination is summarized in Box 26.1.
(b) Accessory tests: resisted (a) extension and (b) flexion of the fingers.
CHAPTER 26 - CLINICAL EXAMINATION 433
Box 26.1 Summary of clinical examination 1. History
2. Inspection
3. Functional examination Passive tests
• • • •
flexion extension pronation supination
4. Palpation
5. Accessory tests
Figure 26.7
Accessory test: Tinel's sign.
Resisted tests:
• • • • • •
flexion extension pronation supination flexion wrist extension wrist
THIS PAGE INTENTIONALLY LEFT BLANK
Interpretation of the clinical examination of the elbow 1----------------.. Traumatic arthritis Monoarticular steroid-sensitive arthritis Haemarthrosis Crystal synovitis Septic arthritis Osteoarthrosis Rheumatoid-type arthritis
1-------... Loose body Pulled elbow
1--------.. Extension limitation in
Interpretation of the clinical , examination of the elbow
tennis elbow
Bicipital bursitis
1--------,,.. Epicondylar bursitis Radiohumeral bursitis Bicipital bursitis
1-------... Sprain of the upper radioulnar joint
Ligamentous lesion Olecranon bursitis
Biceps lesion Brachialis lesion
Resisted flexion is positive
Brachioradialis lesion
Rupture of biceps C5-C6 root lesion
Resisted extension is positive
Triceps lesion Anconeus compartment syndrome Rupture of triceps C7 palsy Radial palsy Fracture of olecranon
Pronator teres lesion Golfer's elbow
Biceps lesion Supinator brevis lesion
Golfer's elbow
C7 root palsy
Resisted extension of wrist is positive
Extensor carpi radialis brevisl longus (tennis elbow) Extensor carpi ulnaris lesion Extensor digitorum lesion C7 root palsy Radial palsy
435
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
Disorders of the inert structures
Limited range of movement 437 The capsular pattern 437 Traumatic arthritis 437 Arthrosis 439 Monoarticular steroid-sensitive arthritis CrystaI synovitis 439 Haemarthrosis 439 Rheumatoid-type arthritis Septic arthritis 440
439
439
The non-capsular patterns 440 Limitation of flexion or extension in isolation 440 Acute limitation of supination and extension in children
443
Limitation of pronation
Full range of movement
443
Pain on full passive supination Ligamentous lesions 444 Pain on full passive pronation Bursitis
445
LIMITED R ANGE OF MOVEMENT
443
443 444
The capsular pattern at the elbow is characterized by limitation of flexion and extension (Fig. 28.1), flexion being usually more limited than extension, although equal
limitation
of
both
movements
does
occur.
Rotations remain full and painless except in advanced arthritis, in which they can be painful at the end of the range. The following conditions are the most common.
TRAUMATIC ARTHRITIS A traumatic arthritis presents as an isolated condition at the joint between humerus and ulna, hence there is iso lated impairment of flexion and extension. The arthritis
F p
s
E Figure 28.1 The capsular pattern. F, Flexion; E, extension; P, pronation; S, supination. 437
438 SECTION FIVE - THE ELBOW
can be the result of either trauma (not necessarily severe)
Technique:
or - in middle-aged or elderly patients - overuse of the
prone on a couch with a small pillow under the elbow.
joint.
intra-articular injection. The patient lies
The arm is held by the side with the forearm fully
The patient usually states that, immediately follow
supinated. In this position the joint lines between
ing an injury or the day after having done heavy work
humerus and radius and the radial side of the olecranon
or exertion, the elbow hurts diffusely. The pain is quite
are both easily felt. A 2 ml syringe is filled with triamci
constant, there is stiffness and difficulty in moving the
nolone acetonide 10 mg / ml and a 2 cm thin needle fitted.
joint.
The needle is inserted at the joint line and aimed slightly
Clinical examination shows the capsular pattern: flexion and extension movements are markedly limited and painful; rotations are of full range and painless. On palpation, some swelling may be detected. If the swelling came on immediately after the accident, it is probably caused by blood and this should be aspirated at once. If not, the effusion is secondary and disappears as soon as the arthritis subsides. There are two situations that are worthy of attention.
Fracture of the olecranon The olecranon lies superficially and is therefore very vul nerable. Injury to the elbow, and especially a fall on a bent
oblique under the olecranon (Fig. 28.2). Rest in flexion. Another rather old fashioned but still
valuable treatment is rest in flexion. It can be used in those patients who for some reason cannot receive an injection. As soon as the patient is seen, the elbow is immobilized in as much flexion as possible by means of a collar-and-cuff bandage. Every day the elbow is flexed more, until full movement can be achieved; thereafter it is held in this position for 2 weeks. The elbow is then rested in slightly less flexion. Three days later the joint is re examined and, if the range of flexion is still full, the forearm is allowed to extend a little farther. Some 6 weeks
elbow, may result in fracture of the olecranon. It is, of course, tender to touch and marked articular signs are found on examination: warmth, swelling and limitation of passive movement in the capsular pattern. Resisted movements are also positive in that isometric extension, an action of the triceps muscle, is painful and weak (see also p. 453). Radiography confirms the fracture and its type: it is mostly displaced but stable and then requires surgery.
When it is not displaced, immobilization
suffices.l
Fracture of the head of the radius Should pronation and supination both hurt in an acute traumatic arthritis at the elbow, the head of the radius is almost certainly fractured. A radiograph confirms the diagnosis and immobilization or surgery is the treatment.2 Fracture of the radial head and neck is not uncommon. It occurs in one-third of all elbow fractures and is most common in females.3
TREATMENT Traumatic arthritis recovers spontaneously but this may take several months. Treatment by massage and / or exercises just irritates the joint and are therefore contraindicated. The treatment of choice consists of two intra-articular injections of 20 mg of triamcinolone acetonide. The injec tion is given when the patient is first seen. The arm is kept in a sling for a couple of days. A week later a second injection is given and the joint should have recovered in
2 weeks' time. Figure 28.2
Intra-articular injection.
CHAPTER 28
later the patient has reached the stage in which the arm can be worn in a sling. After 2 or 3 months movements of the elbow should be full and painless.
-
DISORDERS OF INERT STRUCTURES 439
but it results in hardly any change in the amplitude of movements. The patient may be pain-free for many months, whereupon the injection can be repeated without fear of steroid arthropathy because the elbow is not a weight-bearing joint.
ARTHROSIS This condition may come on spontaneously in late middle age4 and is often bilateral. It may also occur as the result of a fracture,S repeated minor injuryti or a loose body in the joint? The patient, most often a male,8 complains that, after he uses hjs elbow excessively, the joint aches slightly. He may also find the inability to fully straighten the arm incon ven ient. On examination a slight capsular pattern is found with a hard end-feel on flexion. The end-feel on exten sion is also hard but this is because of capsular contrac ture and is not the normal bone-to-bone end-feel. There may be coarse crepitus. The radiograph may show the arthrotic changes although a positive radiograph can also be compatible with full range and painless function at the joint. The differential diagnosis is neuropathic arthropathy,9 which presents with gross painless limitation of move ment in the capsular pattern. An arthrotic joint does not of itself give rise to the sort of symptoms that warrant treatment. What may happen
CRYSTAL SYNOVITIS Gout (uric acid crystals) and pseudogout (calcium pyrophosphate crystals) seldom affect the elbow joint during a first attack (in only 4.5% of gout cases)lO but more frequently causes acute olecranon bursitis.ll During further development, polyarticular attacks may occur, in which case the elbow joint is affected in 30% of cases. The sudden unprovoked onset and the shiny red appearance of the joint are characteristic. The following diagnostic criteria may be useful in gout. When uric acid crystals are found in the synovial fluid during microscopic, chemical or histological exami nation, or tophi are seen on the ears, the diagnosis is certain, as it also is when two of the following four crite ria are present: history of a typical attack of gout at the big toe; history of two typical attacks of gout at another joint; clinical picture of tophus; remission within 48 hours of the acute attack after the administration of colchicine or phenylbutazone.12
is that on top of the arthrosis, a traumatic arthritis devel ops as the result of overuse. This can be treated as out lined earlier. Loose bodies are quite common and may also complicate the arthrosis (see below).
HAEMARTHROSIS Haemarthrosis may occur after an injury to the joint, especially an intra-articular fracture or a direct contu sion
MONOARTICULAR STEROID-SENSITIVE ARTHRITIS
of
the joint
capsule,
or,
less commonly,
in
haemophilic patients. Bleeding into the joint leads to gross swelling
and
a
marked
capsular pattern.13
Aspiration must be carried out immediately to avoid A seronegative arthritis may occur, confined to one elbow
destruction of cartilage.
joint. The pain is spontaneous in onset and the elbow very soon starts to swell. A marked capsular pattern is found and, in due course,
RHEUMATOID-TYPE ARTHRITIS
some limitation of pronation and supination may occur. In the acute and subacute stages, the end-feel is of muscle
Polyarticular rheumatoid arthritis may affect the elbow
spasm. The joint is warm to the touch and synovial thick
joint. Apart from the gross swelling, a rapidly ensuing
ening can be found on palpation over the head of the radius laterally. In advanced cases muscle atrophy may also be seen. If, after some years, crepitus is present, it is of the silky type. On radiography, decalcification and later erosion of cartilage may be visible. Treatment with intra-articular triamcinolone suspen sion (see earlier) is symptomatically very effective in monoarticular steroid-sensitive arthritis; it stops the pain
limitation of extension is typicaJ.l4 The elbow is also one of the sites of predilection, together with the knee and shoulder, for chondromatosis. Pigmented villonodular synovitis occurs most commonly at the knee, followed by elbow and ankleJs In these and the other rheumatOid-type arthritides, systemic medication is required, and sometimes even a surgical approach. Good results have been reported with total elbow arthroplasty.16-23
440 SECTION FIVE - THE ELBOW
F
SEPTIC ARTHRITIS
s
p
A bacterial infection of the elbow joint is always very serious. It may lead not only to total destruction of the joint but may also endanger life.24 It can be the result of an open injury to the joint (e.g. open fracture), penetration of a foreign body (e.g. rose or bramble thorns during gardening or fruit picking) or direct inoculation of a bacterium during intra-articular injection, especially injection of a steroid suspension. It can also be caused by haematogenous dis semination from focal infections: dental abscess, cystitis, urethritis, skin infections. These causes are very depend ent on the patient's resistance to infections: patients with diabetes, renal failure or a deficient immune system (e.g. rhematoid arthritis) are more likely to suffer from haematogenous dissemination followed by a septic arthritis.25--27
E
The symptoms start suddenly and are easily recog nized. The joint shows the signs of a hyperacute inflamma tion: much pain, gross swelling, redness, warmth and gross limitation of movement in the capsular pattern. There are also general symptoms, such as mgh fever, a toxic appearance, pallor, loss of appetite and rigors. Treatment consists of systemic antibiotic therapy and daily local aspiration28 and drainage by arthroscopy.29
Figure 28.3
Example of a non-capsular pattern with limitation of flexion.
female gymnasts with hyperextension and valgus of the elbow.33-35 The history is quite typical: the youngster states that the elbow joint locks suddenly, usually in flexion. It is impossible to straighten the elbow to full range, because of pain. In a few days, the condition gradually subsides. It is possible that there has been one or more of these attacks in the past, with pain-free episodes in between. Clinical examination during an attack shows a
LIMITATION OF FLEXION OR EXTENSION IN ISOLATION
non-capsular pattern: limitation of passive extension F p
Loose body in the joint A loose body in the elbow joint is not uncommon, and may hinder normal movements. It prevents the joint either from moving into full flexion, leaving extension free (Fig. 28.3), or from moving into full extension, leaving flexion free (Fig. 28.4). It then changes the hard end-feel of extension into a rather soft one. Three different clinical pictures can be considered, depending on the age group in which they appear: adolescents, adults or the elderly. In adolescence. A loose body is the common cause of
elbow trouble in adolescents and is the only non-trau matic cause of arthrosis encountered in a young person. The condition does not occur before the age of 14 and usually results from osteochondritis dissecans, mostly on the humeral capitellum,3Q,31 or an intra-articular cmp frac hlre, conditions that may lead to exfoliation of one or
E
more fragments of bone covered by articular cartilage.32 Osteochondritis dissecans is not uncommon in young
Figure 28.4
Example of a non-capsular pattern with limitation of extension.
CHAPTER 28
-
DISORDERS OF INERT STRUCTURES 441
with a soft end-feel. During a pain-free period, exami nation is negative; the diagnosis is suggested by the typical history. Radiography confirms the diagnosis and shows the number and the position of the loose fragments. If the patient is seen during an attack, manipulative reduction can be carried out (for the technique, see p. 442). However, arthroscopic36,37 or surgical removal of the loose piece(s) should always be advised for the following reasons: as the loose body has an osseous nucleus and still lies within its nutrient synovial fluid, it may grow and the condition may worsen at each attack. One should also realize that the loose body is considerably larger than is displayed by a radiograph, as it is covered with radiotranslucent cartilage. If surgery is not performed, loose bodies may finally cause gross arthrosis. Limitation of extension may considerably hinder activities and should therefore be prevented. In a normal joint in adulthood. The cause of loose body
Figure 28.5 Location of a loose body in a normal joint. Left, loose body in the anterior part of the joint limiting fiexion. Right. loose body in the posterior part of the joint limiting extension.
formation in adults is usually traumatic, the injury having chipped off one or more pieces of cartilage. Middle-aged patients who develop a loose body may have multiple cartilaginous fragments in the joint that do not show on radiography; these do not tend to cause arthrosis. The history is not as typical as it is in youngsters: the patient does complain of attacks of pain at the elbow, during which exertion increases the pain but gradual unlocking in the following days does not occur, hence the. importance of the clinical examination. Unless these patients are properly examined, they are thought to suffer from tennis elbow. A very clear non-capsular pattern is found with limi tation either of flexion or extension, depending on the position of the fragment. If the loose body lies in the tri angle formed by the humeral capitulum, the head of the radius and the base of the coronoid process of the ulna, extension is slightly limited, while flexion remains full and painless. The end-feel on passive extension is soft. When the loose piece of cartilage lies anteriorly, flexion is quite limited, the fragment catching between the ante rior aspect of the humerus and the tip of the coronoid process (Fig. 28.5). A loose body that limits extension can usually be reduced. Manipulation under strong traction shifts the loose piece of cartilage to a position at the back of the joint. It then no longer blocks movement, which becomes normal again. The manipulation can be repeated each time derangement occurs. Nothing else should be done, unless recurrence is very frequent, in which case removal during arthroscopy would be a possibility.39,40 A loose body that limits flexion cannot be reduced by manipulation but limitation of flexion, unless gross, is not
of major concern. The alternatives then are: arthroscopic or surgical removal or nothing, depending on the patient's age, preference and functional disablement.41 If nothing is done, there is some danger that the loose body will become embedded and be responsible for a perma nent limitation of flexion. Technique: manipulative reduction of a loose body. The
patient adopts the sitting position on a couch. The arm is abducted to the horizontal and the elbow bent to a right angle. An assistant grasps the patient's arm just proximal to the elbow with both hands and fixes the arm against the couch. A second assistant steadies the patient's thorax with a hand on the lower ribs; the other hand holds the shoulder at the affected side against the couch. When assistants are not available, the patient's body and arm can be fixed with straps. In this manipulation different elements are incorpo rated: traction, movement from flexion towards exten sion, and rotation movements, either pronation or supination (Figs 28.6 and 28.7). The manipulator puts the contralateral foot against that of the first assistant vertically below the patient's elbow. This is the fixed point around which pivoting takes place as the elbow is moved from flexion towards extension. The patient's lower forearm just proximal to the wrist is then grasped with both hands. The position of the hands is slightly different depending on the chosen rotation (Fig. 28.6). The use of the manipulator'S body weight is then able to exert the traction required to distract the joint. Pivoting on the foot, movement is gradually made from flexion towards extension while the patient's forearm is moved either in pronation or
442 SECTION FIVE - THE ELBOW
(a)
(b)
(c)
(d)
Figure 28.6 Manipulative reduction of a loose body. (a) Starting position; (b) ending position using the pronation technique (easiest and most commonly used). (c) Details of position of hands for this technique. (d) Details of position of hands for the supination technique (more difficult and less often necessary). This technique is not shown in general view. Use straps to fix the patient when assistants are not available.
supination through the full range. At the last moment as
alternative rotation can be tried. Treatment should be
extension is approached, the manipulator's trunk is side
stopped when the end-feel has become normal- i.e. hard.
flexed away from the patient to exert maximal traction.
One does not expect to reach a painless range of move
Extension movement is not performed beyond the
ment during the manipulation session but the change in
degree of limitation; if this should happen it would, of
end-feel indicates that the loose fragment has moved. The
course, result in a traumatic arthritis of the joint. After each attempt, extension is re-examined. The
slight traumatic reaction consequent upon the original subluxation of the loose body will subside in the days to
chosen rotation is continued for as long as the signs
come. The patient is seen after a couple of days and, if
improve. When no further improvement is found, the
necessary, the manipulation is repeated.
CHAPTER 28 - DISORDERS OF INERT STRUCTURES 443
result of forced distal traction at the forearm.42 Very often the typical history, of a nervous mother pulling her stubborn child roughly by the hand, is elicited. This manoeuvre is immediately followed by the child having pain and limitation of movement; the elbow is held flexed at about 90° and in pronation.43 The head of the radius is pulled down into the annular ligament. As a result the radius moves verti cally downwards. The subsequent disturbance of the lower radioulnar joint is responsible for the limitation of supination. If a radiograph not of the elbow but of the wrist was taken, it would show the position of the radius. Ultrasonography of the radiohumeral joint
J Figure 28.7 The movements in manipulative reduction of a loose body. The illustration shows the three elements in the technique: traction, movement from flexion towards extension and rotation.
In an arthrotic joint in middle or old age. Again the
history is very indicative. The patient is middle aged or elderly and possibly mentions of a slight aching in the elbow as the result of the arthrosis. In addition attacks of pain are reported that last about a week. The symptoms come on gradually (in the course of some hours) and dis appear even more gradually (in the course of some days). Between the attacks, the elbow presents a capsular pattern with a hard end-feel at the end of the achievable range, the result of the arthrosis. During the attacks the limitation becomes of the non-capsular type with a soft
shows that the distance between the radial head and the capitulum is increased, probably because of the interpo sition of the annular ligament.44 Reduction is easy. Sometimes spontaneous reduction occurs just by bringing the forearm into supination and flexion, as in examining for passive flexion of the elbow.45,46 When this does not happen, manipulation is performed. Technique: reduction of a 'pulled elbow'. The child is
asked to stand against a wall. The upper arm is abducted and the elbow flexed to a right angle. The manipulator grasps the child's lower forearm with the ipsilateral
hand
and
pushes
the
radius upwards
towards the humerus by pressing the elbow against the wall. In the meantime, the forearm is rapidly rotated to and fro to the end of the range in either direction (Fig. 28.8). Suddenly, on full supination, the radial head reduces with a palpable click.
end-feel and particularly restricted. The fragments are osseous and visible on radiographs. However, it is possible to have loose bodies in the joint without having attacks of internal derangement. Manipulative treatment can be performed during the attacks, although it is not strictly necessary because the condition subsides spontaneously. It is sufficient to explain the mechanism to the patient. Alternatively, arthroscopiC removal can be considered.
Limitation of extension in tennis elbow In some cases of tennis elbow a slight limitation of passive extension may be found with a softish end-feel. The primary signs of tennis elbow will of course suggest the diagnosis (see pp. 454--465).
ACUTE LIMITATION OF SUPINATION AND EXTENSION IN CHILDREN This condition called 'pulled elbow' or 'nursemaid's elbow', occurs in children under 8 years of age as the
Figure 28.8 Manipulative reduction of the 'pulled elbow'. This illustration shows the two elements incorporated in the technique: compression and rotation.
444 SECTION FIVE - THE ELBOW
LIMITATION OF PRONATION
LIGAMENTOUS LESIONS
An inflammation of the bursa lying under the insertion of
Isolated minor ligamentous lesions at the elbow are not
the bicipital tendon onto the radial tuberosity may cause
common. Injury to one or another ligament usually
pain at the anterior aspect of the elbow.47 Examination
results in a reaction as a whole - traumatic arthritis.
shows limitation of passive pronation with a soft end
In sportsmen however, especiaI1y overhand throwers,
feel. The condition can be treated with infiltration of
the ulnar collateral ligament comes repeatedly under
20 mg of triamcinolone suspension (see p. 444).
tension, i.e. the anterior part.49 This may lead to ulnar col
Karanjia and Stiles48 describe two cases of bursitis at
lateral ligament insufficiency and sometimes sympto
the distal insertion of the biceps. The swelling is cystic
matic valgus instability.50,51 This condition is often
and may compress the median nerve to cause median
complicated by irritation of the ulnar nerve.52
nerve irritation.
Rarely, radiography may show calcification in a collat eral ligament. This condition may result in slight limita tion of extension. It does not respond to treatment.
FULL R ANGE OF MOVEMENT
After dislocation of the elbow, total rupture of the
PAIN ON FULL PASSIVE SUPINATION Occasionally the proximal radioulnar joint may become sprained as the result of overuse. As the pain is felt at the outer side of the elbow, the patient may be misdiagnosed as
suffering
from
tennis
elbow.
On
examination,
however, full but painful passive supination (Fig. 28.9) is the only positive finding. This lesion has no tendency to spontanous cure. Treatment consists of one or two intra-articular injec tions with 20 mg of triamcinolone suspension. The second injection is given 2 weeks after the first. The patient is cured in a few weeks' time. As this joint lies within the common joint capsule, the same technique as described earlier is used.
medial collateral ligament is common.53 Although this leads to medial instability of the elbow joint, it does not cause persistent problems. 54 Surgical intervention may be necessary when conser vative treatment fails and in a patient who wants to return to highly competitive sports.55 In young throwing athletes repetitive high valgus stress and pull by the common flexor tendon may result in subtle stress fracture of the medial epicondyle epi physis. It becomes manifest with pain at the medial aspect of the elbow and diminished throwing distance and effectiveness. The medial epicondyle is very tender to touch and a slight capsular pattern may be found. This lesion is called 'medial epicondylar stress lesion' or
'little league elbow'.56,5 7
Lesion of the lateral collateral ligament rarely occurs as the result of repetitive isolated varus stress but mostly
F P
s
after complete elbow dislocation.58 It may lead to pos terolateral rotatory instability giving rise to symptoms such as clicking, snapping and locking.41 Tests, such as the lateral pivot shift or posterolateral rotatory drawer test, have been devised for confirming the diagnosis.59 In recurrent problems, surgical reconstruction or repair seems to give good results.60
PAIN ON FULL PASSIVE PRONATION This sign usually accompanies the primary signs of a bicipital tendinitis (see below) and indicates the lesion to lie at its attachment to the radial tuberosity. In the unusual circumstances in which bicipital tendinitis is absent, pain on passive pronation should be regarded as an articular sign, indicating either involvement of the E Figure 28.9 Pain on full passive supination: P, pronation; S, supination; F, flexion; E, extension.
radioulnar joint or a bicipitoradial bursitis.61 Bursitis can be treated with infiltration of triam cinolone acetonide. The same technique is used as for
CHAPTER 28 - DISORDERS OF INERT STRUCTURES 445
bicipital tendinitis but the infiltration is done somewhat
Differential diagnosis must be made between a
more proximally between the tendon and the bone of the
traumatic bursitis and an infected bursa. Septic bursitis
radius (see p. 444).
presents with heat and redness of the skin and pain on resisted extension of the elbow.62,63 Analysis of the bursal fluid obtained through aspiration may be helpful. It is a general experience that aspiration alone will not
BURSITIS
prevent the fluid from reaccumulating because of con
Olecranon bursitis
tinued movements of the elbow. Local anti-inflammatory
Because the bursa is superficial it is very vulnerable.
measures are usually necessary and sufficient. Arthro
The lesion can be provoked by repetitive direct pres
scopic excision can be used when conservative treatment
sure, for example leaning the elbow on a table, or by
fails.64 Septic bursitis should be treated immediately with
falling heavily onto the bent elbow. It is often associated
antibiotic therapy and I or drainage. Sometimes, in the
with occupational or sports trauma, or systemic condi
most stubborn cases, surgical excision is necessary.6S
tions, such as rheumatoid arthritis, gout, tuberculosis and
rheumatic
diseases
xanthomatosis).62,63
(e.g.
chondrocalcinosis,
The symptom is pain at the posterior aspect of the elbow. The signs depend on the type of bursitis present. In acute cases, from trauma or infection, there is swelling
Epicondylar and radiohumeral bursitis Cyriax66 (his p. 175) describes superficial epicondylar bursitis, secondary to rheumatoid arthritis of the elbow joint. It gives rise to vague aching at the lateral aspect of the elbow and can be mistaken for tennis elbow. The
over the olecranon which varies in size from a slight dis
condition becomes clear when resisted movements of the
tension to an egg-sized swelling. A variable amount of
wrist seem to be negative.
heat and redness is also found. In more chronic cases,
Radiohumeral bursitis, also giving rise to vague
slight swelling is the only sign. The functional examina
symptoms around the elbow, can be detected only if
tion is usually negative, although full passive flexion may
calcification has made it radiographically visible.
cause some discomfort, described as 'tight'. Palpation
Bicipital radial bursitis is the most important condition
reveals tenderness over the tip of the olecranon. In
affecting the deep bursae. It may hinder the pronation
chronic lesions palpable thickening of the bursal wall
movement (see above) and is sometimes difficult to differentiate from a distal biceps tendinitis.61,67
may be present.
REFERENCES 1. Cabanela ME, Morrey BF. F ractures of the olecranon. In: Morrey BF
(ed) The Elbow and its Disorders, 3rd edn. Saunders,
Philadelphia, 2000:365-379.
11. Tompkins RB. Nonrheumatoid inflammatory arthritis. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Pruladelprua, 2000:793-794.
2. Geel GW, Palmer AK. Radial head fractures and their effect on
12. Wallace SL, Robinson H, Masi AT et al. Preliminary criteria for
the distal radio-ulnar joint. Rationale for treatment. Clin Orthop
the classification of the acute arthritis of primary gout. Arthritis
Rei Res 1992;275:79-84.
3. Morrey BF. Radial head fracture. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia, 2000:341-364.
4. Doherty M, Preston B. Primary osteoarthritis of the elbow. Ann Rheum Dis 1989;48:743.
5. Smjth FM. The Elbow, 2nd edn. Saunders, Philadelphia, 1972. 6. Hellmann DB, Helms CA, Genant HK. Chromc repetitive
Rheum 1977;20:895.
13. O'Driscoll SW, Morrey BF, An KN. Intra-articular pressuring capacity of the elbow. Arthroscopy 1990;6:100. 14. Luthra HS. Rheumatoid arthritis. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia,
2000:781-783. 15. Cloud SR. Intraarticular truotepa held effective in pigmented
trauma: a cause of atypical degenerative joint disease. Skeletal
villonodular
Radial 1983;10:236.
Western Region Meeting, Wellcome Trend Rheum 1981;3(2).
7. Morrey BF. Primary degenerative arthritis of the elbow. Treatment by ulnohumeral arthroplasty. J Bone Joint Surg 1992;74B(3):409-413. 8. Minami M, Kato S, Kashiwagi D. Outerbridge - Kasruwagi's method for arthroplasty of osteoarthritis of the elbow: 44 elbows followed for 8-16 years. J Orthop Sci 1996;1:11. 9. Morrey BF. Primary degenerative arthritis of the elbow: ulno humeral arthroplasty. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Pruladelprua, 2000:799.
10. Dieppe PA, Calvent P. Crystals and Joint Disease. Chapman & Hall, London, 1982:145.
synovitis. American
Rheumatic
Association
16. Maloney WJ, Schurman OJ. Cast immobilization after total elbow arthroplasty. Clin Orthop Rei Res 1989;245:117. 17. Ewald FC, Scheinberg RD, Poss R et al. Capitello-condylar total elbow arthroplasty: two to five year follow-up in rheumatoid arthritis. J Bone Joint Surg 1980;62A:1259. 18. Sjoden G, Blomgren G. The Souter-Strathclyde elbow replace ment in rheumatoid arthritis. 13 patients followed for 5 (1-9) years. Acta Orthop Scand 1992;63(3):315-317. 19. Morrey BF, Adams RA. Semiconstrained arthroplasty for the treatment of rheumatoid arthritis of the elbow. J Bone Joinl Surg 1992;74A(4):479-490.
446 SECTION FIVE - THE ELBOW
20. Ruth JT, Wilde AH. Capitellocondylar total elbow replacement. A long-term follow-up study. J Bone Joint Surg 1992;74A(1):95-100. 21. Brady 0, Quinlan W. The Guildford elbow. J Hand Surg
23. Schneeberger AG, Adams RA, Morrey BF. Semiconstrained total for
the
treatment
of
drome. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia, 2000:273-276.
distal humeral nonunion. J Bone Joint Surg 1992;77B:67. replacement
elbow' in a child. A case report. c/in Orthop Rei Res 1992;284: 153-155. 46. Letts RM. Dislocations of the child's elbow: pulled elbow syn
1993;18B(3):389-393. 22. Morrey BF, Adams RA. Semiconstrained elbow replacement for
elbow
45. Triantafyllou SJ, Wilson SC, Rychak JS. Irreducible 'pulled
post-traumatic
47. Bourne M, Morrey BF. Partial rupture of the distal biceps tendon. c/in Orthop Rei Res 1991;271:143. 48. Karanjia NO, Stiles PJ. Cubital bursitis. J Bone Joint Surg
osteoarthrosis. J Bone joint Surg 1997;79A:1211. 24. Veys EM, Mielants H, Verbruggen G. Reumatologie. Omega,
1988;70B:832. 49. Jobe F W, Stark H, Lombardo SJ. Reconstruction of the ulnar
Ghent, 1985:112. 25. Meijers KA, Dijkmans BA, Hermans J et al. Non-gonococcal infectious arthritis: a retrospective study. J Infection 1987;14:
collateral ligament in athletes. J Bone Joil1t Surg 1986;68A:115B. 50. Pappas AM, Zawacki RM, Sullivan TJ. Biomechanics of baseball pitching: a preliminary report. Am J Sports Med 1985;13:216.
13-20. 26. Goldenberg DL, Reed JI. Bacterial arthritis. NEJM 1985;312:764.
51. Jobe FW, Nuber G. 1986 T hrowing injuries of the elbow. Clil1 Sports Med 1985;5:521.
27. Ho G. Bacterial arthritis. Curr Opin RheumatoI1992;4:509. 28. Mielants H, Dhondt E, Goethals L et al. Long-term functional
52. Conway JE, Jobe FW, Glousman RE, Pink M. Medial instability
results of non-surgical treahnent of common bacterial infections
of the elbow in throwing athletes: surgical treatment by ulnar collateral ligament repair or reconstruction. J Bone joint Surg
of jOints. Scand J RheumatoI1981;11:101. 29. Butters KP, Morrey BF. Septic arthritis. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia,
53. Josefsson PO, Johnell 0, Wendeberg B. Ligamentous injuries in dislocations of the elbow
2000:811-813. 30. McManama GB, Micheli LT, Berry MY et al. The surgical treat ment of osteochondritis of the capitellum. Am J Sports Med
joint.
Clin
OrtllOp Rei Res
1987;221:221. 54. Josefsson PO, Johnell 0, Gentz CF. Long-term sequelae of sinlple dislocation of the elbow. j Bone Joint Surg 1984;66A:927.
1985;13(1):11. 31. Angelo RL. Arthroscopy. Advances in elbow arthroscopy.
55. Jobe FW, Elattrache NS. Diagnosis and treatment of ulnar col lateral ligament injuries in athletes. In: Morrey BF (ed) The
Orthopedics 1993;16(9):1037-1046.
32. Lindholm TS, Osterman K,Vankka E. Osteochondritis dissecans of the elbow, ankle and hip: a comparative survey. Clin Orthop
Elbow and its
Disorders, 3rd edn. Saunders, Philadelphia,
2000:549-555. 56. Blohm 0, Kaalund S, Jakobsen BW. 'Little league elbow' - acute
Rei Res 1980;148:245.
33. SiJlger R, Roy S. Osteochondrosis of the humeral capitulum.
traction apophysitis in an adolescent badminton player. Scal1d
I
Med Sci Sports 1999;9(4):245-247.
Am j Sports Med 1984;12(5):351.
34. Jackson OW, Silvino N, Reiman P. Osteochondritis in the female
57. Bennett JB, Mehlhoff TL. Articular injuries in the athlete. In: Morrey BF (ed) The Elbow alld its Disorders, 3rd edn. Saunders,
gymnast's elbow. Arthroscopy 1989;5:129. 35. Maffulli N, Chan 0, Aldridge MJ. Derangement of the articular surfaces of the elbow in young gymnasts. J Pediatr Orthop
Philadelphia, 2000:565. 58. F reeman BL. Recurrent dislocations. In: Crenshaw AH (ed) Campbell's Operative Orthopaedics, 7th edn. Mosby, St. Louis,
1992;12(3):344-350. 36. Andrews JR, Carson We. Arthroscopy of the elbow. Arthroscopy
1987:2212. 59. O'Driscoll SW, Bell OF, Morrey BF. Posterolateral rotatory insta
1985;1:97. 37. Boe A, MoIster A. Albueartroskopi. Tidsskr Nor LCEgeforen 38. Morrey BF. Loose bodies. In: Morrey BF (ed) The Elbow and its 39. O'Driscoll SW, Morrey BF. Elbow arthroscopy for loose bodies. 40. O'Driscoll SW, Morrey BF. Arthroscopy of the elbow. Diagnostic
and therapeutic benefits and hazards. J
Bone Joint Surg
62. Canoso JJ, Scheckman PR. Septic subcutaneous bursitis, report of sixteen cases. J RheumatoI1979;6(1):96. 63. Ho G Jr, Tice AD, Kaplan SR. Septic bursitis in the prepatellar
1992;74A(1):84-94. 41. O'Driscoll SW, Morrey BF, Korinek S, An KN. Elbow subluxa tion and dislocation: a spectrum of instability. c/in Orthop Rei
and olecranon bursae: an analysis of 25 cases. Ann Intern Med 1978;89(1):21. 64. Kerr DR, Carpenter CWo Arthroscopic resection of olecranon
Res 1992;280:186-197.
and prepatellar bursae. Arthroscopy 1990;6(2):B6.
42. Illingworth C. Pulled elbow. BMJ 1975;i:672. 43. Choung W, Heinrich SO. Acute annular ligament interposition into the radiocapitellar joint in children (nursemaid's elbow).
65. Reilly JP, Nicholas JA. The chronically inl f amed bursa. Clin Sports Med 1987;6(2):112-114.
66. Cyriax J. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft
J Pediatr Orthop 1995;15:454.
B,
Saengnipanthkul
S,
Laupattarakasem W, Jirawipoolwon P. Ultrasonography of pulled elbow.
61. Karanjia NO, Stiles PJ. Cubital bursitis. j Bone joint Surg 1988;70B:832.
Orthopedics 1992;15(7):855-859.
Mahaisavariya
lateral rotatory instability of the elbow. j Bone Joint Surg 1992;74A:1235.
Disorders, 3rd edn. Saunders, Philadelphia, 2000:890-900.
W,
bility of the elbow. j Bone Joint Surg 1991;73A:440. 60. Nestor B, O'Driscoll SW, Morrey BF. Surgical stabilization for
1992;112(4):493-494.
44. Kosuwon
1992;74A:67.
I Bone Joint Surg 1993;75B(3):421-422.
Tissue Lesions, 8th edn. Bailliere Tindall, London,1982.
67. Morrey BF. Bursitis. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia, 2000:901-90B.
Disorders of the contractile structures
CHAPTER CONTENTS Resisted flexion of the elbow
Pain 447 Weakness
447
451
Resisted extension of the elbow
Pain 451 Weakness
451
453
Resisted supination Resisteq pronation
453 454
Pain on resisted extension of the wrist
454
Tennis elbow 454 Lesion of the extensor carpi ulnaris muscle 465 Lesion of an extensor digitorum muscle 465 Weakness on resisted extension of the wrist Resisted flexion of the wrist
Pain 466 Weakness
468
466
Unlike the shoulder, combined lesions here are quite rare. Therefore positive resisted movements usually indjcClt� a lesion of one contractile structure only.
465
RESISTED FLEXION OF THE ELBOW PAIN
The biceps and brachialis muscles are tested during resis ted flexion, which should be performed with the elbow bent at a right angle - the neutral position between flexion and extension and also the one in which elbow flexion strength is maximap,2 - and the forearm held in active supination. This is the best position to test the biceps muscle,3 which is more often strained than the brachialis. Electromyographic studies confirm a decreased activity of the biceps when flexion is performed in pronation.4--6
Biceps muscle If the biceps muscle is at fault, resisted supination will also be painful. There are four possible localizations, indicated by the site of the pain (Fig. 29.1). Pain at the shoulder. If resisted flexion and resisted supination elicit pain at the shoulder, the lesion should be sought in the upper extent of the long head of the biceps, either in the bicipital groove, or higher up in its intra articular course or even at its attachment to the glenoid labrum. Rupture of the long head of biceps is one of the com monest tendinous ruptures. It causes scarcely any symp toms, except the appearance of a round ball of muscle at the lower part of the arm when the patient flexes his elbow. Resisted flexion remains painless and strong, the brachialis muscle still functioning as the strongest flexor of the elbow - only 8% of elbow flexion strength and approximately 21% of forearm supination strength is lost? Treatment is not required. Pain at the mid-arm. The lesion may lie in the muscle belly itself, usually in the lower half. It is very often the result of a single excessive strain. The patient complains of anterior brachial pain during flexion movements. The symptoms may continue indefinitely, especially in those 447
448 SECTION FIVE - THE ELBOW
2
3
4
Figure 29.1 Sites of lesions in the biceps: 1, tendon in bicipital groove; 2, muscle belly; 3, musculotendinous junction; 4, tenoperiosteal insertion.
patients who go on exerting their arm. Even when the patient is prepared to take relative rest, spontaneous cure may require 2 years to occur. A lesion in the belly of the biceps presents with two particular features: (a) it usually lies at the posterior aspect of the muscle belly - therefore the tender spot must be palpated with a pinching grip; (b) the site is not always especially tender to the touch - it may therefore be difficult to find the exact localization by palpation. Diagnostic infiltration with a local anaesthetic may then be very helpful and, in cases of recent onset, the infiltra tion may even prove curative. Even if this is not the case, it shows exactly where the lesion lies so that the therapist knows where to give deep transverse massage or friction (the latter, more common term to be used throughout), a treatment which is curative in a few weeks, except in very chronic cases -lesions which have lasted for more than 5 years may sometimes prove intractable. Technique: deep friction to the biceps belly. The patient is in a half-lying position and the forearm rests on the thigh, so that the muscle belly is well relaxed. The therapist grasps the muscle belly at the point of the lesion with the ipsilateral hand in a pinching grip, holding the fingers well flexed, which enables the poste-
Figure 29.2
Deep friction to the biceps muscle belly.
rior aspect of the muscle to be reached (Fig. 29.2). The hand is then pulled anteriorly. This results in a transverse friction to the muscular fibres, which can be felt to pass under the fingers. The hand is then brought back to the starting position without losing contact with th.e patient's skin. The manoeuvre thus has two phases: an active phase, when the hand is pulled anteriorly, and a passive phase, when the hand is brought backwards again. Pain at the lower arm. Palpation with a pinching grip shows the lesion to lie at the musculotendinous junction but again it is only possible to be sure of this after diag nostic infiltration with a local anaesthetic. Tendinitis at the body of the lower tendon of the brachial biceps does not occur. Deep transverse friction is, in our experience, the only treatment. Without proper treatment the lesion may go on causing pain indefinitely, having occurred at a point where the natural mobility of muscle is restricted by the presence of tendinous strands. Technique. The same technique is used as described earlier. The position of the hand and fingers, as well as the amplitude of the movement, are adapted to the volume of the structure at the musculotendinous junction.
Pain at the elbow. W hen pain is felt at the anterior aspect of the elbow, probably with some radiation down the front of the forearm as far as the wrist, a lesion at the tenoperiosteal insertion to the radial tuberosity should be suspected.
CHAPTER 29 - DISORDERS OF THE CONTRACTILE STRUCTURES 449
Apart from the usual signs on examination, a localiz ing sign is present - pain at full passive pronation. This is the result of the bicipital insertion being pinched between the radial tuberosity and the shaft of the ulna as the radius turns over the ulna during pronation. Palpation is not necessary and would even be negative as tenderness cannot be elicited by probing with a finger. The treatment of choice is infil tration with triamci nolone. Because it is difficult to infiltrate the entire lesion accurately in the absence of localizing tenderness, up to three infiltrations may be necessary. The alternative treatment is deep transverse friction. Cure takes about 2 weeks, and the treatment is quite painful, in that the lesion lies deeply and is difficult to reach. Technique: infiltra tion of the distal insertion of the
The patient lies prone on the couch. The upper arm is passively held in exter!'al rotation by the side. The forearm is put in full pronation which turns the biceps.
radius so that the radial tuberosity, where the insertion lies, points upwards. The joint line between humerus and radius is palpated. The posterior edge of the ulna is easily felt. A point is chosen 2-3 cm further distally from the joint line and just laterally to the ulna. A 2 ml syringe is filled with triamci nolone and a thin needle 2 em l ong, is fitted. The needl e is inserted at the chosen point and pushed verticall y downwards until it hits the shaft o f the radius, either directly or through a tendinous structure (Fig. 29.3). In the former case, the needle has to be partly withdrawn and reinserted in a slightly different direction in order to feel the tendinous resistance. Then a series of droplets is infiltrated at the tendinous insertion according to the usual infiltration technique. The patient should be warned of moderate after-pain and to avoid flexion and supination movements for a week. Follow up is after 2 weeks and, if the tests are not completely negative, a second infiltration is given. I n most cases, one o r two infiltrations suffice.
Fi gure 29.3
biceps,
Infiltration of the distal insertion of the
450 SECTION FIVE - THE ELBOW
Technique: friction to the distal insertion of the biceps.
The patient sits on the couch with the elbow bent to a right angle and supinated. The therapist sits and with the contralateral hand palpates for the radial tuberosity, searching the radiohumeral joint line and descending 2 cm along the shaft of the radius. At that level the thumb is moved anteriorly to identify the tuberosity deeply under the muscles of the forearm. The thumb is held well flexed and placed medially to the biceps tendon. The fingers give counterpressure at the dorsal aspect of the elbow. The ipsilateral hand, which grasps the patient's forearm just about the wrist, is used to perform a prona tion movement. The forearm is pronated until the biceps tendon passes under the therapist's thumb. The tendon now lies medial to it. Friction is thus performed by this indirect movement. During this part of the movement, the pressure on the tendon is augmented (active phase). The forearm is then brought back to the supinated posi tion, while the pressure is released (passive phase). These repeated movements result in a transverse friction (Fig. 29.4), which is continued for 15 minutes. The therapist must make sure that neither the median nerve nor the brachial or radial arteries are compressed during the manoeuvres.
Brachialis muscle Resisted flexion of the elbow is painful, certainly with the forearm in pronation, the position in which the biceps does not work. Resisted supination is negative.
Again the tender area is difficult to find but it usually lies in the distal third of the muscle belly, just dorsal to the bicipital tendon. It is therefore not impossible for passive flexion also to hurt because this pinches the injured part of the msucle. A diagnostic infiltration may prove necessary. Treatment consists of 2 or 3 weeks' deep transverse friction. Technique: deep friction. The same technique is used as for the brachial biceps muscle. The distal part of the brachialis muscle can be palpated just dorsally to the bicipital tendon. The muscle is well relaxed and friction performed with a pinching grip. During treatment, the therapist should make sure that no nervous (paraesthesia) or arterial (paleness of fingers) symptoms arise, which would indicate that either the ulnar nerve or the brachial artery is being contacted. In such a case, the position of the hand must be altered.
The brachialis muscle and heterotopic ossification. Myositis ossificans is a benign condition, characterized by heterotopic bone forma tion, which occurs after injury to muscle fibres, connective tissue, blood vessels and underlying periosteum. s I t occurs most often in males aged between 15 and 30 years and presents with the following triad of symptoms: pain in the affected muscle, a palpable mass and a fl exion contracture.9 The history of severe contusion is helpful in the early evalu ation of these patients, before radiographic changes are evident.lO When, after an injury, usually fracture,ll pain in the elbow region increases and the range of movement grad ually decreases,12 this m9y indicate the development of myositis ossificans. An increasing firm mass in the brachialis muscle is mostly palpable in the middle or distal segment of the arm and becomes visible on the radiograph in the course of a few weeks.13 A technetium bone scan is clearly positive. 14 When myositis ossificans has fully developed, only a little movement to either side of the right angle is possible and even rotations are markedly limited. Warning Osteogeni c sarcoma may also present w i th the formation of a mass i nvadi ng the muscle.15 The characteri stic radio graphi c appearance of the sarcoma provides the di agnosi s.
F i g u r e 29.4
Deep friction to the distal insertion of the biceps.
Myositis ossificans does not respond to conservative treatment and may disappear spontaneously in the course of 2 years. Lipscomb et a/16 have stated that myo sitis ossificans in the upper extremity is very likely to resorb completely. I f not, surgical excision may be performed.
CH APTER 29
Most people attribute the occurrence of myositis to previous treatments (e.g. massage, mobilization). Cyriax does not believe that the development of myositis is the result of treatment but depends on the type of trauma that caused the muscular lesion. Therefore it would be unwise to give treatment unless a full passive range of movement was present at the elbow joint. If a traumatic arthritis is present, the best approach is to treat the joint until full recovery. If the brachialis muscle still gives some trouble and if resisted flexion is still positive, a radiograph should be taken. If this is negative, treat ment with deep transverse friction can be started and will be curative very quickly.
Brachioradialis muscle We have never encountered a lesion of the brachioradi alis muscle but a case has been described by BarbaixY The patient, following exertion, experienced supra condylar pain at the radial aspect of the elbow occurring during activities which included elbow flexion and simultaneous rotations. The pain could be elicited on passive extension, which was slightly limited, and on resisted flexion of the elbow. Accessory examination showed resisted supination with the forearm in full pronation more painful with a flexed elbow than with an extended one. Diagnosis was confirmed with echog raphy and the patient responded well to infiltration with triamcinolone acetonide. These clinical findings are compatible with an earlier electromyographic study showing electrical activity with flexion, especially with the forearm rotated in pronation. 1 8
-
DISORDERS OF THE CONTRACTILE STRUCTURES 451
Cyriax27 (his p. 173) mentions a case of a complete rupture of the distal tendon of the biceps from the radial tuberosity without a fracture.
RESISTED EXTENSION OF THE ELBOW PAIN
Triceps muscle Lesions of the triceps muscle are rare. Three possible localizations can be differentiated by palpation (Fig. 29.5): the musculotendinous junction, which is the most common site; the body of the tendon; the tenoperiosteal junction at the olecranon. For all the sites treatment consists of deep transverse friction. The tenoperiosteal junction responds equally to deep transverse friction and infiltration. Technique: infiltra tion at the tenoperiosteal junction.
The patient lies prone with the slightly flexed arm by the side. A small pillow is placed under the elbow. A 1 ml syringe is filled with triamcinolone acetonide and a 2 cm needle is fitted. The tip of the ol ecranon is palpated and the tender point located. The needle is inserted 1 cm proximal to it and directed towards the olecranon (Fig. 29.6). Tendinous resistance should be felt
WEAKNESS
Neurological conditions Weakness of elbow flexion usually results from a cervical root palsy, either C5 or C6. In palsy of the fifth cervical root, resisted abduction and external rotation of the shoulder are also weak. In sixth cervical root palsy, resisted extension of the wrist is also weak.
Rupture Rupture of the distal insertion of the biceps (3% of all bicipital ruptures) usually accompanies an avulsion of the radial tUberosity.1 9 Avulsion of the tendon of biceps at its distal insertion is reported increasingly in the current literature. 2o-24 It follows a single excessive exertion and leads to ecchy mosis and pain at the anterior aspect of the elbow. Resisted flexion is only slightly weakened. On contrac tion of the muscle a gap is palpable. Early surgical repair is the treatment of choice. Excellent results are reported.25,26
H""-+- 2
Fi gure 29.5 Sites of lesions of the triceps: 1, musculotendinous junction; 2, body of the tendon; 3, tenoperiosteal insertion.
452 SECTI ON FIVE - THE ELBOW
patient's forearm. The tender spot in the triceps tendon is palpated and then the index finger, reinforced by the middle finger, is placed at the medial side of the tendon. Counterpressure with the thumb is then applied at the lateral aspect of the proximal part of the forearm (Fig. 29.7). The therapist abducts the arm and then brings it back into the side. This is the active phase and is followed by relaxation while bringing the arm back into abduction. Such repeated movement results in a transverse friction to and fro over the lesion.
Resisted extension of the elbow and painful arc
F i g u re 29.6
Another possibility is that resisted extension of the elbow elicits pain at the shoulder in the C5 distribution. This has the same significance as a painful arc at the shoulder. As a result of the contraction of the triceps muscle, the humerus is pulled upwards towards the acromion. A tender structure, lying between the head of the humerus and the roof of the joint, especially an inflamed subacromial bursa, may be painfully squeezed by this movement.
Infiltration at the tenoperiosteal of the triceps.
before hitting bone. Infiltration is then carefully per formed by several withdrawals and reinsertions of the needle and maintaining bony contact. Technique: friction to the musculotendinous junction,
The patient sits next to the couch with the arm rested, the elbow held in 90° flexion. The therapist sits at a right angle to the patient's arm. With the contralateral hand the patient's elbow is grasped while the other hand stabilizes the
body of tendon and tenoperiosteal junction.
F i g u re 29.7
Anconeus compartment syndrome Abrahamsson et al28 reported a case of lateral elbow pain caused by a chronic compartment syndrome of the anconeus muscle. The symptoms were lateral elbow pain and muscular dysfunction during heavy work. The pain was reproduced by repeated extension of the elbow and pronation of the forearm. There was a slightly bulging mass and pronounced tenderness of the anconeus muscle which were successfully treated by fasciotomy.
Deep friction to the triceps.
CHAPTER 29 - DISORDERS OF THE CONTRACTILE STRUCTURES 453
WEAKNESS
Painful weakness Total or partial rupture of the triceps tendon This has been reported as a rare injury - the triceps is the least commonly ruptured tendon.29 ,3o The tear is from the tenoperiosteal junction although a lesion at the musculo tendinous junction has been reported.31 A palpable gap, with complete weakness of arm extension is pathogno monic of triceps rupture and early surgical repair is the treatment of choice.32 The same signs may be found in triceps avulsion fractures, which occur on rare occasions in weightlifters.33 Fracture of the olecranon. If the pain is the result of an injury and resisted extension of the elbow is painful and weak, the possibility of a fracture of the olecranon must be considered. Local tenderness and marked articular signs at the elbow joint will also be present: warmth, swelling and limitation of passive movements in the cap sular pattern. In most cases, conservative treatment is sufficient.34
Painless weakness Among other neurological disorders a radial palsy and a C7 root palsy are the commonest. Radial palsy. Apart from known traumatic causes, a radial palsy is quite often the result of pressure from a crutch or sleeping with the inner side of the arm pressed against a hard edge ('Saturday-night paralysis'). In this case, resisted extension of the wrist is also very weak and may even result in wrist-drop. The condition is painless and recovers spontaneously in the course of 3-6 months. Some severe cases require neurosurgical repair (see p. 557).
Fi gure 29.8
Infiltration of the supinator brevis.
inhibits the function of the biceps. The muscle is not found to be particularly tender and therefore an infiltra tion with a local anaesthetic should be given (Fig. 29.8). This may effect cure, but treatment with deep transverse friction (Fig. 29.9) is usually necessary. It is successful in lor 2 weeks.
root palsy. This is usually the result of a C6 disc pro trusion, compressing the C7 nerve root. The history points towards a neck problem, and cervical examination is positive. The triceps muscle may be found weak in iso lation or in conjunction with weakness of the flexor muscles of the wrist and, in severe cases, the adductors of the shoulder.
C7
RESISTED SUPINATION
Painful resisted supination usually occurs in conjunction with pain on resisted flexion, in which case the lesion lies in the biceps muscle. If resisted flexion is not positive, the supinator brevis muscle must be at fault. The latter condition is quite rare. To confirm the diagnosis, the test is repeated with the elbow held actively in full extension - a position which
Figure 29.9
Deep friction to the supinator brevis.
454 SECTION FIVE - THE ELBOW
Technique: friction to the supinator brevis. The patient sits at the couch. The elbow is bent to a right angle, pronated and placed on the couch. The therapist sits at a right angle to the patient's arm and palpates for the shafts of radius and ulna. The tender spot is found in between the two bones. The supinator, being a flat muscle, cannot be felt on palpation, so anatomical knowledge is required to be able to palpate in the region of it. The therapist then places the thumb on the most tender area and gives counterpressure with the fingers at the medial aspect of the forearm. The friction is performed by an oblique movement perpendicular to the course of the muscular fibres, a movement that starts proximally on the radius and ends more distally on the ulna.
RESISTED PRONATION
Pain on resisted pronation usually indicates golfer's elbow - a lesion in the common flexor tendon - in which case, resisted flexion of the wrist must also be painful. The fact that the pronator teres muscle partly originates from this tendinous complex at the medial epicondyle explains why resisted pronation may be positive. Very occasionally, the lesion lies in the pronator teres muscle itself. Palpation discloses tenderness in the muscle belly, usually at its midpoint. In this unusual lesion, treatment consists of a few sessions of deep trans verse friction. Technique: friction to the pronator teres muscle. The patient sits with the arm rested on the couch. The thera pist sits at a right angle to the patient's arm. The elbow is held in 90° flexion and the forearm in neutral position between pronation and supination. The therapist pal pates at the anterior aspect of the forearm for the muscle belly, which may be facilitated by an active contraction by the patient. The fingertips of two or three fingers of the contralateral hand are then placed on the tender area and counter-pressure with the thumb at the lateral aspect of the forearm is given. The forearm is stabilized with the other hand (Fig. 29.10). The friction movement is begun underneath the muscle and the fingers pulled over the muscle towards the therapist. This is the active phase. The fingers are then brought back to the previous posi tion (passive phase). The sequence is repeated.
PAIN ON RESISTED EXTENSION OF THE WRIST TEN N IS ELBOW
The term 'tennis elbow' has been used to describe a multiplicity of conditions of the elbow.
Fi gure 29.10
Deep friction to the pronator teres.
Renton35 in 1830, was the first to describe a patient with pain along the outer forearm which increased on using the hand. In 1873, Runge, a German physician, wrote an article on 'writer's cramp'. He distinguished the condition from a case of 2 years' inability to write, associated with tenderness on the lateral condyle of the humerus. Rest and electrotherapy had no effect and he then cauterized the skin over the tender area, after which the patient became well. He thought the cramp to be the result of a traumatic inflammation of the peri osteum in this location, caused originally by a forcible supination effort and kept chronic by the continual pull of the extensor muscles attached to the lateral condyle.36 Morris (1882)37 compared a condition named 'lawn tennis arm' to rider's sprain - a lesion of the adductor longus muscle at the hip and Major also called the con dition 'lawntennis elbow'.38 An annotation in the Lancet (1885) drew attention to the number of sufferers from 'tennis elbow', whose plaintive letters had recently appeared in the lay press. From then on the term 'tennis elbow' has been used to describe symptoms at the outer aspect of the elbow. Remak (1894)39 and Bernhardt (1896)40 agreed that it was a periosteal tear from occu pational overuse of the extensor muscles that arise from the lateral condyle. Coudere (1896)41 called it a 'rup_ tured epicondylar tendon', Fere (1897)42 'epicondyl algie', Franke (1910)43 'epicondylitis'. In 1921, Schmidt44
CHAPTER 29
suggested superficial epicondylar bursitis, thereby incriminating the bursa described by Schreger in 1825.45 In 1922, Osgood46 and in 1932, Carp47 believed the lesion to lie in the radiohumeral bursa, and extra-articular bursa under the extensor tendons, which was first described by Monro in 1788.48 In 1936, Cyriax49 compiled a list of no fewer than 26 different types of lesion to which the name tennis elbow had been given by 91 authors during the previous 63 years. He presented a synopsis of the opinions held on the cause of tennis elbow and stated that a condition, the symptoms and signs of which are as constant as those of tennis elbow, may well be supposed to have but one background and, as a corollary, but one type of treatment. An enormous number of articles on tennis elbow have been published in the ensuing years, describing different pathological entities such as radiohumeral bursitis, radiohumeral synovitis, irritation of the syn ovial fringe, degeneration of the annular and collateral ligaments, fibrillation of the articular cartilage, osteoarthrosis of the radiohumeral joint, osteochondritis dissecans, aseptic necrosis of the radial head, stenosis of the orbicular ligament, chondromalacia of the radial h ead and capitulum, calcific tendinitis of the extensor muscles, myofasciitis, traumatic periostitis of the lateral epicondyle, enthesopathy of the lateral epicondyle of the humerus, among others.50-59 A new concept was introduced in 1972 when Roles and Maudsley described the 'radial tunnel syndrome'60 (see p. 560). The most encompassing classification is perhaps that of O'Neill et al61 who state that 'tennis elbow or lateral epicondylitis consists clinically of pain localized in the region of the lateral aspect of the elbow with tenderness in the vicinity of the lateral epicondyle'. This vague description illustrates how unsure most authors are about the pathogenesis of tennis elbow. Most authors consider tennis elbow as a local condi tion in relation to the lateral epicondyle of the humerus. However, some authors have described this condition as resulting from a cervical problem and they claim cura tive results with treatment to the neck. Gunn et al62 con sidered a tennis elbow to be caused by a reflex localization of pain from radiculopathy at the cervical spine. Several authors agreed with this point of view.63-65 Weh66 believes that the idea of a local clinical assessment of tennis elbow should be broadened to an overall vision of a functional chain of cervical spine, shoulder and elbow, in which local reflex inhibition of muscles innervated by the seventh nerve root and a lim itation of movement of the cervical spine are causative elements. It is quite certain that elbow pain may have a cervical origin. This should not be designated 'tennis
-
DISORDERS OF THE CONTRACTILE STRUCTURES 455
elbow' but instead 'referred elbow pain' from the cervi cal spine. If clinical examination shows the elbow pain to be evoked by movements at the elbow, then the lesion must be sought there. In contrast, if cervical examina tion is positive, this means that cervical movements must be the cause of pain in the elbow region ('the' pain). We agree with those who consider tennis elbow as a lesion in the radial wrist extensors at the elbow. This is a logical deduction from what is found at clinical examina tion of the elbow, the primary sign being pain on resisted extension of the wrist. Tenni s elbow i s characteri zed by pai n on resisted extensi on of the wrist
Terminology 'Tennis elbow' is technically a misnomer, since it most often occurs in non-tennis players: less than 5% of the patients play tennis.67-69 And even in a population of 500 tennis players complaining of lateral elbow pain, Grachaw and Pelletier found tennis elbow present in only 39.7%.70 This accords with Kramer's findings.71 Even the term 'epicondylitis' is not right: at least 10% of the lesions do not lie at the epicondyle itself. Of all the patients seen in a general medical practice, 0.5% suffer from 'tennis elbow'.72 The condition is there fore important enough to try to define it properly. Th e lesion lies at the elbow but in the structures controlling wrist extension and radial deviation. Theoretically, the lesion could also lie in the ulnar deviators or in the extensors of the fingers but this is much less common and should be separately named: for example lesion of the extensor carpi ulnaris muscle, lesions of the extensor digitorum muscle.
Pathological features It is generally believed that tennis elbow is an overuse phenomenon caused by repeated contractions of the radial extensors of the wrist,52 ,73 and especially of the extensor carpi radialis brevis.74 Posttraumatic causes have also been described.75 In the early stages, when the tissue atempts repair, and often just as the tear begins to unite, continued muscular contraction pulls the healing surfaces apart once more. This results in the formation of a painful scar with self-perpetuating inflammation (Cyriax27 p. 178). Cyriax's view was confirmed by Coonrad and Hooper in 1973.67 More recent observations during surgery have forced Nirschl to classify this condition mostly under the heading 'tendinosis' rather than tendinitis: surgical inspection shows a typically 'grayish color and homo genous and generally edematous and friable tissue'
456 SECTION FIVE - THE ELBOW
indicating angiofibrob1astic invasion - fibroblasts and vascular granulation-like tissue.76-78 Inflammatory cells are usually not found.79
extensor carpi radialis brevis - the structures involved in tennis elbow (Fig. 29.11).
Palpation History The patient is usually between 30 and 60 years,80,81 and seldom under 20 or over 70. As the lesion is the result of overuse, the patient does not notice the pain the moment a tennis elbow develops but a few days later. A pain is described starting at the outer aspect of the elbow and radiating down the posterior aspect of the forearm, very often as far as the dorsum of the hand. Pain may be felt in the long and ring fingers. It is evoked by grasping, pinch ing and lifting - the movements that involve extension of the wrist and in which the wrist extensors merely act as stabilizers of the joint. In a few weeks, the symptoms develop to the point that even light objects have to be dropped as the result of sudden painful twinges. Patients may be encountered who have constant pain, which may be worst at night and followed by waking in the morning with the elbow feeling stiff.
•
Functional examination Nine out of the 10 tests of the elbow are negative and one is positive: resisted extension of the wrist. It should be remembered that the elbow must be held in full extension in order to avoid a false-negative result. Tennis elbow
=
9 tests negative
The exact location is revealed by palpation. The pa1pa tory manoeuvres must be confined to the structures at fault: the extensor carpi radialis longus and brevis. In that the lateral aspect of the elbow is very often tender to the touch, even in those without a lesion, palpation is sometimes misleading. One elbow should be compared with the other and also one possible location is com pared with another. In corpulent women, it may be difficult to define the lateral epicondyle. The palpation techniques are identical to the friction techniques (see Treatment, below) although it might sometimes be necessary to put the elbow into more extension to be able to reach the tender spot. Practice shows that a tennis elbow has four different localizations (Fig. 29.12). Double lesions, however, are not at all uncommon. On palpation from proximal to distal, a tender spot at one of the following places can be found:
+
•
1 test positive
Our experience has shown that, if resisted extension of the wrist causes such a sharp twinge that the patient has to let the hand go, this points to a lesion at the tenoperi osteal junction. Resisted extension of the wrist with and without the fingers held actively flexed are then com pared. Active flexion of the fingers inhibits the action of the finger extensors. In most instances both versions will be equally positive, which shows the wrist extensors to be at fault. Rarely resisted extension of the wrist with the fingers held actively flexed will be negative, which impli cates the finger extensors. If one or more finger extensors are strained, the resisted extension of the different fingers will show which tendon is involved. The next approach is to differentiate the radial exten sors from the ulnar extensor by two accessory tests. Resisted radial deviation is compared with resisted ulnar deviation, the wrist being held in the neutral position between flexion and extension. In the rare circumstance that resisted ulnar deviation is painful, the lesion lies in the extensor carpi u1naris muscle. Much more frequently resisted radial deviation is painful, which indicates a lesion in either the extensor carpi radialis longus or the
•
•
just proximal to the epicondyle along the supracondy lar ridge at the anterior aspect - i.e. the origin of the extensor carpi radialis longus. This structure feels like a muscular rath er than a tendinous tissue (type I) at the anterior aspect of the lateral epicondyle - the tenoperiostea1 origin of the extensor carpi radialis brevis. In this instance palpation must be precise at the origin of the tendon itself. Palpation of the lateral or posterior aspect of the epicondyle may also be positive which is merely 'associated' tenderness. This disappears as soon as the lesion is cured. The tenoperiosteal variety at the epicondyle itself is by far the most common localization of tennis elbow (type II) level with the radiohumeral joint line and over the head of the radius - the body of the tendon of the extensor carpi radialis brevis, lying in between other tendinous structures (type III) level with the neck of the radius and a few centimetres distally - the upper part of the muscle bellies of the extensor carpi radialis longus and brevis (type IV).
Experience shows that type I occurs in 1% of cases, type II in 90%, type III in 1% and type IV in 8% (Cyriax:27 p. 178).
Treatment of type' (supracondylar) tennis elbow Treatment of this type is quite simple. It responds very well to deep transverse friction and should be cured in three to six treatments, performed two or three times a week. Infiltrations are futile.
CHAPTER 29
-
DISORDERS OF THE CONTRACTILE STRUCTURES 457
Positive resisted wrist extension with fingers relaxed
Resisted wrist extension with fingers flexed
2
3
=
Figure 29.11
Figure 29.12 Localizations of tennis elbow: 1, supracondylar (type I); 2, tenoperiosteal (type II); 3, tendinous (type III); 4, muscular (type IV).
Tennis elbow
Which tendon?
4
Palpation
Clinical examinalion of tennis elbow.
Technique: deep friction. The patient sits with the arm resting on the couch. The elbow is held in 90° flexion and in supination. The therapists sits lateral to the patient and uses the contralateral hand, the tip of the thumb of which is placed on the anterior aspect of the humerus just prox imally to the lateral epicondyle. The thumb is kept well flexed and is held perpendicular to the shaft of the humerus. The fingers apply counterpressure at the posterior aspect of the arm (Fig. 29.13). Friction is imparted by an up-and-down movement of the entire hand, resulting in a movement of the thumb parallel to the axis of the humerus. The manoeuvre has two phases: an active phase during the downwards movement and a passive phase when the hand is brought upwards again.
Treatment of type 1/ (tenoperiosteal) tennis elbow Treatment of the tenoperiosteal type of tennis elbow varies from very easy to very complicated. The choice of treat ment depends on different factors, such as age, activities and duration of the symptoms. As the condition tends to resolve spontaneously, this possibility should be presented to the patient. Active treatment consists of infiltration with triamcinolone and Mills's manipulation. Recurrent or refractory cases may need other approaches, including infiltration with a sclerosant solution, percutaneous tenotomy and partial immobilization - taping and bracing.
The tenoperiosteal variety is the only type of tennis elbow that has a tendency for spontaneous cure82 (Fig. 29. 14); this may take a year in patients under 60 and up to 2 years when the patient is older than this. After full spontaneous recovery, a second attack is rare. However, infiltration of any steroid solu tion inhibits the mechanism of spontaneous cure. The patient should be told about the possibility of sponta neous recovery, certainly if seen after symptoms have been present for some time. Waiting, meanwhile sparing the elbow as much as possible may be the preferred option. Cyriax27 (his p. 179) explains the mechanism of spontaneous recovery as follows: As the result of the large amount of contractions of the extensors of the wrist, that put tension on the healing breach, the gap between the two edges gradually widens. Finally the two surfaces cease to lie in apposition and the tension on the scar ceases. The gap now fills with fibrous tissue. The painful scar is now embedded and heals with permanent length ening of some tendinous fibres. In consequence the strain no longer falls on that part of the tendon. Recurrence is prevented by this structural alteration. Because several muscles are attached here, slight permanent lengthening of the section of tendon relevant to only one muscle does not weaken the power to control the wrist. Natural evolution.
Infiltration with triamcinolone suspension Until 1952 there was no alternative to deep transverse friction in the treatment of tendinous lesions. For many
458 SECTION FIVE - THE ELBOW
Figure 29.14
Figure 29.13
Deep friction in supracondylar tennis elbow.
years a way to abate a localized area of unwanted trau matic inflammation has been sought. In 1952, Cyriax and Troisier83 suggested the use of steroid infiltration as a treatment for tennis elbow. After the infiltration, the scar remains in place but the inflammation ceases. Because the steroid is a suspension of insoluble particles, its action is confined to the structure which is infiltrated without much effect or spread to the adjacent structures. In the following decades, steroid infiltration gained a bad reputation. Some authors therefore advise that the injection be given so that the solution will bathe the underlying tendon rather than be injected into the tendon itself.84 This technique may easily lead to the develop ment of lipoatrophy and depigmentation of the skin. All these side effects can be avoided by using the smallest possible amount of a weak steroid and precise infiltration into the tendon itself. Technique: infiltra tion. The patient sits with the elbow resting on the couch. The joint is flexed at a right angle and held in full supination. The boundaries of the lesion are now meticulously defined by palpation. A 1 ml tuberculin syringe is filled with triamcinolone suspension and fitted with a thin needle 2 cm in length. The thumb is placed at the tender spot. The needle is thrust in vertically until it pierces the tendinous insertion and hits bone (Fig. 29.15). As one droplet is infiltrated, the appearance of a tiny bulge is felt for with the palpating thumb, confirming that the correct spot has been found.
Mechanism of spontaneous cure of tenoperiosteal tennis elbow.
By half-withdrawing and reinserting the needle at slightly different angles, the entire lesion, which must be envisaged as a three-dimensional object, is infiltrated. Each time a droplet is injected, its exact position should be determined using the thumb. Considerable pressure sometimes has to be exerted on the syringe. The patient is warned against possible severe discom fort for 24 hours, which it may be possible to reduce by the application of ice. Complete rest should be taken for a week and relative rest for another week. Follow-up is after 2 weeks with re-testing, even if there is the impres sion that cure has been achieved. The examination is repeated carefully and, if it turns out to be negative, no more need be done. If the elbow still aches or if the clini cal examination is not 100% negative, infiltration should be repeated. Results. Full relief is obtained in all cases but only two thirds remain well. On re-examination after 10 days to 2 weeks they are subjectively and objectively cured - the pain has gone and the tests are completely negative. It is important that these two prerequisites are fulfilled, otherwise the condition is apt to recur. The effectiveness of steroid infiltration was demon strated by the findings of Coonrad and Hooper 67 in 1973. They reported on 317 patients with tennis elbow and 22 patients with golfer's elbow (a lesion of the common flexor tendon at the medial epicondyle; see p. 466). Of these 339 patients, 290 were treated with one to 13 injec tions (different products and dosage). Only 12 patients responded insufficiently and were sent for surgery, during which no abnormality was found that could have been the result of the steroids injected. This was confirmed by Troisier in 1991:84 in a series of 257 cases,
CHAPTER 29 - DISORDERS OF THE CONTRACTILE STRUCTURES 459
(b)
(a)
infiltration of corticosteroids gave full relief in all cases, but the rate of recurrences was 66.7%, although 67% of these recurred only once or twice. Hay et al performed a multicentre pragmatic random ized controlled trial of local corticosteroid injection and naproxen in 164 patients. They came to the conclusion that early local corticosteroid injection is much more effective in the first weeks than treatment with naproxen or placebo but that the outcome at 1 year was equal in all groups.S6 This confirms the findings by Assendelft et als7 and Verhaar et al.ss The remaining third are well for 2-6 months but then relapse. A new infiltration will again cure them for the same period of time but they go on relapsing at regular intervals. This can continue for years because, as the result of the steroid, the mechanism of spontaneous cure has ceased to work. These patients are sent for manipulation, which will be curative in quite a number of cases, the other more refractory ones requiring other approaches. Mills's manipulation. Several authors, such as Cyriax, Mills, Mennell, Stoddard and Kaltenborn, have pro posed manipulation as a treatment for tennis elbow.49,89-93 Although it is based on different patholog ical premises, they found that manipulative treatment could lead to good results. Manipulation, preceded by deep transverse friction, was Cyriax's treatment of choice before infiltration with steroids was found effec tive in 1952. He intended to maximally stretch the exten sor carpi radialis brevis tendon in order to try to pull apart the two surfaces of the painful scar. This would
Figure 29.15
Infiltration in tenoperiosteal tennis elbow. Viewed (a) from behind and (b) from the front.
thus imitate and speed up the mechanism of sponta neous recovery (see p. 458). Several manipulations have been compared and it seems that Mills's manipulation, as described by Cyriax and for the indications which he describes, has the greatest potential to stretch the affected tendon with th e least potential for harm to the joint.94 Mills was an orthopaedic surgeon who described his manipulation technique in 1928 with the intention of realigning a torn bit of the annular ligament, which he regarded as out of place.s9 Cyriax later discontinued the use of his own initial manipulation method and advocated the use of his modification of Mills's manoeuvre. The manipulation is preceded by deep transverse friction because of its desensitizing and softening effect, which makes the actual manoeuvre less painful and therefore more tolerable. Friction alone is ineffective. This second type of tennis elbow is the only tenoperi osteal tear in the body that is not treated by deep trans verse friction alone, and the only one for which manipulation has any effect. Some authors claim good results with stretching of the wrist extensors as home exercise following the treatment.95 Contraindication. Mills's manipulation should not be performed when extension of the elbow is limited, either as the result of an existing capsular pattern (arthritis or arthrosis) or as the result of a limitation of extension in a non-capsular pattern (loose body disorder), because of the danger of provoking a traumatic arthritis. If the extension seems limited but is so because of pain alone, a careful manipulation may be tried and, if this does not set
460 SECTION FIVE - THE ELBOW
up an irritation or reaction of the joint, there is no danger in doing th is at each treatment session. Technique: preparative deep friction. The patient sits with the elbow flexed to 900 and in full supination. The therapist sits facing the patient's arm and grasps the el bow with the contralateral h and. The fingers give counter pressure at the medial aspect of the elbow. The thumb is well flexed and the thumb tip placed on the tender spot at the lateral edge of the epicondyle. The thumb is then brought over the anterior aspect of the epi condyle and imparts friction by moving medially over the bone (Fig. 29.16). The amplitude of the friction is only a few mill imetres. Pressure is exerted vertically down wards. The therapist should start gently, because of the painfulness of the condition, and gradually increase the pressure. After 1 0-15 minutes' friction the manipulation follows. Technique: manipula tion. The patient sits on a chair and the therapist stands behind. The patient's arm is abducted and also put in internal rotation. The forearm is then full y pronated and the wrist flexed. The patient's hand is grasped with the ipsilateral hand by bringing the thumb between the patient's thumb and index finger, so that the therapist's thumb is on the patient's palm. Consequently the fingers come to l ie at the dorsum of the hand. This position enables the therapist to maintain full flexion at the patient's wrist at the moment of the manip ulation. The contralateral hand is then placed on top of the olecranon (Fig. 29.17). By moving both hands in opposite directions, the elbow is extended and the extensor muscles are thus stretched. The therapist focuses attention on the patient's hand, which should be forced into full flexion. As the manoeuvre proceeds the body weight is brought to the other leg, so that the body moves away from the elbow. In this position the therapist is able to keep the patient's el bow and wrist in the required position. A quick thrust towards elbow extension (Fig. 29.18) is then performed by moving both hands in opposite directions. A crack is very often heard, indicating the rupturing of some tendinous fibres. This manipulation is carried out once at each attendance. It usually takes eight to 15 sessions for the patient to be cured but some cases require 20-30 treatments and not every tenoperi osteal tennis elbow responds well. Troisier8 5 reported a series of 131 cases to which good and excellent results were achieved in 63% by deep transverse friction and manipulation.
Refractory tennis elbow. The great majority of this com monest variety of tennis elbow can be cured by the two described procedures. If the l esion seems refractory or if it frequentl y recurs, less usual measures can be used.
Fi gure 29.16
Preparative friction prior to Mills's manipulation
. •
The intention here is no longer to reduce inflammation of the scar but to provoke the formation of dense adhesive scarring, which engulfs the original scar, by the irritant effect of the h ypertonic dextrose. The beneficial result may also be the result of the powerful destructive effect of phenol on the small unmyelinated pain fibres.96 After-pain is considerable and may last several days, after which the condition graduall y improves. The effect may only be expected after 2-3 weeks. The symptoms Infiltra tion with a sc/erosant solution.
CHAPTER 29 - DISORDERS OF THE CONTRACTILE STRUCTURES 461
(b)
(a) Figure 29.17
Mills's manipulation for tenoperiosteal tennis elbow (a). (b) Details of hand position.
should disappear after one infiltration; if not, a second is unlikely to help. Tenotomy. If all other means have been tried without lasting effect, a percutaneous tenotomy under local anaesthesia is worth consideration. This is a very simple operation, performed on an ambulant patient. The extensor carpi radialis brevis tendon at the anterior aspect of the lateral epicondyle is divided across its whole width. It is immediately followed by Mills's manipulation to ensure complete separation of the two cut ends. This treatment again imitates the mechanism of spontaneous cure. A study by Daubinet, of 18 tennis elbow patients who did not respond to conservative treatment, showed the effectiveness of insertion tenotomy of the extensor carpi radialis brevis.96 This was confirmed by Troisier,BS who found that percutaneous tenotomy performed only in patients with recurring pain after temporary cure reduces the rate of recur rences to 1 3% . In a recent prospective long-term follow up study Verhaar et al claim gratifying results and a low rate of complications with lateral extensor release as a simple outpatient procedure. They consider it as the
operation of choice for the treatment of long-standing tennis elbow.97 Grundberg and Dobson claim good to excellent results with percutaneous release of the common exten sor origin for long-standing symptoms.99 Nirschl states that a release, including percutaneous tenotomy, may alter the attachment of the extensor carpi radialis brevis, since a large part of the origin is derived from the exten sor aponeurosis.75 Other authors have come to the same conclusion.1 00, 101 If tenotomy fails, an unexpected outcome is that treat ment can be started again from the very beginning. The
Fi gure 29.18
Mills's manipulation for tenoperiosteal tennis elbow.
462 SECTION FIVE - THE ELBOW
lesion, which did not hitherto respond lastingly to infiltration with triamcinolone, may become amenable and will be helped with one or two further infiltrations. Technique: tenotomy. The exact spot is palpated. Using the same infiltration techni que as for treatment with steroids the whole tender area is infiltrated with 1 ml of a 2% xylocaine solution. Some of the fluid is reserved to inject subcutaneously in order to render the skin anaes thetic. After a minute, resisted extension of the wrist is re tested. If the correct spot has been chosen, this movement should be completely painless. A small thin double-edged tenotome is then thrust in through the skin into the dense tendinous tissue in the same way the needle was introduced - vertically. The tenotome is moved further down until it touches bone (Fig. 29.1 9). By moving the tip of the tenotome up and down along the bone of the epicondyle in a perpendicu lar way, the tendon of the extensor carpi radialis brevis is divided transversely across its entire width. The small lancet is then removed and the bleeding, if present, stopped by pressure. Mills's manipulation is then carried out to ensure com plete separation of the two cut ends. No further treatment is needed. Suture is not necessary as the opening in the skin is only a few millimetres long. The patient should be warned of serious after-pain which may last for a few days. The elbow should not be exerted for a week and follow up is after 2 weeks. Most of the traumatic arthritis, which sometimes results after a tenotomy, will have disappeared by then. If this is not the case, an intra-articular injection with 20 mg of triam cinolone acetonide should be given. If the operation is not successful and resisted extension of the wrist remains painful after, say, a month, a further infiltration with 10 mg of triamcinolone acetonide should be given at the tender spot, which is usually localized at both cu t ends. Extracorporal shock wave therapy. Attempts are made with extracorporal shock wave therapy (ESWT) to treat resistant cases. The patient receives 500-3000 shock waves of 0.08-0.12 mJ / mm2 three times at weekly inter vals. Some authors consider it as a useful conservative alternative in the treatment of tennis elbow.102,103 The results seem to be considerably better for lateral than for medial epicondylitis.1 04 Bracing and taping. Through the years, tape and braces have been used to treat injuries suffered by athletes. In the early stages of the use of external support systems, physicians and certified athletic trainers used mostly trial and error and intuition to provide support for the injured area. Nowadays the interest in
Fi gur e 29.19
Tenotomy.
this aspect of preventive sports medicine has increased, and sound scientific principles have been used to improve the design and effectiveness of external support systems.lOS,1 06 At the elbow, a constricting band can be applied to the proximal part of the forearm (Fig. 29.20). It acts as a counterforce brace, constraining full muscular expansion, therefore decreasing intrinsic muscular force to the sensitive area in the forearm extensors. This has the inten tion of causing the extensor mechanism on the lateral
CHAPTER 29
-
DISORDERS OF THE CONTRACTILE STRUCTURES 463
An alternative treatment is deep transverse friction, which is difficult, painful and not always curative. It is performed with a pinching grip (Fig. 29.23). Technique: in filtra tion
of the
extensor carpi radialis
The patient sits with the elbow rested on the couch. The elbow is flexed to a right angle and supinated. A 10 ml syringe is filled with 0.5% procaine and a 5 cm, thin needle is fitted. The tender spot is held pinched up by the therapist'S thumb and index finger. The needle is inserted obliquely through the belly of the brachioradialis muscle until the point strikes the radius. It is then slightly withdrawn to lie between the fingertips (Fig. 29.24). The solution is now infiltrated fanwise with different withdrawals and reinsertions so that the entire lesion is covered. After 5 minutes, resisted extension of the wrist is re tested. This movement should no longer hurt; if it does, the lesion was not entirely reached. The infiltration will be repeated at the next attendance and concentrated at the 'forgotten' areas. The patient must be warned that a temporary weak ness of extension of the hand is possible, because the infiltration of a local anaesthetic may paralyse the deep branches of the posterior interosseous nerve. m uscle belly.
Figure 29.20
Counterforce brace for tennis elbow.
side of the elbow to work at the point where the band is attached, rather than at its point of origin on the lateral condyle. It is generally accepted as a valuable method for preventing recurrence because it causes improvement in wrist extension and grip strength with positive biome chanical effects.l 07-109 There are, however, authors who do not support these ideas.11 0
Treatment of type 11/ (tendinous) tennis elbow Deep transverse friction is the better treatment here and should be successful in six sessions, performed two to three times a week. The patient sits at the couch with the ann resting on it. The elbow is held in 1350 extension and in nearly full pronation by the ipsilateral hand. The tendon of the extensor carpi radialis brevis now overlies the head of the radius. The therapist takes hold of the patient's elbow with the contralateral hand. Counterpressure is given at the medial aspect of the elbow with the fingers. With the flexed thumb palpation is made for the tender spot. The thera pist starts with the thumb at the medial aspect of the tendon and the friction is given by pulling the thumb towards him, so that it slips over the tendon (Fig. 29.21). The thumb is then relaxed and the same movement started again. The therapist must make sure that the amplitude of the friction movement is not diminished or stopped by the hand coming in contact with the couch. The patient's forearm is therefore best supported with a cushion, which leaves the elbow free. Technique: deep friction.
Treatment of type IV (muscular) tennis elbow The treatment of choice is infiltration with 10 ml of a local anaesthetic in the upper part of the belly of the extensor carpi radialis muscles. Two to four weekly infiltrations usually give lasting relief (Fig. 29.24).
Special circumstances. There are two rare types of lateral elbow pain that are worth considering here. Tenoperiosteal lesion
of the
extensor carpi radia lis
This is encoun tered from time to time. If the limitation is in the cap sular pattern involvement of the capsule is suggested. This possibility has recently been confirmed by arthro scopic examination.11l In that case the capsule sh ould be treated first. I f the limitation is of a non-capsular pattern, it may be caused either by a l oose body limiting mostly extension or by a cyst. The loose body can be manipulated. A cyst gives rise to a few degrees' limitation of passive extension of the elbow. The end feel is softish, even sometimes a bit springy. Palpation usually reveals a cystic swelling under the origin of the tendon. This type of tennis elbow has been shown to be refrac tory to any of the treatments described above. When a thick needle is thrust in, cystic fluid can be aspirated. Immediatt ly afterwards, passive extension becomes of full range. A triamcinolone solution is now infiltrated, 1 ml at the origin of the tendon and 1 ml at a deeper place where the cyst has been detected. The patient is seen again after 2 weeks and, if necessary, treatment is repeated. bre vis with limitation o f m o vement.
Radial tunnel syndrome. Some authors consider the so called radial tunnel syndrome to be a type of tennis elbow (see p. 560).
464 SECTION FIVE - THE ELBOW
Fi gure 29.21
Deep friction in tendinous tennis elbow: (a) starting position; (b) ending pOSition.
LESION OF THE EXTEN SOR CARPI U LN ARIS M U SCLE
Occasionally, resisted extension and resisted ulnar devi ation of the wrist are painful at the outer aspect of the elbow. This indicates a lesion of the e xtensor carpi ulnaris muscle usually at its tenoperiosteal origin at the posterior aspect of the lateral epicondyle of the h umerus (Fig. 29.25) or, more rarely, at the olecranon. Palpation will of course d isclose the exact site of the lesion.
Treatment consists of either infiltration with triam cinolone suspension or deep transverse friction. LESION OF AN EXTENSOR DIGITORUM M U SCLE
Lesions of the extensors of the fingers do occur but are quite uncommon. The diagnosis is made too often and is probably the result of a misinterpretation of the clinical examination - resisted extension of the fingers, and espe cially of the middle finger, is often found to be positive in
CHAPTER 29 - DISORDERS OF THE CONTRACTILE STRUCTURES 465
Fi gur e 29.22
Fi gure 29.23
Treatment of tennis elbow.
Deep friction to the extensor carpi radialis muscle bellies.
Fi gure 29.24
Infiltration of the extensor carpi radialis muscle bellies.
Fi gure 29.25
The extensor carpi ulnaris muscle.
466 SECTION FIVE - THE ELBOW
tennis elbow and apparently is a consequence of the close relationship of the extensors of wrist and fingers in the region of the elbow. When a lesion of the extensor digito rum does occur, resisted extension of the wrist with the fingers held actively flexed should be negative. Treatment consists of either infiltration with triam cinolone (origin) or deep transverse friction.
WEA K NESS ON RESISTED EXTENSION OF THE WRIST
Painless weakness of extension of the wrist can be the result of a radial palsy, a C5 disc protrusion compressing the C6 nerve root Of, rarely, a C6 disc protrusion com pressing the C7 nerve root. Painful weakness also occurs at the moment that a painful twinge is elicited in type II tennis elbow.
Fi gure 29.26
RESISTED FLEXION OF THE WRIST
Occasionally, and only in long-standing cases, calci fication may be seen on radiography. As this is merely a radiological finding without clinical significance, it may be ignored and does not influence the therapeutic approach.
PAIN
Resisted flexion of the wrist (with the elbow held in extension) causing pain at the medial aspect of the elbow indicates a lesion of the common flexor tendon, which originates mainly from the medial epicondyle and is known as golfer 'S elbow. The disorder is not as common as tennis elbow69 and is much less disabling. The patient , aged between 40 and 60 years, describes a pain that may radiate down the upper part of the forearm at the ulnar side. As in tennis elbow, it follows a series of repeated (often occupational) strains,11 2 rather than a single injury. Resisted pronation of the elbow is sometimes positive as well, because the pronator teres muscle partly originates from the common flexor tendon. Rarely, the pain is only evoked by resisted pronation and / or resisted flexion of one or two fingers. This may occur in very localized lesions and depends on which structure is affected. Palpation of the common flexor tendon is necessary to find the exact spot, which is usually very localized. There are two possible sites (Fig. 29.26): •
•
The tel1operiosteal variety: the tender spot is found at the anterior aspect of the medial epicondyle of the humerus at the origin of the common flexor tendon. The musculotendinous variety: the tender spot is 5 mm farther down, level with the inferior edge of the epicondyle. This is the musculotendinous junction (the common tendon diverging immediately below its origin into the muscle belly).
Sites of lesions in the common flexor tendon: 1, tenoperiosteal; 2, musculotendinous.
Treatment Tenoperiosteal junction . The treatment of choice is one or two infiltrations with 1 ml of triamcinolone suspension (Fig. 29.27). The alternative is deep transverse friction (Fig. 29.28). Very often six to twelve sessions, two to three times a week, are needed. The results of surgical treat ment are poor.113 ,1l4 Technique: in filtra tion. The patient lies on the couch with the upper arm abducted and externally rotated so that the elbow lies on the lap of the therapist , who sits next to the patient. The elbow is held in almost full exten sion and in full supination. The tender spot is sought at the anterior aspect of the medial epicondyle. A 1 ml tuberculin syringe is fitted with a fine 2 cm needle. The needle is thrust vertically downwards until the resistance of the tendon is felt and bony contact made. The whole affected area is infiltrated by means of a series of with drawals and reinsertions so as to fill a three-dimensional area. The thumb continuously palpates to make sure that the whole area has been covered. Technique: deep friction. The patient lies in the same position as for the infiltration, again with the elbow held in full extension and supination by the therapist's ipsilateral arm and hand, of which the thumb palpates for the most prominent point at the medial side. This is the medial epi condyle. At its anterior aspect the origin of the common flexor tendon can be found.
CHAPTER 29
Transverse friction is performed with the index finger of the other hand, reinforced with the middle finger. Counterpressure is given with the thumb at the lateral aspect of the el bow. Friction is produced by a movement of the entire arm, which results in a flexion-extension movement at the wrist. Musculotendinous junction. Deep transverse friction is performed two to three times a week. It is the only suc cessful treatment and usually leads to recovery in four to eight sessions.
Fi gur e 29.27
Fi gure 29.28
-
DISORDERS OF THE CONTRACTILE STRUCTURES
467 1
W hen on palpation the teno periosteal junction is found, the finger is then moved 5 mm distally. The ulnar border of the index finger now lies in contact with the distal border of the epicondyle. The structure feels like a soft, muscular and round mass. The index finger now moves to the medial aspect of the muscle and the transverse friction movement is per formed by pulling the hand towards the therapiSt's body. The elbow may be slightly flexed. This relaxes the musculotendinous junction, which can be penetrated more deeply. Technique: deep friction.
Infiltration of the tenoperiosteal junction.
Deep friction to the tenoperiosteal junction.
468 SECTION FIVE - THE ELBOW
Refractory golfer's elbow
WEAKN ESS
Sclerosant infiltration. Medial epicondylitis that does not respond properly to the usual approach can be infiltrated with sclerosant solution (PDG) in order to create dense scarring which engulfs the original scar so that muscular contraction force is no longer transmitted.
Weakness of flexion of the wrist is usually the result of a C6 disc protrusion, compressing the C7 nerve root and occurs in combination with weakness of extension of the elbow and occasionally of adduction of the shoulder.
Counterforce brace . A medial counterforce brace can be applied. It helps to diminish the forces acting on the origin of the common flexor tendon.
REFERENCES 1 . McGarvey SR, Morrey BF, Askew LJ, An K N . Reliability of
isometric strength testing - temporal factors and strength variation. Clin Orthop 1984;185:30l . 2. Motzkin NE, Cahalan TD, Morrey BF, An KN, Chao EYS. Isometric and isokinetic endurance testing of the forearm complex. Am J Sports Med 1991;19:107. 3. Kapandji IA. Physiologie Articulaire, Tome 1: Membre Superieur, 5th edn. Maloine, Paris, 1987. 4. Stevens A, Stijns H, Reybrouck T et al. A polyelectromyograph ical study of the arm muscles at gradual isometric loading.
1 9 . Hempel K, Schwenke K, Ober Abrisse der distalen Bizepssehne. Arch Orthop Unfal/chir 1974;79:313. 20. Leighton MM, Bush-Joseph CA, Bach BR Jr. Distal biceps
21.
22.
Electromyogr Clin NeurophysioI 1973;13:465. 5. Maton B, Bouisset S. The distribution of activity among the
23.
muscles of a single group during isometric contraction. Eur J Appl PhysioI 1977;37: 1 0 l . 6. Funk DA, A n K N , Morrey BF, Daube J R . Electromyographic
analysis of muscles across the elbow joint. J Orthop Res
24.
1987;5:529. 7. Mariani EM, Cofield RH, Askew LJ, Li G, Chao EYS. Rupture of
the tendon of the long head of the biceps brachii, surgical versus nonsurgical treatment. Clin Orthop Rei Res 1 988;228:233. 8. Gilmer W, Anderson L. Reactions of the somatic tissue which progress to bone formation. South Med J 1 959;52:1432. 9. Huss CD, Puhl JJ. Myositis ossificans of the upper arm. Am I Sports Med 1 980;8(6) :419. 1 0. Weinstein L, Fraerman S. Difficulties in early diagnosis of
myositis ossificans. lAMA 1 954;154:994. 1 1 . Morrey BF. Ectopic ossification about the elbow. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia, 2000:437-446.
25. 26.
brachii repair: results of dominant and nondominant extremi ties. Clin Orthop 1995;317: 114-12l. Le Huec JC, Moinard M, Liquois F et al. Distal rupture of the tendon of biceps brachii: evaluation by MRI and the results of repair. I Bone Joint Surg 1996;78B:767-770. Hang DW, Bach BR Jr, Bojchuk J. Repair of chronic distal biceps brachii tendon rupture using free autogenous semitendinosus tendon. Clin Orthop 1996;323:1 88-1 9 1 . Straugh RJ, Michelson H, Rosenwasser M P. Repair of rupture of the distal tendon of the biceps brachii. Review of the literature and report of three cases treated with a single anterior incision and suture anchors. Am J Orthop 1997;26: 151-156. Morrey BF. Injury of the flexors of the elbow: biceps in tendon injury. In: Morrey BF (ed) The Elbow alld its Disorders, 3rd edn. Saunders, Philadelphia, 2000:468-478. Baker BE, Bierwagen D. Rupture of the distal tendon of the biceps brachii. J Bone Joint Surg 1 985;67A:414. Agins HJ, Chess IL, Hoekstra DV, Teitge RA. Rupture of the distal insertion of the biceps brachii tendon. Clin Ortllop 1988;234:34.
27. Cyriax JH. Textbook of Orthopaedic Medicine, vol 1. Diagllosis of Soft Tissue Lesion, 8th edn. Bailliere Tindall, London, 1982. 28. Abrahamsson SO, Sollerman C, Soderberg T et al. Lateral elbow
pain caused by anconeus compartment syndrome, a case report. Acta Orthop Scand 1 987;58:589. 29. Bach BR Jr, Warren RF, Wickiewicz TL. Triceps rupture, a case
12. Orzel JA, Rudd TG. Heterotopic bone formation: clinical, labo
report
ratory, and imaging correlation. J NucL Med 1 985;26: 125. 13. Donatelli R, Wooden MJ. Orthopaedic Physical Therapy. Churchill Livingstone, New York, 1989. 14. Freed )H, Hahn H, Meneter R, Dillon T. The use of the three phase bone scan in the early diagnosis of heterotopic ossification (HO) and in the evaluation of didronel therapy.
15(3):725-727.
Paraplegia 1 982;20:208.
and
literature
review.
Am
J
Sports
Med
1 987;
30. Herrick RT, Herrick S. Ruptured triceps in a powerlifter pre
senting as cubital tunnel syndrome: a case report. Am J Sports Med 1987;15:514. 31. Wagner JR, Cooney WP. Rupture of the triceps muscle at the
musculotendinous junction: a case report. I Halld Surg 1 997;22A:34 1 .
15. Pritchard DJ, Krishnan Unni K. Neoplasms of the elbow. In:
32. Carpentier E, Tourne Y. Avulsion traumatique du tendon tricipital
Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia, 2000:886--888. 16. Lipscomb A, Thomas E, Johnson R. Treatment of myositis ossificans traumatica in athletes. Am I Sports Med 1 976;4:111 . 17. Barbaix E. Radial epicondylitis due to a lesion of the brachio radialis muscle. Geneeskd Sport 1 995;28(6):169-170. 18. De Sousa OM, De Moraes JL, De Moraes VFL. Electromyographic study of the brachioradialis muscle. Anat
brachial. a propos d'un cas. Ann Chir Main Memb Super
Rec 1 961;139:125.
1992;11(2) :163--165.
.
33. Louis OS, Peck D. Triceps avulsion fracture in a weight-lifter. Orthopedics 1992;15(2):207-208. 34. Nuber GW, Din1ent MT. Olecranon stress fractures in throwers.
A report of two cases and a review of literature. Clin Orthop ReI Res 1 992;278:58-61 . 35. Renton J. Observations on acupuncturation. Edillb Med J 1830;34:100.
CHAPTER 29 - DISORDERS OF THE CONTRACTILE STRUCTURES 469
36. Runge F. Zur Genese und Behandlung des Schreibekrampfes. Berl Klil1 Wochellschr 1 873;10:245. 37. Morris H. Rider's sprain. Lancet 1882;ii:557. 38. Major HP. Lawntennis elbow. BMf 1 883;2:557. ' 39. Remak E. Beschiiftigungsneurosen. Urban & Schwarzenberg, Vienna, 1 894. 40. Bernhardt M. Ober eine wenig bekannte Form der Beschaftigungsneuralgie. Neural ZentralbI 1 896;15:13. 41 . Coudere A. E tude sur un nouvel accident professionnel des maftres d'armes dfi a la rupture probable et partielle du tendon epicondylien. These de Bordeaux, 1896. 42. Fere G. Note sur I'epicondylalgie. Rev Med 1897;17:144. 43. Franke F. Ober Epicondylitis Humeri. Dtsch Med Wochenschr 1910;36:13. 44. Schmidt I. Bursitis calcarea am Epicondylus externus Humeri. Arch Orthop Unfallchir 1921;19:215. 45. Schreger GB. De Bursis Mucosis Subcutaneis. Palmand Enke, Erlangen, 1825. 46. Osgood RB. Radiohumeral bursitis, epicondylitis, epicondyl algia (tennis elbow). Arch Surg Chic 1 922;4:420. 47. Carp L. Tennis elbow caused by radiohumeral bursitis. Arch Slirg 1932;24:905. 48. Monro A. Description of all Bursae Mucosae of the Human Body. Elliott, Edinburgh, 1 788. 49. Cyriax JH. The pathology and treatment of tennis elbow. J Bone Joint Surg 1936;18:92 1 . 50. Bosworth D M . The role of the orbicular ligament i n tennis elbow. J Bone Joint Surg 1955;37A:527. 51. Goldie 1. Epicondylitis lateralis humeri (epicondylalgia or tennis elbow). Acta Chir Scand 1964;Suppl 339. 52. Friedlander HL, Reid RL, Cape RF. Tennis elbow. Clin Orthop Rei Res 1 967;51:109. 53. Nirschl RP. Tennis elbow. Orthop Clin North A m 1973;4: 767-787. 54. Boyd HB, McLeod AC. Tennis elbow. J Bone Joint Surg 1 973; 55A:1183. 55. Gardner RC. Tennis elbow: diagnosis, pathology, and treatment. Clin Ort/lOp Rei Res 1 970;72:248. 56. La Freniere JG. Tennis elbow - evaluation, treatment and pre vention. Phys Ther 1979;59:742. 57. Kamien M. A rational management of tennis elbow. Sports Med 1990;9(3):173. 58. Wittenberg RH, Schaal S, Muhr G. Surgical treatment of persist ent elbow epicondylitis. Clin Orthop Rei Res 1992;278:73-80. 59. Ernst E. Conservative therapy for tennis elbow. Br J Clin Pract 1992;46(1):55-57. 60. Roles NC, Maudsley RH. Radial tunnel syndrome. J Bone Joint Surg 1972;54B:499. 61 . O'Neill J, Sarkar K, Uhtoff HK. A retrospective study of surgi cally treated causes of tennis elbow. Acta Orthop Belg 1980; 46:189. 62. Gunn CC, Milbrandt WE. Tennis elbow and the cervical spine. Can Med Assoc J 1976;114:803. 63. Bouillier de Branche B. E tude de 58 dossiers de tendinites epy condyliennes traitees par manipultions cervicales. Ann Readapt Med Phys 1986;29:75. 64. Maigne R. Les manipulations dans Ie traitement des epi condylites: Ie facteur cervical, Ie facteur articulaire. Al1n Readapt Med Phys 1 986;29:57. 65. Murray-Leslie CF, Wright V. Carpal tunnel syndrome, humeral epicondylitis, and the cervical spine: a study of clinical and dimensional relations. BMJ 1976;1:1439-1442. 66. Weh L. Funktionelle Phanomene bei der Epicondylopathia Hemeri radialis. Disch Z Sportmed 1989;8:276.
67. Coonrad RW, Hooper WR. Tennis elbow: its course, natural history, conservative and surgical management. J Bone faint Surg 1973;55A:1177. 68. Kivi P. The etiology and conservative treatment of humeral epicondylitis. Scan J RehabiL Med 1982;15:37-41 . 69. Gellman H. Tennis elbow (lateral epicondylitis). Orthop Clin North Am 1992;23(1):75-8 1 . 70. Grachaw WK, Pelletier D . A n epidemiologic study of tennis elbow. Am J Sports Med 1979;4:234. 71 . Kramer J, Schmitz-Beuting J. Oberbelastungsschaden am Bewegungsapparat bei Tennisspielern. Dtsch Z Sportllled 1979;2:44. 72. Lamberts H. De morbiditeitsanalyse-1972 door de groep spraktijk Ommoord: een nieuwe ordening van ziekte - en probleemgedrag voor de huisartsgeneeskunde. II. Huisarts Wet 1975;18:7. 73. Rodineau J. L'epicondylalgie ou 'tennis elbow'. J Traumat Sport 1988;4:192. 74. Funk DA, An KN, Morrey BF, Daube JR. Electromyographic analysis of muscles across the elbow joint. J Orthop Res 1987;5:529. 75. Nirschl RP. Muscle and tendon trauma: tennis elbow tendinosis. In: Morrey BF (ed) The Elbow and its Disorders, 3rd edn. Saunders, Philadelphia, 2000:523-535. 76. Nirsch! RP, Pettrone F. Tennis elbow: the surgical treatment of lateral epicondylitis. J Bone Joint Surg 1979;61A:832. 77. Nirsch! RP. Lateral and medial epicondylitis. In: Morrey BF (ed) Master Techn iques in Orthopedic Surgery: The ELbow. Raven Press, New York, 1994: 129-148. 78. Kraushaar B, Nirschl R. Tendinosis of the elbow (tennis elbow): clinical features and findings of histological, immuno histochemical, and electron microscopy studies. ] Balle faint Surg 1999;81A:259. 79. Regan W, Wold LE, Coonrad R, Morrey BF. Microscopic histopathology of lateral epicondylitis. Am J Sports Med 1992;20:746. 80. Neviaser TJ, Neviaser RJ, Neviaser JS, Ain BR. Lateral epi condylitis: results of outpatient surgery and immediate motion. Contemp Orthop 1985;11:43. 8 1 . Nirschl RP. Prevention and treatment of elbow and shoulder injuries in the tennis player. Clin Sports Med 1998;7:289. 82. Mens JM, Stoeckart R, Snijders CJ, Verhaar JA, Stam HJ. Tennis elbow, natural course and relationship with physical activities: an inquiry among physicians. J Sports Med Phys Fitness 1999;39(3):244-248. 83. Cyriax J, Troisier O. Hydrocortisone and soft-tissue lesions. BMJ 1952;ii:966.
84. Kerlan RK, Glousman RL. Injections and techniques in athletic medicine. Clin Sports Med 1989;8(3):541-560. 85. Troisier O. Les tendinites epicondyliennes. Rev Prat 1 991; 41(18):1 65 1 . 86. Hay EM, Paterson SM, Lewis M, Hosie G, Croft P. Pragmatic randomised controlled trial of local corticosteroid injection and naproxen for treatment of lateral epicondylitis of elbow in primary care. BMJ 1999;319(7215):964-968. 87. Assendelft WI, Hay EM, Adshead R, Bouter LM. Corticosteroid injections for lateral epicondylitis: a systematic overview. Br J Gen Pract 1 996;46(405):209-216. 88. Verhaar JA, Walenkamp GH, van Mameren H, Kester AD, van der Linden AI. Local corticosteroid injection versus Cyriax type physiotherapy for tennis elbow. ] Bone faint S u rg 1 996;78B(1):128-132. 89. Mills GP. Treatment of tennis elbow. BMJ 1 928;i:12. 90. Mills GP. Treatment of tennis elbow. BMJ 1 937;ii:212.
470 SECTION FIVE - THE ELBOW
9 1 . Mennell J M . Joint Pain - Diagnosis and Treatment using Manipulative Techniques. Little, Brown, Boston, 1964. 92. Stoddard A. Manipulation of the elbow joint. Physiotherapy 1971 ;57:259. 93. Kaltenborn FM. Manual Therapy for the Extremity Joints, 2nd edn. Olaf Norlis, Oslo, 1 976. 94. Kushner S, Reid DC. Manipulation in the treatment of tennis elbow. J Orthop Sports Phys Ther 1986;7(5):264. 95. Solveborn SA. Radial epicondylalgia ('tennis elbow'): treat ment with stretching or forearm band. A prospective study with long-term follow-up including range-of-motion measure ments. Scand ] Med Sci Sports 1997;7(4):229-237. 96. Gildenberg PL, De Vaul RA. Management of chronic pain refractory to specific therapy. In: Yomans JR (ed) Neurological Surgery, 3rd edn. Saunders, Philadelphia, 1 990:4144. 97. Daubinet G. L'epicondylite rebelle: technique et protocol per sonnels de tenotomie des epicondyliens. J Traumatol Sport 1988;4:201 . 98. Verhaar J, Wa]enkamp G, Kester A, Van Mameren H, Van Der Linden T. Lateral extensor release for tennis elbow. j Bone Joint Surg 1 993;75A(7): 1034-1043. 99. Grundberg AB, Dobson JE Percutaneous release of the common extensor origin for tennis elbow. c/in Orthop 2000;376:137-140. 100. Baumgard SH, Schwartz DR. Percutaneous release of the epi condylar muscles for humeral epicondylitis. Am ] Sports Med 1 982;10:233. 1 0 1 . Yerger B, Turner T. Percutaneous extensor tenotomy for chronic tennis elbow: an office procedure. Orthopaedics 1985;8:126 1 . 102. Haupt G. Use of extracorporeal shock waves in the treat ment of pseudarthrosis, tendinopathy and other orthopedic diseases. J UroI 1 997;158(1):4- 1 1 . 1 03. Hammer DS, Rupp S , Ensslin S , Kohn D , Seil R. Extracorporal shock wave therapy in patients with tennis elbow and painful heel. Arch Orthop Trauma Surg 2000; 120(5-6):304-307.
1 04. Krischek 0, Hopf C, Nafe B, Rompe }D. Shock-wave therapy for tennis and golfer's elbow - 1 year follow-up. Arch Ort/lOp Trauma Surg 1999;119(1-2):62-66. 1 05. Rovere GD, Curl WW, Browning DG. Bracing and taping in an office sports medicine practice. Clin Sports Med 1989;8(3):497. 1 06. Snyder-Mackler L. Effects of standard and aircast telmis elbow band on integrated electromyography of forearm extensor musculature proximal to bands. Alii J Sports Med 1 989;2:278. 1 07. Groppel JL, Nirsch} RP, Pfantsch E, Greer N . A mechanical and electromyographical analysis of the effects of varioLls joint counterforce braces on the tennis player. Am J Sports Med 1986;14:1 95. 1 08. Wadsworth CT, Nielsen DH, Burns LT, Krull JD, Thompson CG. The effect of the counterforce armband on wrist extension and grip strength and pain in subjects with tennis elbow. J Orthop Sports Phys Ther 1989;11:192. 109. Savoie E Percutaneous release in the surgical treatment of lateral epicondylitis. Presented to the 3rd International Meeting of the Society for Tennis Medicine. New Haven, Connecticut, June 1 997. 1 1 0. Knebel PT, Avery DW, Gebhardt TL et a/. Effects of the forearm support band on wrist extensor muscle fatigue. j Orthop Sports Phys Ther 1999;29(11):677-685. 1 1 1 . Baker C, Cummings P. Arthroscopic management of miscella neous elbow disorders. Operative Techniques Sportsl/led 1998;6:16. 1 12. O'Dwyer KJ, Howie CR. Medial epicondylitis of the elbow. Int Orthop 1995;19(2):69-71 . 113. Kurvers HAJM, Verhaar JAN. Golfelleboog of epicondylitis medialis, Verslag Nederlandse Orthopaedische Vereniging. Tijdschr Geneeskd 1993;137(23): 1 1 66. 114. Kurvers H, Verhaar J. The results of operative treatment of medial epicondylitis. ] Bone joint Surg 1995;77 A:1374.
SECTION SIX
The wrist, thumb and hand
SECTION CONTENTS 30. Applied anatomy of the wrist, thumb and hand
Joints, joint capsules and ligaments
Rheumatoid arthritis 501 Arthrosis 501 The non-capsular patterns 502 Full range 504 Excessive range 507 Disorders of the contractile structures Resisted extension 510 Resisted flexion 513
473
473
Muscles and tendons 476 Nerve structures 480 31. Clinical examination of the wrist, thumb
and hand 483 Referred pain 483 History 483 Inspection 484
35.
Functional examination Palpation 488 Accessory tests 489
Examination of the fingers
490
32. Interpretation of the clinical examination 33. Disorders of the lower radioulnar joint
Disorders of the inert structures The capsular pattern 495 Traumatic arthritis Arthrosis
493
Disorders of the inert structures The capsular pattern 533
Monoarticular steroid-sensitive arthritis 496 Rheumatoid arthritis 496 The non-capsular patterns 496 Limited supination 496 Painful supination 496 Disorders of the triangular fibrocartilage complex 497 Disorders of the contractile structures 499
The capsular pattern Traumatic arthritis
499 499
499
521
Arthrosis 522 Disorders of the contractile structures Pain 524 Weakness 528 36. Disorders of the hand and fingers
495
Disorders of the inert structures Limited range 499
521
524
495
495
496
34. Disorders of the wrist
Disorders of the thumb
Disorders of the inert structures Rheumatoid arthritis 521 Traumatic arthritis 521
484
510
497
533 533
Rheumatoid arthritis 534 Traumatic arthritis 534 Arthrosis 534 Gout 535 Non-capsular pattern 535 Unreduced dislocation 535 Disorders of the contractile structures Dorsal interosseous muscles 535 Thenar muscles 536 Rexor tendons 536 Trigger finger 536 Tendon rupture 537 Dupuytren's contracture $udeck's atrophy
538
538
535
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Joints, joint capsules and ligaments Distal radioulnar joint 473 Wrist joint
474
Carpometacarpal joints 476 Trapezium-first metacarpal joint Metacarpophalangeal joints Interphalangeal joints 476 Muscles and tendons 476 Extrinsic muscles and tendons Intrinsic muscles 479 Nerve structures
480
Median nerve 481 Ulnar nerve 481 Radial nerve
473
482
476
476
Applied anatomy of the wrist, thumb and hand
477
The anatomy of wrist, thumb and hand is complex because of the presence of many different functional joints: the distal radioulnar joint, the wrist joint (con taining the radiocarpal and the intercarpal joints, the carpometacarpal joints, the trapezium-first metacarpal joint), the metacarpophalangeal joints and the interphal angeal joints. The contractile structures can be divided into extrinsic and intrinsic muscles. the former - the long tendons - are quite regularly affected, while the latter are clinically of less importance.
JOINTS, JOINT CAPSULES AND LIGAMENTS DISTAL RADIOULNAR JOINT The joint is a pivot one between the head of the ulna and the ulna (sigmoid) notch of the radius. The joint line is L-shaped with its shortest part between radius and ulna and its longest part between the distal ulna and the artic ular disc. It has a loose capsule, reinforced with some ligaments, that allows rotation movement of the radius about the ulna. The two bones are held together mainly by the triangular fibrocartilage complex (TFCC) and to a lesser degree by the interosseous membrane and the pronator quadratus muscle (Fig. 30.1). The TFCC contains different parts: (a) the triangular fibrocartilage, which has a central component - the artic ular disc - and two adjoining ligaments, the dorsal and palmar radioulnar ligaments; (b) a meniscus homologue (ulnocarpal meniscus); (c) the ulna collateral ligament; (d) the ulnolunate and ulnotriquetral ligaments; and (e) the sheath of the extensor carpi ulnaris tendon. The articular disc, lying between the radius and the styloid process of the ulna, separates the distal radioulnar joint from the radiocarpal joint. The dorsal and palmar radioulnar ligaments take their origin at the dorsal and palmar borders, respectively, of the joint at the radius and join to insert at the base of the ulna styloid process, so surrounding the articular disc. The most ulnar and distal part of the TFCC is thickened - a meniscus homologue - and inserts into the triquetral and hamate bones and the base of the fifth metacarpal. The ulnolunate and ulnotriquetral ligaments take their origin 473
474 SECTION SIX - THE WRIST, THUMB AND HAND
Ulnolulate ligament
UCL
Ulnotriquatral ligament
Meniscous homologue + ulnar collateral ligament + fibres from tendon sheath
of extensor carpi ulnaris
Palmar radiolunar ligament Articular disk Dorsal radiolunar ligament
Fig. 30.1
The distal radioulnar joint. Fig. 30.2
The triangular fibrocartilage complex.
at the ulnar styloid process and the ulnar aspect of the
radius and the articular disc articulate with the proximal
palmar radioulnar ligament and pass to the lunate and
row of carpal bones to form a condylar joint (radiocarpal
triquetral bones, respectively. The sheath of the extensor
joint) which has its concave surface at the radial side.
carpi ulnaris tendon takes part, with a strong attachment
The joint moves along two axes: anteroposterior for ulnar
(subsheath), in the posterolateral aspect of the TFCC. The TFCC has a stabilizing effect on the distal radio ulnar joint (Fig. 30.2). This distal articulation allows pronation-supination movements of the forearm, inevitably in combination with movement at the upper radioulnar joint, around an axis which runs through the head of the ulna. The distal end of the radius makes a circumferential gliding move ment around and in front of the head of the ulna (see p. 420). Pronation has an amplitude of ± 85° and is stopped by the radius impacting against the ulna and by tension in the interosseous membrane. Consequently, there is an elastic end-feel. Supination ceases at an angle . of 90° when the posterior aspect of the ulna notch of the radius is brought into contact with the styloid process of the ulna through the extensor carpi ulnaris tendon. Its end-feel is also elastic.
�r-,--':'>'--;�'-ff---I'--- Capitate WRIST JOINT The wrist joint consists of two rows of carpal bones. The proximal row contains (from radius to ulna) the scaphOid, lunate, triquetral and pisiform bones, and the distal row
Hamate
--�--'1'ii�
Triquetral
-----1-��
���'J.---+--- Scaphoid
Lunate ------f--t��.-::-;
the trapezium, trapezoid, capitate and hamate (Fig. 30.3). The wrist joint is complex: there are two components, proximal and distal. Proximally the distal part of the
¥+-I--- Trapezium ��V-+---- Trapezoid
Fig. 30.3
The carpal bones.
CHAPTER 30 - APPLIED ANATOMY 475
Fig. 30.4 The two axes of movement in the wrist jOint: 1, anteroposterior axis along which ulna/radial deviation takes place; 2, transverse axis along which flexion/extension takes place.
and radial deviation, and transverse for flexion and extension (Fig. 30.4).
Fig. 30.6 The dorsal ligaments. The arrows emphasize the direction of the ligamentous fibres at the joint lines.
Distally, the intercarpal joint is between the proximal and distal rows of bones (Fig. 30.5), is an open S-shape and acts as a hinge. It should not be considered as an independent joint becaus� its function is to augment the mobility of the carpal bones and thus allow greater mobility at the wrist. Movements are restricted by collateral (Fig. 30.5), palmar and dorsal ligaments (Fig. 30.6).
Radial and ulnar collateral ligaments. The radial collat
eral ligament, between the styloid process of the radius and the scaphoid bone, is taut when the hand is brought into ulnar deviation. The ulnar collateral ligament, between the styloid process of the ulna and the trique tral and pisiform bones, is under tension during radial deviation of the hand. Dorsal ligaments. There are two
groups of dorsal
ligaments: • Those which join the radius to the proximal row of 9
carpal bones - the dorsal radiocarpal ligaments. Their
--\'1\-- 10
fibres are aligned more or less in the same axis as the forearm. They are under tension in flexion. 13
12
• Those which join the bones of the proximal and
distal row of bones - the intercarpal ligaments. Their direction is more or less transverse to the carpus. They are taut during flexion of the wrist. Palmar ligaments. On the palmar aspect of the wrist, a
complex system of ligaments joins the different carpal bones to the radius and the ulna. These palmar liga 11
ments are of little clinical importance and are taut during extension of the wrist.
Movements Fig. 30.5 The wrist and collateral ligaments (right hand dorsal view): 1, pisiform; 2, triquetrum; 3, lunate; 4, scaphoid; 5, hamate; 6, capitate; 7, trapezoid; 8, trapezium; 9, ulna; 10, radius; 11, metacarpal; 12, ulnar
collateral ligament; 13, radial collateral ligament; A, radiocarpal joint line; B, intercarpal joint line; C, carpometacarpal joint line.
The amplitude of radial deviation is only 15°, whereas ulnar deviation has an amplitude of approximately
45°, the wrist being held in the neutral position between flexion and extension. Flexion and extension both have
476 SECTION SIX - THE WRIST, THUMB AND HAND
a range of 85°, with the wrist in the neutral position between radial and ulnar deviation. Flexion-extension have an end-feel of an elastic, cap sular type. Radial and ulnar deviation have an end-feel that is quite hard but is clinically of less importance.
CARPOMETACARPAL JOINTS The joints between the distal row of carpal bones and the second to fifth metacarpal bones are scarcely mobile, except for the joint with the fifth metacarpal, which permits slight movement in a palmar direction neces sary to allow opposition of the fifth finger. They are
Fig. 30.8
Flexion and extension of the metacarpophalangeal joint.
provided with dorsal and palmar carpometacarpal ligaments, the fibres of which are in line with the axis of the metacarpal bones. Intercarpal ligaments 'tie' the bones together.
METACARPOPHALANGEAL JOINTS The metacarpophalangeal joint of the thumb is different from that of the other fingers. It is a hinge and allows only a flexion movement (80-90°) and in hypermobile
TRAPEZIUM-FIRST METACARPAL JOINT
individuals some extension.
The shape of the articular surfaces of both the trapezium
fifth fingers is a 'ball-and-socket' joint with a slack joint
and the first metacarpal bone ('saddle') allows move ment in two directions: abduction-adduction and oppo sition-reposition (Fig. 30.7). The joint capsule is slack so as to allow free movement but strong ligaments control the range. Two sesamoid bones are often embedded in the palmar part of the capsule.
The metacarpophalangeal joint of each of the second to capsule, which is reinforced by strong palmar ligaments and collateral ligaments. The collateral ligaments are taut when the joint is flexed. Tbe possible movements are flexion (90°, Fig. 30.8) and extension (sometimes to 90°, dependent on the laxity of the joint capsule), as well as abduction and adduction (the index finger having the greatest mobility). The rotatory movements are not clinically important.
proximal
A
B'
INTERPHALANGEAL JOINTS The interphalangeal joints are hinges that allow flexion ulnar
without extension, except in some individuals for the interphalangeal joint of the thumb and the distal inter phalangeal joint of the fingers. In the proximal interpha
B
langeal joints, the range of flexion is more than 90° and increases from the index to little finger in which flexion can be 135°, which allows a 'fist' to be made. Distally the amplitude of flexion varies between
A'
80° and 90°, the little finger again being the most mobile. The joint capsules are reinforced by palmar and collateral ligaments. The slight rotatory movements possible at the inter phalangeal joints are not important from a clinical point of view.
MUSCLES AND TENDONS Fig. 30.7 The two axes of movement in the trapezium-first metacarpal jOint: (upper), A-A' for abduction/adduction, B-8' for opposition/reposition; (lower) shows an example of a saddle-shaped jOint. =
=
Clinically, the long tendons of the wrist, thumb and fingers - the tendons of the extrinsic muscles - are of
CHAPTER 30 - APPLIED ANATOMY 477
more importance than the small muscles of hand, thenar
Table 30.1 The extensors
and hypothenar - the intrinsic muscles.
Muscle
EXT RINSIC MUSCLES AND TENDONS
Abductor pollicis longus Extensor pollicis brevis Extensor carpi radialis longus Extensor carpi radialis brevis Extensor pollicis longus Extensor indicis proprius Extensor digitorum communis Extensor digiti minimi Extensor carpi ulnaris
As lesions are usually well localized, a topographical description of the tendinous structures is necessary. An understanding of exactly where they lie and where they insert is important.
Dorsal aspect
Innervation Peripheral nerve
Nerve root
Radial Radial Radial Radial Radial Radial Radial Radial Radial
C7-C8 C7-T1 C6-C7 C7 C7-C8 C6-C8 C6-C8 C6-C8 C7-C8
On the dorsal aspect of the wrist six osteofibrous tunnels can be distinguished (Fig. 30.9), which contain the tendon sheaths of the extensors of the wrist and fingers (Table 30.1) and the abductor of the thumb. Tunnel 1. This contains the tendons of the abductor
pollicis longus and the extensor pollicis brevis. •
Both muscles lie in a common tendon sheath and have a further function: radial deviation and palmar flexion of the wrist. Together they form the radial border of the 'anatomical snuffbox'. Tunnel 2. The second tunnel contains the tendons of
The abductor pollicis longus inserts partly at the base of
extensor carpi radialis longus and brevis. They diverge
the first metacarpal bone, radial to the extensor pollicis
level with the carpus.
brevis and partly into the trapezium. Its main function is abduction of the thumb, a movement that takes
•
place between the trapezium and the first metacarpal. •
The extensor pol/icis brevis
perform dorsiflexion of the wrist. In conjunction with
proximal phalanx of the thumb and is responsible for
the flexor carpi radialis muscle, it produces radial
extension of the thumb. Additionally, because oOts in abduction.
inserts into the dorsal
bone and combines with the extensor carpi ulnaris to
inserts at the base of the
close relationship with the abductor longus, it helps
The extensor carpi radialis longus
and radial aspect of the base of the second metacarpal
deviation. •
The extensor carpi radialis brevis attaches to the dorsal and radial aspect of the base of the third metacarpal bone. It extends the wrist and brings it back from ulnar deviation into a neutral position.
Tunnel 3. The third tunnel contains the tendon of the
extensor pollicis longus, which runs along the ulnar aspect of the dorsal tubercle of the radius and then deviates 45° towards the thumb. Level with the carpus it passes over the tendons of the second tunnel and so forms the ulnar border of the anatomical snuffbox. It then continues over the dorsal aspect of the thumb towards the base of the distal phalanx. Its main function is to extend the thumb, although is also helps in exten sion of the wrist and abduction of the thumb. Tunnel 4. Five different tendons are found here: the
tendon of the extensor indicis proprius and the four tendons of the common extensor digitorum. •
The extensor indicis proprius:
the fibres of the extensor
indicis proprius blend with the dorsal aponeurosis of the index finger. It extends the index finger. •
The extensor digitorum: the tendons of the extensor digitorum merge with the dorsal aponeurosis of the second to fifth fingers and extend the fingers, especially
The extensor tendons and their sheaths (numbers indicate the tunnels described in the text). Fig. 30.9
the proximal phalanges. Their secondary functions are extension and ulnar deviation of the wrist.
478 SECTION SIX - THE WRIST, THUMB AND HAND
Tunnel S. This contains just one tendon, the extensor
digiti minirni, which runs over the distal radioulnar joint and then parallel to the fifth tendon of the extensor digi torum into the dorsal aponeurosis of the fifth finger. Its function is identical to that of the extensor digitorum. Tunnel 6. The extensor carpi ulnaris lies in a groove at
the ulnar aspect of the head of the ulna. It then crosses the lateral aspect of the carpus to insert in the dorsal and ulnar aspect of the base of the fifth metacarpal bone. On account of its position, it functions mainly as a strong ulnar deviator of the wrist and also acts as an opponent to the abductor pollicis longus. Its extension function is very much secondary.
Palmar aspect On the palmar aspect of the wrist lie the tendons of the flexors of wrist and fingers (Table 30.2). These are
Fig. 30.10 Boundaries of the carpal tunnel: 1, trapezium; 2, scaphoid; 3, hamate; 4, pisiform.
enclosed by the carpal tunnel and the tunnel of Guyon, which are of great importance. the palm and helps in palmar flexion of the wrist as
The carpal tunnel. The palmar aspect of the carpus is
concave and covered with the transverse carpal liga ment, also called the flexor retinaculum. An osteo
well as tensing the palmar fascia. •
fibrous canal is thus formed, of which the palpable
fi�gers; in doing this they separate each of the deep
bones and distally the trapezium and hamate bones
flexor digitorum tendons in two. Their functions are
(Fig. 30.10). The canal lies thus more distally and more
mainly flexion of the proximal phalanges of the
towards the ulnar aspect than is often thought - at the Within the carpal tunnel are found: the median nerve;
fingers and ulnar deviation of the wrist. •
superficial extensor digitorum and insert at the base of
licis longus, in separate sheaths; and the superficial and
the distal phalanges of the second to fifth fingers. The
deep flexors of the digits, within a common tendon
•
muscle flexes the fingers and also the wrist. •
The tendinous structures (Fig. 30.12) are:
The flexor carpi radialis traverses the carpal tunnel along the scaphoid bone and inserts at the palmar
The tendons of the deep flexors of the fingers run through the carpal twmel in a common tendon sheath with the
the tendons of the flexor carpi radialis and the flexor pol
sheath (Fig. 30.11).
The flexor carpi ulnaris
flexor carpi ulnaris. Distal to the pisiform, the tendon
34
the wrist and helps in radial deviation.
The palmaris longus muscle is absent in 15%
attaches to the pisiform, which
some consider a sesamoid bone in the tendon of the
aspect of the base of the second metacarpal. It flexes •
5
6
of indi
viduals. It is inserted into the palmar aponeurosis in 8
Table 30.2 The flexors Muscle
Flexor carpi radialis Palmaris longus Flexor digitorum superficialis Flexor digitorum profundus Flexor carpi ulnaris Flexor pollicis longus
Innervation Peripheral nerve
Nerve root
Median Median Median Median Ulnar Ulnar Median
C7-T1 C7-T1 C7-T1 C7-T1 C7-C8 C7-C8
in
insert into the middle phalanges of the second to fifth
boundaries are proximally by the scaphoid and pisiform
heel of the hand.
The tendons of the superficial flexors of the fingers run, a common sheath, through the carpal tunnel and
Fig. 30.11 Transverse section of the carpal tunnel: 1 , flexor poliicis longus; 2, flexor carpi radialis; 3, median nerve; 4, transverse ligament of carpus; 5, superficial flexor digitorum; 6, ulnar artery; 7, ulnar nerve; 8, deep flexor
digitorum.
CHAPTER 30 - APPLIED ANATOMY 479
6
Fig. 30.12 The flexor tendons: 1, flexor carpi radialis; 2, palmaris longus; . flexors of the fingers (4 tendons); 4, deep flexors of the fingers 3, superficial (4 tendons); 5, flexor carpi ulnaris; 6, flexor pollicis longus.
divides into two ligamentous structures: the piso
Fig.30.13 The tunnel of Guyon: 1, pi Siform ; 2, hamate; 3, ulnar nerve.
hamate ligament (which covers the tunnel of Guyon) and the pisiform-fifth metacarpal ligament. Together with the flexor carpi radialis, the flexor carpi ulnaris flexes the wrist and, with the extensor carpi uln�ris, performs ulnar deviation of the wrist. •
deeper head and the adductor pollicis with its transverse and oblique head . •
The flexor pollicis longus originates with a radial head at the anterior aspect of the radius, just distal to the insertion of the supinator brevis muscle and also from the interosseous membrane. There is an additional humeral head at the medial epicondyle. It runs lateral to the flexor carpi radialis muscle under which it crosses proximal to the wrist and then
The hypothenar muscles are the abductor digiti minimi, flexor digiti minimi brevis and opponens digiti minimi.
•
The lumbrical muscles:
there are four lumbrical
muscles. They originate at the radial aspect of the tendons of the deep flexor digitorum muscle and insert at the dorsal aponeurosis of the fingers and at the joint capsules of the metacarpophalangeal joints.
runs in a separate tendon sheath through the carpal tunnel to insert at the base of the distal phalanx of the thumb. It flexes the thumb and slightly flexes and radially deviates the wrist.
Table 30.3 The intrinsic muscles Muscle
The tunnel of Guyon. This tunnel lies between the pisi
form and the hamate bone and is covered by the piso hamate ligament, which is a continuation of the flexor carpi ulnaris tendon. The ulnar nerve and artery are also enclosed within this tunnel (Fig. 30.13).
INTRINSIC MUSCLES (Table 30.3) Apart from the dorsal interossei, the intrinsic muscles of the hand are seldom strained. •
The thenar muscles:
these are clinically less important
and include the abductor pollicis brevis, opponens pollicis, flexor pollicis brevis with its superficial and
Abductor pollicis brevis Oppens pollicis Flexor pollicis brevis Superficial head Deep head Adductor poliicis Abductor digiti minimi Flexor digiti minimi brevis Opponens digiti minimi Lumbricals Radial two lumbricals Ulnar two lumbricals Dorsal interossei Palmar interossei
Innervation Peripheral nerve
Nerve root
Median Median
C8-T1 C6-C7
Median Ulnar Ulnar Ulnar Ulnar Ulnar
C8-T1 C8-T1 C8-T1 C8-T1 C8-T1 C8-T1
Median Ulnar Ulnar Ulnar
C8-T1 C8-T1 C8-T1 C8-T1
480 SECTION SIX - THE WRIST, THUMB AND HAND
•
They flex the metacarpophalangeal joints and extend
proximal phalanges, where they attach into the extensor
the interphalangeal joints.
aponeurosis of the fingers. The first dorsal interosseus
The palmar interossei:
the three palmar interossei
adduct the fingers towards the middle finger, flex the
goes to the radial aspect of the index finger. The second dorsal interosseus goes to the radial aspect of the middle
metacarpophalangeal joints and extend the inter
finger, the third to the ulnar aspect of the middle finger.
phalangeal joints of the fingers (Fig. 30.14).
The fourth dorsal interosseus goes to the ulnar aspect of the fourth finger.
The dorsal interossei
The dorsal interossei abduct the fingers away from the
More important are the four dorsal interossei. They orig
middle finger (Fig. 30.14). They also flex the meta
inate from the sides of the five metacarpal bones, each
carpophalangeal joints and extend the interphalangeal
having two heads, each in the side of two adjacent
joints.
metacarpal bones (Fig. 30.15). They course towards the
The palmar aponeurosis The palmar aponeurosis of the hand is a continuation of the flexor retinaculum (the reinforcement of the distal part of the antebrachial fascia, also called transverse liga
I
I
111 / I Fig. 30.14 (Left) Abduction, four dorsal interossei; (right) adduction, three palmar
ment of the carpus) and consists of transverse and longi tudinal fibres. The latter are part of the tendon sheaths of the flexor tendons (deep transverse metacarpal liga ments) and also connect to the capsules of the meta carpophalangeal joints. The aponeurosis is also connected to the deep fascia of the hand, which is attached to its skeleton. Together with the ligaments, septa and fasciae, the palmar aponeurosis forms a functional unit. During a strong grip it fixes the skin of the palm to the metacarpal bones and protects the soft tissues of the mid-hand.
NERVE STRUCTURES
interossei. The three most important nerves in the wrist and hand are the median, ulnar and radial nerves. The median nerve
Fig. 30.15
The dorsal interossei.
Fig. 30.16
The median nerve.
CHAPTER 30 - APPLIED ANATOMY 481
is most frequently affected in the carpal tunnel, whereas the ulnar nerve becomes compressed in the region of Guyon's tunnel. Lesions of the radial nerve at the wrist are less common.
MEDIAN NERVE The median nerve enters the hand through the carpal tunnel, in between the tendons of the flexor pollicis longus and flexor digitorum superficialis. Distal to the transverse ligament, the nerve divides into two branches (Fig. 30.16). A short motor branch goes to the thenar eminence, where it usually supplies the abductor pollicis brevis and opponens pollicis muscles, and sometimes the flexor pollicis brevis and the first and second lumbri cal muscles. The sensory palmar digital branches inner vate the palmar surface and the dorsal aspect of the distal phalanges of the thumb, the second and third fingers and the radial half of the fourth finger. Fig. 30.18
ULNAR NERVE Proximal to the wrist, the palmar cutaneous branch of the
The ulnar nerve: palmar branch.
The ulnar nerve, together with the ulnar artery, passes between the pisiform and the hook of the hamate through
ulnar nerve arises and runs across the palmar aspect of
the tunnel of Guyon. As it leaves the tunnel it divides into
the forearm and wrist, outside the tunnel of Guyon, to
a mainly sensory superficial terminal branch, which sup
supply the proximal part of the ulnar side of the palm. A few centimetres more distally, the dorsal cutaneous
plies the distal ulnar border of the palm of the hand and the palmar surfaces of the fifth and ulnar half of the
branch arises and supplies the ulnar side of the dorsum
fourth finger (Fig. 30.18) and a deep terminal branch,
of the hand (Fig. 30.17), the dorsal aspect of the fifth
which is entirely motor and innervates nearly all of the
finger and the ulnar half of the fourth finger.
small muscles of the hand.
Fig. 30.17
The ulnar nerve: dorsal cutaneous branch.
Fig. 30.19
Terminal digital branches of the superficial radial nerve.
482 SECTION SIX - THE WRIST, THUMB AND HAND
RADIAL NERVE At the el bow, the radial nerve divides into the posterior interosseous nerve (a deep motor branch), which inner vates the extensor muscles of the wrist and fingers, and the superficial radial nerve (a superficial sensory
branch), which lies under the tendon of the brachio radialis muscle. In the hand, the superficial radial nerve divides into terminal digital branches that supply the dorsolateral aspect of the hand and the dorsal aspect of the first three and a half fingers, except the distal phalanges (Fig. 30.19).
Clinical examination of the wrist, thumb and hand
CHAPTER CONTENTS Referred pain History
483
483
Inspection
484
Functional examination
484
Distal radioulnar joint 484 The wrist 484 The thumb 486 The intrinsic muscles of the hand: dorsal and palmar interossei 488
Palpation
REFERRED PAIN
488
Accessory tests
489
Examination of the fingers
Passive movements Resisted movements Palpation 491
490 491
490
When a patient refers to the wrist as the site of symptoms, an area is indicated in which there are many structures that could be responsible. The region that patients call the wrist contains: • • • • • • •
The The The The The The The
distal radioulnar joint wrist joint tendons that control the wrist trapezium-first metacarpal joint tendons that control the thumb tendons that control the fingers intrinsic muscles of the hand.
When a patient feels pain proximal to the distal radioulnar joint, this is usually described as being in the forearm. The same applies distally, where pain is described as being in the fingers. Pain is usually the result of a local lesion although more proximal causes, such as cervical, shoulder girdle and shoulder disorders, as well as problems at the elbow, may refer pain to the distal part of the upper limb. However, in a lesion in the distal part of the limb, the patient is able to point accurately to the exact site of the lesion and it is only when the clinical examination of the wrist and hand is negative that the lesion should be sought more proximally. Paraesthesia, being a 'nerve symptom', may result either from lesions higher up in the segment (e. g. cervical spine or thoracic outlet) or from local lesions (e. g. ulnar nerve problem or carpal tunnel syndrome).
HISTORY
The history is seldom distinctive and therefore examina tion must be relied on for diagnosis. However, some questions are important. The patient describes the symptoms that are experienced in the wrist, thumb, hand or fingers. They are variable and may include pain, paraesthesia, numbness and weakness.
• What is the problem?
483
484 SECTION SIX - THE WRIST, THUMB AND HAND
Especially when a capsular pattern is found during the examination, the possibility of a fracture must be considered. Or did it start after a par ticular exertion? Most ligamentous, muscular or tendinous lesions result from overuse. The symptoms may have started spol1tal1eously, as usually happens in arthrotic or arthritic disorders. How has the problem developed? Because of the distal localization of the lesion, its evolution can only be judged in terms of the intensity of the symptoms, or in terms of their appearance or disappearance but not in terms of reference of the symptoms.
• How did it start? Was there an injury?
•
INSPECTION
The typical articular deformities of arthrotic or arthritic changes in the joints are well known. Local swelling may be found. In dorsal subluxation of a carpal bone, the bony projection is visible when the wrist is held in flexion. A cyst on the dorsal aspect may mimic such a subluxation. The same applies to mal-united fractures, where bony outcrops may be visible on inspec tion. Palpation or disappearance of a fluid collection after puncture will help to reveal the difference. Another important item is generalized swelling. Swelling coming on quite soon after a trauma, for example a fall, is very suggestive of a fracture of a carpal bone. Spontaneous swelling occurs in rheumatoid arthritis and is quite often bilateral. In long-standing rheumatoid arthritis, multiple large ganglia may also occur. In arthrosis at the trapezium-first metacarpal joint, the thumb is often visibly fixed in adduction; osteophytes can be seen and felt. There may be changes in the colour of the hands, which may suggest a circulatory disorder, for example Raynaud's syndrome, or a cervical rib pressing on the subclavian artery or vein.
FUNCTIONAL EXAMINATION
Many different structures - inert and contractile lie close together and have to be examined. It should be clear that by passive testing, which is meant to examine the inert structures, either stretching or pinching may elicit symptoms. In some instances, painful move ment of a contractile structure is provoked - for example of a tendon within its sheath. The wrist, thumb and hand are examined by 21 tests (Box 31.1). Q
Box 31.1 Tests for the wrist. thumb and hand The distal radioulnar joint 2 passive movements The wrist 4 passive movements 4 resisted movements The thumb
1 passive movement 4 resisted movements The hand 6 resisted movements of the fingers
DISTAL RADIOULNAR JOINT
The two movements described below test the integrity of the distal radioulnar joint. Painful supination is also a localizing sign in tendinitis of the extensor carpi ulnaris in the groove at the distal part of the ulna. The normal end-feel of both movements is capsular (elastic). Passive pronation. The patient holds the elbow in 90° flexion. The examiner grasps the patient's forearm just proximally to the wrist with both hands. The heel of the contralateral hand is placed on the palmar aspect of the ulna, the fingers of the other hand at the dorsal, aspect of the radius. Pronation is performed by a simultaneous movement of both hands (Fig. 31.1a). Passive supination. The examiner changes the position of the hands and puts the fingers of the contralateral hand onto the palmar aspect of the radius and the heel of the other hand on the dorsal aspect of the ulna. Supination is again performed by a movement of both hands (Fig. 31.1b).
THE WRIST Passive movements (Fig. 31.2)
The normal end-feel of flexion and extension is capsular (elastic). If these movements are positive, the examiner must be able to tell whether the condition is of the capsular or the non-capsular type (see eh. 34). flexion. The patient holds the elbow flexed to a right angle. The examiner takes hold of the patient's forearm with the contralateral hand, in order to achieve good fixation. With the other hand the patient's hand is grasped and the wrist is flexed to the end of its range. The movement stretches the structures on the dorsal aspect of the wrist (ligaments, tendons) and pinches some structures on the palmar aspect (Fig. 31.2a). o
Passive
Passive extension. Using the same grip, the examiner can bring the wrist into extension. Extension stretches the palmar tissues and pinches other tissues dorsally (Fig. 31.2b). Q
CHAPTER 31 - CLINICAL EXAMINATION 485
(a)
(b)
Figure 31.1 Passive pronation (a) and supination (b).
(a)
(b)
-
(c)
(d)
Figure 31.2 Passive movements of the wrist: (a) flexion; (b) extension; (c) radial deviation; (d) ulnar deviation.
486 SECTION SIX - THE WRIST, THUMB AND HAND
Passive radial deviation. The examiner brings the patient's hand into radial deviation, which stretches the structures at the ulnar side of the wrist - the ulnar col lateral ligament and the extensor carpi ulnaris (Fig. 31.2c). o
Passive ulnar deviation. The examiner brings the patient's hand into ulnar deviation, stretching the structures at the radial side of the wrist - the radial collat eral ligament and the tendons in the first tunnel (the exten sor pollicis brevis and abductor pollicis longus) (Fig. 31.2d). o
Resisted movements
For the resisted tests (Fig. 31.3) the patient's elbow is kept in extension. This puts more stress on the contractile structures of the wrist and makes it possible to detect even the slightest tendinous and muscular lesions. Resisted flexion. The patient's hand is held in the neutral position. The examiner's contralateral arm is passed under the patient's in order to hold the patient's elbow in extension and fixes the forearm with the hand. The other hand is placed under the patient's hand and creates resistance at the palmar aspect. This test examines the flexors of the wrist and fingers the flexor carpi radialis, flexor carpi ulnaris, flexor digito rum superficialis and profundus (Fig. 31.3a). o
Resisted extension. Fixation of the patient's forearm is as in the previous test. The examiner creates resistance at the dorsal aspect of the patient's hand. This tests the extensors of the wrist and fingers - the extensor carpi radialis longus, extensor carpi radialis brevis, extensor carpi ulnaris, extensor digitorum com munis, extensor indicis proprius and extensor digiti minimi (Fig. 31.3b). o
Resisted radial deviation. Resistance is applied at the radial aspect of the patient's hand - the thumb is not involved - and tests the radial deviators of the wrist - the extensor carpi radialis longus and brevis and flexor carpi radialis (Fig. 31.3c). o
Resistance to ulnar devi ation is applied at the ulnar aspect of the hand and tests the ulnar deviators of the wrist - the extensor carpi ulnaris and flexor carpi ulnaris (Fig. 31.3d). o
Resisted ulnar deviation.
THE THUMB Passive movement Backwards movement during extension. The patient flexes the elbow to a right angle and pres ents the hand with the palm upwards. The examiner o
(a)
(c) Figure 31.3
(d) Resisted movements of the wrist: (a) flexion; (b) extension; (c) radial deviation; (d) ulnar deviation.
CHAPTER 31 - CLINICAL EXAMINATION 487
takes hold of it with the ipsilateral hand and fixes it. With the other hand the thumb is brought into exten sion. Then the thumb is moved backwards so as to stretch the anterior part of the capsule of the trape zium-first metacarpal joint (Fig. 31.4). Resisted movements
The resisted movements of the thumb are shown in Fig. 31.5. Resisted extension. The patient presents the hand with the thumb upwards and it is fixed by the examiner 's contralateral hand. Resistance is then applied with the thumb of the other hand at the dorsal aspect of the distal phalanx. Extension tests the exten sors of the thumb - the extensor pollicis longus and extensor pollicis brevis (Fig. 31.5a). o
Resisted flexion. Resistance is applied to the palmar aspect of the distal phalanx of the patient's thumb and tests the flexors of the thumb - the flexor pol licis longus and brevis (Fig. 31.5b). o
Figure 31.4 Passive movement of the thumb.
(a)
(b)
(c)
(d)
Figure 31.5 Resisted movements of the thumb: (a) extension; (b) flexion; (c) abduction; (d) adduction.
488 SECTION SIX - THE WRIST, THUMB AND HAND
Resisted abduction. Resistance is applied to the distal part of the first metacarpal bone and tests the abductors of the thumb, the abductor pollicis longus and brevis (Fig. 31.5c). adduction. This movement tests the adductor of the thumb - the adductor pollicis (Fig. 31.5d). o
Resisted
THE INTRINSIC MUSCLES OF THE HAND: DORSAL AND PALMAR INTEROSSEI Squeezing with the index and middle fingers. The patient presents the hand in the horizontal position with the dorsal aspect upwards. The examiner puts an index finger between the patient's index (II) and middle (III) fingers and asks for a squeeze on it so testing the palmar interosseus of the index finger and the dorsal radial interosseus of the middle finger (Fig. 31.6a). o
(a)
Squeezing with the middle and ring fingers. Squeezing of the examiner's finger between the patient's middle (III) and ring (IV) fingers: the examiner carries out the test as before, with the finger between the patient's middle and ring fingers, so testing the dorsal ulnar interosseus of the middle finger and the palmar interosseus of the ring finger (Fig. 31.6b). Squeezing with the ring and little fingers. The examiner's finger is squeezed between the patient's ring (IV) and little (V) fingers. The dorsal interosseus of the ring finger and the palmar interosseus of the little finger are tested (Fig. 31.6c). o
Resisted separation of
the index and
(b)
middle
The examiner resists the separation of the patient's fingers at the distal phalanges, which tests the dorsal interosseus of the index finger and the dorsal ulnar interosseus of the middle finger (Fig. 31.7a). fingers.
Resisted separation of the middle and ring fingers. This assesses the dorsal radial interosseus of the middle finger and the dorsal interosseus of the ring finger (Fig. 31.7b). Resisted separation of the ring and little fingers. This tests the palmar interosseus of the ring finger and the abductor of the little finger in the hypothenar, abductor digiti minimi (Fig. 31.7c).
(c)
Figure 31.6 Squeezing the fingers: (a) II-III; (b) III-IV; (c) IV-V. PALPATION
Palpation with the joints at rest helps to find the exact localization of lesions in ligaments, tendons or muscles. Palpation is also performed for warmth, swelling and synovial thickening. Palpation during movement may reveal crepitus. Fine creaking during movement of a tendon in its sheath indi-
cates roughening of the gliding surfaces, the result of overuse. This is quite common in the tendons or muscle bellies of the structures that pass through the first and third tunnels, namely the abductor and extensors of the wrist. Coarser crepitus can indicate tuberculosis or advanced rheumatoid disease.
CHAPTER
31
-
CLINICAL EXAMINATION
(a)
(b)
(e)
Figure. 31.7 Resisted separation of the fingers: (a)
II-III;
489
(b) III-IV; (e) IV-V.
ACCESSORY TESTS
These tests (Fig. 31.8) are not part of the standard exami nation. They are only done when there is a need for more information about the patient's problem. Resisted extension of the wrist with the fingers held actively flexed. The patient is asked to flex the fingers and to press the fingertips in the palm of the hand. In this position resisted extension of the wrist is repeated (Fig. 31.8a).
Resisted extension of each finger separately.
Resistance
is applied at the distal phalanx (Fig. 31.8b). Resisted flexsion of each finger separately.
Resistance is
applied at the distal phalanx (Fig. 31.8c). Tests for carpal tunnel syndrome. These are described on pp.569-571. The clinical examination of the wrist, thumb and hand is summarized in Box 31.2.
490 SECTION SIX - THE WRIST, THUMB AND HAND
Box 31.2 Summary of clinical examination of the wrist. thumb and hand History Inspection Functional examination Lower radioulnar joint 1. Passive pronation 2. Passive supination Wrist joint 3. Passive flexion of the wrist 4. Passive extension of the wrist 5. Passive radial deviation of the wrist 6. Passive ulnar deviation of the wrist Wrist muscles and tendons 7. Resisted flexion of the wrist 8. Resisted extension of the wrist 9. Resisted radial deviation of the wrist 10. R esisted ulnar deviation of the wrist
(a)
Trapezium-first metacarpal joint 11. Passive backward movement during extension Thumb muscles and tendons 12. R esisted extension of the thumb 13. Resisted flexion of the thumb 14. Resisted abduction of the thumb 15. Resisted adduction of the thumb Intrinsic hand muscles 16. Squeeze II and III 17. Squeeze III and IV 18. Squeeze IV and V 19. Spread II and III 20. Spread III and IV 21. Spread IV and V
Palpation Accessory tests
EXAMINATION OF THE FINGERS
(b)
This examination (summarized in Box 31.3) is performed only when the patient clearly presents with a problem in the fingers. PASSIVE MOVEMENTS
Passive movements are performed at the metacarpo phalangeal joints of thumb and fingers, at the inter phalangeal joint of the thumb and at the proximal and distal interphalangeal joints of the fingers. There are four tests for each joint: with one hand the examiner fixes the proximal bone and with the other at the distal bone the joint is brought into flexion. Extension: with one hand the examiner fixes the proximal bone and with the other at the distal bone the joint is brought back to the starting position.
• Flexion:
•
(c)
Figure 31.8 Accessory tests: (a) resisted extension of the wrist, with fingers flexed; (b) resisted extension of one finger; (c) resisted flexion of one finger.
CHAPTER
Bo>l, 31.3 Summary of the functional examination of the fingers Passive movements
•
1. Passive flexion
31 - CLINICAL EXAMINATION 491
forced into radial deviation, thereby using the distal bone as a lever. Ulnar deviation: the same technique is used but now the joint is forced into ulnar deviation.
2. Passive extension 3. Passive rotation in one direction 4. Passive rotation in the opposite direction 5. Passive radial deviation 6. Passive ulnar deviation
Resisted movements 7. Resisted flexion 8. Resisted extension
Palpation
RESISTED MOVEMENTS
Resisted movements test the tendinous structures in the fingers - the long flexor and extensor tendons. There are two tests; in both, resistance is applied at the distal phalanx (see p. 489).
10. For synovial thickening
•
•
Extension is usually not possible, except in very mobile or hypermobile individuals. Rotation in one direction: with one hand the examiner fixes the proximal bone. The other taking hold of the distal bone, brings the joint into slight flexion and rotates it in one direction. Very little movement is possible. Rotation in the opposite direction: the same manoeuvre is performed but this time the rotation goes in the opposite direction. There are two tests for the collateral ligaments: the proximal bone is fixed with one hand; with the other the joint is kept in extension and
• Radial deviation:
with one hand the examiner takes hold of the patient's wrist and hand; the other is used to give resistance against the patient's attempt to flex the finger. Resistance is given at the palmar aspect of the distal phalanx. Extension: the examiner again fixes the patient's wrist and hand. With the other hand at the distal phalanx the patient's attempt to extend the finger is resisted.
• Flexion:
9. For fluid
•
PALPATION
Palpation can be done at the level of the different joints and seeks to detect: which may be found in joint or ligamentous dis orders. Synovial thickening which accompanies rheumatoid-type arthritis. It is best palpated at the level of the collateral ligaments.
• Fluid •
THIS PAGE INTENTIONALLY LEFT BLANK
Interpretation of the clinical examination of the wrist, thumb and hand P-------...� Traumatic arthritis Arthrosis Rheumatoid-type arthritis Monoarticular steroid-sensitive arthritis
1-------.... Limitation of supination Painful supination Disorders of the triangular fibrocartilage complex
493
494 SECTION SIX - THE WRIST, THUMB AND HAND
1-----------------... Traumatic arthritis
(scaphoid fracture) Rheumatoid-type arthritis Early arthrosis
1-----------------... Carpal subluxation Aseptic necrosis Ununited fracture
Interpretation of the clinical examination of the wrist
Isolated arthrosis
1---------p Ganglion Periostitis Stress fracture
1---------... Ulnar coliateral ligament Radial coliateral ligament Dorsal ligaments Extensor carpi radialis longus Extensor carpi radialis brevis Extensor digitorum Extensor indicis proprius
Polyneuropathy C6 root lesion Radial lesion Flexor carpi radialis
Resisted wrist flexion is positive
Flexor carpi ulnaris Pisotriquetral disorders Flexor digitorum profundus C7 root lesion
Abductor pollicis longus and extensores poliicis
Resisted movements of the thumb are positive
Abductor pollicis longus and extensor poliicis brevis Extensor poliicis longus Trigger thumb Neurological lesion Tendinous rupture Interosseus muscles
Resisted movements of the hand are positive
Thenar muscles Flexor tendons Trigger finger Rupture of long flexor tendon
CHAPTER CONTENTS Disorders of the inert structures The capsular pattern 495 Traumatic arthritis 495 Arthrosis 496
Disorders of the lower radioulnar joint
495
Monoarticular steroid-sensitive arthritis
496
Rheumatoid arthritis 496 The non-capsular patterns 496 Limited supination 496 Painful supination 496 Disorders of the triangular fibrocartilage complex 497
Disorders of the contractile structures
497
DISORDERS OF THE INERT STRUCTURES Lesions of the lower radioulnar joint are quite uncommon. They lead to pain felt at the wrist which can be elicited by undertaking passive pronation and supination, which put the dorsal and palmar radioulnar ligaments, respectively, under tension,l-3 as well as the capsule.4
THE CAPSULAR PATTERN The capsular pattern of the lower radioulnar joint pres ents with pain at the end of range of the two movements (pronation and supination, Fig.
33.1) and indicates an
arthritis.
TRAUMATIC ARTHRITIS Occasionally, traumatic arthritis may develop. It is not the result of a single injury but of repeated and exces sive pronation/ supination movements. There is con stant pain, aggravated by certain movements. Swelling may be seen at the ulnar side of the distal forearm. Treatment consists of one or two intra-articular injections of
10 mg of triamcinolone acetonide. p
Figure 33.1
s
The capsular pattern of the lower radioulnar joint.
495
496 SECTION SIX - THE WRIST, THUMB AND HAND
ARTHROSIS When a fracture of the distal part of the radius fails to uni te properly, arthrosis at the distal radioulnar joint may follow. Mal-union of the distal part of the ulna does not give rise to persistent problems5 and painless ulnar styloid non-union is a frequent incidental radiographic finding.6 The patient feels discomfort with movement of the joint. On examination, the extremes of both rotations are uncomfortable. The condition may be helped by strap ping the distal part of the forearm; if this does not help, intra-articular triamcinolone may be tried.
MONOARTICULAR STEROID-SENSITIVE ARTHRITIS An arthritis may develop without provable cause such as rheumatoid or traumatic arthritis. Furthermore, the con dition will worsen when attempts are made to mobilize the joint. Such a condition responds particularly well to intra-articular triamcinolone?
RHEUMATOID ARTHRITIS The distal
radioulnar joint may become affected,
often bilaterally, in the evolution of a rheumatoid condi tion.8,9
Triamcinolone
suspension
injected
intra
articularly once or twice a year may keep the joint free from symptoms. Rheumatoid arthritis may result in ligamentous laxity. At the distal radioulnar joint this regularly leads to the
Figure 33.2
Injection of the radioulnar joint: 1, extensor digiti minimi.
so-called caput ulnae syndrome, including dorsal sublux ation of the distal part of the ulna, supination of the carpus on the forearm and palmar dislocation of the tendon of the extensor carpi ulnaris.10-13
Technique: intra-articular injection. The patient sits at the couch with the arm lying in pronation. A 1 ml syringe filled with triamcinolone acetonide and fitted with a 2 cm
THE NON-CAPSULAR PATTERNS LIMITED SUPINATION
needle is used. The joint line, which is very short, is
After a mal-united Colles' fracture, shortening of the
identified just radially to the head of the ulna. Gliding
radius may be responsible for an irreversible limitation of
movements between the ulna and radius may help to
supination only, with the end-feel of a bony block. The
find it. As the extensor digiti minimi tendon lies just
movement may be painful in recent cases but should
dorsal to the joint line, care must be taken to avoid punc
become painless in due course. This progression may be
turing it (Fig.
speeded up by mobilization.
33.2).
The needle is inserted vertically downwards at the midpoint of the joint line, about
5 mm proximal to the
lower edge of the ulna. It is thrust down and will hit bone at about
PAINFUL SUPINATION
1.5 cm. It is then manoeuvred about in an
oblique direction towards the radius, until it slips beyond
In tenosynovitis of the extensor carpi ulnaris, passive
it without resistance. The injection is then carried out.
supination may be painful at the end of the range. This is
CHAPTER 33
-
DISORDERS OF THE LOWER RADIOULNAR JOINT 497
a localizing sign, indicating that the lesion lies in the
gross instability occurs. Instability is found when the lig
groo\te at the base of the ulna. It is a bizarre sign, for
amentous components of the TFCC proper - the dorsal
which no clear anatomical explanation can be given. The
and palmar radioulnar ligaments - become affected.23
tenosynovitis will, of course, be diagnosed by interpret
Early surgery is then preferred.24,2s Chronic disorders of
ing resisted movements at the wrist (see p.
the TFCC, often combined with instability, require
5 11-512).
arthroscopic26-28 or open repair,29 including ulnar short ening. 30,31 The results are good.32
DISORDERS OF THE TRIANGULAR FIBROCARTILAGE COMPLEX The classification as devised by Palmer shows that the
DISORDERS OF THE CONTRACTILE STRUCTURES
triangular fibrocartilage complex (TFCC) can become affected as the result of trauma or degeneration.14 It
Resisted pronation and supination are not tested in the
results in ulnar-sided wrist pain.IS The traumatic condi
standard functional examination, because they are not
tions (class
relevant at this level. However, resisted pronation can
1) follow hyperpronation or axial load-and
distraction injury to the ulnar part of the wrist (e.g. fall
be performed as an accessory test in order to examine
on an outstretched extremity16) and include perforation
the pronator quadratus muscle. Having said this, a
and avulsion17 with or without fracture.18 The degenera
lesion of this structure has never been described and it
tive disorders (class
2) result from chronic injuries after
does not seem to exist. Resisted pronation movement
repetitive loading on .the ulnar side of the wrist.19 They
also tests the common flexor tendon (in the case of
vary from triangular fibrocartilage wearing to chondro
golfer's elbow) and the pronator teres muscle but in
malacia
lesions of these gives rise to pain felt near the elbow (see
and
ligament
perforation.2o
Degenerative
changes in the TFCC often accompany those in the distal radioulnar joint.21 High-resolution ultrasonogaphy has
pp.
466 and 454).
Resisted supination does not test any structure in the
an acceptable accuracy in the diagnosis.22 The treatment
wrist region, testing only those at the elbow - the brachial
of choice for acute injuries is conservative, except when
biceps and supinator brevis.
REFERENCES 1. Kihara H, Short W H, Werner FW, Fortino MD, Palmer AK. The stabilizing mechanism of the distal radioulnar joint during pronation and supination. ] Hand Surg 1995;20A(6):930-936. 2. Van der Heijden EP, Hillen B. A two-dimensional kinematic analysis
of
the
distal
radioulnar
joint.
J
Hand
Surg
1996;218(6):824-829.
rheumatoid arthritis. Hand Clinics 1989;5:249-256. 13. Linscheid RL. Biomechanism of the distal radioulnar joint. Clin Orthop Rei Res 1992;275:46-55.
14. Palmer AK.
Triangular fibrocartilage complex
lesions:
a
classification. J Hand Surg 1989;14A:594-606.
3. Ward LD, Ambrose CG, Masson MV, Levaro F. The role of the distal radioulnar ligaments, interosseous membrane, and joint capsule in distal radioulnar joint stability. J
12. O'Donovan TM, Ruby LK. The distal radial ulna joint In
Hand
Surg
2000;25A(2);341-351. 4. Kleinman WB, Graham TJ. The distal radioulnar joint capsule: clinical anatomy and role in posttraumatic limitation of forearm rotation. J Hand Surg 1998;23A(4):588-599. 5. Cooney W P, Dobyns JD, Linscheid RL. Complications of Colles' fractures. ] Bone Joint Surg 1980;62A:613. 6. Burgess RC, Watson HK. Hypertrophic ulna styloid non unions. Clin Orthop Rei Res 1998;228:215. 7. Cyriax JH. Textbook of Orthopaedic Medicine, vol!, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:182.
8. Feldon P, Millender LH, Nalebuff EA. Rheumatoid arthritis in
15. Buterbaugh GA, Brown TR, Horn Pc. Ulnar-sided wrist pain in athletes. Clin Sports Med 1998;17(3):567-583. 16. Palmer AK. The distal radioulnar joint. In: Lichtman OM (ed) The
Wrist and its
Disorders.
Saunders, Philadelphia, 1988:
220-231. 17. Adams BD, Samani JE, Holley KA. Triangular fibrocartilage injury: a laboratory model. ] Hand Surg 1996:21A(2):189-193. 18. Lindau T, Adlercreutz C, Aspenberg P. Peripheral tears of the triangular fibrocartilage complex cause distal radioulnar joint instability
after
distal
radial
fractures.
]
Hand
Surg
2000;25A(3):464-468. 19. Chidgey LK. The distal radioulnar joint: problems and solu tions. J Am Acad Orthop Surg 1995;3(2):95-109. 20. Loftus JB, Palmer AK. Disorders of the distal radioulnar joint
the hand and wrist. In: Green DP (ed) Operative Hand Surgery,
and
3rd edn. Churchill Livingstone, New York, 1993:1587-1690.
Lichtman OM, Alexander AH (eds) The Wrist and its Disorders,
9. Blank JE, CaSSidy C. The distal radioulnar joint in rheumatoid arthritis. Hand Clinics 1996;12(3):499-513. 10. Bachdahl M. The caput ulnae in rheumatoid arthritis: a study of the morphology, abnormal anatomy, and clinicaJ picture. Acta Rheumatol Scand 1963;5:1-75.
11. Straub LR, Ranawat CS. The wrist in rheumatoid arthritis surgical treatment and results. J Bone Joint Surg 1969;51A:1-20.
triangular fibrocartilage
complex:
an
overview.
In:
2nd edn. Saunders, Philadelphia, 1997:385-414. 21. Yoshida R, Beppu M, Ishii S, Hirata K. Anatomical study of the distal radioulnar joint: degenerative changes and morphologi cal measurement. Hand Surg 1999;4(2):109-115. 22. Chiou HJ, Chang CY, Chou Y H et al. Triangular fibrocartilage of wrist: presentation on high resolution ultrasonography. ] Ultrasound Med 1998;17(1):41-48.
498 SECTION SIX - THE WRIST, THUMB AND HAND
23.
Stuart PR, Berger RA, Linscheid RL, An KN. The dorsopalmar
28.
689-699. 24.
29.
Bednar JM, Osterman AL. The role of arthroscopy in the treat ment of traumatic triangular fibrocartilage injuries. Hand
26. 27.
Minami A, Kato H. Ulna shortening for triangular fibrocarti lage complex tears associated with ulnar positive variance. J Hand Surg 1998;23A(5):904-908.
Zelouf OS, Bowers W Ho Treatment of acute injuries of the tri angular fibrocartilage complex. In: Lichtman OM, Alexander
Bowers WHo Instability of the distal radioulnar articulation. Hand Clinics 1991;7:311-327.
30.
Clinics 1994;10(4):605-614.
25.
Berger RA. Arthroscopic anatomy of the wrist and distal radioulnar joint. Hand Clinics 1999;15(3):393-413, vii.
stability of the distal radioulnar joint. J Hand Surg 2000;25A(4):
31.
Beyermann K, Krimmer H, Lanz U. TFCC (triangular fibrocar
AH (eds) The Wrist and its Disorders, 2nd edn. Saunders,
tilage complex) lesions. Diagnosis and therapy. Der Orthopiide
Philadelphia, 1997;415-428.
1999;28(10):891-898.
Bednar JM. Arthroscopic treatment of triangular fibrocartilage
32.
Terry CL, Waters PM. Triangular fibrocartilage injuries in
tears. Hand Clinics 1999;15(3):479-488, ix.
pediatric and adolescent patients. J Hand Surg 1998;23A(4):
Zelouf DS, Bowers WHo Arthroscopy of the distal radioulnar
626-634.
joint. Hand Clinics 1999;15(3):475-477, ix.
CHAPTER CONTENTS Disorders of the inert structures 499 Limited range: the capsular pattern 499 Traumatic arthritis 499 Rheumatoid arthritis 501 Arthrosis 501 Limited range: the non-capsular patterns Full range 504 Excessive range 507 Disorders of the contractile structures Resisted extension 510 Resisted flexion 513
Disorders of the wrist 502
510
Lesions at the wrist itself often have a traumatic cause either a single injury or overuse. If the symptoms appear spontaneously, arthritis usually of the rheumatoid type, is the most frequent cause. Usually the history will not be of great help and clin ical and/ or radiological examination is more reliable. The patient will indicate more or less precisely where the lesion lies, in that referred pain in this part of the upper limb is rare.
DISORDERS OF THE INERT STRUCTURES l!IMITED�RANGE: THE CAPSULAR P.A1iiTERN �:;- ···· "
:?
"'i'
The capsular pattern is an equal degree of limitation of flexion and extension (Fig. 34.1). In advanced arthritis, fixation of the wrist in the midposition takes place.
TRAUMATIC ARTHRITIS Uncomplicated traumatic arthritis is almost non-existent. The finding of a posttraumatic arthritis is very suggestive of a fracture.
Warning A capsular pattern last i n g for more t h a n 2 days after trauma makes fractu"re, either of a carpa l bone or of the e p i p hysis of the radius, a strong possib i lity.
The radiographic picture in fracture is unreliable - in the first 2 weeks it may remain negative because the fracture is hairline. Also, because of the shape of the bone it is very difficult to interpret anteroposterior and lateral views. However, the clinical picture of a fracture is so evident that the diagnosis should not be missed. Any case of traumatic arthritis of the wrist lasting for longer than 2 days should be considered as a fracture even if radiography is negative. 499
500 S ECTI O N S I X - T H E WRI ST, TH U M B A N D H A N D
flexion
radial-----� deviation
_______ ulnar deviation
extension
Fig. 34.1
The capsular pattern at the wrist.
History and examination The history is an injury, varying from a simple thrust to a fall onto the outstretched dorsiflexed hand. Immediately afterwards, quite severe and constant pain develops and prevents hand movement. At first, the pain is localized; later it may spread over the entire wrist. Inspection shows generalized swelling of the wrist. On examination, a capsular pattern is found: passive flexion and extension are very painful and limited, the latter being the result of a protective muscle spasm which comes on with a vibrant twang clearly felt when the end-feel is assessed. Passive deviation of the wrist towards the painful side also increases the pain - a com pression phenomenon that provides further evidence of a bony lesion. Careful palpation of the bones will show where the fracture lies in that the damaged bone is very tender to touch. Tenderness is most often elicited in the anatomical snu ffbox,l which implicates the scaphoid . Indeed, the scaphOid is the carpal bone most often fractured,2 because it spans the joint between the proximal and distal rows of carpal bones and is most vulnerable: scaphOid fracture comprises between 51 and 78% of all carpal fractures.3-6 They typically affect young men in their most active and productive years.7 According to Gasser,8 fractures of the scaphOid represent nearly 2% of all fractures. They are very rare under the age of 15 and reach a peak incidence in young adults, aged between 15 and 30 years.9 Scaphoid fractures most easily occur during loading of a wrist which is extended or hyperextended, possibly in combination with ulnar deviation. During dorsi flexion the palmar ligaments [the radiocapitate and radioscaphoid ligaments] tighten and draw the scaphOid
against the radius, thus stabilizing the bone. As the prox imal pole is strongly stabilized, excessive loading and extension movement of the wrist cause bending forces on the distal pole which may result in fracture.lO,]] Scaphoid fractures are classified by Johnson et at (mentioned by Mayfield12-13) as type I (stable), type II (unstable with moderate ligamentous damage) or type III (unstable with severe ligamentous damage and perilunar instability). Fractures may occur at any level in the scaphoid but the more proximal the fracture, the greater the chance of avascular necrosis of the proximal fragment.14 The main reason for this is the special nature of the scaphoid's blood supply, which has been thoroughly investigated in recent decades. The main blood supply to the scaphoid enters the distal pole and proceeds proximally towards the proximal pole.IS Gelberman and Menon16 stated that the scaphoid receives most of its nutrition from the palmar and dorsal branches of the radial artery (Fig. 34.2). Some 20-30% of the vascularity of the distal pole is provided by the palmar branches, entering the bone distally at the tuberosity. The remainder of the vascular supply comes from dorsal branches that enter through the dorsal ridge in the middle third of the bone.17,18 A displaced scaphOid fracture, which occurs in 30% of cases, also presents problems.19,2o Displacement of more than 1 mm is associated with a 55% incidence of non union, not necessarily symptomatic,21 and a 50% risk of avascular necrosis of the proximal pole.22 Because of the danger of the development of avascular necrosis, it is important to recognize a scaphoid fracture as quickly as possible.
Warning It is important to d i a g nose a scaphoid fracture as soon as possib l e in order to avoid avascu lar necrosis. In post traumatic arthritis last i n g longer than 24 hours the condit i o n should be regarded as a fracture until the contrary has been established.
An initial negative radiograph does not alter the clinical diagnosis: it may take up to 2 weeks before radiography can confirm the diagnosis.23 Fractures that are difficult to show on radiography can usually be diagnosed with trispiral tomography or CT with axial and para-axial views. Bone scans, if positive, are not specific but a negative bone scan 72 hours after trauma excludes an occult scaphOid fracture.24-26 Magnetic resonance imaging, although not superior to bone scintigraphy,27 is also valuable in the early diagno sis of occult fractures28 and has a high sensitivity.29
CHAPTE R 34
Fig. 34.2
Vascular supply to the scaphoid.
Treatment Treatment consists of immediate immobilization of the wrist, which is protective and can decrease the inci dence of non-union and avascular necrosis.3D The best posi tion remains unclear. Several dissection studies have come to different conclusions.31-34 Immobilization seems to be best performed with a thumb-spica cast, holding the thumb in the palmar abducted position and the wrist in the midposition but with an element of deviation towards the site of the fracture which, for the scaphoid, would be radial deviation. This helps to press the fractured surfaces together and stimulates the healing process.lO The time necessary for a scaphoid fracture to heal is variable, from a minimum of 6 weeks to as long as 9 months35 but 90% of fresh fractures heal with adequate treatment.3D Fractures of the other carpal bones can occur. Frequently, multiple radiographic views and/ or follow up studies with tomograms or bone scans may be neces sary for a definitive diagnosis.36 Displaced fractures may require open reduction and internal fixation, either with crossed Kirschner wires or with a special (Herbert) screw.37, 38
RHEUMATOID ARTHRITIS The wrist can become affected by any type of rheumatic disorder - for example systemic lupus erythematosus, progressive systemic sclerosis, psoriatic arthritis, gout, pseudogout, ankylosing spondylitis, Reiter's syndrome, infectious arthritis, sarcoidosis - but rheumatoid arthri tis is one of the commonest, frequently affects both wrists39 and often follows involvement of the fingers.
-
D I S O R D E R S O F T H E WRIST
501
Magnetic resonance imaging can be a useful technique to ascertain the criteria for diagnosis and progression of rheumatoid arthritis, and to assess the effects of treat ment.4D In the acute stage a capsular pattern is found on examination, together with swelling, warmth and syn ovial thickening. The more chronic cases present with, in addition to pain, a very gross limitation of movement and may even end up with virtual ankylosis in slight flexion. At this stage, there is no longer any warmth and even the swelling has diminished. In the acute stage, the patient can be treated locally by immobilization of the wrist for some weeks. In the sub acute and chronic stages, triamcinolone is a much better approach. One infiltration of 20 mg of triamcinolone acetonide is given at all the different areas of synovial thickening and/ or tenderness, which are first precisely identified by palpation. Although treatment is very painful, the results are spectacular and symptoms at the wrist tend not to recur.
ARTHROSIS Primary arthrosis may come on spontaneously as age advances. This is an uncommon degenerative condition. Much more common is the arthrosis that is secondary to severe injury or overuse of the wrist (e. g. professional causes). The patient complains of stiffness and of some discom fort on certain activities. On examination a moderate capsular pattern is found, with a hard end-feel and crepitus when passive move ments are performed. The radiograph shows osteophytes, sclerosis of the bony margins and diminished joint spaces, and some times diffuse cystic change. It should be realized that minor arthrosis, visible on a radiograph, does not always interfere with the function of the wrist. Watson et a141,42 examined 4000 radiographs of wrists of which 210 showed some form of degenerative arthri tis. In 95% the scaphoid was involved. Three patterns were recognized (in order of frequency): (a) scapho lunate advanced collapse pattern (SLAC wrist) with destructive changes at the scaphoradial, capitolunate and scaphocapitate joints - 55%; (b) 'triscaphe' arthritis with involvement of the scaphotrapezial and/ or scaphotrapezoidal joints - 20%; (c) combination of SLAC wrist and triscaphe arthritis - 10%. The remaining 5% affect the joints between the lunate bone and the triquetrum, ulna and radius, respectively.43 Because the disability is usually minor in arthrosis, treatment is seldom necessary. In rare instances where fairly heavy loads are imposed on the joint, arthrodesis may be warranted.44
502 SECTI O N S I X - T H E WRI ST, TH U M B A N D H A N D
LIMITED RANGE: THE NON-CAPSULAR PATTERNS CARPAL SUBLUXATION
Subluxation of a carpal bone, most often the capitate, occurs quite frequently. The diagnosis is purely clinical and, once the condition is· recognized, it can be dealt with successfully by conservative management. Recurrence is not at all uncommon and may ultimately cause problems. History and examination The patient complains of pain on certain movements at the dorsal aspect of the wrist, especially when weight is put on an extended wrist. The symptoms may come on spontaneously or as the result of a minor injury in flexion. On examination, signs of internal derangement are found (Fig. 34.3): one movement, most often extension, is limited with - certainly in acute cases - an end-feel of muscle spasm. Other movements are full ni.nge, although often painful - the result of over-stretching of the irritated ligaments (see p. 506). The bony subluxation may be made visible and palpable if the wrist is held in flexion. Local tenderness is found in the ligaments around the subluxated bone. The radiograph is negative: the edge of the sublux ated bone appears merged with the others and cannot be visualized separately on the radiograph, nor can its position be measured against the superimposed margins of the other bones (Cyriax:45 p. 184). The clinical examination supplies the diagnosis. The joint is bl ocked in one direction only, which is typical for internal derangement. On inspection the displacement is visible and immediate reduction during manipulation confirms the tentative diagnosis of a carpal sublu xation. flexion
radial deviation
ulnar deviation
extension Fig. 34.3
The non-capsular pattern in carpal subluxation.
Differential diagnosis Limitation of wrist extension does not necessarily indi cate carpal subluxation and differential diagnosis should be made from the following disorders:
ganglion at the dorsum of the wrist usually feels softer on palpation. It does not respond to manipulative treatment but can be diagnosed and treated by puncture.
• A
•
•
KienbOck's disease, un-united fracture and isolated arthrosis have a different history and can easily be detected on radiography (see p. 504). Palmar subluxation, mostly of the lunate bone, is very exceptional. It gives rise to (slight) limitation of flexion and may compress a palmar branch of the median nerve, causing paraesthesia in the corresponding territory (see p. 569).
Treatment Treatment consists of manipulative reduction, which restores extension. Because of the accompanying sprain of the dorsal ligaments, flexion often remains painful. A few sessions of deep transverse friction will resolve this problem. The patient should be told that if the condition recurs, further manipulation is necessary. Repeated recurrence may indicate instability and can be treated with infiltra tion of a sclerosant solution into the ligaments attached to the subluxated bone, in order to tighten them up and so to prevent the bone from moving dorsally again. Basic technique: manipulation for carpal subluxation.
...;..... . �r_-----.
-----
It could be supposed that the condition is ligamentous, adhesions being ruptured during manipulation. This does not fit with the behaviour of a ligamentous adhe sion in which limitation would be slight and only in the direction that stretches the ligament. In addition the condition would not recur after a successful manipulation.
The patient sits on a couch, the arm held in abduction against the back of the couch. An assistant grasps the patient's upper arm just proximally to the elbow and holds it firmly against the couch. One foot is placed for wards for the manipulator'S benefit: the latter will place a foot against it. The manipulator stands level with the patient's hip, between the couch and the patient's arm and places the ipsilateral foot against the assistant's foot, which will later enable a lean sideways and use of body weight for the pull required to obtain traction on the wrist joint. With the ipsilateral hand, the patient's forearm is grasped just proximally to the radiocarpal joint, with the thumb on the dorsal aspect of the forearm. With the contralateral hand, the patient's wrist is held with the thumb dorsally on the subluxated bone.
CHAPTER 34
The aim of the manipulation is to perform a gliding movement between the rows of carpal bones during trac tion. The technique is executed as follows. The manipula tor leans sideways but makes sure that the pull is only with the distal hand so as to obtain traction on the wrist. After the slack has been taken up, both hands are moved vertically up and down in opposite directions (Fig. 34.4). The little finger of the contralateral hand is kept in the palm of the patient's hand to control movement: the manoeuvre should result in a pure gliding movement and flexion-extension should be avoided. This gliding movement is performed several times in one manoeuvre. The movements of the wrist are then re examined and the manipulation repeated until a full range of extension has been restored or until no further benefit results. If there is no immediate result, the attempt should not be abandoned too quickly. It may sometimes help slightly to change the position of the patient's hand during the manoeuvre and to build in a bit more flexion or extension or radiaLor ulnar deviation. When this technique does not lead to full recovery, the next manoeuvre is tried. Second technique: manipulation for carpal subluxation.
This technique is never used first but is introduced only when the bone is partially reduced. The aim is to perform a squeezing of the wrist during traction. The patient, the assistant and the manipulator main tain the same position as in the previous technique. The
-
D I S O R D E R S OF T H E W R I ST
503
manipulator's distal hand is now moved slightly down wards, so that it grasps the patient's hand at the level of the bases of the metacarpal bones. Using the other hand, the patient's wrist is approached from above and encir cled with thumb and index finger. The metacarpopha langeal joint of the index finger is placed on the subluxated bone. The manipulator's forearm is held vertically (Fig. 34.5). The manipulator leans sideways, applying traction with the distal hand and, having taken up the slack, executes a short and sharp squeezing manoeuvre. Although the manipulative thrust is a pure squeezing, there is an involuntary downwards movement of the hand, which helps reduction. This technique can be repeated several times. Alternative technique: manipulation for carpal sublux ation. The patient stands next to the couch, with the forearm, stabilized by the other hand, placed on the couch, the distal part level with the edge. The manipu lator stands in front of the patient and grasps the hand in such a way that one thumb, reinforced with the other, is placed dorsally on the subluxated bone, while one index finger, reinforced by the other, is placed on the palmar aspect of it. The little fingers are placed in the palm of the patient's hand, in order to prevent flexion-extension movements during the manipulation (Fig. 34.6). Traction is applied with both hands and, after having taken up the slack, an anteroposterior glide is performed with emphasis on downwards movement. Several move ments are performed and the patient is re-examined after each manoeuvre.
OTHER JOINT PROBLEMS
The three following disorders, all visible on the radi ograph, give rise to limited extension only.
Fig. 34.4
Basic manipulation for carpal subluxation.
Fig. 34.5
Second manipulative technique for carpal subluxation.
504 SECTI O N S I X - T H E WRI ST, T H U M B A N D HAN D
In the early stage, radiographs may remain negative, except for the ulnar minus variant.61 Later, sclerosis and deformity of the lunate bone are clearly shown.60 Lichtman et a158,62 have modified Stahl's63 original radi ographic classification: normal architecture with evidence of a linear compression fracture. Stage II: normal outline, but definite density changes within the lunate. Stage III: collapse or fragmentation of the lunate and proximal migration of the capitate bone. Stage IV: generalized degenerative changes within the carpus, localized disappearance of articular cartilage at the lunate-capitate joint, very occasionally with osteophyte formation.
• Stage I: • • •
Fig. 34.6
Alternative manipulation for carpal subluxation.
Aseptic necrosis of the lunate bone (Kienbock's disease) Avascular necrosis of the lunate was first described by Peste in 1843.46 The condition was then forgotten until 1910, when Kienbock recorded lunatomalacia, which he assumed had a vascular traumatic aetiology.47 Other authors48-51 have recognized this condition as avascular necrosis and have attributed the loss of blood supply to primary circulatory problems (e. g. aseptic embolus), lig amentous injury and fracture.52 The condition may also result from acute trauma or repeated microtrauma53 and anatomical variations of either ulna - short ulna (also called negative ulnar variance)54,55 - or radius56 resulting in overpressure at the lunate bone. Current thinking on the aetiology of Kinbock's disease considers the avascular necrosis to be the result of inter ruption of the vascularization of the lunate bone follow ing excessive shear forces caused by acute trauma or repeated microtrauma. This happens more easily in those lunate bones that are supplied by only one single volar or dorsal blood vesseJ.57 The patient, between 20 and 40 but usually a male in his twenties,58,59 complains of pain and stiffness in the region of the wrist, which may vary from moderate to constant, severe and incapacitating. He may also mention reduced strength in the hand.6o The symptoms will have come on spontaneously or as the result of a minor injury and usually interfere very significantly with work-related activities. On clinical examination, the pain is elicited during passive movements of the wrist. Different movements may become limited, especially dorsiflexion - a clear non-capsular pattern.
Trispiral tomograms can also show sclerosis, fragmen tation and proximal pole collapse, and technetium-99 bone scan demonstrates intense uptake in the region of the lunate.64 MRI is another useful investigation that allows early diagnosis.65 Because there is no effective conservative approach, treatment remains a difficult problem. Immobilization is now considered obsolete. There is no effective surgery, although different treatments have been proposed and different authors claim good results. Depending on the stage the following procedures are used: (a) revascularization;66 (b) lunate decompres sive procedures - shortening of the radius,67 lengthen ing of the ulna,68 lateral closing wedge osteotomy, intercarpal arthrodesis (e.g. triscaphe, scaphocapitate or capitate-hamate fusion); (c) excision of the lunate;69,7o (d) salvage procedures - proximal row carpe'=tomy71,72 . and wrist arthrodesis. Avascular necrosis in other carpal bones has been described but is rare?3,74 Un-united fracture This leads to pseudarthrosis and also gives rise to limita tion of extension. Isolated arthrosis This comes on some years after an un-united fracture, especially of the scaphoid bone. The projecting osteo phytes can be seen and felt. Extension is very limited but the condition is not necessarily painful.
FULL _
RJ:\N��> -.
. .
-
'-"' ..... �_ ��__ ,.., �" .�.
."
'-"��� .
:1.'.. ... "
..__
' ..
.# �
HA, .&.1:::-
"'�
__
" ". .ti.: ... ....... _ ....i.
:
LIGAMENTOUS LESIONS
Ligamentous injuries range from minor sprains with no instability, which are discussed here, to complete rupture with gross instability?5
CHAPTER 34 - D I S O R D E RS OF T H E WRIST
Sprain of the ulnar collateral ligament This· disorder is the result of an injury causing a fracture, either a Colles' fracture or fracture of the styloid process of the ulna. The fracture has healed but pain remains at the ulnar aspect of the wrist. On inspection, the deformity of the radius is visible and passive radial deviation causes pain at the ulnar aspect of the wrist. The symptoms can be quickly relieved by an infiltra tion of triamcinolone. Untreated spontaneous recovery takes place in the course of a year.
505
Sprain of the radial collateral ligament This rare disorder results in pain felt at the radial aspect of the wrist during passive ulnar deviation. A more common cause of these symptoms is a tendinous lesion in the extensor pollicis brevis and abductor pollicis longus tendons. Differential diagnosis is easy, because in ten dinitis resisted movements are also positive. Radial collateral sprain responds well to treatment with either one infiltration of triamcinolone or several sessions of deep transverse friction.
A 1 ml syringe, filled with 10 mg of triamcinolone acetonide, and a 2 cm needle are used. The patient's arm rests in pronation on the couch. The hand is brought into slight radial deviation. The tender spot is identified, and the infiltration given with bony contact and ligamentous resistance (Fig. 34.7).
The patient sits with the fore arm in the neutral position and the hand on the couch. The wrist is brought into slight ulnar deviation. The tender spot is palpated and 10 mg of triamcinolone acetonide is infiltrated using a 2 cm needle (Fig. 34.8). During infiltration, ligamentous resistance and bony contact should be felt. Care must be taken to avoid puncture of the radial artery.
Fig. 34.7
Fig. 34.8
Technique: infiltration.
Infiltration of the ulnar collateral ligament.
Technique: infiltration.
Infiltration of the radial collateral ligament.
506 SECT I O N S I X - T H E WRIST, T H U M B A N D HAN D
Sprain of the dorsal ligaments The most common minor lesions are usually the result of overuse but may also occur when long-standing carpal subluxation causes irritation of the overstretched ligaments. Pain is felt at the dorsal aspect of the wrist on full passive flexion. Other tests are negative. Careful palpa tion reveals the exact site of the lesion. Most of the lesions are found in the lunate-capitate ligament but occasion ally also in the radiolunate, capitate-third metacarpal or ulnar-triquetral ligament. Treatment consists of several sessions of deep trans verse friction which should lead to complete cure, independent of how long symptoms have been present. In the rare case in which it is not clear whether the symp toms are caused either by a pure ligamentous sprain or by irritation of the ligaments from carpal subluxation, manipulation may be tried. If it proves ineffective, deep transverse friction is substituted. Even in the chronic stage of a dorsal ligamentous lesion at the wrist, the only effective treatment is deep transverse friction. Other treatments, such as steroid injections, immobilization or operation, are of no use. In order to avoid permanent problems, and because these lesions are often multiple, friction must be given to all the sprained ligaments. Palpation should therefore be performed carefully until all the tender spots have been found. Technique: deep transverse friction. The patient sits with the hand over the edge of the couch. The therapist sits facing the patient's wrist, which is flexed with one hand within the limits of pain. Friction is imparted with the other hand; the direction depends on the course of the ligamentous fibres. For a radiocarpal or carpometacarpal ligament the direction is ulnar-radial. The friction is given with either the index finger, reinforced with the middle finger, or with the thumb (Fig. 34.9). As the lesion is very localized, the therapist must make sure that the finger remains deeply in between the extensor tendons and does not pass over it. An intercarpal ligament is given friction with the thumb and in the proximal-distal direction.
Rupture of a dorsal ligament A dorsal ligament, usually the capitate-third metacarpal ligament, may rupture as the result of a severe flexion injury and usually causes permanent instability. The wrist hurts for about a month, after which all symptoms cease, although after considerable exertion the pain may recur for a few days. When the wrist is held in full flexion, a depression may be palpated at the point of the lesion. The bone no longer moves in concert with its neighbours.
Fig. 34.9
Friction to the dorsal carpal ligaments.
The symptoms can be quickly abolished by partial immobilization (taping) but the instability remains. A series of three sclerosant infiltrations, at weekly intervals, may be tried and may sometimes considerably increase the stability of the wrist (Cyriax:45 p. 185).
CH APTER 34 - D I S O R D E R S OF THE W R I ST
GANGLION
A ganglion is a fluid-filled cavity that originates from joint capsule or tendon sheath. It is very common at the wrist. It occurs dorsally, most often over the scapholunate joint, as well as at the palmar aspect, usually at the trapezioscaphoid joint.76 Its aetiology has been debated for many years and various hypotheses have been pre sented: retention cyst, herniation of tendon or capsular synovia, bursal transformation, neoplasia, or mucinous degeneration of fibrous tissue, the last of these the most widely accepted theory.?7 The main complaint is the presence of a swelling that was not there before. It may sometimes be painful either at rest or during movement. The size may vary and so does its consistency: it can be either very soft or quite hard, giving the impression of a bony structure. When the ganglion grows, the neighbouring tissues may become compressed and there may be pressure on nervous tissue as well (see pp. 565-569). Many techniques have been used to treat this condi tion, varying from crushing the ganglion (e.g. pressure with the thumbs or a firm slap with a book) to aspiration and infiltration with a steroid or sclerosant solution. These measures usually lead to temporary cure but recurrences are frequent because the cause has not been treated. More consistent results are obtained by surgical removal, although the risks with surgery may be more undesirable than the minor symptoms associated with the presence of a ganglion?8 PERIOSTITIS AND STRESS FRACTURES
Pain at the dorsal aspect of the wrist may occur as the result of repetitive extension movements during weight bearing, as frequently happens in gymnastics or other high-energy sports which may lead to a periostitis at the distal epiphysis of the radius or the proximal carpal bones/9,8o described as 'wrist impingement' syndrome81 or 'stress reaction'.82 The pain is elicited each time the patient puts weight on an extended wrist. On examination, passive extension of the wrist is found to be full but painful, all other movements being negative. Careful palpation shows the lesion to lie at the inferior border of the radius or at the scaphoid and lunate bones. Periostitis responds well to local infiltration with 10 mg of triamcinolone acetonide, provided that further irritation is avoided . This can be done by avoiding the extremes of wrist movement in the loaded position or by the application of a splint or a cast, if necessary. Surgery can be performed in recurrent cases or to avoid long-term complications.83
507
Repetitive compressive loading may result in stress fractures of the distal part of the radius, the scaphoid and capitate bones. Scintigraphy and magnetic reso nance imaging are diagnostic and immobilization in a cast is therapeutic.84,85
. EXCESSIVE RANGE LIGAMENTOUS IN STABILITY
According to Ekenstam instability of the wrist is 'a con dition of altered joint kinematics in which one or several carpal bones are permitted abnormal patterns of motion as a result of bony abnormalities, ligamentous lesions or joint laxity' .86 Carpal instability remains a very controversial topic. Since 1943, when Gilford et al87 first mentioned instability of the wrist, many authors have worked on the subject. They have developed several hypotheses and proposed different methods of classification. This variability indi cates the difficulty in reaching a consensus on such a vague topic as 'instability' in the complex area that is the wrist. There is still a lack of standardization in evaluation methods and in the findings and radiographic criteria. Arthroscopy, however, has helped to provide a clearer picture of the possible underlying mechanisms.88 Aetiology Wrist instability is generally believed to be caused by posttraumatic stretching or rupture of one or several radiocarpal or intercarpal ligaments. The injury is usually hyperextension combined with radial or ulnar deviation and/ or pronation or supination.89 According to some authors, however, it can also be the result of anatomic changes and malalignment subsequent to radial or carpal fracture. Other possible causes of liga mentous laxity are degenerative and inflammatory con ditions (i.e. crystal synovitis, rheumatoid arthritis), as well as iatrogenic causes.90 Epidemiology and classification Epidemiological data on carpal instability are still not available, although wrist injuries occur in 28.6% of all accidents.91 Several methods of classification have been described.92 Taleisnik93,94 has proposed a theory based on the columnar concept of Navarro.95 This concept recognizes three vertical columns in the wrist: (a) the central (flexion/ extension) column contains two blocks - one on the lunate bone and one on the trapezium, trapezoid, cap itate and hamate bones; (b) the radial column comprising the mobile scaphoid bone; (c) the ulnar (rotating) column
508 S E CTI O N S I X - T H E WRIST, T H U M B A N D H A N D
which includes the triquetral bone and the pisiform. Taleisnik therefore classifies wrist instability as being radial, ulnar or proximal.96 This concept does not mention the transverse or peri lunar patterns (stages I-IV), which were later described by Mayfield et al97 and the more recently discussed mid carpal instability, proximal row instability and miscellaneous instability. , The Mayo Clinic proposes a classification, based on the work of Amadio, Cooney, Dobyns and Linscheid. 98-102 The Lichtman classification103 deviates from the colum nar wrist concept and the consequent longitudinal classification system, It is based on the 'carpal ring concept' - the distal and proximal rows are joined by two links: on the radial side the mobile scaphotrapezial joint and on the ulnar side the rotatory triquetrohamate joint. This concept includes the perilunate and midcarpal instabilities. Other classification systems, for example the Barton classification, have also been proposed. We consider Saffar's classification92 a clinical and useful approach. 1. Static or dynamic instabilities Dynamic instability only shows when, during movement of the wrist or under specific loading, symptoms can be elicited . Static instability is fixed, cannot be corrected by the patient and shows an abnormal position of the bone. 2. Location of instability • Proximal row instability is the most frequent type of instability: a) Scapholunate: there is a malalignment between the scaphoid and the lunate. This condition may lead to arthrotic changes. b) Triquetrolunate is the result of a complete or partial rupture of the triquetrolunate ligament. c) Or both. • Midcarpal instability: a) Ligament attenuation or tear after a light trauma in hyperlax persons: it results in a malalignment between the proximal and middle row of carpal bones. b) Ligament tear after rotational injury: there is a rupture or elongation of the ligaments that stabilize the mid-carpal joint. • Proximal instability (radiocarpal) with the two Taleisnik's stages: a) Stage 1: ulnar gliding of the entire carpus b) Stage 2: ulnar gliding of the entire carpus with scapholunate separation. Clinical diagnosis Although posttraumatic wrist pain occurs frequently, instability does not. The patient is examined thoroughly
and only when the history and the physical findings are compatible with carpal instability should the diagnosis be made. The patient has a history of past trauma with or without fracture or of past inflammatory disease. Complaint of wrist pain is mostly made during or after activity, which may be accompanied by a feeling of weakness or of snapping during movement. Information about the type of injury should be obtained but the patient often does not recall such features.104 The local ization of the pain is also very informative and points towards specific possibilities. The passive movements are full or even excessive in range and, although they are per formed very gently, they may cause pain at the end of the movement. Provocative tests can be performed:lOS 1 For scapholunate instability • The scaphoid bell sign: the examiner grasps the patient's scaphoid bone between thumb and index finger and controls its movement while the patient is actively moving from radial to ulnar deviation. The movement of the scaphoid should be smooth. If this is not the case, the test is considered positive. • Watson's test:106,107 the examiner puts the patient's hand in ulnar deviation. With the other hand the scaphOid bone is grasped between thumb (on the tubercle) and index finger. The hand is then brought into radial deviation and resists flexion movement of the scaphoid by the thumb. In instability this results in the proximal pole shifting backwards, which can be felt at the dorsal aspect (Fig. 34.10).
Figure 34.10 Watson's instability test: pressure is exerted on the palmar aspect of the scaphoid during movement from ulnar to radial deviation.
CHAPT E R 34
• o
-
D I S O R D E R S OF T H E WRIST
509
Lane's test (the scaphoid shift test):108 the examiner assesses the anteroposterior gliding of the scaphoid.
2 For triquetrolunate instability • Kleinman's shear test109 the examiner grasps the patient's distal forearm and puts the fingers on the most distal and dorsal aspect of the ulna. The thumb is placed on the pisiform bone. The ulna is so stabilized and a posterior pressure exerted on the pisiform. Pain may be produced (Fig. 34.11). • Linscheid's testllO the examiner grasps the patient's distal forearm and puts the finger on the most distal and radial aspect of the radius. The thumb is put at the ulnar aspect on the triquetral bone (Fig. 34.12). The radius is stabilized and pres sure exerted laterally on the triquetrum. Pain may be produced. 3 For midcarpal instability • Midcarpal shift testYl the examiner exerts axial compression to the wrist via the hand and asks the patient to actively move the wrist. A painful click may be produced. The click will not be present when pressure is brought to bear on the pisiform or during active contraction of the hypothenar muscles. • Apprehension testl 12 when the capitate bone is glided in a posterior direction, pain and/ or apprehension is produced.
Figure 34.12 Linscheid's test: the radius is stabilized and pressure is exerted on the triquetra I bone in a radial direction.
•
Metacarpal gliding:l13 the wrist is placed in ulnar deviation and the metacarpals glided in a palmar direction. Pain may be elicited.
4 For radiocarpal instability • Medial radiocarpal drawer test 114 pressure is exerted on the posterior aspect of the triquetral bone and counterpressure is on the radius. The test is positive when painful . • Ulnar sag: the ulnocarpal sag has increased. Technical investigations may include arthrography, arthroscopy, CT scanning, MR imaging and scintigraphy. Treatment Treatment is still controversial and is very much surgeoll-, physician- or therapist-related. Therapy varies from con servative treatment to a range of different surgical tech niques. Asymptomatic or slightly symptomatic cases are usually treated conservatively, including immobilization, anti-inflammatory drugs and gradual physiotherapy. Clearly symptomatic, persistent or recurrent cases are often treated surgically. Therapeutic evidence should be looked for in the years to come.
Figure 34.11 Kleinman's test: the dorsal aspect o f the wrist i s stabilized and pressure exerted on the pisiform bone in a dorsal direction.
Conclusion Posttraumatic wrist pain, if not the result of a fracture, is most often the outcome of a soft tissue lesion, such as ligamentous sprain or tendinous strain or of local bony
51 0 SECT I O N S I X - T H E WRIST, T H U M B A N D H A N D
Box 34.1 Summary o f disorders o f the inert structures of the wrist Limited range The capsular pattern • Traumatic arthritis • Rheumatoid arthritis • Arthrosis
Non-capsular patterns • Carpal subluxation • Other joint problems Full range • Ligamentous lesions • Ganglion • Periostitis and stress fractures Excessive range • Ligamentous instability
damage, such as periostitis. The standard clinical exami nation may show an unusual pain pattern or excessive or abnormal range of motion, in which case a ligamentous rupture or elongation could be suspected. A closer look at the wrist, with eventually accessory stress tests, may suggest instability which should be confirmed by further technical investigations. The examiner should not over estimate this problem: symptomatic wrist instability does occur but is not very frequent compared with ordinary soft tissue lesions. The disorders of the inert structures of the wrist are summarized in Box 34.1.
DISORDERS OF THE CONTRACTILE STRUCTURES
Figure 34.13
Differentiation between the wrist and finger extensors.
finger extensors. When an extensor of the wrist is at fault it is possible to differentiate between the radial extensors and the ulnar extensor by testing resisted radial and ulnar deviation (Fig. 34.13). Extensor carpi radialis longus and/or brevis A lesion of the extensor carpi radialis longus and I or brevis (Fig. 34.14) is usually the result of overuse. us, 116 The patient complains of local pain during activity. Resisted extension and radial deviation of the wrist are painful at the dorsal and radial aspect of the joint. Full passive flexion may also cause pain but is usually negative.
Tendinitis and tenosynovitis of the wrist are often encountered. Their frequency is the consequence of the long course of the tendons over the wrist, the role played by these tendons in the mobilization and stabilization of the wrist and overuse of the hand in daily life as well as in professional and sporting activities.
RESISTED EXTENSION PAIN
Pain on resisted extension indicates a lesion of either the wrist or the finger extensors. The movement hurts near the wrist, which shows that the distal part of either muscle group is implicated. Differentiation between wrist and finger extensors can be made by testing extension first with the fingers relaxed and then actively flexed, which inhibits the action of the
Fig. 34.14
The extensor carpi radialis longus (1) and brevis (2).
CHAPTER 34
-
D I S O R D E RS OF T H E WRIST
51 1
On palpation (in full flexion) two different localiza tions can be found. Tenderness is elicited at the insertion of the tendons at the base of the second (longus) and/or third (brevis) metacarpal bones. Sometimes the lesion lies in the distal part of the tendon(s), level with the carpus. Treatment consists of either deep transverse friction three times a week, in which case full recovery should be obtained within 2 weeks, or one or two infiltrations with triamcinolone suspension, provided the lesion is very localized. For the duration of treatment, the patient should avoid exertion that causes pain. Exercises, passive movements, immobilization and surgery are not indicated. Technique: deep transverse friction. The patient sits with the arm resting on the couch, the hand lying over its edge. The therapist sits lateral to the patient's hand. To stretch the tendon the patient's wrist is flexed but this should not provoke pain. The index finger of the other hand, reinforced with the middle finger, is placed on the tender spot. Counterpressure is applied with the thumb at the ulnar aspect of the wrist (Fig. 34.15). The friction starts at the radial side of the tendon and, when the finger has passed over the tendon, the movement restarts. This results in a to-and-fro movement, the active phase being the movement towards the therapist.
This treatment is only applied to insertion tendinitis on the base of the second and/ or third metacarpal bones. Ten milligrams of triamcinolone
Technique: infiltration.
Figure 34.16
Infiltration of the extensor carpi radialis longus and brevis.
acetonide are infiltrated at the tender area, using a 2 cm needle. The infiltration is given when tendinous resist ance is felt and the needle is in contact with the bone. If the palpating finger is kept on the tender spot during the whole procedure (Fig. 34.16), the exact location of the infiltration can be confirmed. Extensor carpi ulnaris The muscle is the second most common site of teno synovitis in the upper limb.l17,llS A lesion of the extensor carpi ulnaris (Fig. 34.17) may develop after strain or overuse or as the result of a rheumatoid condition, in which instance the tendon may be warm to the touch, swollen or nodular. On examination, pain at the dorsal and ulnar aspect of the wrist is elicited by testing resisted extension and resisted ulnar deviation. Passive radial deviation may also cause pain at the ulnar side. Palpation is performed with the hand in radial deviation, in order to locate the tender area. The lesion has three possible localizations (in order of frequency); at the tenoperiosteal junction at the base of the fifth metacarpal; at the part of the tendon
Figure 34.15
Friction to the extensor carpi radialis longus and brevis.
Figure 34.17
The extensor carpi ulnaris.
51 2 S E CT I O N S I X - T H E WRI ST, T H U M B A N D H A N D
between the triquetral and the head of the ulna; and at the groove in the distal extremity of the ulna. In the last, pain is also elicited at the extreme of passive supination. This was for Cyriax a puzzling phenomenon, which he regarded as a localizing sign (Cyriax:45 p. 186). It is explained by Bowers et al: 'The arrangement of the fibrous septa about the ECU [extensor carpi ulnarisl creates an angular approach of the tendon to its insertion in the position of full supination. This angle results in an ulnar translocation stress on the tendon sheath during ECU contraction, particularly with the forearm in supina tion and the wrist ulnarly deviated' .ll9 In mechanical tenosynovitis, either 2 weeks of deep transverse friction or one or two infiltrations with triam cinolone suspension will effect a cure. Infiltration is per formed only at the tenoperiosteal j unction. Mobilization, exercises or immobilization do not afford any help. Surgery is seldom necessary. Rheumatoid tenosynovitis is treated by infiltration of a steroid suspension along the tendon, between the tendon and its sheath. Posttraumatic rupture of the subsheath or of the exten sor retinaculum may result in recurrent subluxation of the tendon. The patient feels a sudden snap on certain movements, for example active supination with the wrist slightly flexed. This can be felt during palpation of the tendon. Surgical reconstruction is indicated.12o deep transverse friction. The patient's pronated arm rests on the couch. The therapist, sitting at the medial aspect of the patient's arm, stretches the tendon by bringing the patient's hand into radial devia tion. Depending on the extent of the tenderness, friction is applied with the fingertips of one, two or three fingers, or the index finger is reinforced by the middle finger (Fig. 34. 18). Counter-pressure is applied to the radial and distal aspect of the forearm. The finger is placed at the palmar aspect of the tendon and then moved u pwards over the tendon. Repetition of this movement results in up-and-down friction. Technique:
Figure 34.18
Friction to the extensor carpi ulnaris,
explains the phenomenon of 'transmitted stress' which is particularly present at this level. Resisted extension and ulnar deviation of the wrist may be positive in lesions of the inert structures (DRUJ and TFCC). The reverse also holds: passive supination may hurt in a lesion of the extensor carpi ulnaris (see above and also p. 496). The phenomenon can be reduced to a minimum by making sure that all examination tests are performed in a starting position which is technically correct (see Ch. 31). Extensor indicis proprius Lesions of the extensor indicis proprius are rare and result from overuse.
Technique: infiltration at the tenoperiosteal junction.
The patient's forearm rests on the couch in the same posi tion as for �riction. Ten milligrams of triamcinolone ace tonide are infiltrated with a 2 cm needle at the insertion of tendon at the fifth metacarpal bone, while one finger of the other hand ensures that the agent is placed at the right spot (Fig. 34.1 9). The extensor carpi ulnaris and its related structures This structure is closely connected to the distal radioulnar joint (DRUJ) and to the triangular fibrocartilage complex (TFCC). The distinct subsheath blends proximally with the capsule of the DRUJ and distally with the TFCC and
Figure 34.19
Infiltration of the extensor carpi ulnaris,
CHAPT E R 34 - D I S O R D E R S OF T H E WRIST
Pain at the dorsal and radial aspect of the wrist is felt on resisted extension with the fingers relaxed but disap pears when the fingers are held actively flexed. The lesion becomes obvious when each finger is separately extended against resistance. Palpation shows the lesion to lie at the carpal extent of the tendon. Crepitus during movement is occasionally felt. A few sessions of deep transverse friction are curative. Extensor digitorum Tenosynovitis, either mechanical or rheumatoid, may occur at the level of the carpus - where the tendons lie in a common sheath - and gives rise to pain felt locally at the dorsum of the wrist. Resisted extension of the fingers provokes this symptom as does passive flexion, which stretches the tendon. Rheumatoid tenosynovitis is characterized by a discrepancy between (pronounced) symptoms and (moderate) signs. Palpation shows the exact location and, in rheumatoid conditions, reveals swelling as well. Crepitus accompanies mechanical tenosynovitis. The mechanical type responds to either infiltration with 10 mg of triamcinolone acetonide between the tendon and tendon sheath or a number of sessions of deep transverse friction. In the rheumatoid type, triamci nolone injection is the only effective treatment.
WEAKNESS
Painless weakness on resisted extension of the wrist should lead to a full neurological examination of the upper limbs. Combination with weakness of other muscle groups helps to determine the causative lesion. Although other conditions may cause painless weakness, those given below are the most common. Bilateral weakness If examination shows that only wrist extension is weak, lead poisoning is a possibility. Involvement of motor function in the peripheral nervous system is one of the main features, in addition to those arising from haematopoietic, central nervous, gastrointestinal and renal involvement.121 If lead poisoning is not the cause, either carcinoma of the bronchus or one of the general neurological diseases should be suspected . Unilateral weakness Unilateral weakness of wrist extension may result from a lesion of either a nerve root or a peripheral nerve. Combination with weakness of other muscles provides more information: the cause lies at the C6-C8 nerve roots or at the radial nerve.
• •
•
•
51 3
C6 root palsy: in a C6 root palsy, flexion of the elbow is weak as well. C7 root palsy: weakness of extension of the wrist is exceptional in C7 root palsy but extension of the elbow and flexion of the wrist are normally found to be weak. C8 root palsy: this is suspected when the extensor carpi ulnaris and flexor carpi ulnaris are weak. Consequently, the hand deviates radially when resis ted extension of the wrist is tested. Extension and adduction of the thumb are also weak. Radial palsy: pressure on the radial nerve in the arm gives rise to radial palsy. The causes may be pressure by a crutch in the axilla, the edge of a chair or, in acute circumstances, fracture of the humerus at midshaft (see p. 557).
RESISTED FLEXION PAIN
The first question that arises is: is there a lesion of either the flexors of the wrist or the flexors of the fingers and, if a wrist flexor is at fault, is it the radial or the ulnar tendon? Radial and ulnar deviation, tested against resist ance, as well as resisted flexion of each finger in turn, should define the affected structure (Fig. 34.20). Flexor carpi radialis Lesions of the flexor carpi radialis (Fig. 34.21) are not very common122 but typically occur in women (75% of cases)123 and are the outcome of overuse, either athletic or occupational. Pain is felt at the palmar aspect of the wrist during movements such as grasping and lifting with the fingers outstretched. On examination, resisted flexion and resisted radial deviation of the wrist are painful. Tenderness can be pal pated either over the whole distal extent of the tendon or at the insertion of the tendon at the base of the second metacarpal bone.124
Pain on resisted flexion
Figure 34.20
Differentiation between the wrist and finger flexors.
51 4 SECT I O N S I X - T H E WRI ST, T H U M B AND H A N D
tendon and, during the active phase, the fingers are moved to the radial aspect. The patient sits and places the supinated forearm on a high couch, the wrist slightly extended. A 1 ml syringe is filled with 10 mg triam cinolone acetonide and fitted with a 2 em needle. The tendon and its insertion at the base of the second metacarpal bone are difficult to identify through the muscles of the thumb. Therefore, the base of the second metacarpal is palpated at the dorsum by the index finger while the thumb presses on the palmar side. The needle is inserted through the thenar muscles and directed towards the palpating index finger (Fig. 34.23). Before it touches bone, the resistance of a tendinous structure is felt. Infiltration is then performed .
Technique: infiltration.
Figure 34.21
The flexor carpi radialis.
Tenoperiosteal lesions respond well to both infiltration with triamcinolone acetonide and deep transverse fric tion, although friction through the thenar musculature is not easy, quite uncomfortable and time consuming. Tendinous lesions are better treated with friction as the lesion is usually too extensive. The patient sits with the supinated arm lying on the couch and the hand over its edge. The therapist faces the patient and extends the patient's wrist with the ipsilateral hand. With the fingers of the other hand friction is imparted to either the body of tendon or the insertion on the second metacarpal bone (Fig. 34.22). Friction is started at the ulnar aspect of the
Technique: deep transverse friction.
Figure 34.22
Friction to the flexor carpi radialis.
Flexor carpi ulnaris Tendinitis is more common at the ulnar flexor tendon (Fig. 34.24) than at the radial flexor tendon because of the greater mobility at the ulnar side.1 25 This lesion usually arises after a single excessive strain. Usually, the patient can precisely locate the symp toms to the palmar and ulnar aspect of the wrist. Pain is elicited during resisted flexion and resisted ulnar devia tions of the wrist. Palpation discloses the exact site of the lesion: distal to the pisiform bone - at the tenoperi osteal junction at the fifth metacarpal bone - or proximal to the pisiform bone in the body of the tendon.
Figure 34.23
Infiltration of the flexor carpi radialis.
CH APTER 34 - D I S O R D E R S OF T H E WRIST
51 5
2 cm needle is used . The tender area is located by pal pation. The operator keeps the thumb on the painful spot during the whole procedure. After the needle i s inserted, tendinous resistance should b e felt before a series of droplets are deposited in contact with the bone (Fig. 34.26).
Figure 34.24
The flexor carpi ulnaris.
Both deep transverse friction (four to six treatments) and infiltration with triamcinolone suspension are effective. Technique: deep transverse friction. The patient sits with the arm held in supination and the hand hanging over the edge of the couch. The therapist, facing the patient, extends the patient's wrist with the contralateral hand and imparts friction with the thumb of the other hand. Counterpressure is given at the dorsal aspect of the patient's wrist (Fig. 34.25). Friction starts at the radial aspect of the tendon and finishes at the ulnar aspect.
This technique is particularly useful for a lesion at the insertion of the tendon onto the fifth metacarpal bone. The patient's hand is brought in the same position as for friction. A 1 ml syringe, filled with 10 mg of triamcinolone acetonide and fitted with a
Technique: infiltration.
Figure 34.25
Friction to the flexor carpi ulnaris.
Pisotriquetral disorders Disorders of the joint between the pisiform and the palmar surface of the triquetrum may occur and, because of the attachment of the tendon to the pisiform bone, give rise to the same signs as in flexor carpi ulnaris tendinitis . Helal 126 and Buterbaugh et al127 describe a local disorder as well as pisotriquetral insta bility. If such a disorder is suggested intra-articular steroid is required Ys In recu rrent cases, surgical removal of the pisiform may be necessary.129 Flexor digitorum profundus A lesion of the flexor digitorum profundus is ei ther a mechanical tenosynovitis or a rheumatoid tenovaginitis. The former results from overuse. The pain is brought on by testing resisted flexion of the fingers. The lesion lies over an area of 3-4 cm above the level of the carpus on the palmar aspect of the lower forearm. It is treated by deep transverse friction (see below) or by injection of a steroid suspension between the tendons. A rheumatoid tenovaginitis is usually confined to one flexor tendon near the carpus. Early in its progress, diffuse swelling and local warmth on the palmar aspect of the forearm are the only signs. Later tenderness of the tendon may be found over a greater extent than occurs in overuse. After a few weeks, the swelling becomes nodular and local warmth persists.
Figure 34.26
Infiltration of the flexor carpi ulnaris.
... .,
51 6 S E CT I O N S I X - T H E WRI ST, TH U M B A N D H A N D
The symptoms abate after one or two infiltrations with triamcinolone. Swelling on a digital flexor tendon may sometimes lead to compression of the median nerve distal to the carpal tunnel, thus causing a partial syndrome (see p. 572). Technique: deep transverse friction (mechanical tenosyno
The patient sits at the couch with the forearm supinated, the hand hanging over the edge of the couch. The therapist approaches the patient's arm from the radial side. With the ipsilateral hand the wrist and fingers are brought into extension. The friction is applied with two or three fingertips of the other hand. Counterpressure is maintained with the thumb at the radial aspect of the patient's forearm (Fig. 34.27). Friction starts at the ulnar side of the tendons and ends at the radial aspect, the therapist pulling the fingers towards him or herself.
WE A KNESS
Apart from more general neurological conditions, weak ness of wrist flexion is frequently the result of a C7 or C8 nerve root lesion. C7 root palsy: there is in addition marked weakness of extension of the elbow; the triceps jerk is seldom affected. C8 root palsy: both the extensor carpi ulnaris and the flexor carpi ulnaris are weak. The result is that the wrist moves radially when resisted flexion is tested. Resisted extension and adduction of the thumb are also weak.
•
vitis).
•
Disorders of the contractile structures are summarized in Box 34.2.
Box 34.2 Summary of disorders of the contractile structures
.-
Pain Exte nsion Extensor carpi rad i a l i s l o n g us/brevis Extensor ca rpi u l na ris Extensor i n d icis proprius Extensor d i g itorum Flexion Flexor carpi rad i a l is F l exor carpi u l naris F l exor d i g itorum profu ndus
Weakness Extension - bi latera l Lead poiso n i n g B ronchus carcinoma Other n e u ro l ogical co nditions Exte nsion - u n i latera l Nerve root: (6-(8 Rad i a l nerve Flexion
Figure 34.27
N e rve root: C7, (8 Other n e u rolog ica l cond itions
Friction to the fiexor digitorum profundus.
REFERENCES 1.
Calandra
H,
Goldner RD, Hardaker WT. Scaphoid fractures:
assessment and treatment. Orthopedics 1992;15(8):931-937. 2.
Larsen CF, Bmndum fractures
in
V,
Odense,
Denmark.
Acta
Orthop
Scand
Borgeskov S, Christiansen B, Kjcer AM et al. Fractures of the carpal bones. Acta Orthop Scand 1966;37:276.
4.
distal pole of the carpal scaphoid following fracture - a rare 5.
Leslie
jJ,
Dickson RA. The fractured carpal scaphoid. J Bone
Joilll SlIrg 1 98 1 ;63(B):225.
J.
Fractures of the carpal bones. I n :
Livingstone, New York, 1993:799-860. 7.
A m adio Pc.
Scaphoid fractures. Orthop Ciill North A 1'1
1992;23(1):7-17. 8.
Gasser H . Delayed union and pseudoarthrosis of the carpal navicular: treatment by compression screw osteosynthesis.
Sherman SB, Greenspan A, Normal A . Osteonecrosis of the complication. Skeletal Radial 1983; 9 : 1 89.
Amadio pc, Taleisnik
Green D P (ed ) Operative Hand Surgery, v o l 1 . Churchill
Skov O. Epidemiology of scaphoid
1992;63(2):216-218. 3.
6.
J Bone Joint Surg 1 985;47A:249. 9.
Green MH, Hadres AM, LaMont RL. Scaphoid fractures in
10.
Weber ER, Chao EYS. An experimental approach to the mech
children. J Hand Surg 1984;9A:536. anism of scaphoid waist fractures.
, Hal/d Surg 1978; 3 : 1 42-148.
CHAPTE R 34 - D I S O R D E R S OF T H E WRIST
11.
Mayfield JK. Mechanism of carpal injuries. Ciin Orthop Rei Res
36.
;[ 980;149:45-54. 12.
tures. I Bone loint Surg 1993;75B(1):61-65.
Johnson RP, Mayfield JK, Kilcoyne RF. Scaphoid fractures and
fracture-dislocations - pathomechanics and perilunar instabil
37.
1 6. 17.
38.
Ta leisnik J,
Wrist and its Disorders, 2nd edn. Saunders, Philadelphia, 1997:1 89-233. 39.
Rodman Gp, Schumacher R (eds) Pril11er all the Rheulllatic
40.
Cimmino MA, Bountis C, Silvestri E, Garlaschi G, Accardo S.
Diseases, 8th edn. Arthritis Foundation, Atlanta, 1983.
Kelly PJ. The extraosseous and intraosseous
blood supply of the scaphoid bone. I Bone loint Surg 1 966; 48A: 1 1 25.
An appraisal of magnetic resonance imaging of the wrist in
Gelberman RH, Menon J. The vascularity of the scaphoid bone.
rhe u m a toid arthritis.
I Hand Surg 1980;5A:508-513.
1 80-195.
Barber H . The intraosseous arterial anatomy of the adult
41.
human carpus. Orthopedics 1972;5:1-19. 1 8. 19.
Szabo RM, Manske D. Displ aced fractures of the scaphoid. Ciin
42.
Herbert TJ. Scaphoid fractures and carpal instability. Proc Roy Dabezies EJ, Mathews R, Faust DC. Injuries to the carpus: frac
tuberosity. I
23.
44.
Buul
MMC,
van
Beek
EJR,
Broekhuizen A H .
Nielsen PT, Hedeboe J, Thommasen P. Bone scintigraphy in the
Tiel-van
The
SLAC
wrist:
sca pholunate
Clayton ML, Ferlic DC. Arthrodesis of the arthritic wrist. Ciill
Folgezustande: Entartungsformen und Kompressionsfrakturen. 48.
Buul
MMC,
Beckenbaugh RD, Shives TC, Dobyns JH, Linscheid RL. Kienbock's disease: the natural history of Kienbock's disease and consideration of lunate fractures. Ciill Orthop Rei Res
49.
Roolker
W,
Verbeeten
P,
A keson WHo The vas
1980;5A:272-278. 50.
J r,
Fu FH, Imbriglia JF. An anatomical Shldy of the lunate bone in
5;1.
Almquist EE. Kienbock' disease. Hand Ciin 1987;3:141-148.
52.
Mikkelsen SS, Gelineck J. Poor function after nonoperative
53.
Joji S , Mizuseki S , Katayama K , Tsuge S , Ikuta Y. Aetiology o f
scintigraphy in suspected scaphoid fracture. Eur I Nucl Med Bretlau T, Christensen OM, Edstrom
j,
Kienbock's disease. Orthopedics 1985;8:483-487. BWB
Broekhuizen AH. Magnetic resonance imaging versus bone 1996;23(8):971-975.
Gelberman RH, Bauman TD, Menon
cularity of the lunate bone and Kienbock's disease. I Halld Surg
tures of the scaphoid. I Hand Surg 1984;9B : 1 89-190.
treatment of Kienbock's disease. Acta Orthop Scand 1987;58:24 1 .
Thomsen HS, Lausten
Kienbock's disease based on a study of the condition among
GS. Diagnosis of scaphoid fracture and dedicated extremity MRl. Acta Orthop Scand 1999;70(5):504-508.
patients with cerebral palsy. I Hand Surg 1993;18B(3) :294-298. 54.
Breitenseher MJ, Metz VM, Gilula LA et aL. Radiographically
occult scaphoid fractures: value of M R imaging i n detection.
Weber ER, Chao EY. A n experimental approach to the mecha Bongers KJ, Ponsen RJG. Operative and nonoperative manage
Gelberman RH, Salamon PB, Jurist JM, Posch JL. Ulnar vari ance in Kienbock's disease.
55.
Radiology 1997;203(1) :245-250. Fisk GR. The wrist. I Bone loint Surg 1984;66B:396. nism of scaphoid wrist fractures. I Hand Surg 1978;3A:142.
f Bone Joint Surg 1975;57A:674-676.
Lanzer W, Szabo R, Gelberman R. Avascu lar necrosis of the lunate and sickle cell anemia. Ciin Orthop Rei Res 1984;187: 168-171 .
56.
Tsuge S, Nakamura R. Anatomical risk factors for Kienbock's
57.
Alexander CE, Alexander AH, Lichtman DM. Kienbock's
disease.
f Hand Surg
1993;18B(1) :70-75.
ment of fractures of the carpal scaphoid: five years' experience.
disease and idiopathic necrosis of carpal bones. In: Lichtman
Neth J Surg 1980;32(4) :142.
DM, Alexander AH (eds) The Wrist and its Disorders, 2nd edn.
Cooney WP, Dobyns JH, Linscheid RL. Fractures of the scaphoid: a rational approach to management. Ciin Orthop Rei
Res 1980;149:90.
Saunders, Philadelphia, 1997:329-346. 58.
A lexander
AH,
Mack
GR,
Gunther SF.
Alexander AH, Lichtman DM. The Kienbock's dilemma - how to cope. In: Nakamura R, Linscheid RL, Miura T (eds) Wrist Disorders: Current Concepts and Challenges. Springer, Tokyo,
1982;75:860. Cooney WP, Dobyns JH, Linscheid RL. Fractures of the
Res 1986;202:79.
DM,
plasty. I Hand Surg 1982;7A :343-347. 59.
supported by dissection and clinical practice. I Roy Soc Med
scaphoid: a rational approach to management. Ciin Orthop Rei
Lichtman
Kienbock's disease - update on silicone replacement a rthro
King RJ, MacKenney RP, Elnur S. Suggested method for closed treahnent of fractures of the carpal scaphoid: hypothesis
35.
FL.
1980;149:98-106.
Stein F, Miale A, Stein A. Enhanced diagnosis of hand and
27.
34.
B a l let
Fortsch Rontgenstrahlen 1910;16:78-103.
Bull Hasp I Dis 1984;44:477-484.
33.
HK,
Kienbock R. Uber traumatische Malazie des Mondbeins und ihre
Tiel-van
Stordahl A, Schjoth A, Woxholt G et aL. Bone scanning of frac
32.
Watson
46.
26.
31 .
wrist
47.
wrist disorders by triple phase radionucleide bone imaging.
30.
L i m i ted
arterial anatomy of the human carpus, part 1 : the extraosseous
Scand 1983;54:303-306.
29.
TR.
vascularity. J Halld Surg 1983;8A:367.
Gelberman RH, Panagis JS, Taleisnik J, Baumgartner M. The
evaluation of fracture of the carpal scaphoid bone. Acta Orthop
28.
ML, Johnson
Orthop Rei Res 1984;187:89. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagllosis of Soft Tissue Lesions, 8th edn. Baill iere Tindall, London, 1 982. Peste: [Discussion] Bull Soc Anat Paris 1 843;1 8 : 1 69-170.
45.
radionuclide bone scintigraphy. Neth I Surg 1 990;42:50-52.
25.
Goodman
advanced collapse pattern of degenerative arthritis. I Halld
Diagnostic problems of scaphoid fractures: the value of 24.
HK,
J Halld Surg 1981;6A :223-233. 43.
Bone loint Surg
1993;75B(3) :423-425. 22.
Watson
Surg 1984;9A:358-365.
Mody BS, Belliappa PP, Dias JJ, Barton NJ. NOl1lmion of fract;'lres of the scaphoid
Watson HK, Hempton RF. Limited wrist arthrodesis. Part I:
arthrodesis. Part II: Intercarpal and radial carpal combinations.
Orthop Rei Res 1988;230:30.
tures of the scaphoid. Orthopedics 1982;5:1510. 21 .
Semin Arthritis Rheum 2000;30(3):
The triscaphoid joint. I Hand Surg 1980;5A:320-327.
.soc Med 1974;67:26. 20.
Markiewitz AD, Ruby LK, O'Brien ET. Carpal fractures and dislocations. In: Lichtman DM, Alexander A H (eds) The
its Disorders, 2nd edn. Saunders, Philadelphia, 1997:67-69. Donatelli R, Wooden MJ. Orthopaedic Physical Therapy. Churchill Livingstone, New York, 1989:226.
15.
Herbert TJ. Use of the Herbert bone screw in surgery of the wrist. Ciin Orthop Rei Res 1986;202:79.
Mayfield JK. Pathogenesis and pathokinetics of wrist ligament instability. In: Lichtman DM, Alexander AH (eds) The Wrist and
14.
Tiel-van Buul MMC, van Beek EJR, Broekhuizen AH et al. Radiography and scintigraphy of suspected scaphoid frac
ity. Unpublished study, 1974. 13.
51 7
60.
1 992:79-87.
Lind J, Hansen LB. Lunahlm malaci. Nord-Med 1 991;106(10): 258-260.
51 8 SECTI O N S I X - TH E WRI ST, T H U M B AND H A N D
6 1 . McCue FC, Mayer Y. Rehabilitation of common athletic
87. Gilford W, Bolton R, Lambrinudi C. The mechanism of the wrist joint. Guy's Hasp Rep 1 943;92:52-59.
injuries of the hand and wrist. Clin Sports Med 1989;8(4):73 1 . 62. Lichtman DM, Mack G R , MacDonald RI et a/. Kienbock's disease: the role of sil icone replacement arthroplasty. J BOl1e
88. Ruch DS, Bowling J. Arthroscopic assessment of carpal insta bility. Arthroscopy 1998;14(7):675-681 . 89. Mayfield JK. Pathogenesis and pathokinetics o f wrist ligament
Joint SlIrg 1 977;59A:899-908. 63. Stahl F. On lunatomalacia (Kienbock's d isease), a clinical and
instability. In: Lichtman DM, Alexander AH (eds) The Wrist and
roentgenological study, especially on its pathogenesis and
its Disorders, 2nd edn. Saunders, Philadelphia, 1997:55-72.
the late resu lts of immobilization treatment. Acta ChiI' Scnlld
90. Larsen CF, Amadio Pc, Gilula LA, Hodge Jc. Analysis of carpal instability. 1. Description of the scheme. j Hand Surg
1 947;(suppl)126:1-133. 64. Sundberg SB, Linscheid RL. Kienbock's disease: results of treatment
with
ulnar
lengthening.
Clin Orthop Rei Res
1995;20A:757-764. 9 1 . Angermmm
P,
Lohmann M. Inju ries to the hand and wrist. A
study of 50,272 injuries.
1984;187:43-51 . 65. Jackson MD, Barry DT, Geiringer SR. Magnetic resonance
/ Hand Surg 1993;18B:642-644.
92. Saffar P. Classification of carpal instabilities. I n : Bi.ichler U (ed)
imaging of avascu lar necrosis of the lunate. A rch Phys Med
Wrist Instability. Federation of European Societies for Surgery
Rehabi/ 1 990;71(7):510.
of the Hand, Martin Dunitz, London, 1996:29-33.
66. Guo J . Vascu lar bundle implantation into bone for aseptic necrosis of the lunate. Al1n Plast Surg 1996;36(2) : 1 33-138.
/ Hal1d SlIrg
The
ligaments
of
the
wrist.
j Halld Surg
94. Taleisnik J . Post-tra umatic carpal instabili ty. Clill Orthop Rei Res 1980;149:73-82. 95. Navarro A. Luxaciones del carpo. All Fac Med (Mon tevideo)
1 982;7:348. 68. Arm istead RB, Linscheid RL, Dobyns JH, Beckenbaugh RD. Ulnar lengthening in the treatment in Kienbock's disease.
/ Hand Slirg 1985;10A:1008. WD.
Prox i m a l
1988;70A(6):944-949. 99. Amadio Pc. Epidemiology of hand and wrist injuries in
tomy. Orthop Trans 1978;2:216(abstract). Engber
SlIrg 1980;5 :226-24 1 . 9 8 . Amadio P c . Pain dysfunction syndromes. j Balle joint Surg
71 . Briggs BT, Cooney Wp, Linscheid RL. Proximal row carpec BW,
97. Mayfield JK, Johnson RP, Kilcoyne RF. Carpal dislocations: pathomechanics and progressive perilunar instabil ity. j Hand
J Bone joillt Surg 1961 ;43B:245. 70. Bianco RH. Excision of the lunate in Kienbock's disease: long term resu l ts.
1921 ;6:113. 96. Taleisnik J. Carpal instability. In: Tubiana R (ed) TI,e Hand. Saunders, Philadelphia. 1985:986-1000.
j Bone joillt Surg 1982;64A:170. 69. Gil lespie HS. Excision of the l unate bone in Kienbock's disease.
72. Begley
J.
1976;1 : 1 1 0-1 18.
67. Almquist EE, Burns JF. Radial shortening for the treatment of Kienbock's disease: a five to ten year follow-up.
93. Ta leisnik
row
carpectomy
in
advanced Kienbock's disease. / Hand Slirg 1 994;19A: 1 0 1 6-1 018.
73. Rahme H. I diopathic avascular necrosis of the capitate bone case report. Hand 1983;15(3):274-275.
sports. Hand Clin 1990;6(3):379-381 . 1 00. Linscheid RL, Dobyns JH, Beabout JW, Bryan RS. Traumatic instability of the wrist: d iagnosis, classification and patho mechanics. ] Bone Joint Surg 1 972;54A:1612-1632.
74. Murakami 5, Nakajima H. Aseptic necrosis of the capitate bone
1 0 1 . Linscheid RL, Dobyns JH, Beckenbaugh RD, Cooney Wp, Wood MB.
in two gymnasts. AI1I j Sports Med 1984;12(2):1 70-1 73. 75. Jones WA . Beware the sprained wrist: the incidence and d iag nosis of scapholunate instability. / Bone Joint SUl'g 1988;70B:293.
76. Schultz RJ, Kearns RJ. Tumors i n the hand. j Halld Surg
Instability patterns of the wrist. I Halld Surg
1983;8A:682-686. 102. Cooney WP, Dobyns JH, Linscheid RL. Arthroscopy of the wrist:
anatomy
and
classification
of
carpal
instabil ity.
Arthroscopy 1990;6:1 33-140.
1 983;8:803-806. 77. Angelides AC, Wal lace PF. The dorsal ganglion of the wrist: its
103. Lichtman D M . Introduction to the carpal instabilities. In:
pathogenesis, gross and m kroscopic anatomy, and surgical
Lichtman DM, Alexander AH (eds) The Wrist and its Disorders,
treahnent. ] Hand Surg 1976;1:228.
2nd edn. Saunders, Philadelphia, 1997:187.
78. Bogu m i l l
G P.
Tu mors of the
wrist.
In:
Lichtman
DM,
Alexander AH (eds) The Wrist and its Disorders, 2nd edn. 79. Linscheid RL, Dobyns J H . Athletic injuries o f the wrist. Clin Gabel
GT.
Gymn ast's
wrist.
Hand
Clin
8 1 . Snook G. Injuries in women's gymnastics. A five year study. 82. Roy 5, Carne D, Singer K. Stress changes of the distal radial young
gymnasts.
1 987:3 : 1 03-1 1 1 . 1 0 7 . Watson HK, Ashmead D , Makhoulf MY. Examination o f the
Alii j Sports Med 1979;7(4):242. in
1996:35-44. 1 06. Watson HK, Black DM. Instability of the wrist. Hand Clill
1990;6:493-505.
epiphysis
Buchler U (ed ) Wrist Illstability. Federation of E u ropean Societies for Surgery of the Hand, Martin Dunitz, London,
Orthop Rei Res 1 985;198:1 41-15 1 . J H,
loint Surg 1988;70A:1 262-1268. 1 05. Dumontier C. The clinical diagnosis of wrist instability. In:
Saunders, Philadelphia, 1997:563-581 .
80. Dobyns
1 04. Taleisnik J . Current concepts review. Carpal instabil ity. j Bone
A liI J Sports Med 1 985;
13:301-308. 83. Le TB, Hentz VR. Hand and wrist injuries in young athletes.
Hand Clin 2000;16(4):597-607. 84. Read MT. Stress fractures of the distal radius in adolescent gymnasts. Br j Sports Med 1981;15:272-276.
scaphoid. ] Hand Surg 1988;13A:657-660. 1 08. Lane
LB.
The
scaphoid
shift
test.
I
Hand
Slirg
1993;18A:366-368. 1 09. Ambrose L, Posner MA. Lunate-triquetral and midcarpal joint instabili ty. Hand Clin 1992;8:653-668. 1 1 0. Linscheid RL, Dobyns J H . Physical examination of the wrist.
85. Hanks G, Kalenak A, Bowman L et al. Stress fracture of the
In: Post M (ed) Physical Examination of the Musculoskeletal System. Year-Book, Chicago, 1987:80-94.
carpal scaphoid: a report of four cases. j Bone Joint Surg
1 1 1 . Lichtman DM, Schneider JR, Swafford AR, Mack GR. Ulnar
1989 ;71A:938-941 .
86. Ekenstam FA. Wrist stability / wrist instabili ty. I n : Buchler U (ed) Wrist Instability. Federation of European Societies for Surgery of the Hand, Martin Dunitz, London, 1996:25.
midcarpal instability - clinical and laboratory analysis. J Hand
Surg 1 98 1;6A:515-523. 112. Johnson RP, Carrera GF. Chronic capitolunate instability. I Balle
Joint Surg 1986;68A: 1 1 64-1176.
CHAPT E R 34 - D I S O R D E R S O F T H E W R I ST
113. Truong NP, Mann FA, Gilula LA, Kang Sw. Wrist instability series: increased yield with clinical-radiologic screening criteria. Radiology 1 994;192:481-484. 11 4. Schernberg F. Le Poigl1et - Anatomie Radiologique et Chirurgie. Masson, Paris, 1992.
T, Itoman M .
1 2 1 . Linden MA, Manton WI, Stewart M, Thai ER, Feit H. Lead poisoning from retained bul lets. Anll Surg 1982;195:305. 122. Bishop AT, Gabel GT, Carmichael Sw. Flexor carpi radialis tendonitis.
Part I: Operative anatomy. ] BOlle Joil1t Surg
1994;76A: 1 009-1013.
115. Grundberg AB, Reagan DS. Pathologic anato m y of the forearm: Intersection syndrome. J Hand Surg 1 985;10A(2):299. 1 1 6. Futami
51 9
Extensor carpi u l naris syndrome.
Findings in 43 patients. Acta Orthop Scand 1 995;66(6):538-539. 117. Wood MD, Dobyns JH. Sports related extraarticular wrist syndrome. Clin Orthop Rei Res 1986;202:93-102.
118. Crimmins CA, Jones NF. Stenosing tenosynovitis of the exten sor carpi ulnaris. Ann Plast Surg 1995;35(1):105-107. 119. Bowers WH, Zelouf DS. Treatment of chronic disorders of the distal radioulnar joint. In: Lichtman DM, Alexander AH (eds)
The Wrist and its Disorders, 2nd edn. Saunders, Philadelphia, 1 997:440. 120. Inoue G, Tamura Y. Recurrent dislocation of the extensor carpi ulnaris tendon. Br J Sports Med 1998;32(2) : 1 72-174.
1 2 3 . Gazarian A , Foucher G. La tendinite du grand palmaire: 11 propos de vingt-quatre cas. Arm ChiI' Main Melllb Super
1992;11(1):14. 124. Gabel G, Bishop AT, Wood MB. Flexor carpi radialis tendinitis.
J Bone Joint Surg 1994;76A : 1 0 1 5-1 018. 125. K u l u n d D N . The Injured A thlete, 2 n d edn. Lippincott, Philadelphia, 1988:30. 126. Helal B. Racquet players pisiform. Hand 1978;10:87-91 . 127. Buterbaugh GA, Brown TR, Horn Pc. Ulnar-sided wrist pain in athletes. Clin Sports Med 1 998;17(3):567-583. 128. Palmieri TJ. Pisiform area pain treatment by pisiform excision.
J Hand Surg 1982;7:477-480. 129. Carroll RE, Coyle MP. Dysfunction of the pisotriquetral joint: treatment by excision of the pisiform. J Hand Surg ] 985; 10A:703-707.
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
Disorders of the inert structures
Disorders of the thumb
521
Rheumatoid arthritis 521 Traumatic arthritis 521 Arthrosis 522
Disorders of the contractile structures Pain 524 Weakness
524
528
Disorders affecting the base of the thumb may cause pain over the radial aspect of the wrist. This is why the trapezium-first metacarpal joint and its neighbouring tendinous structures are tested in examination of the wrist.
• ,,"-
'<-1:r�..--; '-"-"�""
DISORDERS OF THE INERT STRUCTURES
The only relevant passive test for the first carpometa carpal joint is backward movement during extension. Pain and I or limitation indicate a capsular lesion. In the majority of cases, it is the anterior aspect of the capsule that is affected and the joint is found to be tender anteriorly. The three following conditions are quite common.
RHEUMATOID ARTHRITIS
Both first carpometacarpal joints are frequently affected in rheumatoid arthritis and respond well to intra articular triamcinolone. Surgery is seldom necessary and, if so, resection anthroplasty is preferred.7
TRAUMATIC ARTHRITIS
The patient describes an injury to the thumb (usually overstretching) or some overuse, possibly occupational, after which the thenar area and the radial side of the wrist are painful, especially on movement. On examination, pain is elicited during the passive move ment and limitation can also be found. The radiograph is negative.7 Spontaneous recovery may take many months. The condition can be treated either by intra-articular triamcinolone or by 2 weeks' treatment with deep trans verse friction on alternate days. The friction is directed to the anterior and anterolateral capsuloligamentous structures. Techniques.
See arthrosis below. 521
522 SECTION SIX - THE WRIST, THUMB AND HAND
ARTHROSIS
This condition is very common and occurs most fre quently in middle-aged or postmenopausal womenl,2 and may affect 30% of women over 50.3,4 The condition is often bilateral, sometimes in association with arthrosis at the distal interphalangeal joints of the fingers. The patient complains of pain in the thenar area, which has come on spontaneously and is felt on certain move ments. As the disease progresses, the pain may become constant. Swelling may be seen because of subluxation of the base of the metacarpal bone and also synovitis. Later, instability, weakness of grip and pinch, and Z- and adduction deformity of the thumb may develop.s The deformities are commonly asymptomatic as well. On examination, slight limitation of movement and crepitus may be felt, especially when the joint is axially compressed and then circumducted - the 'grind' test.6 The radiograph shows clear signs of sclerosis of the bone and also osteophytes. The picture, however, is not always compatible with the clinical signs.7 Later in pro gression deformity and subluxation of the joint may be seen.
ment reconstruction, tendon interposition procedures,ll-14 arthrodesis,lS-17 resection arthroplasty without prosthesis or with implantl8-26 or total trapeziometacarpal implant arthroplasty.27-3o intra-articular injection, The patient lies supine on a high couch. The physician takes the out stretched hand on the knee, the thumb uppermost. With one hand the joint is palpated in the anatomical snuff box. Caution is necessary not to mistake the edge between the metacarpal bone and an osteophyte for the joint line. With the other hand, slight traction (arrow in
Technique:
TREATMENT
The treatment that is chosen depends on the stage of the arthrosis and the functional disability of the joint (see Table 35.1). In early arthrosis, deep transverse friction to the anterior and lateral aspect of the capsule can cause the pain to cease but does not influence mobility. Later in the course of the condition, intra-articular tri amcinolone can be tried. It usually has only a temporary result, except when a traumatic arthritis has supervened, in which the long-term results of triamcinolone are very effective. In a recent randomized, prospective, placebo controlled double-blind study Reeves and Hassanein have found that dextrose prolotherapy was clinically effective and safe in the treatment of pain which occurs with joint movement and limitation of range in osteoarthritis of the thumb and finger joints.s In severe cases, and after all conservative means have failed, surgery should be considered,9,1Q including ligaTable 35,1 Summary of treatment of capsular disorders Deep friction
Intra-articular injection
Surgery
Rheumatoid arthritis Traumatic arthritis Moderate arthrosis
Rheumatoid arthritis
Traumatic arthritis Early arthrosis
Severe arthrosis
Figure 35.1
Intra·articular injection.
CHAPTER 35 - DISORDERS OF THE THUMB 523
Fig. 35.1) and ulnar deviation is performed to open the joint: If the patient relaxes well the joint line can be identified by a small gap, which is marked by the use of the nail of the palpating thumb. A 1 ml syringe, filled with 10 mg triamcinolone ace torude, is fitted with a thin needle, 2 cm long. Traction is applied again. The needle, inserted at the marked line, is directed at an angle of 60° to the horizontal. At about 1 cm, the tip of the needle is felt to enter the joint capsule. If it strikes bone at less than 1 cm, it is not intra-articular and should be adjusted until it is felt to enter the joint. The injection is then given. The injection is stopped when considerable resistance is encountered, which may happen after 0.5 ml has entered the joint. The patient should be warned of after pain which may last for up to 24 hours. Exertion should be avoided for a few days, and review made after 2 weeks. One to two injections should suffice.
position, so as to stretch the anterior capsule. Pain should be avoided. The joint line between the trapezium and the first metacarpal is identified. It should not be confused with the joint line between the scaphOid and the trapezium, which lies just a centimetre more proximal. With the thumb of the other hand, the friction is per formed parallel to the joint line. Counterpressure is taken by the fingertips on the proximal interphalangeal joints of the supporting hand (Fig. 35.2a). Technique: deep transverse friction to the anterolateral
The patient sits with the supinated arm resting on the couch, the hand hanging over its edge. The thera pist extends the patient's wrist and brings the dorsum of the ipsilateral hand in contact with the dorsum of the patient's hand; with the thumb the patient's thumb is directed into extension and a slightly backwards
capsule. The patient's forearm is brought into neutral position. With the contralateral hand the therapist brings the patient's wrist into ulnar deviation and the thumb into flexion, which stretches the capsule. Friction is imparted at the joint line and parallel to it with the thumb of the other hand. Counterpressure is given with the fingers on the ulnar aspect of the patient's hand (Fig. 35.2b). It is necessary to make sure that the thumb remains palmar to the extensor pollicis brevis tendon, in that the lesion lies at the anterolateral aspect of the joint. Friction is given two to three times a week for about 2-3 weeks. The results are good in traumatic arthritis and early arthrosis.
(a)
(b)
Technique:
deep
transverse friction
to the anterior
capsule.
Figure 35.2 Friction to the anterior (a) and anterolateral capsule (b).
524 SECTION SIX - THE WRIST, THUMB AND HAND
DISORDERS OF THE CONTRACTILE STRUCTURES PAIN RESISTED EXTENSION
This movement seldom causes pain in isolation. Because the extensor brevis and abductor longus tendons lie together in one tendon sheath, in the majority of the cases resisted abduction is also painful. Abductor pollicis longus, and extensor pollicis longus and brevis (first and third tendon sheaths)
Tenosynovitis of these tendons, also known as 'intersec tion syndrome',3" 32 occurs at the point where they curve arOlmd the shaft of the radius just above the wrist and causes pain at the dorsal and radial aspect of the lower forearm. The lesion may also lie somewhat more proxi mally in the muscle bellies - 'myosynovitis'. This condi tion has only one other parallel in the body - myosynovitis with crepitus of the tibialis anterior muscle belly. It always results from occupational overuse or after unusual efforts and can be quite disabling. It is most common in weight lifters and rowers.33 The patient mentions crepitus during wrist move ments. On examination, resisted extension and resisted abduction of the thumb are painful and some passive wrist movements can also be painful. Not only do those movements that stretch the tendons (e.g. flexion of the thumb and ulnar deviation of the wrist) increase the discomfort, but every movement of the tendon in the tendon sheath (e. g. thumb extension, radial deviation and flexion or extension of the wrist) may also be painful. On palpation, tenderness and swelling are found over an area of 3-4 cm exactly where the tendons cross the radius. In cases with a recent onset, a silky crepitus during active wrist movements is very common. The differential diagnosis is made from suppurative inflammation of the tendon sheaths; de Quervain's tenosynovitis (see below); early chronic evolutive poly arthritis; arthrosis of the trapezium-first metacarpal joint of the thumb; lesions of the radial collateral liga ment; and tenosynovitis of the extensor carpi radialis longus and I or brevis. After an initial stage with much pain and disability, the condition may evolve towards a more chronic state. Spontaneous cure may take many months and only occurs when the patient gives the wrist complete rest. Treatment with immobilization, infiltration of steroid or local anaesthetic and even surgery often do not lead to
full and permanent recovery. Deep transverse friction (three times a week, over 2 weeks) is successful. All other treatments must be considered obsolete, a view confirmed by Paton in 1 978,34 who has used deep trans verse friction since 1 947 without failure. One of the present authors treated 62 cases - 48 men and 1 4 women - in private practice in the period between 1975 and 1982. The onset was recent (less than 6 weeks) in 55 cases and chronic in 7 (2.6 months on average). Forty-eight of the patients received other treatments, with poor results: steroid infiltration in 16 cases; local anaesthetic infiltration in 4; plaster immobilization in 1 3 (average 1.8 weeks); partial immobilization with tape in 2; ice friction in 4; physiotherapy in 9. Deep trans verse friction - performed three times a week for 15 minutes - led to complete recovery in all but one case, with an average of 6.7 treatments, and 39 patients improved from the first treatment onwards.35 Technique: deep transverse friction. The patient's forearm rests in pronation on the couch, the hand over its edge. With the contralateral hand the therapist brings the patient's wrist and thumb into flexion (Fig. 35.3). This stretches the tendons. The other hand takes hold of the patient's wrist; the thumb then lies flat on the site of the lesion. Movement starts with the thumb at the ulnar side of the tendons. By supination of the arm, the thumb passes over the tendons to the radial aspect. Repeated movement results in a to-and-fro movement.
Abductor pollicis longus and extensor pollicis brevis (first tendon sheath)
This is a lesion of the common tendon sheath of the abductor pollicis longus and extensor pollicis brevis tendons at the wrist. Two conditions can be distin guished - mechanical and rheumatoid - that require the same treatment. Mechanical tenovaginitis. This was first described by Felix de Quervain in 189536,37 and has since been known as de Quervain's disease, tenovaginitis stenosans and styloiditis radii.38 Its incidence has risen considerably in the last decades.39 It occurs mostly in women, with an average age of 47, and almost never before the age of 30.40 A significant association was noted in patients with de Quervain's disease after pregnancy.41 Very often it comes on spontaneously, but it can also result from overuse. Swift repeated movement with exer tion of considerable strength is a possible cause.42 A study by Kauer43 offers a likely explanation for the disorder's frequent occurrence. In an electromyographic study in normal subjects, he noted that the extensor pollicis breVis, abductor pollicis longus and extensor carpi ulnaris muscles isometrically contracted throughout pronated
CHAPTER 35
-
DISORDERS OF THE THUMB 525
mucopolysaccharide, indicating myxoid degeneration, were apparent. They consider these changes as patho gnomonic of the condition. They conclude that de Quervain's disease is a result of intrinsic, degenerative mechanisms rather than extrinsic, inflammatory ones. Recent anatomical45 and ultrasonographic46 studies confirm the observations during surgery47 that the first extensor compartment may contain a septum separating the extensor pollicis brevis tendon from the abductor pol licis longus. During a study of variants of the tendon of the abductor pollicis longus in 110 upper extremities, Melling et al found supernumerary tendons in 80% and also an intertendinous septum in 30%.48 These findings do not interact with the clinical picture but may have consequences for treatment. Pain is felt diffusely at the radial side of the wrist and may radiate down to the thumb and up the lower forearm; the patient finds the symptoms very disabling and they prevent the hand from being used properly. Triggering may complicate the more severe forms49 and demonstrates a more recalcitrant course when treated non-operatively.50 On examination, resisted extension and abduction of the thumb are painful. Passive movements of wrist and thumb also cause pain as they slide the tendon up and down within its irritated sheath, so setting up painful friction. Very occasionally, resisted radial deviation of the wrist also hurts because the thumb tendons assist this movement. Finkelstein's test51 is positive when there is intensified pain on forced ulnar deviation of the wrist while the thumb is opposed to the little finger. Some con sider this pathognomonic.52 Palpation must be performed over a wide area as there are three possible localizations for the lesion:53 at the level of the carpus; at the tenoperiosteal insertion of the abduc tor pollicis longus into the base of the first metacarpal bone; and at the groove on the lower extremity of the radius (Fig. 35.4).
Figure 35.3 Friction to the abductor pollicis longus, and extensor pollicis longus and brevis (a); detail of hand fixation (b).
and supinated dorsiflexion and palmar flexion. The con clusion was that these tendons might serve as dynamic collateral ligaments, supplying further strength to the medial and lateral aspects of the wrist. Their continuous tension may in the end result in overuse, leading to inflammation. Clarke et al compared the histopathological appear ances of the tendon sheath and synovium of 23 patients with 24 controls.44 They did not find inflammation but thickening of the tendon sheath and accumulation of
Figure 35.4 Abductor pollicis longus (the lower of the two tendons) and extensor pollicis brevis (upper tendon).
526 SECTION SIX - THE WRIST, THUMB AND HAND
It should be emphasized that one should not be misled by the localization of tenderness. Very often the styloid process of the radius is more tender than the tendon itself, which has led to the lesion being described as styloiditis radii. This is a misnomer, since it gives the impression that the lesion is bony and lies at the styloid process. That this is not so can be shown during clinical examination and the progress of treat ment: pain increases when resisted movements of the thumb are tested and disappears as the result of treat ment directed to the tendons. Styloiditis radii does not exist and is another example of the phenomenon, named by Cyriax, 'associated tenderness'. Because the lesion is a tenovaginitis, crepitus is always absent and localized swelling can also be palpated. Spontaneous recovery may take 3-4 years. However, treatment is quite simple. This lesion responds remark ably well to one, and only occasionally two, injections with triamcinolone suspension,55 provided the injection is correctly placed between tendon and tendon sheath. Leslie et al found that most wrists for which injection fails have a separate extensor pollicis brevis compart ment at surgical release. They recommend a second, more dorsal injection in patients whose first failed.56 In a controlled, prospective, double-blind study by Zingas et al the accuracy of infiltration in the first extensor com partment was defined and correlated with clinical relief of the disorder. They concluded that only those patients in whom the steroid solution really entered the tendon's sheath were cured. They also found that it was difficult to infiltrate the extensor pollicis brevis subcompart ment. They believed that failure to infiltrate the extensor pollicis brevis compartment could be a reason for unsuccessful therapy.57 Consequently, other treatments, such as deep trans verse friction, immobilization or surgery are obsolete. Decompressive surgery is used in those rare cases that do not respond to conservative treatment. 58 Yuasa and Kiyoshige suggest for those patients who have a septum in the first extensor compartment, decompressing only the extensor pollicis brevis subcompartment. In a series of 16 patients they achieved 100% complete relief.5 9 Rheumatoid tenovaginitis. Here there is a striking dis crepancy between the symptoms and signs. Contrary to a mechanical disorder, which shows little swelling and gross disability, rheumatoid presents with marked thickening of the tendon sheath but not a great deal of pain. The condition responds well to one or two injections with triamcinolone suspension. There is no tendency to recurrence.
The patient lies supine on a high couch, the forearm halfway between pronation and
Technique: infiltration.
supination and supported on the operator's thigh. The wrist is held in ulnar deviation and the thumb slightly flexed. The tendons are easily identified when the patient is asked to actively extend and abduct the thumb. The border between the two tendons is identified and marked. The common sheath containing the extensor pollicis brevis and the abductor pollicis longus tendons is pinched between thumb and index finger. A 1 ml syringe is filled with 5 mg triamcinolone ace tonide and fitted with the thinnest possible needle. A point is chosen just proximal to the base of the first metacarpal bone and the needle is thrust in almost hori zontally between the two tendons so that the tip comes to lie in the common tendon sheath. When the fluid is forced in, the palpating fingers feel a small sausage shaped swelling along the course of the tendons (Fig. 35.5); 0.5 ml of fluid can be injected before counter pressure is experienced on the barrel of the syringe. Because of the risk of lipodystrophy from subcuta neous injection, care must be taken that fluid does not flow back into the subcutaneous tissue when the needle is withdrawn. Extensor pollicis longus
Pain on resisted extension of the thumb is rare and is the consequence of a lesion of the tendon of the extensor pol licis at its carpal extent. Overuse ('drummer boy palsy'), forced wrist extension, direct trauma or distal fractures of the radius may all precipitate an extensor pollicis longus tendinitis.6o Pain is felt over the dorsal aspect of the wrist and can be reproduced by testing resisted extension of the thumb. Treatment consists of deep transverse friction and the condition takes about 2 weeks to cure. RESISTED FLEXION Flexor pollicis longus
Tenosynovitis of the flexor pollicis longus may present at two different sites which can be differentiated by palpa tion: at the level of the first metacarpal (Fig. 35.6), where it responds well to an infiltration of triamcinolone but not to deep transverse friction; and at the level of the carpus, where crepitus may be present. Deep transverse friction is then effective. The patient sits with the hand resting on the couch. By asking the patient to flex the thumb against resistance, the tendon can be palpated and the lesion thus precisely located. The tender spot along the first metacarpal shaft is identified. A syringe filled with 10 mg of triamcinolone suspension fitted with'the thinnest possible 2 cm needle is used. The needle is inserted at the level of the tenderness and infiltrates by Technique: infiltration.
CHAPTER 35 - DISORDERS OF THE THUMB 527
Figure 35.6 The fiexor pollicis longus: 1, level of the first metacarpal; 2, level of the carpus.
the tender spot is identified, which is deep in between the tendons of the flexor carpi radialis and the palmaris longus, level with the carpus. The tendon can be felt when the patient is asked to perform flexion and exten sion of the thumb. Counterpressure is given with the fingers at the dorsum of the patient's wrist (Fig. 35.8). Friction is started at the radial side of the tendon and ended at the ulnar side. The movement is performed by a pronation-supination movement of the forearm.
Figure 35.5 brevis.
Infiltration of the abductor pollicis longus and extensor pollicis
several withdrawals and reinsertions along the inflamed tendon (Fig. 35.7). The patient sits with the hand on the couch. The therapist sits in front of the patient's hand. With the contralateral hand the wrist and thumb are brought into extension. With the thumb of the other hand
Technique: friction.
Figure 35.7
Infiltration of the fiexor pollicis longus.
528 SECTION SIX - THE WRIST, THUMB AND HAND
The tender node can be palpated, just proximal to the head of the first metacarpal bone and is felt to move when the thumb is flexed and extended. Spontaneous cure may occur but takes several months.61 One infiltration with triamcinolone is usually curative. When the condition recurs, simple surgery to split the tendon sheath longitudinally will give lasting relief from symptoms.
Figure 35.8
Friction to the fiexor pollicis longus.
Technique: infiltration. The patient lies supine on the couch and the operator sits adjacent. The patient's hand is placed on the operator's thigh, palm upwards. A tuberculin syringe is filled with 1 ml of a 10 mg/ml tri amcinolone solution and attached to a thin needle, 2 cm long. With one finger the tender node, which lies just proximal to the metacarpophalangeal joint, is identified. The needle is inserted about 1 cm distally and directed toward the palpating finger (Fig. 35.9). Half of the solu tion is infiltrated around, the rest into the nodule. The patient should be warned that there may be con siderable after-pain. The result is evaluated after 2 weeks; a second infiltration is needed only rarely.
WEAKNESS Trigger thumb
A tendinous node frequently forms on the flexor pollicis longus and becomes engaged in the tendon sheath, so preventing voluntary movement in flexion-€xtension. The interphalangeal joint may become fixed in flexion, after which the patient has to passively extend the joint with the help of the other hand. A snap and pain may accompany this. This typical history suggests the diagno sis, because resisted movements of the thumb do not elicit pain.
Weakness of one or several muscles of the thumb may follow either rupture of a tendon or a nerve lesion. RUPTURE
A tendinous rupture is easily detected by clinical examination. Rupture of the extensor pollicis longus tendon occurs rarely after a fracture at the distal extremity of the radius
Figure 35.9 thumb.
Infiltration of the fiexor pollicis longus in trigger
CHAPTER 35 - DISORDERS OF THE THUMB 529
Table 35.2 Nerve lesions and weakness of the thumb Weakness
Muscle
Nerve
Extension
Extensor pollicis longus Extensor pollicis brevis
Radial Radial
Flexion
Flexor pollicis longus Flexor pollicis brevis
Anterior interosseous Ulnar/(median)
Abduction
Abductor pollicis longus Abductor pollicis brevis
Posterior interosseous Median
Adduction·
Adductor pollicis
Ulnar
Opposition
Opponens pollicis
Median
brevis which does not necessarily cause weakness of abduction of the thumb. In advanced cases, weakness of the muscles innervated by the median and ulnar . nerves may be detected. • Median nerve: long-standing compression of the median nerve in the carpal tunnel may lead to slight weakness and wasting of the thenar muscles. • Posterior interosseous nerve: a lesion of the posterior interosseous nerve at the elbow results in weakness of thumb abduction and finger extension (see p. 560). • Ulnar nerve: entrapment of the ulnar nerve in the hand gives rise to weakness of thumb adduction. Disorders of the thumb are summarized in Box 35.1.
(Colles' fracture); it usually happens some weeks later as the result of the tendon being frayed by bony callus.62, 63 It is also seen in patients with advanced rheumatoid arthritis. Surgical repair is the appropriate treatment and, in acute cases, should be done with some urgency to prevent a second rupture, which often follows.64,65
Box 35.1 Summary of disorders of the thumb Disorders of the joint capsule Rheumatoid arthritis Traumatic arthritis Arthrosis
Disorders of the contractile structures Pain
NERVE LESIONS
Nerve lesions causing weakness of the thumb may lie at different levels (Table 35.2). •
•
C8 nerve root: compression of the C8 nerve root, usually caused by a C7 disc protrusion, leads to weak ness of adduction and extension of the thumb. This is accompanied by weakened ulnar deviation of the wrist. Brnchial plexus: when the lower trunk of the brachial plexus becomes affected at the thoracic outlet, for example as the result of compression by a cervical rib, there may be marked wasting of the abductor pol1icis
Resisted extension • Abductor pollicis longus Extensor poliicis longus/brevis • Abductor pollicis longus Extensor poliicis brevis • Extensor poliicis longus Resisted flexion • Flexor pollicis longus • Trigger thumb Weakness Rupture Nerve lesions
REFERENCES 1. Burton RJ, Pellegrini YO Jr. Surgical management of basal
8. Reeves KO, Hassanein K. Randomized, prospective, placebo
joint arthritis of the thumb, Part II: ligament reconstruction with
controlled
tendon interposition arthroplasty. J Hand Surg 1986;l1A:
for
324-332.
trapeziometacarpal) joints: evidence of clinical efficacy. I Altern
2. Pellegrini VD Jr. Osteoarthritis at the base of the thumb. Orthop Ci ill NorthAm 1992;23(1):83-102. 3. Amadio PC Millender LH, Smith RJ. Silicone spacer or tendon spacer for trapezium resection arthroplasty. Comparison of the results. J Hal l d Surg1982;7A:237. 4. Thomson JS. Surgical treatment of trapezio-metacarpal arthro sis. Adv Orthop SlIrg1982;10:105. 5. Menon J. The problem of trapeziometacarpal degenerative arthritis. Ci in Orthop ReIRes1983;175:155. 6. Swanson AB. Disabling arthritis at the base of the thumb: treat ment by resection of the trapezium and flexible (silicone) implant arthroplasty. I Boneloil l t Surg1982;54A:456. 7. Gunther SF. Carpometarcarpal joint of the thumb. In: Lichtman OM, Alexander AH (eds) The Wrist and its Disorders, 2nd edn. Saunders, Philadelphia, 1997;443-458.
double-blind
osteoarthritic
study
thumb
of
and
dextrose
finger
prolotherapy
(DIP,
PIP,
and
Complementary Med2000;6(4):311-320. 9. Kuschner SH, Lane CS. Surgical treatment for osteoarthritis at the base of the thumb. AmJ Orthop1996;25(2):91-100. 10. Poole JV, Pellegrini YO Jr. Arthritis of the thumb basal jOint complex. I Hand Ther 2000;13(2):91-107. 11. Eaton RG, Lane LB, Littler JW, Keyser JJ. Ligament reconstruc tion for the painful thumb carpometarcarpal joint: a long-term assessment. I Hand Surg1984;9A:692.
12. Robinson 0, Aghasi M, Halperin H. Abductor pollicis longus tendon arthroplasty of trapezio-metacarpal joint: surgical tech nique and results. J Hand Surg1991;16A:504-509.
13. Sigfusson R, Lundborg G. Abductor pollicis longus tendon arthroplasty for treatment of arthrosis in the first car pometacarpal joint. Scand ] Plasf Recol1str Surg Hall d Surg
1991;25:73-77.
530 SECTION SIX - THE WRIST, THUMB AND HAND
14. Burton R. AmericanSociety forSurgery of theHandCorrespondence Newsletter, 1995:January. 15. Carroll RE, Hill NA. Arthrodesis of the carpometacarpal joint of the thumb. j Bonejoint Surg 1983;55B:292-294. 16. Stark HH, Moore JF, Ashworth CR, Boyes JH. Fusion of the fi.rst metacarpotrapezial joint for degenerative arthritis. J Bone Joint Surg 1977;59A:22-26. 17. Ishida 0, Ikuta Y. Trapeziometacarpal joint arthrodesis for the treatment of arthrosis. Scand J Plast Reconstr Surg Hand Surg 2000;34(3):245-248. 18. Jervis WHo A review of excision of the trapezium for osteoarthritis of the trapeziometacarpal joint after 25 years. I Bonejoint Surg1973;55B:56-57. PC, Brushart T M, Smith RJ. Treatment of 19. Dell trapeziometacarpal arthritis: results of resection arthroplasty.
] Hand Surg1978;3A:243. 20. Braun RM. Total joint replacement at the base of the thumb preliminary report. J Hand Surg 1982;7:245-251. 21. Wilson J, Bossley C. Osteotomy in the treatment of osteo arthritis of the first carpometacarpal joint. ] Bone Joint Surg 1983;65B:179-181. 22. Holmberg J, Lundborg G. Osteotomy of the first metacarpal for osteoarthrosis of the basal joints of the thumb. Scand J Plast Reconstr SurgHandSurg1996;30(1):67-70. 23. Vandenbrouchke J, De Schrijver F, De Smet L, Fabry G. Simple trapezectomy for treatment of trapeziometacarpal osteoarthritis of the thumb. Clin RheulIJatoI1997;16(3):239-242.
24. Young BT, Rayan GM. Arthroplasty for trapeziometacarpal arthrosis. ] Oklahoma State MedAssoc 1998;91(2):53-59. 25. Hobby JL, Lyall HA, Maggitt BF. First metacarpal osteotomy for trapeziometacarpal osteoarthritis. J Bone Joint Surg 1998;80B(3):508-512. 26. Gibbons CE, Gosal HS, Choudri AH, Magnussen PA. Trapeziectomy for basal thumb joint osteoarthritis: 3- to 19-year follow-up. 1ntOrthop 1999;23(4):216-218. 27. Alnot JY, Saint Laurent Y. Total trapeziometacarpal arthroplasty. Report on seventeen cases of degenerative arthritis of the trapeziometacarpal joint. Anll Chir Main 1985;4:11. 28. Braun RM. Total joint arthroplasty at the carpometacarpal joint of the thumb. Clin Orthop ReIRes 1985;195:161. 29. Alnot JY, Muller GP. A retrospective review of 115 cases of sur gically-treated trapeziometacarpal osteoarthritis. Rev Rhum (English edn) 1998;65(2):95-108. 30. Hannula TT, Nahigian SH. A preliminary report: cementless trapeziometacarpal arthroplasty. ] Hand Surg 1999;24A(1): 92-101. 31. Dobyns JH, Sim FH, Linscheid RL. Sports stress syndromes of the hand and wrist. AmJ Sports Med 1978;6:236-253. 32. Grundberg AB, Reagan DS. Pathologic anatomy of the forearm: intersection syndrome. J HandSurg 1985;10A:299-302. 33. Wood MD, Dobyns JH. Sports related extraarticular wrist syndrome. Gin Orthop Rei Res 1986;202:93-102. 34. Paton HO. Traumatic tenosynovitis of the wrist. BM] 1978;i:789. 35. Missotten J, Stainier P, Bisschop P. Tenosynovite d'e s extenseurs et abducteur du pouce. Kil1l!sitherapie Scientifique 1992;311:35. 36. de Quervain F. Uber eine Form von chronischer Tendovaginitis. Korresp BI SchweizArzte 1895;25:389. 37. de Quervain F. On a form of chronic tendovaginitis by Dr. Fritz de Quervain in la Chaux-de-Fonds. 1895. Am j Orthop 1997;26(9):641-644 (English translation of the original article)
38. T hompson AR, Plewes LW, Shaw EG. Peritendinitis crepitus and simple tenosynovitis: a clinical study of 544 cases in industry. BrJ Ind Med 1951;8:150. 39. Kiefhuber TR, Stern PJ. Upper extremity tendinitis and overuse syndrome in the athlete. Clin Sports Med 1992;11:39-55. 40. Le Viet D, Lantieri L. Tenosynovite de de Quervain. Cicatrice horizontale et fixation du lambeau capsulaire. Rev Chir Orthop ReparAppar Mot 1992;75(2):101-106. 41. Harvey FJ, Harvey Pp, Horsley WM. De Quervain's disease: surgical or nonsurgical treatment. ] HandSurg 1990;15A:83. 42. Armstrong ThJ, Fine LJ, Goldstein SA, Lifshitz YR, Silverstein BA. Ergonomic considerations in hand and wrist tendinitis.
JHandSurg1987;12A:830. 43. Kauer J. Functional anatomy of the wrist. Clin Orthop ReI Res 1980;149:9. 44. Clarke MT, Lyall HA, Grant JW, Matthewson MH. T he histopathology of de Quervain's disease. I Hand Surg 1998;23B(6):732-734. 45. Aldan ZA, Ozturk L, Calli IH. An anatomical study of the first extensor compartment of the wrist. Kaibogaku Zasshi 1998;73(1):
49-54. 46. Nagaoka M, Matsuzaki H, Suzuki T. Ultrasonographic exami nation of de Quervain's disease. J Orthop Sci2000;5(2):96-99. 47. Bahm J, Szabo Z, Foucher G. The anatomy of de Quervain's disease. A study of operative findings. Int Orthop 1995;19(4): 209-211. 48. Melling M, Wilde J, Schnallinger M, Schweighart W, Panholzer M. Supernumerary tendons of the abductor pollicis. Acta Anat 1996;155(4):291-294. 49. Witczak JW, Mesear VR, Meyer RD. Triggering of the thumb with de Quervain's stenosing tendovaginitis. j Hand Surg 1990;15A(2):265. 50. Albertson GM, High WA, Shin AY, Bishop AT. Extensor trigger ing in de Quervain's stenosing tenosynovitis. J Hand Surg 1999;24A(6):1311-1314. 51. Finkelstein H. Stenosing tenovaginitis at the radial styloid process. J BoneJoint Surg 1930;12A:509. l Orthop ReI 52. Pick RY. De Quervain's disease: a clinical triad. Clil Res 1979;143:165. 53. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:188. 54. Giovagnorio F, Andreoli C, De Cicco ML. Ultrasonographic evaluation of de Quervain disease. I Ultrasound Med 1997;16(10):685-689. 55. Weiss Ap, Akelman E, Tabatabai M. Treatment of de Quervain's disease. JHand Surg1994;19A(4):595-598. 56. Leslie BM, Ericson WB, Morehead JR. Incidence of a septum within the first dorsal compartment of the wrist. I Hand Surg 1990;15A:88. 57. Zingas C, Failla JM, Van Holsbeeck M. Injection accuracy and clinical relief of de Quervain's tendinitis. j Halld Surg 1998;23A(1):89-96. 58. Ta KT, Eidelman D, T homson JG. Patient satisfaction and out comes of surgery for de Quervain's tenosynovitis. J Hand Surg 1999;24A(5):1071-1077. 59. Yuasa K, Kiyoshige Y. Limited surgical treatment of de Quervain's disease: decompression of only the extensor pollicis
l d Surg 1998;23A(5):840-843. brevis subcompartment. JHal 60. T horson E, Szabo R. Common tendinitis problems in the hand and forearm. Orthop Clin Norttl Am 1992;23(1):65-74. 61. Schofield CB, Citron ND. The natural history of aduft trigger thumb.) Hand Surg 1993;18B(2):247-248.
CHAPTER 35 - DISORDERS OF THE THUMB 531
62. Engkvist 0, Lundborg G. Rupture of the extensor pol\icis lon&us tendon after fracture of the lower end of the radius - a clinical and microangiographic study. Hand1979;11:75. 63. Kozin SB, Wood MB. Early soft-tissue complications after fractures of the distal part of the radius. J Bone Joint Surg 1993;75A(1):144-153.
64. Schneider LH, Rosenstein RG. Restoration of extensor pol\icis longus function by tendon transfer. Plast Recon Surg 1983;71:533-537. 65. Ferlic DC. Extensor indicis proprius transfer for extensor pollicis longus rupture. In: Blair W, Steyers C (eds) Techniques in Hand Surgery. Williams & Wilkins, Baltimore, 1996:649-653.
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Disorders of the inert structures The capsular pattern
533
Rheumatoid arthritis Traumatic arthritis Arthrosis 534 Gout 535 Non-capsular pattern
534
534
535
Unreduced dislocation
535
Disorders of the contractile structures Dorsal interosseus muscles Thenar muscles 536 Flexor tendons
536
Trigger finger 536 Tendon rupture 537 Dupuytren's contracture 5lideck's atrophy
538
Disorders of the hand and fingers
533
538
535
535
Pain and paraesthesia are two symptoms that are common in the hand. Pain is very often the result of either local trauma or overuse. Precise localization is pos sible in pain that is not referred from a lesion higher up in the limb. Paraesthesia may reflect a proximal lesion and the patient has difficulty in identifying the source of his symptoms.
DISORDERS OF THE INERT STRUCTURES THE CAPSULAR PATTERN
Any of the joints of the fingers may become affected by one or other form of arthritis, which results in limitation of movement with a capsular pattern. The capsular pattern at a finger joint is an equal loss of movement at the beginning and end of the normal range in either direction. Some movement remains possible at the midpoint. Rotations are painful at the extremes of range. In very severe arthritis, rotations may also become limited. The presence of a capsular pattern indicates that an arthritis has developed, the type of which can be defined from the history. The following questions are relevant: •
• •
• •
How did it all start? The possibilities are: no apparent cause, trauma or post-immobilization. A spontaneous onset indicates the possibility of rheumatoid arthritis or of a simple arthrosis. Trauma suggests traumatic arthritis. Are other joints affected as well? If they are, this suggests a rheumatoid condition. Which joints were affected first, the distal or the proximal joints? Arthrosis usually starts at the distal interphalangeal joints, whereas rheumatoid arthritis tends to start at the metacarpophalangeal joints. Is the joint capsule swollen? Swelling often occurs in a rheumatoid or traumatic arthritis. Does the joint change colour? The joint becomes red in gout. 533
534 SECTION SIX - THE WRIST, THUMB AND HAND
RHEUMATOID ARTHRITIS
Rheumatoid arthritis is undoubtedly the most deforming and most incapacitating disorder of the hand.l The symptoms and signs usually develop in the course of a few weeks or months and are often symmetrical. Frequently, the first symptom is morning stiffness of the fingers. The basic functional examination is usually negative, but tenderness to touch can be elicited. The erythrocyte sedimentation rate is markedly raised. Early in the course, a capsular pattern develops and one or more metacarpophalangeal joints or proximal interphalangeal joints of one or both hands show the familiar spindle-shaped swelling. Later, when osseous destruction takes place, a palmar luxation of the fingers occurs and they deviate towards the ulnar side as the result of subluxation in the metacar pophalangeal joints. The fingers may develop the typical buttonhole and swan neck deformities: the former results in hyperextension of the metacarpophalangeal joint, flexion at the proximal interphalangeal joint and exten sion at the distal interphalangeal joint; the latter results in flexion at the metacarpophalangeal joint, hyperextension at the proximal and flexion at the distal interphalangeal joint. The thumb becomes Z-shaped (typical 'ninety ninety' deformity): the metacarpophalangeal joint is fixed in 90° flexion, the interphalangeal joint in 90° extension. The joints are also warm to the touch. Secondary rupture of tendons and ligaments may occur, with subsequent muscular contractures or muscu lar atrophy. Treatment is systemic. Only in the initial stage, when few joints are affected, may intra-articular triamcinolone prove effective. As in any other patient, symptoms may develop that have nothing to do with the patient's rheumatoid arthri tis. Trigger finger, carpal tunnel syndrome and de Quervain's disease are common, and another possibility is a ganglion lying between the heads of the second and third metacarpal bones, which gives rise to vague local aching and responds well to aspiration.2
TRAUMATIC ARTHRITIS
The typical history of direct contusion, indirect sprain or reduced dislocation of a finger joint indicates the presence of a traumatic arthritis - a very common condi tion. A chip fracture may also be responsible for the arthritis. On inspection, a spindle-shaped swelling is often seen, which resembles the swelling of rheumatoid arthritis. Examination further reveals a capsular pattern, and on
palpation warmth may be felt, especially after a severe injury. As the arthritis may be combined with a tendinous lesion, resisted movements of the fingers must also be tested. Traumatic arthritis of the finger joints does not respond satisfactorily to any treatment. Intra-articular injection with a steroid, so useful in traumatic arthritis in the toe joints, affords no corresponding benefit in the fingers. Recovery is spontaneous over 6-18 months, depending on the severity of the original trauma and the age of the patient. Sometimes manual therapeutic techniques may favourably alter the natural course.3 Immobilization is strongly contraindicated.
ARTHROSIS
Occasionally arthrosis in one joint develops as the result of severe injury but more often the condition has a spon taneous onset and affects several joints. Women between 40 and 60 years of age are often affected, and there is a strong familial predisposition.4 Arthrosis begins at the distal interphalangeal joints, and its knobbly appearance is quite different from rheumatoid arthritis. Both hands are usually affected more or less symmetrically. The index, middle and ring fingers are most usually affected. At the base of the distal phalanx, two small rounded bosses on the dorsum of the joint (Heberden's nodes)5 can be seen. A varus deformity may develop at a distal joint, usually at the index. Some years later, the arthrosis may spread to the proximal interphalangeal joints (with the formation of nodes at index and middle fingers - Bouchard's nodes); It seldom reaches the metacarpophalangeal joints. From time to time, a new node forms at an affected joint and the patient will mention some aching or slight pain over 1 or 2 months, during which time the fingertip may occasion ally become pink. The colour is mottled and different from the shiny red of gout. After a month or two the dis colouration passes off and the node ceases to be painful. As the joints of the hand are not weight-bearing, arthrosis is not a very painful condition. The patient merely complains of stiffness and aching especially after exertion. The radiograph clearly shows the usual arthrotic changes - osteophytes and erosion of cartilage. Heberden's nodes and arthrosis cause hardly any symptoms. They are unsightly and may be associated with aching and clumsiness. Since the distal finger joints finally fix in 45° flexion, arthrodesis seldom brings much improvement unless an intractable painful traumatic arthritis supervenes after injury. Some patients are pleased to have the exostoses removed surgically for cosmetic reasons.
CHAPTER 36 - DISORDERS OF THE HAND AND FINGERS 535
GOUT
The hands become involved only very late in the evolu tion of gout. According to Dieppe and Calvent,6 the finger joints are affected in approximately 15% of cases. The onset and the clinical appearance of chronic gout in elderly men may very closely mimic rheumatoid arthritis but diagnosis is not difficult when the patient is known to have gout and describes recurrent attacks. These typically start in the first metatarsophalangeal joint of the big toe, clear up completely and later spread to other joints. The affected joint usually has a shiny red appearance. Tophi in the ears and a raised blood uric acid level finally appear but are of little diagnostic aid in the early, doubtful case. Very characteristic, even diagnostic, is the rapid improvement of the arthritis within 48 hours of colchicine or phenylbutazone administration.
NON-CAPSULAR PATTERN UNREDUCED DISLOCATION
Dislocation is sometimes mistaken for traumatic arthritis at the interphalangeal joint of the thumb. The joint is so swollen that it is not obvious that it is fixed in full exten sion - a clear non-capsular type of limitation. In late cases, reduction is impossible and surgery is required.
DISORDERS OF THE CONTRACTILE STRUCTURES
Strains of muscles and tendons in the hand are not infre quent. They have no tendency to spontaneous cure. Diagnosis is not difficult and conservative treatment leads to good results. All the intrinsic muscles of the hand and their short tendons respond immediately to adequate deep transverse friction but not to infiltrations with steroids. In contrast, friction has no effect on the long flexor tendons in the palm but triamcinolone infiltration is successful? DORSAL INTEROSSEOUS MUSCLES PAIN
A lesion in an interosseous muscle is usually traumatic, either the result of a direct injury or of a fracture of a metacarpal bone. Less commonly it follows overuse (e.g. musicians and typists).
�� 3
2
1
Figure 36.1
Sites of lesions of a dorsal interosseous muscle: 1, in the muscle belly; 2, in the body of the tendon; 3, at the insertion into the dorsal aponeurosis.
There are three possible localizations for the lesion: in the muscle belly; in the tendon where it crosses the metacarpophalangeal joint; and at the insertion into the base of the phalanx (Fig. 36.1). In the muscle belly, the lesion is found between the metacarpal shafts, usually distally. The patient experi ences pain at the dorsal aspect of the hand, elicited by resisted abduction of the extended finger. Passive move ment at the metacarpophalangeal joint may cause pain at the extreme range of movement but, as the pain is not felt at the joint itself and resisted movements are also painful, attention is drawn to the interosseous muscle. Careful palpation reveals the exact site of the lesion. This lesion has no tendency to spontaneous recovery and it only responds - and very impressively - to deep transverse friction: two or three treatments suffice. If the lesion is in the tendon or at the insertion, the pain is accurately felt at one side of one knuckle. The joint may be slightly swollen at the site of the lesion. Passive devi ation of the finger away from the painful side is painful, as well as resisted abduction towards the painful side. Again, palpation must be performed very carefully to determine the exact painful spot. Differentiation from traumatic arthritis is not always easy. Pain on resisted movement clarifies the diagnosis. Differential diagnosis is important because deep trans verse friction will cure a tendon lesion but will have no effect on traumatic arthritis. Untreated, the lesion may go on for years but it responds very well to deep transverse friction. The patient will be cured after four to ten treatments, however long the condition has lasted. Technique: friction to the muscle belly. The patient sits
at the couch with the hand resting on it. The therapist sits opposite the patient. The tender spot between the shafts of the metacarpal bones is palpated for, keeping the finger as parallel as possible to the metacarpals. Friction is imparted with the middle finger, reinforced by the index finger (Fig. 36.2). The movement is pure prona tion-supination, transverse to the muscular fibres. Technique: friction to the tendon. It is sometimes
difficult to get the finger to the exact spot because it lies more or less between the knuckles. Therefore the follow ing procedure is used. With one hand the therapist takes
536 SECTION SIX - THE WRIST, THUMB AND HAND
(b)
(a) Figure 36.2
Friction to (a) the belly and (b) the tendon of a dorsal interosseous muscle.
the patient's hand, with the fingers in the palm of the patient's hand. The tips of the middle and ring fingers lie on the palmar aspect of the knuckle that contains the lesion and push the bone upwards. At the same time the thumb is laid on the dorsal aspect of the adjacent knuckle, which is pushed downwards. This manoeuvre brings the affected tendon within reach of the thumb of the other hand. With the fingers of this hand counter pressure is exerted (Fig. 36.2). The friction is given with the thumb, starting at the palmar aspect of the tendon and ending at the dorsal side of it. The movement is achieved by a supination movement of the forearm. WEAKNESS
Weakness of one or more interosseous muscles is the result of a neurological condition and is often one of the first signs of amyotrophic lateral sclerosis. Weakness and wasting of one interosseous muscle only occurs in cases of localized pressure (usually occu pational) on the deep palmar branch of the ulnar nerve in the palm of the hand (cyclist's palsy).8 A cervical rib can cause pressure on the lower trunk of the brachial plexus: apart from some of the interosseous muscles, the ulnar half of the flexor digitorum profundus and the flexor carpi ulnaris are also usually weak. A first thoracic nerve root lesion may also be responsi ble for weakness of the small muscles of the hand.
THENAR MUSCLES
A lesion of a thenar muscle may follow an abduction sprain of the thumb. The origin of the oblique portion of
the adductor pollicis muscle at the palmar aspect of the base of the (second or) third metacarpal bone is most commonly affected. Resisted adduction of the thumb is painful, as is passive abduction. Treatment consists of a few sessions of deep transverse friction. Technique: friction. The patient sits at the couch, the
supinated arm resting on it and the hand over the edge. The therapist sits opposite the patient. With the contra lateral hand the wrist and the thumb are brought into extension in order to stretch the tendon and to bring it within reach of the fingers (Fig. 36.3). Friction is imparted with the thumb of the other hand, starting at the radial aspect of the insertion and ending at the ulnar aspect. FLEXOR TENDONS
A tenosynovitis may develop in the long flexor tendons in the palm of the hand. The rheumatoid type often presents with coarse crepitus on movements. This chronic tenosynovitis causes few or no symptoms. If necessary, the lesion responds well to infiltration with triamcinolone. TRIGGER FINGER
Swelling in any of the digital flexor tendons may form just proximal to the metacarpophalangeal joint, together ' with narrowing of the tendon sheath and give rise to 'trigger finger'. The third or fourth finger is most com monly involved.
CHAPTER 36
Figure 36.4
-
DISORDERS OF THE HAND AND FINGERS 537
Trigger finger.
TENDON RUPTURE MALLET FINGER
As the result of an injury that flexes the distal interpha langeal joint while it is actively held in extension, the long extensor tendon may rupture (Fig. 36.6) or may become detached (avulsion fracture) from the distal phalanx. Distinction between the two can be made by radiography. Figure 36.3 Friction to the adductor pollicis.
Flexion is free and active but extension requires the help of the other hand, because the swelling engages within the tendon sheath. A snap accompanies dis engagement. The swelling is easily palpated in the palm, just proximal to the head of the metacarpal bone (Fig 36.4 ). Trigger finger can arise spontaneously or can be the result of repetitive minor trauma or a complication of rheumatoid arthritis. If the condition gives rise to painful symptoms infiltration with 10 mg of triamcinolone acetonide in and around the nodule quickly cures these (Fig. 36.5).9-12 If the result is not adequate, the tendon sheath can be slit up either at open surgery - a simple procedure - or percutaneously.13
Figure 36.5
Infiltration for trigger finger.
538 SECTION SIX - THE WRIST, THUMB AND HAND
sO DECK'S
Figure 36.6
Mallet finger.
On examination, the distal joint is held in flexion and the patient is not able to extend it actively. On passive testing, movement is normal. Conservative treatment consists of immobilizing the finger with the proximal interphalangeal joint held in full flexion and the distal interphalangeal joint in full exten sion, so as to completely relax the extensor tendon until union takes place.14 In a retrospective study, Hooyboer and Vuursteen15 evaluated the results of conservative and operative treatment. They suggest that the tendinous repair should be considered to be the treatment of choice in tendon rupture, whereas conservative treatment is better for avulsion fracture.
RUPTURED FLEXOR TENDON
Rarely, a tendon of the flexor digitorum longus may rupture at the level of the base of the distal phalanx. The whole tendon recoils into the palm of the hand. The distal interphalangeal joint cannot be actively flexed. Passive movement remains normal. Surgical repair is indicated.
ATROPHY
Reflex sympathetic dystrophy syndrome (RSDS), or Siideck's atrophy, is a curious disorder that is not uncommon. Different terminology has been used to label the same condition: Siideck's atrophy, causalgia, algodystrophy, algoneurodystrophy, reflex sympathetic dystrophy syndrome (RSDS).22 It is a controversial con dition. The controversy concerns the manner in which the sympathetic nervous system is involved in RSDS. It was redefined in 1996 by an ad hoc International Association for the Study of Pain task force that sug gested changing the name to 'complex regional pain syndrome' (CRPS).23-25 CRPS type 1 is reflex sympa thetic dystrophy; type II is causalgia.26 It occurs most commonly as a complication of major or minor trauma (up to 5% of patients with traumatic injuries) or in patients with myocardial ischaemia (5-20%) or hemiplegia (12-20%).27 Kozin28 stated that RSDS was found to occur most frequently after fracture (25%) or other trauma (27%). In 27% of cases, no specific precipitating event could be identified. Central nervous system or spinal disorders, myocardial ischaemia and peripheral nerve injury are responsible for, respectively, 12, 6 and 4% of cases. The pathogenesis is unclear. Some authors regard it as an injury to the peripheral nerve mechanism; others propose the theory of a central neurological dysfunction, causing abnormal activity in the sympathetic nervous system. The main symptom is posttraumatic pain which is dis proportionate to the injury. It spreads beyond the distriBox 36.1 Summary of disorders of the hand and fing�rs Disorders of the inert structures The capsular pattern Rheumatoid arthritis
DUPUYTREN'S CONTRACTURE
Traumatic arthritis Arthrosis Gout
This disorder, named after G. Dupuytren, 16 is a painless contracture of the palmar aponeurosis. The aetiology is still unknown but it seems to occur more often in combi nation with alcoholism, disorders of the liver, diabetes and epilepsy.17-19 It is common in men after the age of 30, whereas in women it does not occur under the age of 45.20 A small node in the palm of the hand is the initial symptom. Further contraction of the palmar fascia leads to flexion contracture of the fingers, especially the ring and little fingers, which are affected in 85%.21 Once the contracture becomes disabling, because per manent flexion interferes with normal activities, the only treatment is surgery.
The non-capSUlar pattern Dislocation
Disorders of the contractile structures Dorsal interosseous muscle T henar muscle Flexor tendons Trigger finger Rupture of a tendon Mallet finger Ruptured flexor tendon
Dupuytren's contracture Sudeck's atrophy (reflex sympathetic dystrophy syndrome)
CHAPTER 36 - DISORDERS OF THE HAND AND FINGERS 539
bution of any single peripheral nerve, is usually felt dis tally in the arm and is often described as 'burning'. 29 Tenderness is always present and is occasionally associ ated with allodynia and enhanced sensitivity to palpa tion. Swelling of the affected part is often present and pitting or non-pitting oedema may be found. Dystrophic skin changes are seen: nail and hair changes (hypertri chosis), shiny and taut skin and loss of wrinkling. The radiographic changes (patchy osteoporosis) have been well described by Sudeck,30 Kienbock31 and
Hermann et af.32 A bone scan may be useful to arrive at a diagnosis. Differential diagnosis has to be made with septic arthritis, rheumatoid arthritis, systemic lupus erythe matosus, Reiter's syndrome and peripheral neuropathy. The treatment consists of closed active mobilization within the range of pain (physiotherapy)33 and, when this measure does not help, systemic corticosteroids or sympathetic interruption may be tried.34,35 Disorders of the hand and fingers are summarized in Box 36.1.
REFERENCES 1. Tubiana R, Ghozlan R, Minkes CJ. Main rhumatoi"de, Appareil
Disease, 2nd English edn. Churchill Livingstone, Edinburgh,
Locomoteur. Encyclopedie Medicochirurgicale, Paris 1978; 10:14067. 2. Rhoades CE, GeJberman RH, Manjarris JF. Stenosing tenosyn ovitis of the fingers and thumb. Clin Orthop Rei Res 1984;190:236. 3. Mink AJF, ter Veer HI. Vorselaars JACTh. Extremiteiten, Functie ol1derzoek en Manuele Ttlerapie, 6th edn. Bohn, Scheltema & Holkema, Utrecht, 1990;300.
1985:94.
4. Veys EM, MieJants H, Verbruggen G. Reumatologie. Omega
20. Ewing J. Neoplastic diseases. In: Rothman R, Simeone F (eds) A Treatise on Tumors, 3rd edn. Saunders, Philadelphia, 1982:368. 21. Lukes RJ, Collins RD. New approaches to the classification of lymphomata. Br J Cancer 1975;31:1.
22. Alvarez-Lario B, Aretxabala-Alcibar I, Alegre-Lopez I. Alonso Valdivielso JL. Acceptance of the different denominations for reflex sympathetic dystrophy. Ann Rheum Dis 2001;60(1):
5. Heberden W. Commelltaries on the History and Cure of Diseases.
77-79. 23. Marchettini P, Lacerenza M, Formaglio F. Sympathetically
Payne, London, 1802. 6. Dieppe PA, CaJvent P. Crystals and Joint Disease. Chapman &
24. Stanton-Hicks M. Reflex sympathetic dystrophy: a sympatheti
Editions, Ghent, 1985:621.
Hall, London, 1982:145. 7. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. BaiJliere Tindall, London, 1982:194. 8. HaJoua JP, Collin JP, Coudeyre L. Paralysis of the ulnar nerve in cyclists. Anl1 Chir Main 1987;6:282. 9. Panayotopoulos E, Fortis AP, Armoni A, Dimakopoulos P, Lambiris E. Trigger digit: the needle or the knife? J Hand Surg 1992;17B:239.
maintained pain. Current Rev Pain 2000;4(2):99-104. cally mediated pain syndrome or not? Current Rev Pain 2000;4(4):268-275. 25. Stanton-Hicks M. Complex regional pain syndrome (type I,
RSD; type II, causalgia): controversies. Clin ] Pain 2000;16(2
Suppl ):S33- S40. 26. Vie I E, Ripart I. Pelissier J, Eledjam JJ. Management of reflex
sympathetic
dystrophy.
Ann
Med
Interne
(Paris)
1999;
150(3):205-210.
10. Anderson B, Kaye S. Treatment of flexor tenosynovitis of the
27. Davis Sw. Shoulder-hand syndrome in a hemiplegic popula
hand ('trigger finger') with corticosteroids. A prospective study of the response to local injection. Arch Intern Med 1991;151(1):153-156. 11. Lambert MA, Morton RJ, Sloan JP. Controlled study of the use of 10caJ steroid injection in the treatment of trigger finger and thumb. J Hand Surg 1992;17B(1):69-70. 12. Buch-Jaeger N, Foucher G, Ehrler S, Sammut D. The results of
tion: 5 year retrospective study. Arch Phys Med Rehabil 1977;58:3553. 28. Kozin F. The painful shoulder and reflex sympathetic dystrophy
conservative management of trigger finger. A series of 169 patients. Alln Chir Main Memb Super 1992;11(3):189-193. 13. Eastwood DM, Gupta KJ, Johnson DP. Percutaneous release
syndrome. In: McCarty DJ (ed) Arthritis and Allied Conditiol1s, 10th edn. Lea & Febiger, Philadelphia, 1985:1322. 29. Goldstein DS, Tack C, Li ST. Sympathetic innervation and func tion in reflex sympathetic dystrophy. Ann NeuroI2000;48(1):49-59. 30. Siideck P. Uber die akute entziindliche Knochenatrophie. Arch Klin Chir 1900;62:147.
31. Kienbock R. Uber akute Knochenatrophie bei Entziindungs
of the trigger finger: an office procedure. J Hand Surg
processen
1992;17A(1):114-117.
Inaktivitatsatrophie der Knochen) und ihre Diagnose nadl dem
14. Wehbe MA, Schneider LH. 1984. Mallet fractures. J Bone Joint Surg 1984;66A:658.
15. Hooyboer PGA, Vuursteen PJ. De behandeling van de mallet finger; stack-spalk of tenodermodese. Ned Tijdschr Geneeskd 1990;4:134.
an
den
Extremitaten
(falschlich
sogenannte
Rontgenbild. Wien Med Wochenschr 1901;5:1345. 32. Hermann LG, Reinecke HG, Caldwell JA. Posttraumatic painful osteoporosis: a clinical and roentgenological entity. AnI J RoentgenoI1942;47:353.
33. Oerlemans HM, Oostendorp RA, de Boo T et al. Adjuvant phys
16. Dupuytren G. Lefons Orates de Clinique Chirurgicale, vol 1. Bailliere, Paris, 1832. 17. Hueson JT. Dupuytren's contracture. In: Flynn JE (ed) Hand SlIrgery, 3rd edn. Williams & Wilkins, Baltimore, 1982:797. 18. Lamb OW. Dupuytren's disease. In: Lamb DW, Kuczynski K
ical therapy versus occupational therapy in patients with reflex sympathetic dystrophy! complex regional pain syndrome type I. Arch Phys Med Rehabil 2000;81(1):49-56. 34. Kozin F. Reflex sympathetic dystrophy syndrome. Bull Rheum
(eds) The Practice of Hand Surgery. Blackwell, Oxford, 1981:470. 19. James JIP. The genetic pattern of Dupuytren's disease and idio
35. Bushnell TG, Cobo-Castro T. Complex regional pain syndrome:
pathic epilepsy. In: Hueston JT, Tubiana R (eds) Dupuytren's
Dis 1986;36(3):632-638.
becoming more or less complex? Manual Therapy 1999;4(4): 2 21-228.
THIS PAGE INTENTIONALLY LEFT BLANK
SECTION SEVEN
Nerve lesions and entrapment neuropathies of the upper limb SECTION CONTENTS 37. Nerve lesions and entrapment neuropathies of the upper limb Disorders of the spinal accessory nerve 543 Disorders of the brachial plexus 545 Traumatic disorders 546 Space-occupying lesions 546 Thoracic outlet syndrome 546 Plexitis 552 Disorders of the long thoracic nerve 553 Disorders of the suprascapular nerve 554 Disorders of the axillary nerve 556 Disorders of the radial nerve 557 558 Lesions at the proximal and middle part of the upper arm Lesions at the distal part of the upper arm 559 Lesions at the upper part of the forearm 559 Lesions at the distal part of the forearm 561 Disorders of the ulnar nerve 561 Lesions at the elbow 562 Lesions at the wrist 565 Disorders of the median nerve 566 Lesions at the forearm: anterior interosseous nerve 568 Lesions in the carpal tunnel 568 Disorders of the musculocutaneous nerve 573 Disorders of the medial cutaneous nerve of the forearm 573
543
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS o
Disorders of the spinal accessory nerve
Nerve lesions and entrapment neuropathies of the upper limb
S43
Disorders of the brachial plexus S4S Traumatic disorders 546 Space-occupying lesions 546 Thoracic outlet syndrome 546 Plexitis 552 Disorders of the long thoracic nerve Disorders of the suprascapular nerve Disorders of the axillary nerve Disorders of the radial nerve
553 554
556 557
Lesions at the proximal and middle part of the upper arm 558 Lesions at the distal part of the upper arm 559 Lesions at the upper part of the forearm 559 Lesions at the distal part of the forearm
561
' Disorders of the ulnar nerve 561 Lesions at the elbow 562 Lesions at the wrist 565 Disorders of the median nerve
566
Lesions at the forearm: anterior interosseus nerve Lesions in the carpal tunnel
568
Disorders of the musculocutaneous nerve
568
Peripheral nerve lesions in the neck, shoulder girdle and upper limb can occur anywhere along the extraspinal extent of the nerve - between the intervertebral foramen and the most distal nerve endings in the extremities, The function of the nerve becomes impaired either as the result of an entrapment phenomenon, or as the outcome of an injury causing bruising or elongation of the nerve tissue. Entrapment phenomena occur typically at four differ ent sites giving rise to four different mechanisms (see Chapter 2). •
573
•
Disorders of the medial cutaneous nerve of the forearm 573 •
•
Pressure on a distal nerve causes mainly analgesia as well as some paraesthesia in the territory of the nerve. When a nerve trunk or plexus becomes compressed, the release phenomenon - paraesthesia when the pressure ceases - is found. Nerve root compression is characterized by pain and paraesthesia, felt in the corresponding dermatome, and often followed by sensory and motor deficit in the same segment. Pressure on the cervical spinal cord is painless. An early symptom is paraesthesia with multisegmental distribution. When the compression becomes more severe, numbness, incoordination, spasticity and hyperreflexia may occur.
Disorders of the spinal cord and nerve roots are discussed in Chapters 2 and 9.
DISORDERS OF THE SPINAL ACCESSORY NERVE ANATOMY
The accessory nerve is a cranial nerve (XI) and consists of two parts. Its main part is the spinal root, the other is the cranial root. The spinal root takes origin in the spinal cord from a small pillar of nuclei in the anterolateral part of the ante rior horn of the levels CI-CS/C6. The fibres leave the cord between the anterior and posterior rami of the nerve root. They join and form a strand that ascends parallel to 543
544 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
1. Sternocleidomastoid 2. Trapezius
1. spinal nuclei 2. external rarnus 3. internal ramus 4. jugular foramen 5. vagal nerve 6. spinal accessory nerve
1ffil_-2-
Figure 37.2 •
•
Figure 37.1
Anatomy of the spinal accessory nerve.
the spinal cord and enters the skull through the foramen magnum. The cranial root takes its origin in the caudal part of the nucleus ambiguus in the medulla oblongata. Both parts accompany the glossopharyngeal (IX) and vagus (X) nerves in their exit through the jugular foramen. The fibres originating from the nucleus ambiguus then join the vagus nerve and the other fibres - the real spinal accessory nerve - descend towards the muscles they innervate (Fig. 37.1). INNERVATION
The spinal accessory nerve is a pure motor nerve and . innervates the sternocleidomastoid and the trapezIUs muscles (Fig. 37.2). DISORDERS
The spinal accessory nerve can become affected at different levels: •
Within the skull where the cause is usually tumourous.1 ,2 This is uncommon.
Motor innervation by the spinal accessory nerve.
At the level of the exit through the jugular foramen where again, rarely, metastases or schwannomas may affect the nerve.3A At the level of the neck where iatrogenic trauma, for example biopsy of lymph nodes in the posterior triangle, forms the commonest cause of isolated paralysis.5-10 External traumas may also damage the nerve.
Idiopathic spinal accessory neuropathy may occur in isolation or in combination with a disorder of other nerves (glossopharyngeal, vagus, long thoracic or dorsal scapular). Mononeuropathy of the spinal accessory nerve
The patient initially complains of intermittent pain in the shoulder girdle area, which soon may become perma nent.n,12 At the same time, the arm starts to feel weak and heavy, which leads to some functional IOSS. 1 3 Exceptionally, pain is absent. Pain normally lasts for about 3 weeks, after which it disappears spontaneously. On clinical examination of the shoulder, painless limi tation of active arm elevation of about 5-10° is found, which is less than the limitation in neuritis of the long thoracic nerve. Neck, scapular and arm movements do not influence the pain. In severe cases the trapezius muscle may be wasted. The diagnosis is confirmed by asking the patient to adduct both scapulae while the therapist applies counter pressure at the medial border of the inferior scapular angle (Fig. 37.3). In neuritis of the accessory nerve, the scapula on the affected side can easily be pushed away at the side. No treatment exists but spontaneous cure of motor function of the trapezius is the rule and usually takes about 4-8 months, although recovery is sometimes incomplete.1 4
CHAPTER 37
-
NERVE LESIONS OF THE UPPER LIMB 545
Peripheral nerve
Figure 37.3
-
Test to confirm spinal accessory nerve palsy.
.
�
-
'
DISORDERS OF THE BRACHIAL PLEXUS
ANATOMY
The ventral rami of the spinal nerves C5, C6, C7, C8 and T1 unite to form the brachial plexus. Occasionally a prefixed (C4) or postfixed (T2) ramus takes part in the formation of the plexus. Several interconnections lead to the formation of trunks, divisions, cords and branches. Trunks
From the three cords the major peripheral nerves of the upper limb are formed. The lateral cord continues into the musculocu taneous nerve. The posterior cord forms a branch that divides into two separate nerves: the radial nerve and the axillary nerve. The medial cord forms the ulnar nerve. From an anastomosis between the lateral cord and the medial cord the media n nerve is formed. Several other nerves emerge directly from the brachial plexus, either from its supraclavicular or its iniraclavicu lar part. From the supraclavicular part of the plexus originate: the dorsal scapular nerve (innervating the levator scapulae, major rhomboid and minor rhomboid muscles); the long thoracic nerve (innervating the serratus anterior muscle); the thoracodorsal nerve (innervating the latissimus dorsi muscle); the s uprascap ular nerve (innervating the supraspinatus and infraspinatus muscles); the inferior subscapular nerve (innervating the teres major muscle); the subclavian nerve (innervating the subclavian muscle); the lateral pectoral nerve (innervating the upper part of the pectoralis major muscle); and the medial pectoral nerve (innervating the lower part of the pectoralis major muscle as well as the pectoralis minor muscle). From the infraclavicular part of the plexus the follow ing nerves originate: the medial c u taneous nerve of the arm (supplying the anteromedial and posteromedial part of the arm); and the medial cu taneous nerve of the forearm (its anterior ramus supplying the anteromedial aspect of the forearm, and its cubital ramus supplying the postero medial aspect of the forearm) branches of the medial cord of the brachial plexus (Fig. 37.4).
There are three trunks: superior, middle and inferior. The superior tru nk is created by the fusion of the ventral rami of C5 and C6. The middle trunk is the continuation of the ventral ramus of C7. The inferior trunk is formed by the ventral rami of C8 and Tl.
, , , ,
Divisions
superior trunk
The three trunks divide into an anterior and a posterior part. The posterior parts form the posterior cord. The anterior parts form the other cords: the superior trunk continues in the lateral cord and the inferior trunk in the medial cord. The superior and inferior trunks also give off branches for the middle trunk, thus forming in tercon n ections.
, ,
, , , ,
inferior trunk
Cords
The cords are lateral, posterior and medial according to their relation to the subclavian/axillary artery. The lateral cord is formed from fibres of the superior trunk, together with fibres from the middle trunk. The posterior cord results from the fusion of fibres originating from the three trunks. The medial cord is the continuation of the inferior trunk.
axillary n.
ulnar n.
Figure 37.4
The brachial plexus.
546 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
INNERVATION
The brachial plexus is responsible for the complete motor and sensory innervation of the shoulder girdle and upper limb.
the deltoid and supraspinatus muscles, which results in the patient not being able to elevate the arm above the horizontal. Elbow flexion is weak because of paresis of the biceps muscle. Sensation remains normal. Lower brachial plexus palsy
TRAUMATIC DISORDERS
The brachial plexus lies quite superficially within a very mobile shoulder girdle and is closely related to the dif ferent bony structures of neck, shoulder girdle, shoulder and thorax. This situation makes it very vulnerable. Traumatic disorders are therefore one of the commonest causes of brachial plexus dysfunction. As the result of traction injuries (e.g. motorcycle accidents), compression by dislocated (e.g. shoulder luxation15,16) or fractured bones (e.g. fracture of the clavicle17) or by haematomas, and intraoperative or birth injuries, larger or smaller parts of the plexus may become damaged, leading to total or partial syndromes.18 Upper brachial plexus palsy
This is called Erb-Duchenne's paralysis and is defined as a palsy of C5 and C6 and sometimes of C7. There is a motor deficit of the muscles innervated by the nerves originating from these fibres and possibly a sensory deficit in the C5 and C6 dermatomes (lateral and anterior aspects of arm and forearm and radial aspect of hand and fingers) (Table 37.1). The patient cannot bring the arm up and has difficulty in bending the elbow; there is a visible atrophy of the deltoid, supraspinatus and infraspinatus muscles. Middle brachial plexus palsy
If the middle part of the brachial plexus becomes damaged in trauma, the serratus anterior and rhomboid muscles remain unaffected. There is slight weakness of Table 37.1 Affected nerves and muscles in a palsy of the upper part of the brachial plexus Nerve
Muscle
Long thoracic
Serratus anterior
Dorsal scapular
Rhomboids
Suprascapular
Supraspinatus Infraspinatus
Axillary
Deltoid Teres minor
Musculocutaneous
Coracobrachialis Biceps
Radial
Brachioradialis Supinator
This is known as Dejerine-Klumpke paralysis and is not so common but it causes severe disability. The lesion affects the C8 and T1 segments, and quite often also C7. As a result, there is a palsy of the muscles supplied by the ulnar and median nerves as well as the finger extensors and the extensor carpi ulnaris muscle (radial nerve). A complete inability to use the hand follows. There is also sensory deficit in the C8 segment (ulnar aspect of hand and distal forearm).
S PACE-OCCUPYING LESIONS
Metastatic tumours - usually originating from the breast, the lung or the lymphatic system - may invade the brachial plexus. The superior pulmonary sulcus tumour (Pancoast) typically invades the lower trunk of the plexus as well as the sympathetic ganglia at the base of the neck. A lower brachial plexus dysfunction is then accompanied by Horner's syndrome (see p. 656). Aneurysm of the subclavian artery and pseudo aneurysm of the axillary artery are other possible causes of compression of the brachial plexus.
THORACIC OUTLET SYNDROME
Thoracic outlet syndrome (TOS) is a vague term, only suggesting the presence of a disorder within the area of the thoracic outlet. Although it is generally accepted that the aetiology is compression of the plexus and vas cular bundle in the thoracic outlet, different opinions exist about the pathogenesis. This is expressed in the various names that have been given to the syndrome (see Box 37.1).19 The consequence of disagreement on the aetiology is that numerous methods of treatment are advocated. ANATOMY
The thoracic outlet is the space bounded by the upper part of the sternum, clavicle, first rib and the first thoracic vertebra. Towards the centre, it is limited by the trachea and oesophagus. It forms the communicating area at the base of the neck for the passage of blood vessels and nerves from mediastinum and neck to the axilla and into which the dome of the pleura rises upward.2o The vagus,
CHAPTER 37
Bqx 37.1 Synonyms for thoracic outlet syndrome -
Shou lder-hand syndrome F i rst thoracic rib synd rome Cervical rib synd rome Brachiocepha l i c synd rome Scalenus anticus syndrome Humeral head syndrome Costoclavic u l a r synd rome Nocturnal pa raesthetic brachi a l gia Adson's syndrome Hyperabduction synd rome Cervicobrachi a l neurovasc u l a r compression synd rome Fractured clavicle synd rome Pneumatic ha mmer syndrome 'Rucksack' para lysis Effort vein thrombosis Cervicothoracic outlet synd rome Pectora l is minor synd rome Su bcoracoid synd rome Synd rome of the sca lenus medius band Brachi a l p l exus syndrome Pa get-Schroetter synd rome Naffzige r's synd rome Sho u l d e r gird l e syndrome Haven's synd rome Sympathetic a l godystrophy
-
NERVE LESIONS OF THE UPPER LIMB 547
phrenic nerves, sympathetic trunk and thoracic duct also pass through the same openings. The first rib has a flat upper surface. In its anterior portion there are two grooves, which are separated by the tubercle at which the anterior scalene muscle inserts. The more medial groove accommodates the subclavian vein. Behind the muscle, in the posterior groove, both sub clavian artery and brachial plexus are found (Fig. 37.5). The clavicle overlies the first rib just cranial to the pos terior groove. At this site, compression of the neurovas cular structures between first rib and clavicle is possible; this mainly happens to the most medially localized trunks, which contain fibres of C8 and TI, so causing symptoms in the territory of the median and the ulnar nerve. TYPES
According to Cyriax, the syndrome is the outcome of a compression of the most medial branches of the brachial plexus, usually occurring between the clavicle and first rib, seldom as the result of a cervical rib. The compression is usually bilateral, intermittent or continuous and may or may not involve the subclavian artery and vein.21 It
1, brachial plexus; 2, scalenus anterior m uscle; 3, subclavian artery; 4, subclavian vein; 5, first rib; 6, clavicle.
/"o!..r.T;;;���-:9--
3
��!lt-- 4
-+;.--�-- 5
Figure 37.5 A slightly schematic representation of the relationship of neurovascular structures in the thoracic outlet:
548 SECTION SEVEN - NERVE LESI ONS AND ENTRAPMENT NE UROPATHIES
gives rise to a set of neurovascular symptoms, which are rarely present all together. Symptoms of neurological dis turbances are usually found but sometimes only features of vascular compression. 22 The brachial plexus is involved in 98% of cases, the subclavian vein in 1.5%, and the artery in 0.5%. 23,24 Cyriax recognized two main groups of thoracic outlet syndromes based on anatomical and clinical grounds: the cervical rib syndrome and the first rib syndrome. We prefer to substitute for these terms. We make a distinction between the thoracic outlet syndrome caused by anatomical changes and that from postural factors. This approaches the growing agreement about the use of four terms to indicate the presence of the thoracic outlet syn drome:25 true neurologic, arterial and venous TOS - those syndromes that result from compression by a cervical rib (anatomical variety); and non-specific neurologic TOS26,27 - the postural variety.
Figure 37.6 (arrow).
Compression of the subclavian artery with poststenotic aneurysm
Vascular compression.
The compression can be venous
and/or arterial. Anatomical variety
This is caused by structural changes - the presence of a bony cervical rib or a band of fibrous tissue which is found in 0.5% of a normal population. OnJy 5% of them will ever suffer from a thoracic outlet syndrome.28 In a fibrous band, the corresponding transverse process of C7 is larger than usual - a rudimentary cervical rib. A cer vical rib sometimes gives rise to a palpable mass at the base of the neck. Interference with the neurovascular structures usually begins at between 20 and 30 years of age and is thereafter continuous. Structural change and clinical features are frequently bilateral, although often more pronounced at one side. 29 The symptoms are the result of compression of both neurological and vascular structures. Neurocompression. Compression of a nerve trunk can give rise to pain felt at the base of the neck, radiating uni laterally towards the shoulder and arm and even towards the chest. The pain is not very severe and is often associ ated with pins and needles and numbness, which may be felt in all five digits, although most frequently the fourth and fifth fingers are affected together with the ulnar side of the arm and hand. The symptoms often appear or increase shortly after having carried a heavy object but exceptionally they can occur during the activity itself. Some patients complain of disturbed fine motor coordination together with weak ness and dysfunction of the hand. On clinical examination, atrophy of the hypothenar (Tl) or of the thenar muscles (C8), together with weak ness of the interossei (Tl), can be present. Once a cervical rib has started to interfere with a nerve, the compression does not resolve. Therefore the symp toms are continuously present and tend to increase.
Arterial. Compression of the subclavian artery (Fig. 37.6) results in coldness, pallor and easy tiredness of the hand.3D Especially after the arm has been hanging down for a while, the hand may turn white and cold over a period of hours. A diminished pulse may be found. In more severe cases, chronic compressive stenosis of the artery may give rise to claudication of the upper extremity. It may further lead to a poststenotic dilation, sometimes to the formation of an aneurysm. Atheromata arising from these aneurysms or from chronic compres sion injury of the artery can result in peripheral emboliza tion, which may lead to irreversible damage to the hand and even to the entire arm. 23,31-33 The presence of an acute ischaemic syndrome of the upper extremity, usually in a young female, suggests the possibility of a thrombosis in a poststen otic aneurysm.' Venous. If the subclavian vein is impaired, cyanosis, swelling and oedema of the hand and forearm are the indirect signs of this process. Thrombosis of the sub clavian vein may occur.34-36 Postural variety
This category comprises cases that have an almost identi cal clinical pattern but in which there is no cervical rib or fibrous band. It is-characterized by neurological symptoms typically present after lying down for, say, 2-3 hours. It is a benign disorder seldom resulting in vascular disturbance or in muscular atrophy. There are two types, depending on the clinical features. Acute onset. This is unusual, but the diagnosis is impor tant although difficult to make. Frequently the patient' is admitted to the hospital suspected of having had a heart attack. 37
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 549
Young patients with acute onset of symptoms after carrying a heavy load are typical. They complain of a sudden and severe thoracic pain, radiating down the arm, feel faint and have pain on breathing. All such fea tures draw attention to serious visceral disorders (heart attack, pneumothorax). A short time later, the arm and hand blanche. This situation resolves after a few hours so that by the time investigations, such as electrocardio ra phy, radiography of the thorax and possibly laboratory tests, have been done, the symptoms have disappeared and the patient is perfectly normal again.
�
Slow onset. This is the more common type. It is very slow i� progression and has a benign evolution, seldom giving nse to neurological deficit. The diagnosis is often missed although not difficult to establish. It affects the middle aged or elderly, more frequently females. It sometimes occurs in pregnancy. The onset is with pins and needles in the hand and fingers, mainly at night and usually after 2-3 hours of sleep. The process is often bilateral although worse on one side. Paraesthesia may be felt in all digits but may predominate in the median or ulnar distribution. It wakes the patient, who finds that she has to sit up or walk around for a short period of time, rubbing and moving the hands and fingers, to make the symptoms go. The symptoms disap pear after a few minutes, allowing sleep to be continued although recurrence may take place in the early morning hours. The more physical activity during the preceding day, the worse the symptoms at night. In periods of rest or si�kness, when the patient lies down for the whole day, no pms and needles are felt. Some patients also experi ence symptoms during the day, on activities such as knitting, holding a newspaper in front of the eyes or bicycling, all of which require some degree of shoulder elevation. Augmenting the pressure by carrying a heavy object may exceptionally provoke the symptoms as well, but normally only to a mild degree. Cyriax explained this pattern as being the consequence of a diminishing tone in the shoulder muscles, starting in . mIddle age. As a result, the shoulder girdle droops down during the day, resulting in compression of the most medial trunks of the brachial plexus, between the first rib and clavicle. Compression occurs during the day but the symptoms come on mainly at night after the pressure on the nerve has disappeared. He called this the 'release phenomenon' (see p. 2S). The process seldom leads to damage of the nerve parenchyma with subsequent mus cular atrophy because the brachial plexus can recover every night when the pressure is released.
FUNCTIONAL EXAMINATION
The diagnosis is based mainly on the typical history, all passive movements of neck, shoulder and shoulder
Figure 37.7
Sustained shoulder elevation test.
girdle being normal,38 The resisted movements are of normal strength and painless, except for CS or Tl struc tures in the hand, which may be weakened when the compression is the outcome of a cervical rib. This type of characteristic history should always be followed up with the following additional tests. Sustained elevation of the shoulders
The patient sits in a comfortable position and is asked to shrug the shoulders for about 3 minutes (Fig. 37.7). This ca�ses maximum release of pressure and therefore may . bnng on the pms and needles and abolish vascular symp . toms If present. However this test is not always positive when thoracic outlet syndrome is present; in this case, release of pressure must be tried in different positions, either fully raising the arms above the head and main taining this position for 3 minutes (Fig. 37.S) or lying supine with both hands on the head for the same length of time (Fig. 37.9). Auscultation, pulse and blood pressure
The subclavian area should always be auscultated for a bruit, the radial pulse must be checked and blood pressure must be measured. The diagnostic significance, however, is not certain. Other tests
Other tests for thoracic outlet syndrome have been advo cated classically. Although we regard them as less specific
550 SECTION SEVE N - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
a positive test to indicate vascular compression by the scalenus anterior. Modified Adson's test. This is similar to Adson's test but the patient turns the head away from the involved side. In this test, the scalenus medius puts pressure on the vessels. A positive test is thought to imply scalenus medius compression. Roos' test. The patient abducts the arms to 90°, then opens and closes the hands slowly for 3 minutes. Those who are unable to keep their arms and hands elevated because of pins and needles are regarded as suffering from thoracic outlet syndrome. However in carpal tunnel syndrome, active flexion of the fingers can bring on the pins and needles, and therefore this test does not differentiate between these two disorders (Fig. 37.10).
Examination of the cervical spine
Figure 37.8
Alternative sustained shoulder elevation test.
If pins and needles are present in the upper extremities, a full examination of the cervical spine must always be carried out. In thoracic outlet syndrome, the passive movements of the neck are painless and of full range. When a cervical rib is present, weakness and atrophy of the thenar, hypothenar and interosseous muscles may be found. Tests for carpal tunnel syndrome
All the specific tests for a carpal tunnel syndrome must be carried out (see pp. 569-571).
Figure 37.9
Alternative sustained shoulder elevation test.
and reliable, they are mentioned here for completeness. Adson's test,39 the modified Adson's test and Roos' test (elevated arm stress test)40 are regarded by some as totally unreliable, because about 50-60% of the normal population have positive findings.41,42 The patient stands with the arm resting at the side. In this position the examiner feels the patient's radial pulse. Then the patient is asked to take a deep breath and to turn the head towards the involved side. Any change in pulse degree or in blood pressure, prefer ably measured by a Doppler probe, is noted. If there is a change, it means that the subclavian artery is compressed and probably also the brachial plexus. Adson considered
Adson's test.
Figure 37.10
Roos' test.
CHAPTER 37
TECHNICAL INVESTIGATIONS .
It should be emphasized that thoracic outlet syndrome is primarily a clinical diagnosis, based on a full history and a complete clinical examination. Electromyography (EMG) and conduction studies are of little value, for two reasons. First, the range is quite variable in normal patients. Second, because the stimu lating electrode can not be placed proximal to the level of the compression, the compound action potential which is measured does not cross the site of the nerve compres sion. But EMG is helpful for differential diagnosis, in excluding nerve compression at other levels, such as ulnar nerve impingement at the elbow or carpal tunnel syndrome. A radiograph of both the cervical spine and thorax can help to detect a cervical rib, a hypertrophic transverse process of C7 (suggesting a fibrous band) or the forma tion of a clavicular callus. 43 It also helps to exclude a Pancoast's tumour. A CT scan may demonstrate an abnormal fibrous band. Angiography (arteriography and/or phlebography) must be considered but is only indicated when the vas cular symptoms are so severe that surgery is contem plated. Such can be the case when signs and symptoms of arteria I embolism or arterial and/or venous occlusion are present. DIFFERENTIAL DIAGNOSIS Cervical disc protrusions. When a posterolateral cervical disc compresses a nerve root, the cervicobrachial pain is very severe, often worse at night, coming and going without apparent reason. Some articular movements of the cervical spine increase the pain although surprisingly enough, their influence may be only very slight. In posterocentral cervical protrusion with cord com pression, pins and needles are felt in both hands and feet and are brought on or increased by neck flexion. Compression of the ulnar nerve. A lesion of the ulnar nerve provokes pins and needles felt only in the fifth finger and at the ulnar half of the fourth. In compression at the cubital tunnel, some local pain around the elbow may also occur (see p. 562). Compression of the radial nerve. Pins and needles may be felt at the dorsal aspect of the lower arm, and of the 3+ radial digits. Resisted extension of the hand is weak but painless. Sometimes a drop hand is found (see p. 557). Carpal tunnel syndrome. Compression of the median nerve in the carpal tunnel causes paraesthesia felt on the palmar aspect of the thumb, index and middle finger and the radial half of the ring finger. Carpal tunnel tests may
-
NERVE LESIONS OF THE UPPER LIMB 551
be positive, although in 50% they remain negative (see pp. 568-573). Carcinoma of the superior sulcus of the lung (Pancoast's
The coexistence of pins and needles and Pancoast's tumour implies invasion of the brachial plexus, which may give rise to a palsy of the interosseous muscles at the hand. Very often a palsy of the recurrent nerve, causing hoarseness, is also present. Clinical inspection of the face may reveal Horner's syndrome (ptosis of the upper eyelid, enophthalmia and myosis; see p. 322). tumour).
Raynaud's syndrome. This provokes only pain, and no pins and needles. Typically the hand becomes white and then blue in cold conditions.
TREATMENT Anatomical variety
Thoracic outlet syndrome due to a cervical rib or a fibrous band can only be treated surgically. Paraesthesia and pain mostly disappear but wasting and weakness seldom resolve completely. Postural variety
Because of the lack of consensus about the aetiology of this syndrome, various forms of treatment have been described (see Box 37.2). In the light of the mechanism that we consider responsible for the symptoms, the following approach is proposed. Posture and exercise. Cases caused by the first rib can be helped by conservative management. However, the first step in the treatment is a clear explanation to the patient of the pressure and release mechanism of the disorder. He or she should understand that the pins and needles at night are the result of compression during daytime and Box 37.2 Various forms of treatment for thoracic outlet syndrome Active strengthening exercises of the u pper extremity a n d n e c k m uscles Sho u l d e r shru ggi n g exercises Sca p u l a r a d d ucti o n a n d a b d u ction exercises Stretching o f the sca l e n i m uscles Mo b i l izations of the stern oclavicu l a r and acrom ioclavic u l a r joi nts Mob i l i zations of the first a n d second ribs Susta i n ed postures a n d postures of prevention d u ring activities Transcuta neous e l ectrica l n e rve st i m u l ation (TENS) Sca l enectomy Periarter i a l sym pathectomy Removal of the first r i b Removal of the cervical r i b Removal o f a pathologica l fibrous b a n d
552 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
the nerve being fully liberated from the pressure. Lacking such understanding, the patient will mistakenly regard the exercise as harmful and discontinue it. An orthosis designed to elevate the shoulder has been described. It has good results in 77% of patients. 44 Surgery. In cases refractory to conservative treatment, resection of the normal first rib can be performed. 45-48 However, this is major surgery and not always successful in relieving symptoms. This approach also carries poten tial dangers, because of the close relationship to the brachial plexus and subclavian/axillary artery.49,50 Table 37.2 provides a summary and differential diag nosis of the anatomical and postural varieties of thoracic outlet syndrome. Figure 37.11
Shoulder elevation exercise for first rib syndrome.
PLEXITIS
that they come on when the nerve is liberated from the pressure. He or she also should realize that, to get rid of the complaints, pressure on the nerve during the day must always be avoided. To achieve the latter, the patient is asked to keep the shoulders slightly shrugged all day. Carrying loads and wearing heavy coats must be avoided. For some weeks, the following daily exercise must be done in the evening. Seated in an armchair elbows resting on the arms, both shoulders are kept shrugged passively (Fig. 37.11). This brings the pins and needles on after a while but the position is maintained, even if symptoms become more severe. Once they diminish and disappear spontaneously, usually in half an hour, the shoulders are let down. If the exercise is repeated daily, the patient soon finds that the paraesthesia comes on later and later at night and then appears only in the early morning hours and, after some more weeks of exercising at night, finally disap pears completely. Exercises can then be stopped. But the patient must remember to continue indefinitely to keep the shoulders slightly shrugged during the day. As mentioned previously, it is important to explain the release phenomenon in clear terms to the patient, so that he/she understands that the pins and needles are due to
Acute or subacute neuritis of the brachial plexus has been described under different headings: amyotrophiC neuri tis, neuralgic amyotrophy, Parsonage-Turner syndrome, idiopathic brachial plexus neuropathy, brachial neuritis. There is a tendency to use the term 'acute brachial plexus neuropathy' . This rather uncommon parenchymatous disorder of the peripheral nerves, described by Parsonage and Turner,51,52 has no specific cause.53 However, two biopsy studies, mentioned by Stewart (his p. 143),25 may clarify the pathology and pathogenesis of this syndrome. They suggest that the disorder is the result of immune mediated nerve damage following a previous viral infec tion or autoimmune process.54,55 It may develop at any age.56 The onset is with quite sudden central neck pain or pain in one or both scapu lae. After some hours to some days the pain radiates to one or both upper limbs, sometimes as far as the hands. Even in bilateral distribution the picture is asymmetrical and paraesthesia is uncommon. The pain is severe, con tinues for 2-3 months and then gradually diminishes. Sometimes coughing or taking a deep breath may also be painful. It takes another 2 or 3 months before the patient is comfortable.
Table 37.2 Differential diagnosis and summary anatomical and postural varieties
Age Release phenomenon? Pins and needles? Atrophy and weakness? Cold hands? Cynosis and swelling? Treatment
Anatomical
Postural
20-30 years At first All day Thenar/hypothenarlinterossei Possible Possible Surgery
Middle-aged and elderly All the time At night None None No Keeping shoulders slightly shrugged all time; daily exercises in the evening
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 553
Examination in the early stage may show that the neck movements influence the cervicoscapular pain even though the lesion is not articular, but a clear pattern is not found. When neckache has disappeared a full range of move ment is found, with slight local discomfort at the end of range. When the painless arm is tested, one muscle may be found paralysed, usually the infraspinatus. Movements against resistance in the painful limb identify gross w�akness in several muscles. Weakness is maximal within the first few days and is random, not according to the pattern of one root. The muscles most often involved are: serratus anterior, deltoid, supraspinatus and infra spinatus, followed in frequency by biceps and triceps. Frequently weakness of the following muscle combina tions occurs: infraspinatus and triceps, infraspinatus and finger extensors, or infraspinatus and thumb extensors (Cyriax:21 p. 90). However, it is extremely rare for the infraspinatus on the affected side to escape weakness. Sensory abnormalities are much less pronounced than pain and weakness. Analgesics may be necessary during the pain period but the other symptoms and signs recover spontaneously. In the majority of patients, the weakness abates in the next few months after the disappearance of the pain.57 Severe cases also occur. The onset is sudden and leads to complete palsy of most of the muscles in both upper limbs. Such patients are best treated in hospital with adequate pain relief and physiotherapy to prevent muscular contractures.
Figure 37.12
• • • •
Anatomy of the long thoracic nerve.
As the result of direct compression ('backpack injuries') because of its long course along the thorax60 As the result of excessive shoulder activity61,62 In the clinical pattern of an acute brachial plexitis As the result of idiopathic neuritis.
Mononeuropathy of the long thoracic nerve
.DISORDERS OF THE LONG THORACIC NERVE ANATOMY
The long thoracic nerve takes origin in the upper trunk of the brachial plexus from the ventral rami C5, C6 and often C7. It courses behind the brachial plexus and follows the lateral wall of the thorax where it divides into several branches (Fig. 37.12). INNERVATION
The long thoracic nerve is a pure motor nerve and inner vates the serratus anterior muscle (Fig. 37.13). DISORDERS
The nerve can become affected: •
As the result of iatrogenic causes, such as axillary or first rib surgery58,59
In neuritis of the long thoracic nerve the history is identi cal to that in accessory nerve neuritis: spontaneous pain for about 3 weeks. Soon, weakness of the serratus ante rior muscle occurs with winging of the scapula. Examination of the shoulder shows a limitation on active elevation of the arm of about 45-90°. Passive movements are of full range; resisted movements are normal. The diagnostic manoeuvre is to ask the patient to push against a wall with the arms stretched out horizon tally in front of the body (Fig. 37.14). The medial border of the scapula becomes yet more prominent. There is no active treatment. Spontaneous recovery occurs in 4-8 months. Traumatic palsy
An injury in which the scapula is pulled laterally away from the trunk may damage the long thoracic nerve, resulting in a palsy of the serratus anterior muscle. It leads to winging of the scapula, together with limitation on active elevation of the arm between 45-90°. Pressure against a wall accentuates the winging.
554 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
(a)
Figure 37.14
Test to confirm long thoracic nerve palsy.
The condition may resolve spontaneously. Surgical repair, by transfer of the pectoralis major muscle, can be done.63 ' DISORDERS OF THE SUPRASCAPULAR NERVE . " .
'
ANATOMY (b)
The suprascapular nerve takes origin from the upper trunk of the brachial plexus with fibres from the C4 to C6 ventral rami. It courses through the posterior trian gle of the neck, underneath the trapezius muscle. At the level of the scapula it divides in two: one branch goes through the suprascapular notch into the supraspinous fossa, the other travels behind the scapula ' and curves around the spinoglenoid notch towards the infraspinous area (Fig. 37.15). INNERVATION
The nerve is motor and supplies both the supraspinatus and infraspinatus muscles (Fig. 37.16). DISORDERS
Suprascapular nerve dysfunction can be caused by: •
• • • •
Figure 37.13 Motor innervation of the serratus anterior muscle by the long thoracic nerve: (a) lateral view; (b) dorsal view.
Entrapment of the nerve by a ganglion,64,65 a tight ligament or an osteophyte at the level of either the suprascapular notch or the spinoglenoid notch66,67 Sports activities of certain intensity and duration68 Acute brachial plexitis Trauma, e.g. shoulder luxation or scapular fracture69 Idiopathic neuritis.
CHAPTER 37
Suprascapular nerve
Spinoglenoid notch -+=;;;,..o",--:�'-..,.:::!'--�
Figure 37.15
Anatomy of the suprascapular nerve.
Infraspinatus
-
NERVE LESIONS OF THE UPPER LIMB 555
the supraspinatus will be most affected, or at the spino glenoid notch leading to isolated infraspinatus weakness. The patient complains of a fatigue-like pain which may be aggravated by activities that stretch or mobilize the nerve, such as combing one's hair or moving the scapulae. On clinical examination, full passive lateral rotation of the arm may provoke some pain, as may all active and passive scapular movements. Passive horizontal adduction of the arm is also painful. Cervical move ments are normal. Weakness of both resisted abduction and lateral rotation is the most striking sign, together with atrophy of both infra- and supraspinatus muscles. Lateral rotation is weaker than abduction. Compensating hypertrophy of other muscles, such as the teres minor, may occur. An EMG shows a denervation of the infra- and supraspinatus which, together with the history of an injury, confirms the diagnosis. Ultrasonography can be used to show a ganglion. Magnetic resonance imaging is appropriate to diagnose entrapment?O Treatment consists of avoiding all activity that stretches the nerve and steroid infiltration. If this treat ment is unsuccessful, surgical decompression of the nerve at the suprascapular ligament is necessary. In most patients it leads to full relief.71on The patient sits on a chair. The entire spine of the scapula is marked from the medial to the lateral edge. This line is bisected and a second line drawn at a 45° angle in an anterolateral direction. A 2.5 cm mark is made on this second line and a 7 cm needle, fitted to a syringe containing 2 ml of steroid, is inserted vertically downwards at this point until it hits the bone at the base of the scapular spine (Fig. 37.17). The tip of the needle is then moved further anteriorly until it slips in the suprascapular notch. The steroid is injected here.
Technique: injection.
Mononeuropathy of the suprascapular nerve
Figure 37.16 Motor innervation of the supraspinatus (1) and the infraspinatus (2) muscles by the suprascapular nerve.
Suprascapular nerve entrapment
Entrapment is not so uncommon and may be the result of compressive cystic, ligamentous or bony elements. It may occur at the suprascapular notch, in which case
The history is the same as in mononeuritis of the accessory or of the long thoracic nerve. Differentiation can easily be made by clinical examination. Sometimes atrophy of both supra- and infraspinatus muscles is visible on inspection. Weakness of both resisted abduc tion and lateral rotation of the arm is present. Weakness is most marked on lateral rotation. Because the deltoid and the teres minor muscles are intact, active movements of elevation and lateral rotation of the arm remain possible. No specific cure exists. The pain disappears spontaneously within 3 weeks, weakness within 4-5 months.
556 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
Figure 37.17
,
Injection for suprascapular nerve entrapment.
.
DISORDE�S OF THE �� �LLARY �E�VE . , '
�,'
ANATOMY
The axillary nerve takes origin in the posterior cord of the brachial plexus from fibres derived from C5-C6. It passes over the posterior aspect of the shoulder joint and curves medially around the neck of the humerus. A motor branch for the teres minor muscle detaches at the same time as a sensory branch - the upper lateral cutaneous nerve of the arm. The axillary nerve continues as a motor nerve deeply under the deltoid and divides into an ante rior and a superior branch which innervate the deltoid muscle (Fig. 37.18).
Posterior cord
Axillary nerve --'�---i--+-�
To teres minor ----+-"--+---�:iIi
INNERVATION
The axillary nerve is mixed. The motor branches inner vate the deltoid muscle and the teres minor muscle. The sensory branch innervates the skin over the deltoid region and the upper and lateral part of the arm. DISORDERS
Radial nerve -------1/---\-->..-,
Figure 37.18 The axillary nerve and its motor innervation of deltoid teres minor (2) muscles.
(1) and
The axillary nerve: •
Is very vulnerable to trauma: because of its close rela tionship with the shoulder joine3 it can easily become affected following shoulder dislocation or proximal humeral fracture and also by direct contusion.7 4•75
• •
Can be damaged during surgical interventions in the ' shoulder region. Can be affected as part of an acute brachial plexitis (Stewart:25 his p. 168).
CHAPTER 37
This nerve can easily be damaged in a dislocation of the head of the humerus or by a humeral fracture. An unintentional local infiltration with steroid into the axil lary nerve on infiltrating too far distally for infraspinatus tendinitis may cause the same problem. The patient usually complains of pins and needles in the deltoid area. Sometimes extensive visible wasting of the deltoid is present, together with an area of cutaneous analgesia in the mid-deltoid region. According to Cyriax,76 (his p. 153) some patients tend to relax the axillary nerve as much as possible by elevating the scapula at the same side during the first few weeks after the injury. The process is a consequence of spasm of the trapezius and leads to pain on passive side flexion of the neck towards the contralateral side. Deltoid palsy is obvious. Because the supraspinatus muscle is not involved, active elevation of the arm remains possible, but severe weakness is found on resisted abduction. The diagnostic test is to ask the patient to abduct the arm to 90° and to bring it further backwards into hori zontal extension (Fig. 37.19). This is impossible with an axillary nerve lesion. Spontaneous cure is possible but takes about 6 months. Care should be taken to mobilize the shoulder during the recovery so as to avoid an immobilizational arthritis. If no improvement has occurred after 6 months, surgical decompression is needed via a release of the teres minor and major tendinous insertions.
Figure 37.19
Resisted horizontal extension.
-
NERVE LESIONS OF THE UPPER LIMB 557
DISORDERS OF THE RADIAL NERVE ANATOMY
The radial nerve takes origin in the posterior trunk of the brachial plexus and thus contains fibres from C5-TI. It reaches the lateral wall of the axilla and winds around the posterior aspect of the humerus in the groove for the radial nerve. It then pierces the lateral intermuscular septum to enter the anterior compartment of the arm. It lies lateral to the biceps and continues between the biceps tendon and the proximal part of the brachioradialis muscle. At the level of the elbow it divides into a superficial sensory branch (the superficial radial nerve) and a deep motor branch (the deep radial nerve). The latter continues to become the posterior interosseous nerve. The superficial radial nerve lies under the brachioradi alis muscle and follows the lateral border of the radius until at the wrist it divides into terminal digital branches to the dorsoradial part of the hand and the three radial digits. The posterior interosseous nerve winds around the neck of the radius and goes into the dorsal compartment of the forearm. It pierces the supinator muscle through the arcade of Frohse and runs deeply under the extensors as far as the wrist (Fig. 37.20).
Figure 37.20 The course of the radial nerve. 1, Supinator muscle; 2, superfcial radial nerve; 3, posterior interosseous nerve.
558 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
INNERVATION
The motor part of the radial nerve innervates mainly the extensors of the arm and forearm: triceps and anconeus muscles, brachioradialis, extensors of the wrist, supinator and extensors of thumb and fingers. The sensory part supplies the skin of the lateral arm, the posterior part of the forearm, the radial dorsum of the hand and the skin of the dorsal aspect of the proximal and middle phalanges of 3 t radial digits.
The fu l l radia l nerve syn d rome g ives rise to weakness of e l bow extension (triceps, anconeus) and s u p i nation (brachio rad i a lis, s u pinator), and exte nsion of the wrist (extensor carpi radia l i s l o n g u s and brevis, extensor carpi u l na ris). Extension of the fingers at the metaca rpo p h a l a ngeal joints is a lso weak (extensor d igitorum, extensor in d i cis proprius, extensor d i giti m i n i m i), as we l l as abd uction and exte nsion of the th u m b (abd uctor pol licis long us, extensor pol licis l o n g u s and brevis). Sensory deficit may be found at the latera l aspect of the a rm a n d posterior aspect of the forearm as far as the dorsum of the wrist. Paraesthesia is experienced o n the dorsal aspect but not i n the termin a l p h a l a nges of the t h u mb, i ndex a n d m i d d l e fing ers and t h e radia l half of the fourth finger ( F i g . 37.2 1 ).
DISORDERS
The radial nerve is quite frequently affected by pathologi cal conditions. This happens in more generalized diseases, such as poisoning by heavy metals (e.g. lead), but also in more localized lesions, either traumatic or following entrapment of the nerve tissue. The symptoms and signs depend on where, along the nerve, the lesion lies. The radial nerve may become affected at five different sites: the proximal and middle part of the upper arm, the distal part of the upper arm, the proximal part of the forearm and the distal part of the forearm (Table 37.3).
axillary palsy.69 Space-occupying lesions in the axilla or the use of old-fashioned axillary crutches are other (rare) causes.77,78
LESIONS AT THE PROXIMAL AND MIDDLE PART OF THE UP P ER ARM
When the lesion results from an injury - fracture or dis location of the humerus - it is usually combined with an
Figure 37.21
Sensory supply in the hand by the radial nerve.
Table 37.3 The radial nerve and its branches Branching off
Nerve
Supply
Upper third of upper arm
Posterior cutaneous nerve of arm (sensory)
Skin of lateral arm
Middle third of upper arm
Muscular rami (motor)
Triceps Anconeus
Posterior cutaneous nerve of forearm (sensory)
Skin of posterior forearm
Lower third of upper arm
Muscular rami (motor)
Brachioradialis Extensor carpi radialis longus Extensor carpi radialis brevis (Brachialis)
ProximaUorearm (elbow)
Superficial terminal branch (sensory)
Skin of radial dorsum of hand
Deep terminal branch (motor)
Supinator Extensor digitorum Extensor digiti minimi Extensor carpi ulnaris
Posterior interosseous nerve (motor)
Abductor pollicis longus Extensor pollicis longus Extensor pollicis brevis Extensor indicis proprius
Superficial terminal branch 5 dorsal digital nerves (sensory)
Skin of dorsal aspect of proximal and middle phalanges of 3 t radial digits
,
Distal forearm (wrist)
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 559
Examina tion reveals weakness of extension and supihation of the elbow, together with weakness of extension of wrist, fingers and thumb. This results in a characteristic position of elbow and hand - porter 's hand or drop hand. Because of the anastomoses between the posterior cutaneous nerve of the arm - first branch of the radial nerve - and other neighbouring nerves, sensory deficit is not common but when it occurs it is found at the lateral aspect of the arm and posterior aspect of the forearm as far as the dorsum of the wrist. Differential diagnosis must be made from spinal cord, intraspinal and radicular lesions (C7), as well as conditions affecting the brachial plexus, neuritises or myopathies.
LESIONS AT THE DISTAL PART OF THE UP PER ARM
Lesions are more common at the distal than the middle and proximal part of the arm. The palsy may be trau matic - fracture of the humerus,79,8o fracture or disloca tion of the elbow - or may result from a sustained pressure just proximal to the elbow. This is typically the case in a patient who has fallen asleep with the arm over the edge of a chair or has lain all night with the arm resting against the hard edge of a bunk - 'Saturday night paralysis'. The fu 11 radial syndrome develops, except that the triceps and anconeus muscles are unaffected, as is the brachioradialis muscle. The patient awakes with a painless dropped wrist. Sensory disturbances may occur at the dorsal aspect of the forearm when the posterior cutaneous nerve of the forearm is involved, although this area may have over lapping supply from neighbouring sensory nerves - the lateral and medial cutaneous nerves of the forearm. The superficial sensory branch of the radial nerve is responsi ble for cutaneous deficit at the radial and dorsal aspect of the hand, except when anastomoses with either the lateral cutaneous nerve of the forearm - a sensory branch of the musculocutaneous nerve - or the dorsal branch of the ulnar nerve at the hand provide an alternative pathway.
the extensor indicis proprius. When a lesion occurs prox imal to this division, symptoms of both are combined. As the branches supplying the brachioradialis, extensor carpi radialis longus and brevis, and brachialis escape the compression, there is only weakness of supination, extension of the fingers, ulnar deviation of the wrist and extension and abduction of the thumb. DEEP BRANCH OF THE RADIA L NERVE
Conditions such as fracture and/or luxation of the head of the radius or local inflammatory processes, for example chronic bicipitoradial bursitis, may cause compression of the deep branch of the radial nerve where it turns around the head of the radius. The result is weakness of supina tion, ulnar deviation of the wrist and finger extension. POSTERIOR INTEROSSEOUS NERVE OF THE FOREARM
Just below the point where the deep radial nerve comes to lie at the dorsal aspect of the forearm the posterior interrosseous nerve of the forearm branches off and passes through the deep and superficial heads of the supinator brevis muscle (Fig. 37.22 ). When the edge of the upper border of the superficial head has become fibrous, this opening forms the arcade of Frohse,81 also called the radial tunnel. The nerve then passes further down along the interrosseous membrane and irulervates the abductor pollicis longus, extensor pollicis longus and brevis, and extensor indicis proprius muscles. The posterior interosseous nerve can be compressed as the result of: (1) an injury, usually a fracture (or the hard ware used to fix fractures),82,83 or elbow joint dislocation;84 (2) space-occupying lesions, such as synovial proliferations from the elbow joint in rheumatoid arthritis85 or soft tissue tumours,86,8? for example lipomas; or (3) fibrous bands, which can be traumatic in origin (e.g. Volkmann's contracture) or developmental (arcade of Frohse).88-92
LESIONS AT THE UP PER PART OF THE FOREARM
Level with the head of the radius the radial nerve divides in its two terminal branches - the superficial (sensory) and deep (motor) branches (see Fig. 37.20). The latter then forks off into (1) muscular rami running towards the supinator, extensor digitorum, extensor digiti minimi and extensor carpi ulnaris muscles, and (2) the posterior interrosseous nerve of the forearm, which supplies the long abductor and extensors of the thumb as well as
Figure 37.22 muscle.
Course of the posterior interosseous nerve through the supinator
560 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
Many authors believe that compression of the poste rior interosseous nerve at the point where it passes through the arcade of Frohse is a cause of lateral elbow pain and they therefore consider it as a type of tennis elbow. We do not agree that this condition should be con sidered to be a (resistant) type of tennis elbow, because the lesion does not lie in the extensors of the wrist. Hagert et al93 also regarded epicondylitis and posterior interosseous nerve entrapment as 'two different dis orders, which have nothing to do with each other, and which should therefore not be mixed up'. Radial tunnel syndrome
In 1883, Winckworth stated that the posterior interosseous nerve could become compressed where it passes through the supinator muscle.94 Since Roles and Maudsley described the radial tunnel syndrome in 1972, 95 this pathology has become recognized as a cause of resistant tennis elbow.86,88,96--98 This idea is based on the reports of good results after surgical decompression of the posterior interosseous nerve at the radial tunnel,99, l OO Nerve compression by the edge of the superficial supinator muscle seems to occur on passive pronation of the forearm. On active supination the increase of pressure is much greater, which has led to the conclusion that dynamic compression of the posterior interosseous nerve by the edge of the superficial supinator muscle is probably a cause of local nerve irritation and pain. In compression of a predominantly motor nerve, such as the posterior interosseous nerve, the main symptom would be paralysis. Kopell and Thompson, however, state that entrapment of a motor nerve may cause dif fusely localized dull aching pain.lOl The pain would originate from the nociceptive thin or non-myelinated afferent nerve fibres of muscular and extramuscular origin. 1 02 However, the symptoms described by different authors are very similar to those found in tennis elbow: pain at the lateral side of the elbow, radiating distally along the posterior aspect of the forearm. The pain may be constant and can be brought on or aggravated by exertion, especially rotation movements, and the symptoms continue for some time after the causative strain has ceased. There is also diffusely localized pain on resisted supination and/or pronation as well as on resisted extension of the middle finger. Local tenderness is present over the proximal and posterior aspect of the forearm, at the suspected entrapment site. These symp toms and signs correspond with the clinical picture of what we have described as type IV (muscular) tennis elbow (see p. 456). Treatment consists of surgical decompression. After surgery, the pain seems to disappear gradually, in the course of 6-12 months.
Werner analysed the hypothesis that posterior interosseous nerve entrapment can be a cause of lateral elbow pain.103 The following investigations were carried out: patients with suspected posterior interosseous nerve entrapment were operated on by decompression of the nerve and then subjected to a follow-up for 2 years; the topographical anatomy was compared with observa tions at dissections; the epidemiology and symptomatol ogy were compared with that in a series of cases of lateral epicondylitis. He concluded that lateral elbow pain may indeed be caused by dynamic compression of the poste rior interosseous nerve and that it can be relieved by decompression of the nerve where it enters through the supinator muscle. The diagnosis is based solely on palpa tion and on positive resisted supination. Pain on resisted extension of the middle finger seems to be an unreliable test. Electrophysiological examinations (EMG) are of limited diagnostic value. Using Cyriax's methods to examine lateral elbow pain, we have some difficulties in accepting the existence of a radial tunnel syndrome, giving rise to pain. If the main symptom is pain at the lateral aspect of the elbow and the pain is clearly aggravated by a resisted movement, one should think of a lesion of a contractile structure and try to find out what structure is at fault: • •
Pain on resisted supination draws attention to the supinator brevis muscle. Pain on resisted extension of the middle finger does not exclude a tennis elbow, because this test also implicates the extensors of the wrist.
Differential diagnostic tests should be included (see p. 456). Pain on palpation is not reliable: the lateral aspect of the elbow is always tender to the touch and therefore the response to the palpatory manoeuvres may be false positive. We conclude that the diagnosis of radial tunnel syn drome is probably made too often. A clear distinction should be made between the two different conditions: (1) tennis elbow, a lesion in the radial extensors of the wrist, and (2) radial tunnel syndrome (see Table 37.4). Other authors share this view. 104,105 We believe that what has been described in the literature as radial tunnel syndrome very often has nothing to do with the posterior interosseous nerve at all, but is simply a lesion of an extensor of the wrist, the symptoms of which have erroneously been attrib uted to that nerve. We speculate that the good results claimed for surgery may be the outcome of either spon taneous recovery or incidental permanent lengthening of some muscular fibres during operation. In the latter instance, the operation, ostensibly for radial tunnel syn drome, unintentionally becomes an operation for tennis elbow.
CHAPTER 37
-
NERVE LESIONS OF THE UPPER LIMB 561
Table 37.4 Differential diagnosis: type IV tennis elbow and radial tunnel syndrome
Elbow pain
Tennis elbow type IV
Radial tunnel syndrome
Lateral pain on hand movements
Ache at elbow, especially at rest or after repetitive pronation and supination
Resisted test
Pain on wrist extension and radial deviation
Negative
Tenderness
In deep muscles overlying neck of radius
In supinator
Weakness
No muscular weakness
Possible weakness of thumb and index finger
When entrapment of the posterior interosseous nerve at the elbow occurs it should give rise to a dull ache over the lateral aspect of the elbow, eventually radiating down the posterior aspect of the forearm. In due course, weakness will be found of abduction and extension of the thumb and of extension of the index finger. Paraesthesiae are absent. St�wart confirms our view. 1 06 His ideas are also based on clinical findings and have been reinforced following the publication of three studies showing that, in this group of patients in whom pain is the main symptom, there is little evidence for a focal nerve lesion.107-109 He also cites some references that support the value of the diagnostic findings and confirm the good results after operative release, just as we think, not because of the posterior interosseous nerve decompression but because of the release of the lateral extensor aponeurosis from the lateral epicondyle.l10,1l3
LESIONS AT THE DISTAL PART OF THE FOREARM Figure 37.23
The superficial sensory branch of the radial nerve runs under the brachioradialis muscle along the radial artery and further towards the hand. At the level of the wrist it divides in five dorsal digital nerves (Fig. 37.23) and sup plies the skin at the dorsal aspect of the thumb, index, middle and radial half of the fourth finger but not the ter minal phalanges, which are supplied by the median nerve. In the distal part of the forearm the nerve may rarely become affected as the result of external pressure (e.g. damage by handcuffs);1l4,1l5 the result is paraesthesia and sensory deficit over the radial and dorsal aspect of the hand. If the pressure involves the medial and dorsal branch to the thumb, for example after the protracted use of small scissors, the ulnar aspect of the thumb becomes numb.
I
DISORDERS OF THE ULNAR NERVE
ANATOMY
The ulnar nerve takes origin in the lower trunk of the brachial plexus from the spinal nerves C8-n. It runs
Branching of the superficial sensory branch of the radial nerve.
from the axilla down the medial aspect of the upper arm. At mid-humerus it pierces the medial intermuscular septum towards the posterior compartment. It follows the medial head of the triceps onto the retrocondylar groove at the elbow. It then courses under the aponeu rotic arch joining the two heads of the flexor carpi ulnaris muscle - the cubital tunnel - and follows its course towards the wrist, under this muscle (Fig. 37.24). At the wrist it runs through Guyon's tunnel before it divides into its terminal branches. INNERVATION
There are no branches in the upper arm. In the forearm motor branches supply the flexor carpi ulnaris muscle and the ulnar half of the deep flexor digitorum. Sensory branches supply the skin of the ulnar half of the hand. At the wrist the ulnar nerve, as it leaves Guyon's tunnel, divides into a superficial and a deep branch. The deep branch is motor and innervates the hypothenar muscles, the interossei, the two ulnar lumbricals and, on the thenar side of the hand, the adductor pollicis and the deep head
562 SECTION SE VEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
of the flexor pollicis brevis. The superficial branch is sensory and supplies the skin of the little finger and the ulnar half of the ring finger. DISORDERS
Ulnar nerve entrapment is one of the most frequent peripheral neuropathies, especially compression of the nerve at the level of the elbow. As it is a combined motor and sensory structure (Table 37.5) entrapment leads to a gamut of symptoms and signs. The two most frequent localizations of compression are pressure in the cubital tunnel at the inner side of the elbow, and pressure in the area of Guyon's tunnel at the wrist. The f u l l u l n a r nerve syn drome leads to weakness of the u l na r flexors of wrist a n d f i n gers (flexor carpi u l n aris, u l n a r h a l f of flexor d i gitorum su perfi c i a l i s a n d profundus), the hypothe n a r m uscles (abd uctor d i giti m i n i m i , flexor d i giti m i n i m i brevis, opponens d i giti m i n i m i , palmaris brevis), the i ntrinsic muscles of the ha nd (dorsa l a n d p a l m a r i nterossei, u l n a r two l u m b ri c a l s) and part of the the n a r muscles (add uctor p o l l icis a n d deep head of flexor poll icis brevis). Sensory deficit is found i n the u l n a r ha lf of the ha nd and, in the u l n a r two f i n gers, the entire fifth fi nger and the u l n a r h a l f o f the fourth f i n ge r.
Figure 37.24
LESIONS AT THE ELBOW
Anatomy of the ulnar nerve.
In 1877, Panas116 was the first to describe ulnar nerve palsy, in a paper to the Academie de Medecine. Since Table 37.5 The ulnar nerve and its branches Branching off
Nerve
Supply
Upper arm
None
None
Elbow
Muscular rami (motor)
Flexor carpi ulnaris Deep flexor digitorum - ulnar half (Superficial flexor digitorum - ulnar half)
Lower forearm
Palmar cutaneous (sensory)
Skin of ulnar proximal palm of hand
Proximal to Guyon's tunnel
Dorsal digital (sensory)
Skin of ulnar dorsum of hand Skin of dorsal aspect of ulnar 1 t fingers
Muscular ramus (motor)
Palmaris brevis
Distal to Guyon's tunnel
Muscular rami (motor)
Abductor digiti minimi Opponens digiti minimi
Hand
Superficial terminal branch (sensory)
Skin of ulnar distal palm of hand Skin of palmer (and dorsal) aspect of ulnar 1 t fingers
Deep terminal branch (motor)
Interossei Ulnar two lumbricals Adductor pollicis Flexor pollicis brevis (deep head)
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 563
may be the result of recurrent dislocation of the nerve.119,120 The patient notices that from time to time the nerve comes out of its groove and then replaces spontaneously. This phenomenon is sometimes accompanied by a paraesthetic twinge felt in the ulnar aspect of the hand and the ulnar one and a half fingers. Recurrent dislocation may in the end lead to ulnar palsy. A fall on the elbow or a direct blow to the medial aspect of the elbow may bruise the nerve sheath which becomes irritated. The condition is self-perpetuating, as flexion movements continue the trauma. Structural changes may alter the stress on the nerve and thus cause friction on certain movements. These changes are excessive cubitus valgus or alterations of the position of the elbow after mal-united fractures of the medial condyle.12l Humeral trochlear hypoplasia has been described as a rare condition that may result in ulnar nerve palsy.122 Positions of prolonged flexion (e.g. during the night) may in the end set up the known symptoms. This type of ulnar nerve lesion is sometimes known as cubital tunnel syndrome.123 Osborne124 described 'tardy ulnar neuritis', after having observed compression of the ulnar nerve where it pierces the flexor carpi ulnaris. Wadsworth and Williams125 have pointed out that because the medial collateral ligament, behind which the nerve passes, runs from a fixed point at the medial epicondyle to a movable one (the olecranon), the nerve is subject to compression during elbow flexion. The ligament becomes taut and exerts pressure.126 A loose body causing compression of the ulnar nerve is quite uncommon. If a loose fragment in the elbow joint displaces medially at the posterior aspect of the joint, it can compress the ulnar nerve and cause paraesthesia in its territory. A non-capsular pattern will be found on examination. Osteophytes, tumours or ganglia of the nerve may compress the nerve in the cubital tunnel. Idiopathic: the aetiology very often remains unknown.127 In as many as 50% of cases a precipitating cause is not apparent.128
• Friction
•
•
Flexor carpi ulnaris
Aponeurosis
Olecranon
Figure 37.25 The cubital tunnel.
then, several authors have described this lesion as well as the possible surgical treatments. The ulnar nerve courses under the medial head of the triceps muscle towards the posterior aspect of the medial epicondyle (see Fig. 37.24) where it lies superficially in a shallow groove behind this bone (sulcus for the ulnar nerve) and is therefore very vulnerable to direct contu sion. It becomes stretched during flexion of the elbow. The nerve runs further distally in between the two heads of the flexor carpi ulnaris muscle, which form an apo neurotic arch. Together with the medial epicondyle, the olecranon and the medial collateral ligament, this arch forms the cubital tunnel (Fig. 37.25).
•
•
AETIOLOGY
Entrapment of the ulnar nerve - cubital tunnel syndrome - is the second most common compressive neuropathy of the upper extremity, with only carpal tunnel syndrome presenting more frequently. Entrapment of the ulnar nerve at the elbow has several different causes, summa rized in Box 37.3:
• •
DIAGNOSIS Box 37.3 Summary of the aetiology of ulnar nerve palsy Friction Tra u matic Structural Postural Loose body Space-occ u pying lesions U n known
The history is obvious. The patient describes paraesthesia and/or numbness in the ulnar half of the fourth and the entire fifth finger and eventually weakness or clumsiness of the hand. A slight ache may also be felt at the elbow. A history of trauma may be elicited or merely that the symptoms came on spontaneously. In spontaneous onset, further questioning may determine whether the cause is postural.
---
564 SECTION SE VEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
On inspection there may be signs of joint abnormality. Furthermore, there may be wasting of the intrinsic muscles of the hand, the hypothenar muscles or some forearm muscles - flexor carpi ulnaris and deep flexors of the fingers. In severe cases, the patient may present with an ulnar palsy leading to weakness of the ulnar half of the deep flexor digitorum and of the flexor carpi ulnaris muscles, with weakness of the intrinsic hand muscles resulting in a claw hand. On examination, signs are found that immediately draw attention to the ulnar nerve. A few accessory tests may give some further confirmatory information: •
•
•
•
The elbow is brought into maximal flexion and maintained there for a few minutes, which may bring on the pins and needles and indicates a possible postural cause. The elbow flexion test:129 with the patient sitting and both shoulders and arms in the anatomical position, both elbows are fully but not forcefully flexed, with full extension of the wrist. This position is maintained for a few minutes and the patient reports to the examiner at regular intervals whether pain, numbness or tingling occur or increase.1 30 When combined with pressure on the ulnar nerve the test becomes even more sensitive.13] Tests for the sensitivity to light touch and two-point discrimination in the peripheral distribution of the ulnar nerve. Specific testing of the motor function of the abductor digiti minimi, the flexors digitorum profundi to the little and ring fingers and the flexor carpi ulnaris muscles.
Figure 37.26
On palpation of the inner aspect of the elbow, tender ness in the nerve sheath may be found and should be compared with the other elbow. A positive finding sug gests frictional neuritis. Thickening of the nerve sheath indicates recurrent dislocation. Because it is not always clear whether the cause lies either at the elbow or at the wrist, tenderness should also be sought at Guyon's tunnel at the wrist.132 Failure to find a local cause may indicate a neuritis from metabolic problems such as diabetes mellitus, alcoholism, hypothyroidism or lead poisoning. According to McGowan, cited by some authors, l 33,134 ulnar entrapment neuropathy can be classified into three grades: subjective symptoms combined with hypoaesthesia in ulnar fingers. Grade II: weakness and wasting of the interossei, combined with subjective symptoms. Grade III: marked weakness and wasting of the interossei, adductor pollicis and hypothenar muscles, combined with anaesthesia in the ulnar fingers.
• Grade I: • •
A differential diagnosis must be made with other possible proximal causes: cervical myelopathies, anterior horn lesions, polyneuropathies, myopathies, cervical nerve root problems (C7, C8) and thoracic outlet syn drome;Bs or a more distal cause, which is compression in Guyon's tunnel.1 36 Electromyography can be useful;1 37 and alternatively, an infiltration with a local anaesthetic may prove diagnostic.
Steroid infiltration for an ulnar nerve lesion at the elbow.
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 565
TREATMENT Avoidance of postural strains or pressure
The patient's daily activities should be studied to see what causes or influences symptoms. Precipitating or aggravating postures or movements which stretch or compress the ulnar nerve should be avoided. It may be necessary to explain this in some detail to the patient. Some patients can be helped by the use of a night splint, worn for several months.138,1 39 Infiltration
An injection of 1 ml of triamcinolone suspension about the nerve, not into it, will desensitize the nerve sheath and lead to lasting relief in those cases in which the only symptom is paraesthesia and in which conduction has not yet become impaired (Fig. 37.26). Surgery
Surgical treatment may be by simple decompression,1 4o anterior subcutaneous,141,142 intramuscular 1 43-145 or sub muscular1 46 transposition of the nerve, or medial epi condylectomy.1 47-1 52 Transposition or epicondylectomy is performed when structural changes are responsible for the friction and when the causative strains cannot be avoided. Postsurgical early mobilization speeds up the period of recovery. 153,15 4
LESIONS AT THE WRIST
Three different types of compression of the ulnar nerve at the wrist have been described: purely motor, purely sensory and a mixed form, dependent on the site of the compression.155 Consequently, the diagnosis may not be easy. Furthermore, there is the possibility of a Martin Gruber anastomosis (see p. 424) which again makes the diagnosis more difficult. The ulnar nerve, together with the ulnar artery, passes through the tunnel of Guyon. This tunnel lies between two dynamic structures, the pisiform and hamate bones, and is covered by the pisohamate liga ment (Fig. 37.27), which is a continuation of the flexor carpi ulnaris tendon. Proximal to the wrist, the palmar cutaneous branch arises and runs over the palmar aspect of the forearm and wrist outside the tunnel of Guyon to supply the proximal part of the ulnar side of the palm. A few centimetres more distally the dorsal cutaneous branch arises and supplies the ulnar side of the dorsum of the hand, the dorsal aspect of the fifth finger and the ulnar half of the fourth finger (Fig. 37.27). As it leaves the tunnel of Guyon, the nerve divides into a mainly sensory superficial terminal branch, which sup-
Figure 37.27 The ulnar nerve passes through the tunnel of Guyon (upper); but the dorsal cutaneous branch (lower) does not.
plies the distal ulnar border of the palm of the hand and the palmar surfaces of the fifth and ulnar half of the fourth finger (Fig 37.28), and a deep terminal branch, which is entirely motor and innervates nearly all of the small muscles of the hand: palmaris brevis, abductor digiti minimi, opponens digiti minimi, flexor digiti minimi brevis, dorsal interossei, palmar interossei, third and fourth lumbricals, adductor pollicis and the deep head of the flexor pollicis brevis.156
566 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
TREATMENT
This depends on the cause and severity of the lesion. Very often rest and avoidance of the causative strain can be sufficient. In more severe cases, local infiltration with a steroid suspension or surgical decompression may be necessary.
,
. '1
DISORDERS OF THE MEDIAN NERVE. ' •
' ... .
,"
�'
•
-r.
::-�:. � ••�:,
ANATOMY Figure 37.28
Sensory supply in the hand by the ulnar nerve.
AETIOLOGY
The cause may be either intrinsic or extrinsic. Intrinsic causes are a cyst, the most common cause; a lipoma; an abnormal position of the abductor digiti minimi muscle,IS7 or anatomical variation in the flexor carpi ulnaris tendon.1S8 Extrinsic conditions are an injury with or without fractures of the pisiform or hamate bones and professional or sporting overuse.tS9 SYMPTOMS
The symptoms may be compared with those resulting after compression of the nerve at the elbow. Because the ulnar nerve divides into a superficial and a deep branch at the wrist, the symptoms may be purely motor (deep branch) or purely sensory (superficial branch). Sensation over the dorsal aspect of the fingers remains unaltered, because the dorsal sensory branch has an origin proximal to the wrist. Four localizations are possible:160 at the pisiform bone. This causes compression of the superficial and deep branches with sensory and motor deficit (hypothenar and intrinsic hand muscles). Within Guyon 's tunnel, with compression of the deep motor branch, which results in a motor deficit of the hypothenar and intrinsic hand muscles. There is no sensory deficit. Distal to Guyo n 's tunnel, at the hook of the hamate bone; as a result of compression of the deep palmar branch the intrinsic hand muscles are weak.
• Proximal to G uyon 's tunnel,
•
•
The median nerve arises from the junction of the medial and lateral cords of the brachial plexus and thus from the segments C5-Tl. It runs anteriorly towards the elbow, between the biceps and the brachialis muscles and courses medial to the distal biceps tendon and in between the two heads of the pronator teres muscle. It passes under the aponeurotic arch joining the two heads of the superficial flexor digitorum and runs directly to the wrist where it passes into the carpal tulmel before dividing into its terminal branches (Fig. 37.29). INNERVATION
There are no branches in the upper arm. Just distal to the elbow the first branches arise for the pronator teres, the flexor carpi radialis, the palmaris longus and the superficial flexor digitorum. The anterior interosseous nerve of the forearm innervates the pronator quadratus, the flexor pollicis longus and the radial half of the deep flexor digitorum. A sensory branch innervates the skin over the thenar and the radial half of the palm of the hand. After passing the carpal tunnel the digital nerves divide to supply the skin over the 3 t radial digits ana the muscles of the thenar eminence except those innervated by the ulnar nerve (Fig. 37.29).
• In the palmaris brevis m uscle at the distal part of Guyon 's
t � nnel; the superficial branch is compressed and gives nse to a purely sensory deficit.
A fifth type of compression with motor deficit of the first dorsal interosseous and the adductor pollicis muscles has been reported by Yu-Sung et aU61
Figure 37.29
Sensory supply by the median nerve.
CHAPTER 37
-
NERVE LESIONS OF THE UPPER LIMB 567
DISORDERS
The median nerve (Table 37.6, Fig. 37.30) is the most important nerve of the hand, because it renders opposi tion of the thumb possible, combined with a circular pronation movement, as well as flexion of the radial fingers. Palsy of this nerve leads to total incapacity of the hand. The fu l l median nerve syn d rome affects the pronator teres, the flexor carpi rad i a l is, the ra d i a l h a l f of the flexor d i g ito rum su perficia l i s and profundus, the f l exor p o l l icis longus and the pronator q u a d ratus, the thenar (abd uctor po l l icis brevis, superfi c i a l head of the flexor p o l l icis brevis, o p po nens poll icis) and the rad i a l two l u m b ricals. The sensory deficit is detected in the rad i a l h a l f of the p a l m of the hand, the palmar aspect of the thu mb, i n dex a n d m i d d l e fin gers a n d t h e ra d i a l h a l f o f t h e r i n g finger, as we l l as the dorsal aspect of the d i sta l p h a l a n ges of the same fi ngers.
LESIONS AT THE LOWER PART OF THE ARM AND AROUND T HE E LBOW
The median nerve can become damaged as the result of supracondylar fractures or elbow dislocation. It can also become compressed above the elbow by a supracondylar process and the ligament of Struthers, if the latter is present. Thickening or fibrosis of the bicipital aponeuro sis may also cause compression. Below the elbow, the problem is most common at the point where the median nerve and its anterior interosseous branch dip between the two heads of the pronator teres. Thickening of the fascia that holds these two heads together can cause com pression - the pronator teres syndrome.162,163
Figure 37.30
The course of the median nerve.
Table 37.6 The median nerve and its branches Branching off
Nerve
Supply
Elbow
Muscular rami
Pronator teres Flexor carpi radialis Palmaris longus Superficial flexor digitorum
Upper forearm
Anterior interosseous
Flexor pollicis longus Deep flexor digitorum (radial halD Pronator quadratus
Wrist
Palmar cutaneous
Skin of radial palmar aspect of hand
Hand
Common palmar digital Motor palmar digital branch I
Abductor pollicis brevis Flexor pollicis brevis (superficial head) Opponens pollicis Lumbrical I
Motor palmar digital branches I I-III
Lumbrical II
Sensory palmar digital branches I-III
Skin of palmar aspect of 31 radial digits Skin of dorsal aspects of terminal phalanges of 31 radial digits
568 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
The clinical picture includes weakness of the median innervated muscles distal to the pronator teres muscle the flexor pollicis longus and the thenar muscles. Sensory deficit is often present. Pain is certainly not the main complaint. The following accessory tests have been described: • • •
Local pressure during isometric pronation Sustained isometric flexion of the middle finger Tinel's sign: percussion in the area of the pronator teres muscle.
Infiltration of steroid solution in the area of com pression is usually curative. If not, surgical release is performed. Pronator teres syndrome is probably a tunnel syn drome that is easily overestimated. The picture should be confirmed objectively by sensory and electrophysiologi cal examination. When the tentative diagnosis cannot be confirmed, possible compartment syndrome or lesion of the pronator teres muscle should be considered.
LESIONS AT THE FOREARM: ANTERIOR INTEROSSEOUS NERVE
Compression of the anterior interosseous nerve - a branch of the median nerve - is known as the Kiloh-Nevin syndrome. 164,165 The symptoms are pain in the volar aspect of the prox imal forearm, which sometimes worsens at night. After some months of compression, weakness of the flexor pollicis longus, deep flexor digitorum of the index and middle fingers, and pronator quadratus muscles may supervene and cause an inability to write. Diagnosis must be based on clinical examination and not on electromyographic findings.166-169
3
2 --+��-- 4
Figure 37.31
The boundaries of the carpal tunnel (right hand, palmar view):
1, scaphoid; 2, trapezium; 3, pisiform; 4, hamate.
Carpal tunnel syndrome is the most common periph eral entrapment neuropathy. 1 71,m While first recognized by Sir James Paget in 1854,173 it was not until 1942 that Cyriax174 described irritation of the median nerve under the heading 'median perineuritis'. The condition remained further unrecognized until 1946, when more detailed description was given. 1 75, 1 76 Full appreciation of how common the lesion is followed Phalen's article.177 AETIOLOGY
Any factor that provokes an increase in volume of a struc ture within the carpal tunnel may in the end compress the median nerve. The cause may either be local or systemic. On the basis of observation, two types are distinguished: a full syndrome (symptoms in the entire territory of the nerve) and a partial syndrome (symptoms in only a part of the nerve's territory), summarized in Box 37.4. 3
4
5
palmar
LESIONS IN THE CARPAL TUNNEL
The palmar aspect of the carpus is concave and covered with the transverse carpal ligament. An osteofibrous canal, the carpal tunnel, is thus formed, of which the boundaries are the scaphoid and pisiform bones proxi mally and the trapezium and hamate bones distally. The canal thus lies more distally and more towards the ulnar aspect than is often thought, at the heel of the hand (Fig. 37.31). Within the carpal tunnel are found the median nerve, the tendons of the flexor carpi radialis and the flexor pol licis longus, in separate sheets, and the superficial and deep flexors of the digits within a common tendon sheath (Fig. 37.32).
Figure 37.32 Transverse section of the carpal tunnel: 1, flexor pollicis lon�us; 2, flexor carpi radialis; 3, median nerve; 4, transverse ligament of carpus;
5, superficial flexor digitorum flexor digitorum (4 tendons).
(4 tendons); 6, ulnar artery; 7, ulnar nerve; 8, deep
CHAPTER 37
Full syndrome ,
Idiopathic. Half of all cases are idiopathic, mostly women (68%) between 40 and 60 years. 1 78
Subluxation of the lunate bone following a (possibly minor) trauma suddenly fixes the wrist in flexion, immediately followed by paraesthesia in the ter ritory of the median nerve. After some days the patient also experiences numbness and some weeks later may even develop severe weakness of the thenar muscles. Occupational activities, such as repeated use of some tools (e.g. a screwdriver or a plane), or repetitive profes sional activities (e.g. polishing, sanding, massaging, tree felling, stirring with a pestle in a mortar) may cause irri tation of the median nerve. Once irritation has occurred, very little provocation is enough to provoke symptoms. Friction of the nerve may occur after wrist fracture, especially a Colles' fracture, as it becomes caught either by the callus or by the displaced bone. Traumatic.
Inflammatory. This occurs in conditions causing thicken ing of the transverse carpal ligament and the tendons in the carpal tunnel, such as rheumatoid arthritis.1 79 Gout
- NERVE
LESIONS OF THE UPPER LIMB 569
and pseudogout are also possible causes. The former gives rise to so much swelling that the nerve becomes severely compressed; the main symptom is then cuta neous analgesia. Other causes are amyloidosis, haematoma and rubellar polyarthritis. Endocrine. Possible causes are hypothyroidism, 18o with accumulation of myxomatous deposits within the carpal tunnel;1 81 acromegaly;1 82,183 pregnancy 1 84 (20% of preg nant women develop a carpal tunnel syndrome after the 6th month1 85); and menopause. Generalized peripheral neuropathy. This can occur in patients suffering from diabetes186 or uraemia.
The nerve may become compressed by a gan glion187 (e.g. swelling on a digital flexor tendon), benign hlmours (e.g. lipofibroma or neuroma) and malignant tumours.
Tumours.
Vascular conditions. These include conditions such as spontaneous bleeding in haemophiliacs and in patients on anticoagulant therapy; thrombosis of a congenital median artery may also damage the median nerve.
Partial syndromes Box 37.4 Aetiology of carpal tunnel synd rome Full syndrome Idiopathic Tra u matic S u b l uxation of l u nate bone Occupational Friction I n f l a m matory Rheumatoid a rthritis Gout/pseudogout Amyl oidosis Haematoma R u be l l a r polyarthritis Endocrine Hypothyroidism Acromegaly Pregnancy Menopause Genera l ized peripheral neu ropathy Diabetes U raemia Tumours G a n glia Be n i gn tumours:
l i pofibroma neuroma M a l i gn a nt t u m o u rs
Vasc u l a r Haemorrhage:
haemophiliacs anticoagu l a nts
Thrombosis of median a rtery
Partial syndromes Tra umatic 'Stick palsy' Trigger finger
These occur when pressure is exerted on one or several of the most distal terminal branches of the nerve. This can be the result of an injury, incorrect use of a walking stick or a trigger finger (see Ch. 36 and p. 572). H ISTORY AND SYMP TOMS
The condition starts in one hand, very often the dominant one, but becomes bilateral in 30% of cases. The first symp toms are pins and needles felt in the territory of the median nerve (Figs 37.29 and 37.33): the palmar aspect of the thumb, index, middle and radial half of the ring finger, as well as the dorsal aspect of the distal phalanges of these fingers. These symptoms are experienced especially on exertion and rest brings temporary relief. Nocturnal paraesthesiae rarely occur as the only symptom but are mentioned more often in combination with the other complaints (see below). At onset, the symptoms may be vague and diffuse and may involve only one finger usually the middle one. After a while, the typical distri bution becomes clear. After some months, pain develops in about 15% of patients188 and is felt in the palm of the hand and in the forearm. The pins and needles do not follow this proximal reference but remain distal to the point of compression. Slight n umbness in the radial fingers is sometimes present and therefore mentioned by the patient but it is often only detected when sensory deficit is sought during the examination.
570 SECTION SEVEN - NERVE LESIONS AND ENTRAPM ENT NEUROPATHIES
Figure 37.34
Figure 37.33
The median nerve passes through the carpal tunnel to mainly supply the palm of 3t digits.
FINDINGS DURING INSPECTION AND EXAMINATION
Inspection may reveal structural changes - post-fracture, deformities in rheumatoid arthritis, ganglia, bony sub luxations - conditions that could be relevant when the overall clinical picture is considered. In long-standing cases, and very occasionally early in the course of the condition, muscular atrophy of the thenar eminence may occur, involving the opponens pol Ii cis and abductor pollicis brevis muscles. The lateral aspect of the thenar eminence becomes flattened and gives rise to a so-called ape hand. The standard examination of the wrist is usually negative and some accessory tests may then be performed: •
•
The wrist is held in extension, and the examiner presses at the carpal tunnel while the patient actively flexes and extends his fingers; paraesthesiae occur. Phalen 's test177,189 the wrist is kept passively flexed for a m inute and then suddenly extended causing pins and needles (Fig. 37.34).
the wrist is held passively flexed and the thumb, index and long fingers are forcefully flexed as well. Tinel 's test191 percussion of the carpal tunnel gives rise to pins and needles felt distally (Fig. 37.35). The tourniquet test: inflation of a tourniquet for 1 minute gives rise to pins and needles. Tests of sensation: pin-prick, light touch and two-point discrimination (Weber's test) show if sensation is impaired.
• Modified Phalen 's test190
•
In some long-standing or severe cases, the patient may complain of weakness and inability to use the hand. In the assessment of carpal tunnel syndrome the history is most relevant. The precision of the patient's account very strongly implies the possibility of the pres ence of the syndrome. The area of paraesthesia described is exactly that of the median nerve and mention is made of the intermittent appearance and activity dependence of the symptoms.
Phalen's test.
• •
Gellman et a[l92 believe that the most reliable accessory tests are the Phalen's (most sensitive) and Tinel's tests (most specific). They state that a positive result gives a useful clinical indication of the carpal tunnel syndrome but that the diagnosis is not excluded when the tests turn out to be negative. Recent studies tend to conclude that the clinical tests are not sufficiently reliable. Patients should be sent for electrophysiological examination in order to confirm or to exclude the diagnosis.193-194 Weakness of the thumb - abduction (abductor pollicis brevis), flexion (flexor pollicis brevis, superficial head), opposition (opponens pollicis) - and of the two radial lumbricals is found in longstanding or severe compression.
Figure 37.35
Tinel's test.
CHAPTER 37
TECHNICAL INVESTIGATIONS .
These may sometimes be helpful and are more often positive in carpal tunnel syndrome than in other entrapment syndromes.196 Although false negatives and positives do occur, EMG may not only confirm the diagnosis but may also be inter esting from the prognostic point of view: when the distal motor latency between wrist and thumb is more than 7 ms, conservative treatment will probably give only temporary relief.197 Attempts have been made with cross-sectional imaging of the carpal tulmel, both with CT and MR!. According to Zucker-Pinchott et al, 1 98 CT is a promising, useful tool for evaluating soft tissue abnormalities of the wrist. John et al199 illustrated that it is possible to show thickening of soft tissue (e.g. transverse carpal ligament and _synovial flexor tendon sheath). Jetzer et al200 found abnormalities on CT in 78.2% of recent cases of carpal tunnel syndrome, as opposed to 53.1 % positive EMGs in the same cases. Fahr and Sauser201 cited several recent studies describ ing the MRI appearance of the carpal tunnel and stated that, with its improved resolution of soft tissues, MR! may prove to be clinically useful in diagnosis of carpal tunnel syndrome. High-resolution sonography is a low cost alternative to MRI,202,203 and has gained increasing popularity. 204 DIAGNOSTIC IN FILTRATION
A much more simple and very reliable diagnostic approach is by infiltration of 20 mg of triamcinolone sus pension into the carpal tunnel. If diagnosis is right, all symptoms should disappear for at least a few weeks. When symptoms have not disappeared some days after the injection, the diagnosis must be reconsidered. DIFFERENTIAL DIAGNOSIS
Carpal tunnel syndrome must be differentiated from a cervical disc protrusion that compresses a nerve root and from thoracic outlet syndrome with compression of a part of the brachial plexus. Both are often difficult. When distal paraesthesiae are the result of a cervical disc lesion, the symptoms usually come and go in an erratic fashion during the day as well as at night. They are transient and not particularly activity related. The distribution within the fingers is related to a dermatome but the patient cannot localize the paraesthesiae exactly. They are preceded and accompanied by severe root pain and often followed by segmental motor and/or sensory deficit. On examination of the cervical spine, a partial articular pattern is found. The symptoms disappear
-
NERVE LESI ONS OF THE UPPER LIMB 571
spontaneously in the course of a few weeks to a few months (see pp. 185-192). In the early stage of thoracic outlet syndrome, pins and needles are strictly nocturnal and wake the patient usually a middle-aged woman - after some hours' sleep as a result of the decompression of the nerve. The paraes thesiae are felt in all the fingers and do not have any par ticular distribution. Decompression tests of the thoracic outlet are positive (see earlier and Ch. 2). Other differential diagnoses are cervical myelopathy, anterior horn lesions, polyneuropathies, myopathies and arthrosis of the trapezium-first metacarpal joint.
TREATMENT
Treatment is conservative and consists of one or more injections into the carpal tunnel. Surgery is called for in refractory or recurrent cases. Wrist splint, Splinting with the wrist in the neutral posi tion, especially at night, leads to good but possibly only temporary results in about 70% of patients.20s,206 More recent studies show best results with a full-time splint.207 Injection. As a diagnosis of carpal tunnel syndrome can be made in spite of a negative examination, it remains provisional until therapeutic confirmation has been obtained. Relief, even if it is only temporary, after injec tion with triamcinolone acetonide is diagnostic. If paraes thesia is not relieved by injection, the diagnosis must be wrong. If the symptoms do not reappear for several months or years, a later recurrence can be treated with a further injection.
Technique: injection. The patient sits next to the couch. The physician stands medial to the affected hand, that lies palm upwards on the couch. The wrist is held in 45° of extension. The proximal border of the carpal tunnel (pisiform and scaphoid) and the palmar tendons of the wrist are easily detectable in this position. A 2 ml syringe is filled with 20 mg triamcinolone and fitted to a 5 cm needle. The tip of the needle is inserted between the tendons at a point 2 cm proximal to the proximal border of the carpal tunnel and inserted in the direction of the base of the fourth metacarpal bone. It slips, without resistance, between the tendons and under the transverse ligament into the carpal tunnel (Fig. 37.36). At 4 cm depth, the needle lies at the distal aspect of the carpal tunnel. Some fluid is injected and no resistance or painful sensation should be felt. The needle is then slowly with drawn while the syringe is further emptied. All cases of carpal tunnel syndrome respond immedi ately,208 but 60% recur within 3 to 6 months and at 2 years only 8% remain better.209 In a Cochrane review Marshall
572 SECTION SEVEN - NERVE LESIONS AND ENTRAPM ENT NEUROPATHIES
Symptoms still present
I----� Wrong diagnosis?
'---'
Symptoms disappeared
Recurrence after > 6 weeks
Right diagnosis
20 mg triamcinolone
Recurrence after < 6 weeks
Atrophy
Figure 37.37
Treatment of carpal tunnel syndrome.
A controlled prospective trial of steroid injections and splinting,211 showed only 2 2 % of patients asymptomatic after 1 year. Low-dose steroid is as effective as high-dose products.212 Cases with severe symptoms and evidence of motor atrophy responded poorly.
Figure 37.36
Steroid injection in carpal tunnel syndrome.
et al concluded that local corticosteroid injection provides
greater clinical improvement in symptoms 1 month after injection compared to placebo.2IO Recurrences after injec tions with steroid are frequent. If the symptoms recur more than 6 weeks after the injection, one or two further attempts may be made. When the result is still not sufficient or the recurrence is too rapid - within 6 weeks, or more than twice in 6 months - surgical treatment is required. Lasting problems with muscle atrophy are certain indications for surgery (Fig. 37.37).
Surgery. Rapid recurrence is an indication for surgery2 1 3,214 and, in those patients who do not show objective neurologic deficit, surgical division of the trans verse carpal ligament gives very good results.21 5-2 1 7 The long-term results of endoscopic release are similar to those of open release but the former leads to quicker functional recovery.2I8,219 There is no general agreement on the appropriate treatment of those patients who present with thenar atrophy and / or a fixed median sensory deficit. Several authors propose to combine transverse carpal ligament release with internal neurolysis of the palmar half of the median nerve,220-222 but the value of neurolyis has been questioned by the suggestion that internal dissection of the median nerve may lead to an increase in intrafascicular fibrosis.223 A prospective, randomized, double-blind, controlled study compared interfascicular neurolysis and standard release of the transverse carpal ligament for patients with severe symptoms.224 Additional benefit did not result from the extra procedure. This view has been confirmed by others.222,225,226
PARTIAL SYNDROME
Distal to the carpal tunnel the common palmar digital nerve divides into terminal motor and sensory palmar
CHAPTER 37
-
NERVE LESIONS OF THE UPPER LIMB 573
digital branches. In the hand one of these can become compressed, with the result that only part of the territory of the median nerve is involved. There are a number of possible causes. As the result of a direct blow, usually a fall on the hand, the sensory palmar digital branch to the thumb at the level of its carpometacarpal joint may be bruised. Afterwards the patient feels rather painful pins and needles in the thumb only and there is little tendency to spontaneous cure. Traumatic.
'Stick palsy' , In elderly people, the sensory palmar digital branches to the index and middle fingers may become compressed in the palm of the hand, just distal to the carpal tunnel, by incorrect use of a walking stick. This results in pins and needles, felt in these two fingers. Instruction in how to use a walking stock correctly is given.
A trigger lesion that has formed on the proximal part of a flexor tendon in the palm of the hand, just distal to the carpal tunnel, may rarely cause compression of the branch of the median nerve that supplies the middle and ring fingers and give rise to pins and needles at the adjacent surfaces of these two digits. Infiltration or surgery are the possible thera peutic measures. Swelling on a digital flexor tendon,
Musculocutaneous nerve
----I---""'""..AJH Median nerve
To corabrachialis muscle
----+--hllII'j'
To biceps muscle ---
In...u---j�4-- To brachialis muscle Lateral cutaneous nerve of the forearm ---.�'"
DISORDERS OF THE . MUSCULOCUTANEOUS NERVE ANATOMY
The musculocutaneous nerve takes origin in the lateral cord of the brachial plexus and contains fibres from CS to C7. 1t pierces the coracobrachialis muscle and descends in the anterior compartment of the arm between the biceps and brachialis muscles. It runs lateral to the distal biceps tendon and then continues as the lateral cutaneous nerve of the forearm (Fig. 37.38). INNERVATION
The musculocutaneous nerve supplies the coraco brachialis, biceps and bracrualis muscles. The lateral cutaneous nerve of the forearm innervates the skin at the anterolateral aspect of the forearm. A lesion of the musculocutaneous nerve is rare and occurs as the result of an injury in the upper arm. This causes motor deficit with weakness of the flexors of the elbow and sensory deficit over the radial aspect of the forearm. When the lesion is at the forearm, it involves the sensory branch - the lateral cutaneous nerve of the
Figure 37.38
The musculocutaneous nerve.
forearm - and leads to a similar sensory deficit. This sometimes occurs after a paravenous injection.227
�
DiSORDERS OF THE MEDIAL CUTANEOUS OF THE FOREAR M . NERVE � ... �
This nerve can be damaged by extravenous injections at the point where it crosses over the median basilic vein on the anterior aspect of the elbow. The result is numbness lasting some months, with pain and hypersensitivity of the skin, lasting possibly up to a year, over the inner aspect of the forearm.
574 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NEUROPATHIES
RE FERENCES 1.
Christoferson LA, Leech RW, Grossman M . Intracranial neurilemoma of the spinal accessory nerve. S u rg Neu ral 1 982;18 : 1 8-20.
2.
Ohkawa M, Fujiwara N, Takashima H et al. Radiologic manifes tation of spinal accessory neurinoma: a case report. Radiat Med 1996;14:269-273.
3. Kaye AH. Jugular foramen schwannomas. ] Neurosurg 1984;60 : 1 045-1053.
Chong VF, Fan YF. Jugular foramen involvement in naso pharyngeal carcinoma. ] Laryngol OtoI 1 996;110:987-990. 5. King RJ, Motta G. Iatrogenic spinal accessory nerve palsy. A I l IJ
4.
Roy Call S u rg EngI 1 983;65:35-37.
Berry H, MacDonald EA, Mrazek AC. Accessory nerve palsy: a review of 23 cases. Can J Neurol Sci 1991;18:337-341. 7. London J, London NJ, Kay SP. Iatrogenic accessory nerve injury. 6.
Ann Roy Call Surg EngI 1996;78:146-150.
Matz PG, Barbaro NM. Diagnosis and treatment of iatrogenic spinal accessory nerve injury. Ambulatory Surg 1 996;62( 8 ) : 682-685. 9. Nakamichi K, Tachibana S. Iatrogenic injury of the spinal accessory nerve. Results of repair. ] Bone Joint Surg 1998; 8.
80A(11 ) : 1 6 1 6-1 621 . 1 0.
Wiater JM, Bigliani LU. Spinal accessory nerve injury. Ciin Orthop Rei Res 1 999;368:5-16.
11.
Shone GR, Yardley MP. An audit into the incidence of handicap after unilateral radical neck dissection. ] Laryngol Otol
Dawson DH, Hallett M, Wilbourn AJ et al. Entrapmellt 3rd edn. Lippincott-Raven, Philadelphia, 1999. 28. Gilliatt R. Thoracic outlet syndromes. In: Dyck PI, Thomas PK, Lambert EH, Bunge R (eds) Peripheral Neuropathy, 2nd edn. Saunders, Philadelphia, 1984:1409-1424. 29. Bateman J. Neurological pain conditions affecti ng the shoulder. Ciin Orthop Rei Res 1983;173:48. 30. Fechter J, Kuschner S. The thoracic outlet syndrome. 27.
Neu ropathies,
Orthopedics 1993;16(11 ) : 1 243-1 251 .
Pecina M, Krmpotic-Nemanic I, Markiewitz A. Til II Ilel CRC, Boca Raton, 199 1 : 1 3-20. 32. Hood DB, Kuehne J, Yellin AE, Weaver FA. Vascular compli cations of thoracic outlet syndrome. Am ! Surg 1997;63:
31.
Syndrol1les.
913-917.
33. Green RM. Vascular manifestations of the thoracic outlet syndrome. Sem Vasc Surg 1998;11:67-76. 34. McCleery R, Kesterson J, Kirtley J, Love R. Subclavius and anterior scalenus muscle compression as a cause of intermit tent obstruction of the subclavian vein. Ann Surg 1951;133:588. 35. Etheredge S, Wilbur B, Stoney R. Thoracic outlet syndrome. Am ] Surg 1979;138:175.
Sanders RJ, Haug C. Subclavian vein obstruction and thoracic outlet syndrome: a review of etiology and management. AIJIl Vasc Surg 1990;4:397-410. 37. Wood V, Twito R, Verska J. Thoracic outlet syndrome. The results of first rib resection in 100 patients. Orthop Ciill North 36.
1991;105:760-762.
Williams WW, Twyman RS, Donell ST, Birch R. The posterior triangle and the painful shoulder: spinal accessory nerve injury. Ann Roy Call Surg EngI 1996;78:521-525. 13. Remmler D, Byers R, Sheetz J et at. A prospective study of shoulder disability resulting from radical and modified neck dissections. Head Neck S u rg 1 986;8:280-286. 1 4. Petrera JE, Trojaborg W. Conduction studies along the acces sory nerve and follow-up of patients with trapezius palsy. ! Neural Neu rosu rg Psychiatry 1 984;47:630-636. 15. Volpin G, Langer R, Stein H. Complete infraclavicular brachial plexus palsy with occlusion of axillary vessels following anterior dislocation of the shoulder joint. ] Orthop Trauma 12.
1 990;4: 121-123. 16.
Travlos I, Goldberg I, Boorne RS. Brachial plexus lesions asso ciated with dislocated shoulders. ] Bone Joint Surg 1990;728: 68-71 .
Hansky B, Murray E, Minami K, Korfer R. Delayed brachial plexus paralysis due to subclavian pseudoaneurysm after clavicular fracture. Eur J Cardiathor S u rg 1993;7:497-498. 18. Dyck pJ, Thomas PK, Lambert EH, Bunge R. Peripheral Neuropathy, vol II, 2nd edn. Saunders, Philadelphia, 1984. 19. Moore J. Thoracic outlet syndrome. Experience in a metropoli tan hospital. Ciin Orthop Rei Res 1 986;207:29-30. 20. Nichols H. Anatomic structures of the thoracic outlet. Ciin 17.
Orthop Rei Res 1986;207:13-20.
Cyriax J. Textbook of Orthopaedic Medicine, voI r, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982: 1 1 8 . 22. Riddell D, Smith B. Thoracic and vascular aspects of thoracic outlet syndrome. Ciin Orthop Rei Res 1 986;207:31-36. 23. Ruckley C. Thoracic outlet syndrome. BM] 1 983;287:447-448. 24. Bauwens F, Duprez D, Clement D. Thoracic outlet syndrome.
Am 1988;19(1) : 1 31 -146.
38. Parziale JR, Akelman E, Weiss Ap, Green A. Thoracic outlet syndrome. A m J Orthop 2000;29(5) :353-360. 39. Adson A. Surgical treatment for symptoms produced by cervi cal ribs and the scalene anticus muscle. Surg GYllecol Obstet 1947;85:687. 40.
] Surg 1976;132:771-778.
41 . Rayan GM, Jensen c. Thoracic outlet syndrome: provocative examination maneuvers in a typical population. J Shoulder Elbow Surg 1 995;4:113-117. 42. Plewa Me, Delinger M . The false-positive rate of thoracic outlet syndrome shoulder maneuvers in healthy subjects, Acad E1I1erg Med 1998;5:337-342. 43. Kozin F (ed) Painful shoulder and the reflex sympathetic dys trophy syndrome. In: Arthritis and Allied Conditiolls, 9th edn. Lea & Febiger, Philadelphia, 1979 : 1 091-1120. 44. Nakatsudti Y, Saitoh S, Hosaka M, Matsuda S. Conservative treatment of thoracic outlet syndrome using an orthosis. ! Halld Surg 1 995;20B :34-38. 45. 46. 47.
21 .
Med Trends 1 990;5:252-257.
Stewart JD. Focal Peripheral Neuropathies, 3rd edn. Lippincott Williams & Wilkins, Philadelphia, 2000 : 1 33. 26. Wilbourn AJ. Thoracic outlet syndrome: thoracic outlet syn drome is overdiagnosed. Muscle Nerve 1999;22 : 1 30-138.
Roos DB. Congenital anomalies associated with thoracic outlet syndrome: anatomy, symptoms, diagnosis, and treatment. Am
48.
49. 50.
25.
51 .
Hawkes C. Neurosurgical considerations in thoracic outlet syndrome. Ciin Orthop Rei Res 1 986;207:24-28. Luoma A, Nelems B. Thoracic outlet syndrome: thoracic surgery perspective. Neuros urg Ciill North Aln 1991;2:187-226. Sanders RJ. Results of the surgical treatment for thoracic outlet syndrome. Sem Thoracic Cardiovase Surg 1996;8:221-228. Hempel GK, Shutze Wp, Anderson F, Bukhari HI. 770 consec utive supraclavicular first rib resections for thoracic outlet syndrome. A n n Vase Surg 1 996;10:456-463. Wilbourn AJ. Thoracic outlet syndrome: a plea for conser vatism. Neurosurg Ciin North Am 1991;2:235-245. Cherington M, Cherington C. Thoracic outlet synd �ome: reimbursement patterns and patient profiles. Neu rology 1992;42: 943-945. Parsonage MJ, Turner JWA. Neuralgic amyotrophy: the shoulder-girdle syndrome. Lancet1948;1 :973-978.
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 575
52.
Turner JWA, Parsonage MJ. Neuralgic amyotrophy (paralytic brachial neuritis): with special reference to prognosis. Lancet
77.
Rei Res 1993;297:245-246.
1957;2:209-212.
53. McCarty EC, Tsairis P, Warren RF. Brachial neuritis. Clin Orthop Rei Res 1 999;368:37-43. 54.
Cusimano MD, Bilbao JM, Cohen SM. Hypertrophic brachial plexus neuritis: a pathological study of two cases. Ann Neurol
55.
Suarez GA, Giannini C, Bosch EP et al. Immune brachial plexus neuropathy: suggestive evidence of an inflammatory-immune pathogenesis. Neurology 1996;46:559-561 . Zehar.ia A, Mukamel M, Frishberg Y, Weitz R, Mimouni M. Benign plexus neuropathy in children. j Pediatr 1990;116:276-278. Misamore GW, Lehman DE. Parsonage-Turner syndrome (acute brachial neuritis). j Bone Joillt Surg 1 996;78A:1405-1408. Kauppila LI, Vastamaki M. Iatrogenic serratus anterior paraly sis: long-term outcome in 26 patients. Chest 1996;109:31-34. Wilmot C, Watemberg S, Landau 0, Litwin D. Of balloon axil loscopy and avoidance of iatrogenic injury to the long thoracic nerve. Arcll Surg 1997;132:1121-1124. Mumenthaler M. Neu rology, 3rd edn. Thieme, New York,
Raikin S, Froimson M I . Bilateral brachial plexus compressive neuropathy (crutch palsy). j Orthop Trauma 1997;11 : 1 36-1 38. 79. Ogawa K, Vi M . Humeral shaft fracture sustained during arm wrestling: report on 30 cases and review of the literature.
78.
J Trauma 1 997;42:243-246.
1988;24:61 5-622.
56. 57. 58. 59.
60.
Ogawa K, Yoshida A. Throwing fracture of the humeral shaft: an analysis of 90 patients. Am J Sports Med 1998;26:242-246. 8 1 . Frohse F, Frankel M. Die Muskel des menschlichen Armes. [n: Bardelben 's Handbuch der Anatomie des Menschell. Fisher, Jena, 80.
1 908. 82.
83. 84. 85.
1990:410.
Schultz )S, Leonard JAJ. Long thoracic neuropathy from athletic activity. Arch Phys Med RehabiI 1992;73:87-90. 62. Packe� GJ, McLatchie GR, Bowden W. Scapula winging in a sports injury clinic. Br J Sports Med 1993;27:90-91 . 63. Connor PM, Yamaguchi K, Manifold SG et al. Split pectoralis major transfer for serratus anterior palsy. Clin Orthop Rei Res 61 .
1 997;341 : 1 34-142. 64.
Fehrman DA, Orwin JF, Jennings RM. Suprascapular nerve entrapment by ganglion cysts: a report of six cases with arthro scopic findings and review of the literature. Arthroscopy
65.
Moore TP, Fritts HM, Quick De, Buss DD. Suprascapular nerve entrapment caused by supraglenoid cyst compression.
86. 87.
j Shoulder Elbow Surg 1997;6:455-462.
Kiss G, Komar J. Suprascapular nerve compression at the spinoglenoid notch. M uscle Nerve 1990;13:556-557. 67. Holzgraefe M, Kukowski B, Eggert S. Prevalence of latent and manifest suprascapular neuropathy in high-performance volleyball players. Br J Sports Med 1994;28:1 77-1 78. 68. Ringel SP, Treihaft M, Carry M, Fisher R, Jacobs P. Suprascapular neuropathy in pitchers. Am J Sports Med
670-671 .
Spinner M. The arcade of Frohse and its relationship to posterior interosseous nerve paralysis. J Bone Joint Surg 1968;50B: 808. 89. Goldman S, Honet Je, Sobel R, Goldstein AS. Posterior interosseous nerve palsy in the absence of trauma. Arch Neural 1969;21:435-441 .
Bryan FS, Miller LS, Panijayanond P. Spontaneous paralysis of the posterior interosseous nerve. A case report and review of the literature. Clin Orthop Rei Res 1971;80:9-1 2. 9 1 . Nielsen HO. Posterior interosseous nerve paralysis caused by fibrous band compression at the supinator muscle. A report of four cases. Acta Orthop Scand 1976;47:304-307. 92. De Zanche L, Negrin P, Fardin P, Carteri A. Paralysis of the deep branch of the radial nerve due to entrapment neuropathy.
90.
Eur NeuroI 1978;17:56-58. 93.
1990;18:80-86. 69.
De Laat EA, Visser CP, Coene LN, Pahlplatz PV, Tavy DL. Nerve lesions in primary shoulder dislocations and humeral neck fractures: a prospective clinical and EMG study. J Bone
95.
72.
Antoniadis G, Richter H P, Rath S, Braun V, Moese G . Suprascapular nerve entrapment: experience with 2 8 cases. J Neurosu rg 1996;85 : 1 020-1025.
73. Leffert RD. Nerve lesions about the shoulder. Orthop Clin North
96.
Travlos J, Goldberg I, Boome RS. Brachial plexus lesions asso ciated with dislocated shoulders. J Bone Joint Surg 1990;72B:
j Bone Joint Surg 1966;48B:770.
Lister GD, Belsole RB, Kleinert HE. The radial tunnel syn drome. J Hand Surg 1 979;4A:52. 98. Barnum M, Mastey RD, Weiss Ap, Akelman E. Radial tunnel syndrome. Hand Clin 1996;12:679-688. 99. Ritts GD, Wood MB, Lindscheid RL. Radial tunnel syndrome: a ten year surgical experience. Clin Orthop Rei Res 1987;219:201-205. 100.
Gumina S, Postacchini F. Anterior dislocation of the shoulder in elderly patients. J Bone Joint Surg 1997;79B:540-543. 76. Cyriax J. Textbook of Orthopaedic Medicine, vol t Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982.
Minami Y, Yamazaki J, Kato S. Lateral elbow pain syndrome and entrapment of the radial nerve. Nippon Seikeigeka Gakkai Zasshi 1 992;66(4):222-227.
68-71 . 75.
Capener N. The vulnerability of the posterior interosseous nerve of the forearm. A case report and an anatomical study.
97.
Alii 2000;31(2):331-345. 74.
Winckworth CEo Lawn-tennis elbow. BMJ 1883;2:708. Roles NC, Maudsley RH. Radial tunnel syndrome: resistant tennis elbow as a nerve entrapment. J Bone joi n t S u rg 1972;54B:499-508.
70.
893-896.
Hagert CG, Lundborg G, Hansen T. Entrapment of the poste rior interosseous nerve. SCll n d J Plast Reconstr Surg 1977;11: 205-212.
94.
Joillt Surg 1 994;76B:381-383.
Filler AG, Kliot M, Howe FA et al. Application of magnetic resonance neurography in the evaluation of patients with peripheral nerve pathology. J Neuros u rg 1996;85:299-308. 71. Callahan JD, Scully TB, Shapiro SA, Worth RM. Suprascapular nerve entrapment: a series of 27 cases. J Neu rosu rg 1991 ;74:
Lichter R, Jacobson T. Tardy palsy of the posterior interosseous nerve with Monteggia fracture. J Bone Joint Surg 1975;57A : 1 24. Olney BW, Menelaus MB. Monteggia and equivalent lesions in childhood. ] Pediatr Orthop 1989;9:21 9-223. Morris AH. Irreducible Monteggia lesion with radial nerve entrapment. J Bone Joint Surg 1974;56A:1 744. Sjostrand J, McLean WG, Frizell M. The application of axonal transport studies to peripheral nerve problems. In: Omer G Jr, Spinner M (eds) Management of Peripheral Nerve Problellls. Saunders, Philadelphia, 1 980. Wu KT, Jordon FR, Eckert C. Lipoma: a cause of paralysis of the deep radial nerve. Surgery 1974;75:790. Werner CO. Paralysis of the posterior interosseous nerve caused by tumour: brief report. J Balle Joint Surg 1987;69B:
88.
1995;11:727-734.
66.
Poddar SB, Gitelis S, Heydemann PT, Piasecki P. Bilateral pre dominant radial nerve crutch palsy: a case report. Clill Orthop
Thompson WAL. Peripheral E n t raplllent Williams & Wilkins, Baltimore, 1963. 1 02. Matthews PBC. Mammalian Muscle Receptors and Their Central Actions. Edward Arnold, London, 1 972. 101.
Kopell
H P,
Neuropathies.
576 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
1 03.
Werner CO. Lateral elbow pain and posterior interosseous nerve entrapment. Acta Orthop Scand 1 9 79;174(supp l ) :
131.
352-355. 104.
105.
19A(5):817-820.
De Smet L, Van Raebroeckx T, Van Ransbeeck H. Radial tunnel release and telmis elbow: disappointing results? Acta Orthop
132.
Belg 1999;65(4):510-513.
133.
1 999;22(7):960-967.
Stewart JD. Focal Peripheral Neuropathies, 3rd edn. Lippincott Williams & Wilkins, Philadelphia, 2000:290-292. 107. Van Rossum J, Buruma OJ, Kamphuisen HA. Tennis elbow: a radial tunnel syndrome. J Bone Joint Surg 1978;60 B : 197-198. 108. Rosen I, Werner CO. Neurophysiological investigation of pos terior interosseous nerve entrapment causing lateral elbow pain. Electroencephalogr Clin Neu rophysiol 1980;50:125-133. 109. Verhaar J, Spaans F. Radial tunnel syndrome: an investigation of compression neuropathy as a possible cause. J Bone Joint Surg 1991;73A:539-543. 110.
Heyse-Moore GH. Resistant tennis elbow. J Hand S u rg
114. 11 5. 116. 1 1 7.
Atroshi I, Johnsson R, Ornstein E. Radial tunnel release: unpre dictable outcome in 37 consecutive cases with a 1-5 year follow-up. Acta Orthop Scand 1995;66:255-257. Appel H. Handcuff neuropathy. Neu rology 1991;41:955. Cook AA. Handcuff neuropathy among U.S. prisoners of war from Operation Desert Storm. Mil Med 1993;158:253-254. Panas AL. Sur une cause peu connue de paralysie du nerf cubital. Arch Gen Med 1878;2:5. McPherson SA, Meals RA. Cubital tunnel syndrome. Orthop Clin North Am 1992;23(1):111-123.
118.
Bozentka DJ. Cubital tunnel syndrome pathophysiology. Clin Orthop Rei Res 1998;351:90-94.
Lazaro L 3rd. Ulnar nerve instability: ulnar nerve injury due to elbow flexion. Sou thern Med ] 1977;70(1):36-40. 120. Childress HM. Recurrent ulnar-nerve dislocation at the elbow.
119.
722-727.
Rayan GM. Proximal ulnar nerve compression. Cubital tulmel syndrome. Hand Clin 1992;8(2):325-336. 136. Gurnucio CA, Lund H, Young VL, Young AE. Diagnosis and management of uLnar nerve entrapment. Mo Med 1992;89(4): 231-240. 137.
Weinstein SM, Herrin SA. Nerve problems and compartment syndromes in the hand, wrist and forearm. Clin Sports Med
138.
Seror P. Treatment of ulnar nerve palsy at the elbow with a night splint. J Bone Joint Surg 1993;75B(2) :322-327. Hong CZ, Long HA, Kanakamedala RY, Chang YM, Yates L. Splinting and local steroid injection for the treatment of ulnar neuropathy at the elbow: clinical and electrophysiological evaluation. Arch Phys Med Rehabi/ 1996;77(6):573-577. Nathan PA, Myers LD, Keniston RC, Meadows KD. Simple decompression of the ulnar nerve: an alternative to anterior transposition. j Hand Surg 1992;17B(3):251-254. Stuffer M, Jungwirth W, Hussl H, Schmutzhardt E. Subcutaneous or submuscular anterior transpOSition of the ulnar nerve? J Hand Surg 1992;17B(3):248-250. Manske PR, Johnston R, Pruitt DL, Strecker WB. Ulnar nerve decompression at the cubital tunnel. Clin Orlhop Rei Res
1992;11(1):161-188.
139.
140.
141 .
142.
1 992;274:231-237.
Gelberman RH, Eaton R, Urbaniak JR. Peripheral nerve com pression. ] Bone Joint Surg 1 993;75A(12) : 1 854-1878. 144. Plancher KD, McGillicuddy JO, Kleinman WB. Anterior intramuscular transposition of the ulnar nerve. Hand Clin 143.
1996;12(2) :435-444. 145.
Glowacki KA, Weiss AP. Anterior intramuscular transposition of the ulnar nerve for cubital tunnel syndrome. J Shoulder
Joint Surg 1979;51A:130.
146.
Siegel DB. Submuscular transposition of the ulnar nerve. Hand
Minami A, Sugawara M. Humeral trochlear hypoplasia sec ondary to epiphyseal injury as a cause of ulnar nerve palsy.
147.
Clin Orthop Rel Res 1975;108: 1 68-173. 121 . 122.
Bartels RH, Menovsky T, Van Overbeeke JJ, Verhagen WI. Surgical management of ulnar nerve compression at the elbow: an analysis of the literature. ] Neurosu rg 1998;89(5):
135.
1 034-1043. 113.
Alnot JY, Frajman JM. Syndrome de compression chronique du nerf cubital au niveau du coude: a propos de 74 cas. Ann ChiI' Main Memb Super 1992;11(1) :5-13.
1 34.
1984;9B:64-66.
Wadsworth TG. Tennis elbow: conservative, surgical, and manipulative treatment. BMJ 1 987;294:621-624. 1 1 2. Verhaar J, Walenkamp G, Kester A, van Mameren H, van der Linden T. Lateral extensor release for telmis elbow: a prospec tive long-term follow-up study. J Bone Joint Surg 1 993;75A: 111 .
Bednar MS. Ulnar tunnel syndrome. Hand Clin 1996;12(4): 657-664.
Rosenbaum R. Disputed radial tunnel syndrome. Muscle Nerve
106.
Novak CB, Lee GW, Mackinnon SE, Lay L. Provocative testing for cubital tunnel syndrome. ] Hand Surg 1 994;
Prietto CA. Supracondylar fractures of the humerus. j Bone
Elbow Surg 1997;6(2) :89-96. Clin 1996;12(2) :445-448.
Clin Orthop Rei Res 1988;228:227.
Feindel W, Stratford J. The role of the cubital tunnel in tardy ulnar palsy. Can ] Surg 1958;1:287. 124. Osborne GY. The surgical treatment of tardy ulnar neuritis. 123.
] Bone joint Surg 1957;398:782.
Wadsworth TG, Williams JR. Cubital tunnel external compres sion syndrome. BM] 1973;i:662. 126. Toby EB, Hanesworth D. Ulnar nerve strains at the elbow. 125.
] Hand Surg 1998;23A(6):992-997.
Janes PC, Mann RJ, Farnworth TK. Submuscular transposition of the ulnar nerve. Clin Orthop Rei Res 1989;238:225. 128. MacNicol MF. The results of operation for ulnar neuritis. ] Bone 127.
148.
Buehler MJ, Thayer DT. The elbow flexion test. A clinical test for the cubital turulel syndrome. Clin Orthop Rei Res 1988;233:
130.
Rosati M, Martignoni R, Spagnolli G, Nesti C, Lisanti M . Clinical validity of the elbow flexion test for the diagnosis of ulnar nerve compression at the cubital tulmei. Acta Orthop Belg
McPherson SA, Meals RA. Cubital hlnnel syndrome. Orthop Clin North Am 1 992;23(1 ) : 1 1 1-123.
Rombouts JJ, Hoan P, Knoops P. La neuropathie du cubital par compression au coude. Acta Orthop Belg 1992;58(3):301-307. 1 5 1 . Kuschner SH. Cubital tunnel syndrome. Treatment by medial epicondylectomy. Hand Clin 1996;12(2):411-418. 152. Kaempffe FA, Farbach J. A modified surgical procedure for cubital tunnel syndrome: partial medial epicondylectomy. 150.
] Hand Surg 1998;23(3):492-498. 153.
213-216.
1998;64(4):366-370.
Robinson D, Aghasi MK, Halperin N. Medial epicondylectomy in cubital tunnel syndrome: an electrodiagnostic study. J Hand Surg 1992;17B(3) :255-256.
149.
Joint SUl'g 1979;61 B : 158. 1 29.
Craven PR, Green DP. Cubital tunnel syndrome. ] Bone Joint Surg 1980;62A:986.
Seradge H. Cubital tunnel release and medial epicondylec tomy: effect of timing of mobilization. I Hand Surg 1997;22A(5): 863-866.
154.
Weirich SD, Gelbermann RH, Best SA et al. Rehabilitation after subcutaneous transposition of the ulnar nerve: immediate versus delayed mobilization. j Shou lder Elbow Surg 1998; 7(3):244-248.
CHAPTER 37 - NERVE LESIONS OF THE UPPER LIMB 577
155. 156. 157.
158. 159.
Dupont e, Cloutier GE, Prevost Y, Dion MA. Ulnar-tunnel �yndrome at the wrist. / BOlle /oillt Surg 1 965;47A:757. Sunderland S. Nerves alld Nerve Injuries. Churchill Livingstone, Edinburgh, 1978. Fahrer M, Milroy PJ. Ulnar compression neuropathy due to anomalous abductor digiti minimi: clinical and anatomic study. / Halld Surg 1981 ;6:266. al-Qattan MM, Duerksen F. A variant of flexor carpi ulnaris causing ulnar nerve compression. J Anat 1992;180(1 ) : 1 89-190. Noth J, Dietz V, Mauritz KH. Cyclist's palsy: neurological and EMG study in 4 cases with distal ulnar lesions. I Neural Sci
O'Duffy JD, Randall RY, MacCarty CS. Median neuropathy (carpal-tunnel syndrome) in acromegaly: a sign of endocrine overactivity. Ann Intern Med 1973;78:379-383. 183. Jenkins pJ, Sohaib SA, Akker S et al. The pathology of median neuropathy in acromegaly. A n ll Illtem Med 2000; 133(3):
1980;47: 11 1.
185.
Oh SJ. Clillical Electromyography: Nerve Conduction Studies. University Park Press, Baltimore, 1984. 1 6 1 . Yu-Sung Wu, Morris JD, Hogan GR. Ulnar neuropathy at the wrist: case report and review of literature. Arch Phys Med
181.
751-756. 182.
1 97-201 . 1 84.
160.
162.
163.
186.
Rehabi/ 1985;66:785.
187.
Morris HH, Peters BH. Pronator syndrome: clinical and electrophysiological features in seven cases. / Neurol Neuros u rg
188.
Psychiatry 1976;39:461-464.
189.
Aiken BM, Moritz MJ. Atypical electromyographic findings in pronator teres syndrome. Arch Phys Med Rehabil 1987;68: 1 73-175.
Kiloh LG, Nevin S. Isolated neuritis of the anterior inter osseous nerve. BM] 1952;i:850. 165. Stern MB. The anterior interosseous nerve syndrome (the Kiloh-Nevin syndrome). Ciill Ort/wp Rei Res 1984;187:223. 166. Solnitsky O. Pronator syndrome: compression neuropathy of the median nerve at level of pronator teres muscle. Georgetowll
Scalld I Rheumato/ 1996;25:107-108.
Smith EM, Sonstegard DA, Anderson WHo Carpal tunnel syn drome: contribution of flexor tendons. Arch Phys Med Rehabil
191.
Moldover J. Tiners sign: its characteristics and Significances.
1977;158(58):378. ] BOlle Joint Surg 1978;60A:412. 192.
Med Bull 1960;13:232. 193.
De Krom MC, Knipschild PG, Kester AD, Spaans F. Efficacy of provocative tests for diagnOSiS of carpal tunnel syndrome.
194.
Golding ON, Rose OM, Selvarajah K. Clinical tests for carpal tunnel syndrome: an evaluation. B r / Rheu111atol 1986;25:
Lancet 1990;335:393-395.
/ Bone Joint Surg 1981 ;63A:885.
Werner CO, Rosen I, Thorngren KG. Clinical and neurophysi ologic characteristics of the pronator syndrome. Ciin Orthop Rei Res 1985;197:231 .
Vrieling C, Robinson PH, Geertzen JHB. Anterior interosseous nerve syndrome: literature review and report of 11 cases. E u r J Plast Surg 1998;21 : 1 88.
171 .
Bora FW Jr, Osterman AL. Compression neuropathy. Ciin Orthop Rei Res 1982;100:20.
Howard FM. Controversies in nerve entrapment syndromes in the forearm and wrist. Orthop Ciin North Ani 1986;17:375. 173. Paget J. Lectures on Surgical Pathology. Lindsay & B lakiston, Philadelphia, 1854. 174. Cyriax JH. Perineuritis. BM/ 1942;i:578. 1 75. Cannon BW, Love JG. Tardy median palsy: median neuritis: median thenar neuritis amenable to surgery. S u rgery
172.
388-390.
Katz IN, Larson MG, Sabra A et al. The carpal tunnel syn drome: diagnostic utility of the history and physical examina tion findings. Ann In tern Med 1990;112:321-327. 196. Wertsch JJ, Melvin J. Median nerve anatomy and entrapment syndromes: a review. Arch Phys Med Rehabi/ 1982;63:623. 197. Golding ON. Brachial neuralgia and the carpal tunnel syn drome. BMJ 1968;3:803. 198. Zucker-Pinchott B, Hermann G, Srinivasan R. Computed tomography of the carpal tunnel: a radioanatomical study.
195.
J Cornput Assist Tornogr 1981;5:525. 199.
Jolm V, Nam HE, Nahzer He. CT of carpal tunnel syndrome.
200.
Jetzer T, Erickson 0, Webb A. Computed tomography of the carpal tunnel with clinical and surgical correlation. CT Ciin
201 .
Fahr LM, Sauser DO. Imaging of peripheral nerve lesions.
202.
Chen P, Maklad N, Redwine M, Zelitt D. Dynamic high resolution sonography of the carpal tunnel [review]. Ani
Am J NeuraradioI 1983;4:770.
1946;20:210.
Symp 1984;7:2.
Brain WR, Wright AD, Wilkinson M. Spontaneous compres sion of both median nerves in carpal tunnel: 6 cases treated surgically. Lallcet 1947;i:227. 177. Phalen GS. The carpal tunnel syndrome: 17 years' experience in diagnosis and treatment. / Bone Joint Surg 1966;48A:211 . 178. Stevens jC, Sun S, Beard CM, O'Fallon WM, Kurland LT. Carpal tunnel syndrome in Rochester, Minnesota, 1961 to 1980. 176.
Neu rology 1988;38: 1 34-138. 179.
Course
Lectures,
The
Americall
Academy
of
vol 33. Mosby, St Louis, 1 984:489-512. 180. Palumbo CF, Szabo RM, Olmsted SL. The effects of hypothyroidism and thyroid replacement on the development of carpal tunnel syndrome. ] Hand S u rg 2000;25A(4): Orthopaedic Surgeons,
734-738.
Orthop Ciin North Am 1988;19(1):34.
J Roen tgenoI 1997;168:533-537. 203.
Buchberger W. Radiologic imaging of the carpal tunnel. E u r I RadioI 1997;25:1 12-117.
Teefey SA, Middleton WD, Boyer MI. Sonography of the hand and wrist. Sem Ultrasound CT MRI 2000;21 (3) : 1 92-204. 205. Kruger VL, Kraft GH, Deitz Je, Ameis A, Polissar L. Carpal tunnel syndrome: objective measures and splint use. Arch Phys 204.
Spinner M. Management of nerve compression lesions. In: Illstructiollal
Gellman H, Gelberman RH, Tan AM, Botte MJ. Carpal tunnel syndrome: an evaluation of the provocative diagnostic tests. ] Bone loint Surg 1986;68A:735.
Johnson RK, Spinner M, Shrewsbury MM. Median nerve entrap ment syndrome in the proximal forearm. I Hand Surg 1979;4:48. 168. Hartz CR, Linscheid RL, Gramse RR, Daube JR. The pronator teres syndrome: compression neuropathy of the median nerve.
167.
170.
McLennan HG, Outs IN, Walstab JE. Survey of hand symp toms in pregnancy. Med J Aust 1987;147:542-544. Gould JS, Wissinger HA. Carpal tunnel syndrome in preg nancy. Southern Med J 1978;71:144. Wilbourn AJ. Diabetic entrapment and compression neuro pathies. In: Dyck pJ, Thomas PK (eds) Diabetic Neuropathy, 2nd edn. Saunders, Philadelphia, 1999:481-508. Kerrigan JJ, Bertoni JM, Jaeger SH. Ganglion cysts and carpal tunnel syndrome. J Hand Surg 1988;13A:763-765. Crymble B. Brachial neurologia and CTS. BMJ 1 968;3:470. Tsai CY, Yu CL, Tsai ST. Bilateral carpal tunnel syndrome secondary to tophaceous compression of the median nerves.
190.
164.
169.
Purnell DC, Daly DO, Lipscomb PR. Carpal-tunnel syndrome associated with myxedema. Arch I n tern Med 1 961 ;108:
Med RehabiI 1991;72:517-520. 206.
Burke DT, Burke MM, Stewart GW, Cambre A. Splinting for carpal tunnel syndrome: in search of the optimal angle. Arch Phys Med Rehabil 1 994;75 : 1 241-1 244.
578 SECTION SEVEN - NERVE LESIONS AND ENTRAPMENT NE UROPATHIES
207.
208.
Walker WC, Metzler M, Cifu OX, Swartz Z. Neutral wrist splinting in carpal tunnel syndrome: a comparison of night only versus full-time wear instructions. Arch Phys Med Rehabil
218.
2000;81 (4):424-428.
219.
McColl GJ, Dolezal H, Eizenberg N. Common corticosteroid injections. An anatomkal and evidence based review. Aust Fam Phys 2000;29(10) :922-926.
Girlanda P, Dattola R, Venuto C et al. Local steroid treatment in idiopathic carpal tunnel syndrome: short- and long-term efficacy. } Neural 1993;240: 1 87-190. 210. Marshall S, Tardif G, Ashworth N. Local corticosteroid injec tion for carpal tunnel syndrome (Cochrane review). Cochrane
Main 1999;18(2) : 1 1 5-1 2 1 .
Brief R , Brief L P. Endoscopic carpal tunnel release: report of 146 cases. Mt Sinai } Med 2000;67(4):274-277. 220. Curtis RM, Eversman WW Jr. Internal neurolysis as an adjunct to the treatment of the carpal tunnel syndrome. J Balle Joint Surg 1973;55A:733.
209.
213.
224.
Szabo RM, Madison M. Carpal tunnel syndrome. Orthop Clin North Am 1 992;23(1 ) : 1 03-108.
215.
1979;61A:93.
McConnell JR, Bush DC. Intraneural steroid injection as a com plication in the management of carpal tunnel syndrome. Clin
O'Gradaigh 0 , Merry P. Corticosteroid injection for the treat ment of carpal tunnel syndrome. A n n Rheum Dis 2000;59(11):
Orthop Rei Res 1 990;250:181 . 214.
Harris CM, Tanner E, Goldstein MN, Pettee OS. The surgical treatment of the carpal tunnel syndrome correlated with pre operative nerve conduction studies. J Bone Joint Surg
9 1 8-919.
Gelberman RH, Aronon 0, Weisman MH. Carpal tunnel syn drome: a prospective trial of steroid injection and splinting. } Bone Joint Surg 1980;62A: 1 1 8 1 .
212.
221 .
Rhoades CE, Mowery CA, Gelberman RH. Results of internal neurolysis of the median nerve for severe carpal tunnel syndrome. J Bone Joill! Surg 1 985;67A:253. 223. Rydevik B, Lundborg G, Nordborg C. Intraneural tissue reac tions induced by internal neurolysis: an experimental study on the blood-nerve barrier, connective tissues and nerve fibers of rabbit tibial nerve. Scond J Plast Reconstr Surg Hand Surg
Database Syst Review 2000;4:CDOOI554 211.
Lindau T, Karlsson MK. Complications and outcome in open carpal tunnel release. A 6-year follow-up in 92 patients. Chir
Pagnanelli OM, Barrer SJ . Bilateral carpal tunnel release at one operation: report of 228 patients. Neu rosu rgery 1992;31(4): 1030-1033.
216. Haupt WF, Wintzer G, Schop A, Lottgen J, Pawlik G. Long term results of carpal tunnel decompression. Assessment of 60 cases. } Hand Surg 1993;18B(4):471-474. 217. Delaere 0, Bouffioux N, Hoang P. Endoscopic treatment of the carpal tunnel syndrome: review of the recent literature. Acta Chir Belg 2000;100(2):54-57.
222.
1976;10:3.
Lowry WE, Follender AB. Interfascicular neurolysis in the severe carpal tunnel syndrome. Clin Orthop Rei Res 1988;227:25l . 225. Blair S. Avoiding complications o f surgery for nerve compres sion syndromes. Orthop Clin North Am 1988;19(1) : 1 25. 226. Gelberman RH, Pfeffer GB, Galbraith RT. Results of treatment of severe carpal tunnel syndrome without internal neurolysis of the median nerve. J Bone Joint Surg 1987;69A:895. 227. Horowitz SH. Iatrogenic causalgia: classification, clinical findings, and legal ramifications. Arch NeuroI 1984;41:821-824.
SECTION EIGHT
The thoracic spine
SECTION CONTENTS 38. Applied anatomy of the thorax and abdomen The thoracic spine 581 The thoracic cage 585 The abdominal wall 589 39. Clinical examination of the thoracic spine Introduction 593 Referred pain 594 History 599 600 Inspection and palpation 601 Functional examination 607 Accessory tests Technical investigations
581
593
610
40. Interpretation of the clinical examination
613
615 41. Disorders of the thoracic spine: disc lesions Introduction 615 Clinical presentation 616 Symptoms and signs 616 Clinical types of thoracic disc protrusion 618 Treatment
622
Manipulation 622 Oscillatory techniques 630 Sustained traction 630 Sinuvertebral nerve block 631 Rest in bed 631 Surgery: removal of protruded discs Prevention of recurrence 631
631
42. Disorders of the thoracic spine: non-disc lesions
635 Introduction 635 635 Warning symptoms and signs Symptoms 635 Signs 636 Disorders and their treatment 637 Tumours of the thoracic spine 637 Extradural haematoma 641 Thoracic spinal canal stenosis 641 Chest deformities 642 Fracture of a transverse process 648 Spinal infections 648 Lateral recess stenosis 649 Arthritis of the costovertebral and costotransverse joints 650 Arthritis of the thoracic facet joints 650 Paget's disease 651
43. Disorders of the thoracic cage and abdomen Referred pain 655
655
Pain referred from visceral structures 655 Pain referred from musculoskeletal structures not belonging to the thoracic cage 661 Disorders of the thoracic cage and abdomen 661 Disorders of the inert structures 662 Disorders of the contractile structures 664 44. Ankylosing spondylitis of the thorax Clinical findings 669 Further investigations 670 Treatment 670
669
THIS PAGE INTENTIONALLY LEFT BLANK
Applied anatomy of the thorax and abdomen
CHAPTER CONTENTS The thoracic spine
581 581
The vertebra The intervertebral disc 583 The ligaments 583 Facet joints 583 Content of the spinal canal 584
The thoracic cage
585
Bony structures 585 Contractile structures 587 Landmarks 589 Movements of the thoracic spine and cage
The abdominal wall
589
589
THE THORACIC SPINE THE VERTEBRA
The thoracic spine has a primary dorsal convexity (Fig. 38.1) associated with intrauterine life - a phylo genetic kyphosis - whereas the cervical and lumbar spine have a compensatory lordosis. The 12 thoracic vertebrae are intermediate in size between those in the cervical and lumbar regions. They are composed of a vertebral body - a cylindrical ventral mass of bone - continuing posteriorly into a vertebral arch (Fig. 38.2). The typical thoracic vertebral body is heart-shaped in cross-section and has on each of its lateral aspects a superior and inferior costal facet for articulations with the ribs (costovertebral joints). The arch is constructed out of two pedicles and two short
Figure 38.1
Lateral (left) and posterior (right) views of the thoracic spine. 581
582 SECTION EIGHT - THE THORACIC SPINE
(a)
ding transverse process is located approximately one level higher. The oval intervertebral foramina are located behind the vertebral bodies and between the pedicles of the adja cent vertebrae and contain the segmental nerve roots. In the thoracic spine, these are situated mainly behind the inieroposterior aspect of the upper vertebral body and not just behind the disc. This makes a nerve root com pression by a posterolateral displacement less likely at the thoracic level, whereas at the lumbar level nerve root compressions by posterolateral disc protrusions are quite common (Fig. 38.3). The location of the intervertebral foramen depends on the level. In the upper and lower thoracic area, it is level with the tip of the spinous process of the vertebra above, i.e. level above. At mid-thorax there is a difference of about It levels.
7
5
(b)
5
7
(c)
5
Figure 38.2 Lateral and cranial views of the sixth thoracic vertebra (a, b) and lateral view of the twelfth thoracic vertebra (c). 1, vertebral body; 2, vertebral arch; 3, pedicle; 4, lamina; 5, spinous process; 6, articular processes; 7, transverse process.
laminae, the latter uniting posteriorly to form the spinous process. Laminae and spinous processes lie obliquely covering each other like the tiles of a roof, so protecting the posterior cord posteriorly. The pedicles carry the articular and transverse processes. The posterior aspect of the vertebral body and the arch enclose the vertebral foramen. The spinal cord at the tho racic level is rounder and smaller than at the cervical and in consequence the vertebral foramina are also smaller. Where the pedicles and laminae unite the transverse process is found, slightly posterior to the articular process, pedicle and intervertebral foramen. There is also an oval facet for the ribs on all the transverse processes, except for Tll and T12, to which ribs are not attached. The spinous processes at mid-thorax are long and very steeply inclined: each transverse process is at a level one and a half vertebrae higher than the tip of the correspon ding spinous process. In the upper and lower thorax, the spinous processes are less inclined; here, the correspon-
Thoracic motion segment
Lumbar motion segment Figure 38.3 Thoracic discs are smaller and flatter than lumbar discs. The intervertebral foramen is located behind the vertebral body instead of behind the disc.
CHAPTER 38 - APPLIED ANATOMY 583
THE INTERVERTEBRAL DISC .
A fibrocartilaginous disc forms the articulation between two vertebral bodies. The anatomy and behaviour of discs are discussed in the chapter on applied anatomy of the lumbar spine. However, it is worth noting here that thoracic discs are narrower and flatter than those in the cervical and lumbar spine. Disc size gradually increases from superior to inferior. The nucleus is rather small in the thorax. Therefore protrusions are usually of the annular type, and a nuclear protrusion is very rare in the thoracic spine.
although it covers only a part of the posterior aspect of each vertebral body. It has some lateral expansions, which are firmly attached to the discs. The ligamentum flavum, interposed between the laminae, extends laterally as far as the medial part of the inferior articular process. At each level the ligamentum flavum has lateral extensions to both sides to form the capsules of the facet joints. The transverse processes are connected to each other by the intertransverse ligaments. The supra- and inter spinal ligaments bridge the gap between the spinous processes.
THE LIGAMENTS
The longitudinal ligaments run anteriorly and posteriorly on the vertebral bodies (Fig. 38.4). The anterior ligament covers the whole of the vertebral bodies' anterior aspect and some of their lateral aspect. It is firmly connected to the periosteum but only loosely to the discs. The poste rior longitudinal ligament is strongly developed at the thoracic level and is wider than in the lumbar region,
FACET JOINTS
Each facet joint is composed of a superior and an inferior articular process, covered by hyaline cartilage and con nected to each other by a joint capsule which possesses a true synovium. The articular surface of the superior artic ular process points backwards, slightly upwards and out wards. The facet of the inferior articular process faces
3 8
(a)
(c) 2
ilG!r/AI---3 -
(b)
(d)
Figure 38.4 Ligaments of the thoracic spine: posterior (a), anterior (b), lateral (c) and posterior with vertebral arch removed (d). 1, anterior longitudinal ligament; 2, posterior longitudinal ligament; 3, intervertebral disc; 4, ligamentum flavum; 5, intertransverse ligament; 6, supra- and interspinal ligament; 7, radiate ligament; 8, costotransverse ligament.
584 SECTION EIGHT - THE THORACIC SPINE
forwards, slightly downwards and inwards. These articu lations lock the vertebrae together while allowing move ments of flexion-extension, bilateral side flexion and rotation. CONTENT OF THE SPINAL CANAL
The spinal canal is formed by the vertebral foraminae of the successive vertebrae, the posterior aspects of the discs, the posterior longitudinal ligament, the ligamenta flava and the anterior capsules of the facet joints. In con trast to the cervical and lumbar regions, where the canal is triangular in cross-section and offers a large lateral extension to the nerve roots, the thoracic spinal canal is small and circular. It can be divided into three zones: the upper (TI-T3), and lower (TIO-T12) zones are transi tional, respectively, the cervical and the thoracic spine, and the thoracic and the lumbar spine. Between these is the mid-thoracic zone (T4-T9), where the spinal canal is at its narrowest (Fig. 38.5). The spinal canal contains the dural tube, within which are the spinal cord, the spinal nerves and the epidural tissue. Dura mater The dura mater, a blind-ended membraneous sack arising from the occiput and ending at 52 level, has similar characteristics at all levels. It is free within the spinal canal, where it is only loosely attached to the adja cent posterior longitudinal ligament allowing the dura to move and to deform on aIl spinal movements. The anterior part of the dura is largely innervated by a mesh of nerve fibres belonging to different and consecu tive sinuvertebral nerves. This may be the anatomical explanation for the broad and large pain reference com monly found in dural irritation at the thoracic level. Spinal cord The dura mater contains the spinal cord, which ends approximately at the L1 level. The spinal cord occupies the space of the spinal canal maximally at the thoracic level. This, together with its poor vascularization renders the thoracic spine very vulnerable to damage by extradural processes and vertebral trauma. The cord depends for its blood supply on these arterial circles. The inner circle is of three longitudinal arterial channels, which run from the medulla oblongata to the conus medullaris. Their perforating arteries to the spinal cord are larger and more numerous at the cervical and lumbar level than at the thoracic level. Moreover, the inner arterial circle is characterized in the thoracic spine by a lack of anastomoses. One of the two outer arterial circles is located in the extradural space, the other in the extravertebral tissues.
Thoracic spinal canal
Figure 38.5 The small and round thoracic spinal canal is largely occupied by spinal cord and dura.
These give rise to the 'medullary feeders', which arise at the cervical spine mainly from the vertebral arteries, and in the thoracic and lumbar spine from the intercostal and lumbar arteries, which are segmental branches of the aorta. It is at mid and lower thorax that the spinal cord has the least profuse blood supply: the so-called critical vascular zone. When surgery is contemplated here, strict care must be taken not to impede blood flow. Nerve roots and innervation As at the cervical and lumbar level, the thoracic spinal nerves emerge from the cord as a ventral and a posterior ramus, which join together to form the short spinal nerve root. The lateral part of the spinal canal that envelops the nerve root is the radicular canal. n is formed anteriorly by the posteroinferior aspect of the upper vertebra and a small part of the intervertebral
CHAPTER 38
disc, both covered by the posterior longitudinal liga ment. The posterior boundary is formed by the lamina and the superior articular facet. The intraspinal course of the upper thoracic nerve roots is almost horizontal, as in the cervical spine. Therefore a nerve root can only become compressed by its corresponding disc. However, the more caudal in the spine the more oblique the nerve root's course. The T12 nerve root within the spinal canal is at the height of the eleventh vertebral body, and therefore courses downwards, outwards and slightly anteriorly behind the Tll disc and the T12 ver tebral body, to leave the foramen at the inferior margin of body T12. As a consequence, the lowest thoracic nerve roots can be compressed by disc lesions of two consecutive levels (T12 root by Tll or T12 disc). The nerve leaves the spinal canal through the interver tebral foramen just behind the inferior vertebral margin and' the costovertebral joints. Because the intervertebral foramina are quite large at these levels, osseous interfer ence with the nerve roots is seldom encountered in the thoracic spine. Beyond the intervertebral foramen, the nerve root divides into a large ventral and a smaller dorsal branch (Fig. 38.6). The latter gives rise to a medial and a lateral branch, which innervate mainJy the skin of the posterior thorax and upper lumbar region; they also give branches to the erector spinae muscles. The ventral rami do not form plexuses at the thoracic level but retain their seg mental distribution as intercostal nerves, having their course in the costal sulcus of the corresponding rib in which they lie dorsocaudal to the blood vessels. They
-
APPLIED ANATOMY 585
innervate the costotransverse joints, the chest wall, the parietal pleura, the skin of the thorax and the intercostal muscles. As at the lumbar and cervical levels, innervation of the spinal canal is by the sinuvertebral nerve, which arises from the nerve root and re-enters the epidural space. It gives branches to the nervous network of the anterior and posterior longitudinal ligaments. Branches to the dura mater cross the midline and innervate several consecu tive levels, to about four segments cranial and caudal to their points of entrance. This explains why pressure to the dura mater may give rise to pain felt multisegmen tally and even bilaterally (see p. 716).
THE THORACIC CAGE
The thorax is a complex system of bony, cartilaginous, ligamentous, muscular and tendinous structures. Superficial to the thoracic wall are bony and musculo tendinous structures, connecting the upper limb to the trunk. These structures belong to the shoulder girdle and are discussed there (see p. 397). The cranial border of the cage is the superior thoracic aperture. It is bounded by the first thoracic vertebra, the first ribs, the clavicles and the upper edge of the manubrium. The aperture does not lie in a horizontal plane but is inclined ventrally downwards. Inferiorly, the thorax is separated from the abdomen by the diaphragm. BONY STRUCTURES
6
4
5
Figure 38.6 Spinal and intercostal nerve supply: 1, nerve root; 2, ventral ramus and intercostal nerve; 3, dorsal ramus; 4, medial branch; 5, lateral branch; 6, spinal ganglion; 7, sympathetic ganglion.
Twelve pairs of ribs, together with the sternum, the clav icle and the thoracic spine, form the bony part of the thoracic cage (Fig. 38.7). Because the thoracic spine is kyphotic, with the apex of the kyphosis at T7, the thoracic cage is widest in sagittal diameter at this level. The sternum (Fig. 38.8) is composed of an upper part (manubrium), a mid-portion (body) and a caudal part (xiphoid). Because of the overall slightly oblique align ment of the sternum the caudal end projects further anteriorly. The upper part of the manubrium has a depression, the jugular incisura, lying between the sternal heads of both sternocleidomastoid muscles. Its superolateral sides are the sternal joint surfaces of the sternoclavicular joints. A synchondrosis joins manubrium and body. It pro trudes slightly anteriorly and is known as the sternal angle of Louis - an important landmark because the second rib is attached to the sternum at this level. At the caudal end, another synchondrosis connects the xiphoid process to the sternum; it is reinforced by the costo xiphoid ligaments.
586 SECTION EIGHT - THE THORACIC SPINE
Figure 38.7
Posterior (left) and anterior (right) views of the thoracic cage.
The thoracic cage contains twelve pairs of ribs. Each rib consists of a head, a neck and a body (Fig. 38.9). The head consists of the slightly enlarged posterior end, nor mally carrying two hemifacets for the costovertebral joints. The first, eleventh and twelfth ribs have only one full facet here. The body is separated from the head by a thilmer part: the neck. At the junction with the corpus of the rib a tubercle is present, on which another joint surface lies (Fig. 38.10). This is part of the costotransverse joint lying between the rib and transverse process (Fig. 38.11). The two lowest ribs have no articular facet on their
tubercle. The costovertebral and the costotransverse joints are true synovial joints. The anterior portion of the capsule of the costovertebral joint is locally reinlorced by the radiate ligament, which courses between both adja cent vertebrae and the rib. The capsules of the costo transverse joints are locally reinforced by the costotransverse ligaments. A few centimetres beyond the vertebral column, where the curve of the rib is most pronounced, is the costal angle (Fig. 38.9).
5
4
Figure 38.8 The sternum: 1, manubrium; 2, body of sternum; 3, xiphoid; 4, jugular incisura.
Figure 38.9 Rib structure: 1, costal head; 4, costal body; 5, facet surfaces.
2, costal neck; 3, costal angle;
CHAPTER 38 - APPLIED ANATOMY 587
Facet for head of rib
of the cartilage lies at the same level as the manubrioster nal synchondrosis. Since the first rib can hardly be pal pated, the second rib is usually the first bony structure caudal to the clavicle which can be easily defined, even in circumstances where the sternal angle is not pronounced. Therefore it is an important landmark. The rib length increases further caudally, until the seventh rib; then they become progressively shorter. The attachment of the ribs to the sternum is variable. The upper five, six or seven ribs have their own cartilagi nous connection. The length of this varies from about 2 cm for the first rib to about 10 cm for the seventh rib. The cartilage of the eighth rib ends by blending with the seventh. The same situation pertains for the ninth and the tenth ribs, so giving rise to a common band of cartilage and connective tissue. The eleventh and twelfth ribs remain unattached anteriorly but end with a small piece of cartilage. CONTRACTILE STRUCTURES
Facet for tubercle of rib Figure 38.10 Articular facets for the rib joints on the vertebral body and transverse process.
Except for the first and second ribs, all ribs have a groove for the intercostal nerve and blood vessels at their lower margin, which is at the outer aspect confined by a sharp bony edge. All ribs are different from each other in size, width and curvature. The first rib is the shortest. Its anteromedial part lies beneath the medial end of the clavicle. It has two sulci, separated from each other by a tubercle to which the scalenus anterior muscle inserts. Important neuro vascular structures are situated medial and lateral to this tubercle. The second rib is much longer. The medial end
4 Figure 38.1 1 The rib joints. 1, costovertebral joint; 2, costotransverse joint; 3, radiate ligament; 4, costotransverse ligaments.
The muscular and tendinous elements of the thoracic cage are the intercostals and the diaphragm. Superficial to the thoracic cage are the erector spinae muscles, levator scapulae, trapezius, rhomboid, pectoralis minor, subclavius and serratus anterior muscles. The other associated structures, such as the pectoralis major and latissimus dorsi, are discussed in Chapter 3. The intercostal muscles The intercostal muscles connect the ribs to each other and are the primary respiratory muscles. Three different structures can be distinguished: the external and internal intercostals and the intimi. The external intercostal muscles take origin from the lower margin of the upper rib, just superficial to the costal sulcus. Their direction is from cranioposterior to caudoanterior; insertion is into the superficial aspect of the upper margin of the lower rib. Their posterior edges are level with the neck of the rib (Fig. 38.12). The anterior margins are at the junction of the rib and its cartilage; thus, in the most medial part of the intercostal space, an external intercostal is not present. Due to the oblique course of the fibres and the fact that leverage is greatest on the lower of the two ribs, on contraction the muscle pulls the lower rib towards the upper rib, which results in inspiration. The internal intercostals originate from the internal aspect of the upper margin of the lower rib and insert on the inner aspect of the sulcus of the upper rib. The course of their fibres is from caudoposterior to cranioanterior. Their anterior margins are at the edge of the sternum, the posterior margin at the costal angle. They pull the upper rib downwards in forced expiration.
588 SECTION EIGHT - THE THORACIC SPINE
4
Figure 38.12
The intercostal muscles: 1, external intercostal muscles; 2, internal intercostal muscles; 3, diaphragm; 4, endothoracic fascia.
Between the internal and external intercostals lie the intimi. These take origin on the upper aspect of the lower rib and insert just medially to the origin of the external intercostal muscles. Their direction and function are the same as for the internal intercostal muscles. The diaphragm (C3-C4J The diaphragm is a dome-shaped musculotendinous structure which separates the thorax from the abdomen (Fig. 38.13). It is pierced by structures passing from thorax to the abdomen and vice versa.
Its short origin is from the inner aspect of the caudal bony thoracic aperture and can be divided into three different parts, all of which insert into a central tendi nous structure, that forms the roof of the dome. The sternal part is attached to the posterior aspect of the xiphoid process and inserts anteriorly at the middle of the central tendon. The costal part originates from the internal aspect of the six lowermost ribs and their cartilages. It inserts into the lateral part of the central tendon. The origin of the lumbar part is slightly different on the two sides of the midline. To the left, the origin is from the anterior part of the three upper lumbar verte bral bodies; to the right, from the four upper lumbar vertebrae. These tendinous structures create an arch for the aorta and thoracic duct in front of the spine. Anterolaterally to the left, there is an opening in the muscular fibres for the oesophagus. The fibres of lumbar origin insert into the posterior aspect of the central tendon. To the right of the midline posteriorly is an aperture for the passage of the vena cava inferior. Contraction of the diaphragm pulls the central tendon downwards, so producing diaphragmatic inspi ration. The diaphragm also provides a flexible barrier between thorax and abdomen. Other clinically important muscles The following clinically important muscular structures, although inserting on the thoracic cage, belong to the shoulder girdle. They are discussed thoroughly on pages 347-352 .
Figure 38.13
1, diaphragm; 2, external intercostal muscles; 3, internal intercostal muscles.
• •
Trapezius Rhomboid minor and major
CHAPTER 38
• • • • • • •
Levator scapulae S�rratus posterior inferior Subclavius Pectoralis minor Serratus anterior Pectoralis major Latissimus dorsi
LANDMARKS
With the shoulder in neutral position, the superior angle of the scapula is level with the first thoracic vertebra and the posterior end of the first rib (Fig. 3S.14). The inferior angle corresponds to the interspinal level between T7 and TS, whereas the spine of the scapula lies at the level of the T3 spinous process. The medial border of the scapula is approximately 5-6 cm from the midline. MOVEMENTS OF THE THORACIC SPINE AND CAGE
The thoracic vertebral column constitutes the most rigid part of the spine but nevertheless allows some move ment in flexion-extension (in a sagittal plane), side flexion (in a frontal plane) and rotation (in a horizontal plane). Flexion-extension movements take place mainly in the lower thoracic segments, whereas side flexion takes place at all thoracic levels but is slightly increased towards the caudal thoracic area. Rotation takes place mainly at the joints of the upper half of the thoracic spine.
-
APPLIED ANATOMY 589
Rotation is stopped by the posterior ligaments, essen tially by the ligamentum flavum, together with the capsules of the facet joints. This gives rise to an elastic ligamentous end-feel on passive rotation. The degree of vertebral rotation is nevertheless limited by the close and multiple connections between the thoracic spine and the rest of the thoracic cage. Because many of the costal carti lages and ligaments lose part of their elasticity with ageing, the range of rotation is considerably decreased in elderly subjects. On extension, the disc is compressed posteriorly and widens anteriorly, and the nucleus pulposus moves anteriorly. Extension is arrested by the spinous and articular processes, together with tension of the anterior longitudinal ligament as this is stretched. An elastic end-feel is the result. The posterior longitudinal ligament, the ligamentum flavum and the interspinous ligaments relax. Flexion ends with tension in the interspinous ligament, the ligamentum flavum, the capsules of the facet joints and the posterior longitudinal ligament. Side flexion is limited by the impact of the ipsilateral articular processes and by the contralateral ligamentum flavum and inter transverse ligaments. As in the cervical spine, there is a coupling character istic to movement: on side flexion there is always some degree of axial rotation in such way that the spinolls processes move toward the concavity of the lateral Cllr vature. Thus, on side flexion to the right, a rotation to the left occurs. This 'side coupling' is mainly confined to the upper thorax.
THE ABDOMINAL WALL
The abdominal wall is mainly a musculotendinous struc ture with some posterior and inferior bony elements (thoracolumbar spine and pelvis - see ehs 50 and 60). The rectus abdominis muscle, situated bilateral to the midline between the thoracic cage and the pubic sym physis, takes origin from the superficial aspect of the rib cartilage of the fifth, sixth and seventh ribs and inserts into the upper surface of the pubic symphysis and pubic bone (Fig. 3S.15). It is anchored in a fibrous sheath both anteriorly and posteriorly (see below). The muscle assists in anterior flexion of the trunk on the pelvis and vice versa.
Figure 38.14
The shoulder in neutral position: landmarks.
External oblique is the most superficial muscle of the lateral abdominal wall and takes origin from the outer surface of the seven lowermost ribs. Its uppermost attachments alternate with those of the serratus anterior and the lower ones with the costal origin of the latissimus dorsi. The fibres course in a
590 SECTION EIGHT - THE THORACIC SPINE
Internal oblique. This lies deep to the external oblique and superficial to the transversus abdominis muscle (Fig. 38.17). It originates from the superior aspect of the anterior two-thirds of the iliac crest, from the ventral part of the lumbar fascia and from the lateral two-thirds of the inguinal ligament. The fibres have a craniomedial course. They insert into the lower aspect of the three lower ribs and the rectus sheath. Contraction causes an anterior flexion and an ipsi lateral rotation and side flexion of the trunk. Transversus abdominis. The origin is from the internal aspect of the six lowermost ribs, from the lumbar fascia, from the internal surface of the iliac crest and from the lateral third of the inguinal ligament. The direction of its fibres is horizontal (Fig. 38.18) and insertion is into the sheath of the rectus. It assists in contraction of the abdominal wall and may have some function in lumbar stabilization.
Figure 38.15
Rectus abdominis, 1.
caudomedial direction and insert into the external edge of the anterior two-thirds of the iliac crest, into the inguinal ligament and the lateral border of the rectus sheath (Fig. 38.16). Contraction causes anterior flexion of the trunk on the pelvis, rotation of the trunk to the opposite side and ipsilateral side flexion.
2
Figure 38.16
3
Rectus abdominis, 1; external oblique, 2; transversus abdominis, 3.
The ilioinguinal region is the lower ventral part of the abdominal wall. Here the internal and external oblique muscles, the transversus abdominis and the inguinal ligament merge to form the inguinal canal. The last con tains the spermatic cord in the male, the round ligament of the uterus in the female and the ilioinguinal nerve in both sexes. The canal extends downwards and medially, parallel and a little above the inguinal ligament. The boundaries are: in front, the aponeurosis of the external oblique and muscular fibres of the internal oblique in its lateral one-third; behind, the reflected inguinal ligament
3 --+---H
Figure 38.17
4
Rectus abdominis, 1; internal oblique, 3; transversus abdominis, 4.
CHAPTER 38
- APPLIED ANATOMY 591
and the transversalis fascia; above, the arched fibres of the internal oblique and the transversus abdominis; below, the union of the transversalis fascia with the inguinal ligament. Protrusion of peritoneum and/or intestine into the inguinal canal is known as a direct or indirect inguinal hernia (see p. 1038).
,..,----1-+- 4
Figure 38.18
Table 38.1
Transversus abdominis, 4.
Rectus sheath. The fascia of the rectus abdominis muscle is reinforced by the aponeuroses of the oblique abdo minis muscles, which merge in the midline to form the dense fibrous linea alba. In the upper part, the anterior portion of the sheath is formed by the insertion of the external oblique and the internal oblique muscle, which splits, to form a deep and superficial layer. The posterior part is the deep layer of the internal oblique muscle and the insertion of the transversus abdominis. In the lower part, from about halfway between the umbilicus and symphysis, layers of the flat muscles pass anterior to the rectus; behind the rectus is only diaphenous fascia. A summary of the muscles of the thorax and trunk is provided in Table 38.1.
Summary of the muscles of the thorax and trunk
Structure and muscle
Function
Peripheral innervation
External intercostal
inspiration
Internal intercostal
Expiration
Corresponding intercostal nerve Corresponding intercostal nerve
Intimi intercostal
Expiration
Corresponding intercostal nerve
Diaphragm
Inspiration
Phrenic nerve
C4 ( C3-C5 )
Spinal innervation
Thoracic cage
Abdorninal pressure Scapulothoracic Trapezius
Elevates scapula Adducts scapula
Accessory nerve and branches of cervical plexus
C2-C4
Rhomboid
Elevates scapula Adducts scapula
Dorsal scapular nerve
C5
Levator scapulae
Elevates scapula
Dorsal scapular nerve and cervical plexus
C5
Serratus posterior inferior
Pulls lower ribs downwards and dorsally
Intercostal nerves
T9-T12
Subclavius
Depresses scapula
Branch of superior trunk of brachial plexus
Serratus anterior
Rotates scapula
Long thoracic nerve
C5 C5-C7
Pectoralis minor
Depresses scapula
Medial pectoral nerve
C 8-T 1
Middle and caudal intercostal nerves
T6-T11
Intercostal nerves
T5-T12
Intercostal nerves
T 10-T 12
Intercostal nerves
T7-T 12
Fixates scapula Adducts scapula Abdomen Rectus abdominis
Abdominal pressure Flexion of trunk
External oblique
Contralateral rotation of trunk Flexion of trunk Ipsilateral side flexion of trunk
Internal oblique
IpSilateral rotation of trunk Flexion of trunk Ipsilateral side flexion of trunk
Transversus abdominis
Abdominal pressure
592 SECTION EIGHT - THE THORACIC SPINE
BIBLIOGRAPHY Benson M, Byrnes D. The clinical syndromes and surgical treatment of thoracic intervertebral disc prolapse. J Bone Joint Surg 1975;57(4):471-477. Clarys JP, Wylock P, Wilikens P. Uit de k1iniek. Geneeskd Sport 1993;26(1):2-9. Dommisse G. The blood supply of the spinal cord. J Bone Joint Surg 1974;56(2):223-235. Gerritsen B, Heerkens Y. Anatomie in vivo van het bewegingsapparaat. Scientific Publishing, Bunge, Utrecht, 1986. Groen G. De innervatie van de wervelkolom bij de mens. Ned Tijdsch Man Ther 1991;10. The Guarantors of brain. Aids to the Examination of the Peripheral Nervous System. Bailliere Tindall, London, 1986. Guyot). Atlas of Human Limb Joints, 2nd edn. Springer, Berlin, 1990. Hoppenfeld S. Physical Examination of the Spine and Extremities. Appleton-Century-Crofts, Norwalk, Connecticut, 1976. Kapandji lAo Bewegingsleer Deel I. De bovenste extremiteit. Bohn, Scheltema & Holkema, Utrecht/ Antwerp, 1986.
Kapandji IA. Physiology of the Joints. Vol III, The Trunk and the Vertebral Column, 2nd edn. Churchill Livingstone, Edinburgh, 1990. McMinn R, Hutchings R. Atlas vall de Menselijke Anatolllie. Medical Books Europe, Lochem, 1984. Manohar M et al. Thoracic human vertebrae. Quantitative three dimensional anatomy. Spine 1991;16(8):888-901. Netter
F.
The
Ciba
Collection of Medical Illustrations;
Vol 8;
Musculoskeletal System Part I. Ciba-Geigy, Summit, New Jersey, 1987. Sobotta J, Becher H. Atlas der Anatomie des Menscllell; ]. Urban & Schwarzenberg, Munich, 1962. Sobotta J, Becher H. Atlas der Anatomie des Menschell; 3. Urban & Schwarzenberg, Munich, 1967. Troisier O. Semiologie et Traitement des Algies Discales et Ligal11entaires du Rachis. Masson, Paris, 1973:24. White A, Panjabi M. Clinical Biomechanics of the Spine. Lippincott, Philadelphia, 1978. Yong-Hing K, Reilly J, Kirkaldy-Willis W. The ligamentum flavum. Spine 1976;1(4).
Clinical examination of the thoracic spine
CHAPTER CONTENTS ,
Introduction 593 Principal differences between the thoracic and the
lumbar and cervical spines
593
Referred pain 594 Pain referred from musculoskeletal structures
Pain from visceral structures
595
597
History S99 Pain 599 Para.esthesia 600 Anticoagulant treatment and bleeding disorders Inspection and palpation Scoliosis 601
Kyphosis
600
601
Functional examination
601
Standing 601 Sitting 605 ,Lying prone 607 Accessory tests
607
Technical investigations
610
600
INTRODUCTION
Thoracic or abdominal wall pain is a common complaint and a major diagnostic challenge to physician and therapist. The pain is often referred from visceral disorders although the frequency of musculoskeletal lesions of the thorax and the abdomen should not be underestimated. A physician not familiar with the musculoskeletal disorders of the region could be tempted to ascribe unexplained pain to vague lesions such as intercostal neuralgia, neuritis, cardiac neurosis, pleurodynia or rib syndromes. Again the lack of an exact diagnosis leads to inadequate and unsuccessful treatment. The absence of a precise (orthopaediC) diagnosis can be to a certain extent the consequence of the complexity of the region itself. However, another important reason is the lack of an appropriate clinical approach to this part of the body. Thorough examination should not be restricted to the routine visceral examination (e.g. auscultation, percussion and palpation) but also must include proper orthopaedic and neurological tests. Although a large number of reliable technical investigations for detecting all types of visceral disorder are available, the same cannot be said when it comes to musculoskeletal disor ders, for which technical investigations are often of limited diagnostic value. Clinically, the thoracic region is approached in a different way from the cervical or the lumbar spine because it behaves differently in many aspects. PRINCIPAL DIFFERENCES BETWEEN THE THORACIC AND THE LUMBAR AND CERVICAL SPINES Visceral versus musculoskeletal pain
Because referred pain from visceral problems can mimic pain of musculoskeletal origin and vice versa, the first step towards diagnosis must always be to differentiate these two categories. The character of the pain is usually of little help in differential diagnosis, because it has the same features in both. Pain referred from heart, lungs and intestines is usually poorly localized, vaguely delin eated and is referred to a segmental or multisegmental 593
594 S E CTION E I G HT - T H E THORACIC S PI N E
distribution. The behaviour o f the pain may also mislead the examiner. It is a main characteristic for pain in lesions of moving parts to be brought on by posture and movements. This is also the case in thoracic lesions: if the patient's symptoms depend on activity rather than on visceral function, a cause originating from moving parts should be considered. However, it must always be kept in mind that posture, physical activity, a deep breath or a cough may also influence visceral pain in the thorax or abdomen. The best method to achieve differentiation is to work in two complementary ways: exclusion of any visceral disorder through a thorough internal check-up, together with a positive confirmation of a provisional orthopaedic diagnosis (Fig. 39.1). This routine will also safeguard against unnecessary technical investigations and delays in diagnosis and treatment.1-3
in an asymmetrical way. Not so in the thoracic spine. Because of the rigidity of the thorax, such an obvious pattern is seldom found. Very often only one of the six passive movements, usually a rotation, is positive and then only slightly so. Therefore diagnosis in the thoracic spine is more tentative and may have to be based on smaller, subtler abnormalities. • Neurological deficit is seldom encountered in a thoracic
Discal lesions
Discodural and discoradicular interactions are well known causes for cervical and lumbar pain. In a discodural lesion, a shifted component of the disc impinges on the dura and causes pain that has multiseg mental characteristics (crossing the midline and occupy ing several dermatomes). Discodural conflicts are characterized by two sets of symptoms and signs: articu lar and dural (see p. 743). In a discoradicular lesion, the subluxated disc com ponent impinges on the nerve root and its dural sleeve. The pain and paraesthesia that result are strictly seg mental. Discoradicular conflicts are characterized by three sets of symptoms and signs: articular, root and cord. Disc lesions also commonly occur in the thoracic spine but often show characteristics that are quite different from those found at the lumbar and cervical spines. a discodural interaction at the cervical or the lumbar level usually presents with a clear partial articular pattern: some move ments hurt or are limited and others do not, always
• The articular signs are subtle:
•
•
disc lesion: whereas some degree of neurological deficit is a common finding in cervical or lumbar posterolateral disc lesions, muscular weakness is rarely detectable in thoracic discoradicular lesions. Also disturbance of sensation is very rare. This absence of neurological signs is probably the outcome of the location of the nerve root in the intervertebral foramen, where it lies mainly behind the lower aspect of the vertebral body and less behind the disc (see p. 582). There is no tendency for spontaneous recovery: in the lumbar and cervical spines there is usually a spontaneous cure for root pain, which seldom lasts longer than 4 months at the cervical and 12 months at the lumbar level. At the thoracic level, no such tendency exists and constant root pain can persist for many years. Protrusions can usually be reduced: although thoracic disc lesions are more difficult to diagnose, they are easily and effectively cured. Protrusions - no matter how long they have been present, or whether they are posterocentral or posterolateral, or soft or hard - can usually be reduced by one to three sessions of manipulations. Unlike at the lumbar or cervical levels, time is not a criterion for reducibility. Hence a disc displacement may well prove reducible after constant root pain even for several years. Traction is seldom required because the protrusions are usually of the annular type.
Non-discal lesions
In the thorax non-discal musculoskeletal lesions are also frequently encountered. To name but a few: ribs, rib joints, cartilage, intercostal and abdominal muscles. This is in contrast to the cervical and lumbar spines where lesions of the disc are the principal cause of dysfunction and pain.
REFERRED PAIN Discodural Discoradicular Figure 39.1
Non-discal lesion
Routine for differentiation between thoracic and abdominal wall pain.
Both musculoskeletal and visceral lesions can be ' the source of referred pain to the thoracic and I or abdominal wall.
C HAPTER 39 - C L I N I CAL EXAMI NATION 595
PAIN REFERRED FROM MUSCULOSKELETAL .
STRUCTURES Dura mater and nerve roots
Pain originating from the dura mater is referred in a multisegmental way: it crosses the midline and may cover several consecutive dermatomes (see p. 17). A possible explanation for this phenomenon may lie in its multi segmental origin, which is reflected in the great overlap between the fibres of the consecutive sinuvertebral nerves innervating its anterior aspect.4 Recent research has demonstrated that dural pain may spread over eight segments with great overlap between adjacent and con tralateral dura mater.s This may be an explanation for the fact that lower cervical discodural conflicts may produce pain that spreads into the upper thoracic level (Fig. 39.2a) or that lumbar dural pain causes pain in the lower thoracic region (Fig. 39.2b). Pain originating from a nerve root sleeve has a strict segmental reference and is restricted to the borders of the dermatome. Thoracic disc lesions may thus cause referred pain in the thorax, not only as the result of extrasegmental refer ence in the case of a discodural contact but also when a discoradicular interaction has been created. However, cervical and lumbar discal lesions may also be the origin of thoracic referred pain.
(a)
Cervical disc lesions. Some cervical disc lesions may cause pain in the thoracic region. Cervical discodural interactions. Low cervical disco dural interactions very often result in unilateral inter scapular pain, usually felt above T6 and spread over several dermatomes. The pain is also often referred to the sternum and the precordial region. Exceptionally, the pain may be felt only in the anterior chest, so misleading almost all clinicians. It should be remembered that extrasegmentally referred pain of cervical origin never spreads into the upper limb (see p. 17). Cervical discoradicular interactions. A posterolateral disc protrusion compressing the C5, C6, C7 or C8 nerve root gives rise to unilateral root pain characterized mainly by a sharp pain down the upper limb. There may also be some degree of scapular pain, especially in C7 lesions, but this is usually not very severe (see p. 189). The C4 nerve root gives rise to pain in the trapezius area, the infraclavicular chest and the scapular region above the scapular spine.
Thoracic disc lesions. Thoracic discodural and disco radicular interactions are common causes of referred pain in the thoracic and abdominal region.
(b) Figure 39.2
Extrasegmental pain: (a) cervical origin; (b) thoracic origin.
Discodural interactions. It should be noted that extraseg mental pain from a posterocentral thoracic disc protrusion usually remains in the trunk itself, where it can spread anteriorly and I or posteriorly over several segments (Fig. 39.2b). It seldom spreads into the neck or into the buttocks. The pain is usually unilateral and spreads over several segments. Exceptionally it is felt centrally at the spine, radiating bilaterally towards the sides. Discoradicular interactions. A posterolateral impinge ment on the two upper thoracic roots produces pain felt in the arm (Fig. 39.3). If the T1 nerve root is involved, pain may be referred to the ulnar side of the forearm, whereas a T2 nerve root compression gives rise to pain
596 SECTION E I G H T - T H E THORACIC SPI N E
felt over the ilUl.er aspect o f the arm from the elbow t o the axilla, at the anterior aspect of the upper thorax around the clavicle and at the posterior upper thorax around the scapular spine. Clinically the upper two thoracic seg ments belong to the cervical spine and are thus most easily examined with the cervical segments. If the third to the twelfth root is compressed, pain spreads unilaterally as a band around the thorax, some times reaching anteriorly as far as the sternum (Fig. 39.3). The following landmarks may be helpful to determine which root is involved: • •
• •
If pain is felt around the nipple, the T5 nerve root is at fault. Because the epigastrium belongs to the T7 and T8 segments, pain present here arises from structures of the same origin. Pain at the umbilicus and in the iliac fossa may point to a lesion of the T9, TlO and Tll nerve roots. If the Tll or Tl2 thoracic roots are compressed, pain may be referred to the groin or even further down to the testicle.
lumbar disc lesions Discodural interactions. Extrasegmentally referred pain from a lumbar discodural interaction is usually felt in the lumbar area and the abdomen, sometimes radiating into the lower limbs. The pain seldom spreads into the lower thorax.
Segmentally referred pain Discoradicular interactions. from Ll , L2 and L3 nerve roots may be felt in the side and in the groin. Nerves Neuritis. Neuritis of the spinal accessory nerve, the long thoracic nerve and the suprascapular nerve can provoke unilateral pain at the base of the neck and over the scapula. Herpes zoster. In that the thorax is often the seat of a herpes zoster infection, unilateral spontaneous pain of recent onset always calls for a careful inspection of the skin for erythema and grouped vesicles.
Bones
Osseous structures usually do not give rise to much in the way of referred pain; the pain remains typically local. T5
T1
T7
,
T2
,
I
T3
I
T10 '.
T12
',-"
',-"
""
Figure 39.3
Segmental referred pain of thoracic origin.
.
..j)
\.:I
..
CHAPTER 39 - CLI NICAL EXA M I NATION 597
Intense though localized pain is a warning sign and the following conditions should be considered: severe central pain is to be expected for about 2-6 weeks. For the first week there is often girdle pain. Thereafter it gradually disappears. If uncomplicated, spontaneous cure is to be expected within 12 weeks. Vertebral tumours: all types of bony tumour of the vertebrae, primary or metastatic, as well as infec tions, initially provoke local pain in the centre of the back. Contusion or fracture of a rib: the patient can point exactly to the tender spot. The same is the case in malignant invasion. Disorders of the sternum: traumatic disorders and tumours of the sternum may also give rise to local sternal pain.
• Traumatic fracture of a vertebral body:
•
•
•
Joints and ligaments
Ligaments and joints consistently obey the rules of referred pain, which means that the deeper the location of the affected structure and the closer its position to the midline, the more referred pain is to be expected. On the other hand, the further the lesion lies from the spinal axis and the more superficial, the more accurate will be its localization by the pain it provokes. as these are superficially located, the pain is felt locally. Costochondral and chondrosternal joints (Tietze's syndrome and costochondritis): the patient is able to indicate the site of the lesion accurately. Intervertebral facet joints: these give rise to unilateral paravertebral pain, felt deeply and locally, not going further lateral than the medial edge of the scapula. If several joints are affected at the same time, as may be the case in ankylosing spondylitis, the pain spreads more in a craniocaudal direction than mediolaterally; the opposite is true for a disc protrusion. Costovertebral and costotransverse joints: the pain is felt wulaterally between the vertebral column and the scapula. Anterior longitudinal ligament: when tills ligament is affected, pain is usually located anteriorly behind the sternum. Posterior longitudinal ligament: involvement of this ligament causes pain in the back, felt centrally between the scapulae.
• Manubriosternal and sternoclavicular joints: •
•
•
•
•
• Disorders of the costocoracoid fascia or the trapezoid and
conoid ligaments (p. 407): the pain is usually felt in the
infraclavicular fossa.
Muscular lesions
Muscular sprains of intercostal muscles, the abdominals and the muscles of the shoulder girdle usually provoke well-localized pain at the site of the lesion. PAIN FROM VISCERAL STRUCTURES The heart
Pain arising from disorders of the heart can be referred to dermatomes C8-T4, because the heart is derived largely from these segments. Therefore pain can radiate towards the tip of the shoulder, to the anterior chest and to the corresponding region of the back. It may also be referred towards the ulnar side of both upper limbs, though referral to the left side is more common (Fig. 39.4a). Pain from the pericardium always arises from the parietal surface, because this is the only part which has a sensory innervation. The aorta
Pain from the aorta, as in dissecting aneurysm, may be felt behind the sternum or in the abdomen, depending on the exact level of the disorder. It often radiates into the back and may expand as the lesion progresses. The lungs and visceral pleura
These are both insensitive. Therefore pain is caused by either the parietal pleura, as in pleurisy, or invasion of the chest wall by a tumour. The oesophagus
Disorders of the oesophagus (T4-T6) usually give rise to pain felt at any part of the sternum, often radiating between the scapulae into the back (Fig. 39.4b). The diaphragm
The central part of the diaphragm is mainly derived from the third and fourth, and sometimes, although rarely, the fifth, cervical segments. Pain from irritation of the central part of the diaphragm is felt at the tip of the shoulders and the base of the neck. Pain from the peripheral part is felt more locally in the lower thorax and in the upper abdomen at the costal margin (Fig. 39.4c). The stomach and duodenum
Pain from stomach and duodenum (T6-TlO) is most commonly felt in the epigastrium and upper abdomen, sometimes substernally and exceptionally in the lower thoracic part of the back (Fig. 39.4d). The liver, gal/bladder and bile ducts
The liver is derived from the right side of T7-T9. The gall bladder and bile ducts are of right T6-TlO origin. Pain is
598 SECTION E I G HT - T H E THORACIC SPI N E
(a)
Heart
Oesophagus
(b)
(c)
Diaphragm
Stomach
(d)
(e)
Gallbladder
Pancreas
(f )
(g)
Figure 39.4
Kidney-Ovary-Testicles
Pain referred from visceral structures: (a) heart; (b) oesophagus; (c) diaphragm; (d) stomach; (e) gallbladder; (0 pancreas; (g) kidney/ovary/testicles
felt in the right hypochondrium and may radiate towards the inferior angle of the right scapula (T7-T9) (Fig. 39.4e). The pancreas
Patients suffering from a pancreatic disorder complain of upper abdominal pain often referred to the back at T8 (Fig. 39.4f). The spleen
Pain arising from disorders of the spleen is usually felt in the left hypochondrium, sometimes in the left side at low thoracic level (T7-TlO).
The small intestine, appendix and colon
Problem in the small intestine (T9-TlO) give rise to pain felt around the umbilicus. In disorders of the colon (TlO-S5), pain is usually felt in the neighbourhood of the lesion. The appendix is a TlO-Ll structure. The kidneys and ureters
Disorders of kidney and ureters (TlO-Ll) give rise to pain felt posteriorly in the side, at and just below the lower ribs, and at the anterolateral aspect of' the abdomen. The pain often radiates towards the testicles or the labiae (Fig. 39.4g).
CHAPT E R 39 - CLI N I CAL EXA M I NATION 599
Reproductive system
Disorders of the ovaries (Tll-Ll) may result in unilateral low abdominal pain, sometimes felt in the periumbilical area. Testicular problems (Tll-Ll) give rise to scrotal pain, sometimes radiating into the groin and to the side. See Box 39.1 for a summary of referred pain in the thorax and abdomen.
HISTORY
In dealing with pain in the thorax or abdomen, the main goal of history taking is to differentiate between musculo skeletal and visceral problems. As already pointed out, a relationship between the patient's complaints and posi tions or activities does not necessarily exclude a visceral disor
PAIN What made the pain come on?
If the patient mentions an injury to the chest, a bony problem of ribs, sternum or vertebra is likely. In a patho logical fracture a sudden pain may follow a very trivial movement. When the pain has come on without trauma, it is of interest to know what the patient was doing at the time and in which position the body was held. Thoracic disc lesions are, just as lumbar ones, most often the result of a combined flexion-rotation movement. However, in disc lesions a history of such provocation cannot always be obtained, the patient stating that the pain started without any specific activity or posture. Pain that came on after a forceful movement of trunk or arms - such as during sporting activities - may be from a muscular lesion. Arthritis of the costovertebral, costotransverse or facet joints begins spontaneously. When it is the result of ankylosing spondylitis, pain and stiffness often occur in phases and are usually worst in the early morning.
Warning
A pa i n of sponta neous o nset , i nc reasi ng i n i nt ensi ty a nd expand i ng a l l th e t i m e, should b e suspected o f b ei ng caused by a tumour.
Box 39.1 Summary of referred pain in the thorax and abdomen Pain of musculoskeletal origin
Du ra ma ter a nd nerve roots Cervical d isc l esions Thoracic d isc l es i o ns Lum b a r d isc l esions N erves N eu ritis • S p i na l accesso ry nerv e • Lo ng thoracic nerve • S u p rascap u la r nerve Herp es zos ter Bo nes Vert eb ra e • F racture • Bony t u m o u rs • I nfec ti o ns R i bs • Contusion a nd fractu re • M a l i g na nt i nvasion o f a rib
S ternum • F racture • Tu m o u rs Joi nts a nd l i g a m ents M a nu b riost ernal a nd st ernoclavicula r joi nts Costochond ra l a nd chond ros terna l j o i nts Interv ert eb ra l facet j o i nts Costov ert eb ra l a nd costotra nsverse j o i nts Anterio r a nd posteri o r l o ng i tu d i na l l igam ents Costocoracoi d a nd coracoclavic u l a r ligam ents M uscu l a r l es i o ns I nt ercostals P ectora l is m a jo r P ec to ra l is m i no r Subclavius Latissimus d o rsi S erratus posteri o r i nferi o r Abdom i nals Pain of visceral nature
Hea rt Ao rta P l eu ra a nd l u ngs Oesophagus D i a p h ragm S tomach a nd d uod enum G a l l b l a d d er a nd b i l e ducts Panc reas Spl een Small i ntesti ne a nd colon Kid ney a nd u reters G eni ta l s
Where was the pain a t the beginning, where did it spread or shift to and where is it now?
When the pain is felt between the scapulae above T6, a cervical disc problem is most likely. In such cases, clinical
600 SECTION E I G HT - T H E TH ORACIC S PI N E
examination of the cervical spine should be done initially. If this is negative, clinical examination of the thorax follows. A thoracic disc lesion usually gives rise to discomfort felt centrally or unilaterally in the posterior thorax. Here, as in the cervical spine, the pain may be felt centrally at first and then shift more to the side. A shifting pain suggests a shifting (disc) lesion. A posterocentral protrusion interfering with the dura normally results in unilateral extrasegmental referred pain, usually felt in the anterior chest. However, it can also give rise to abdominal pain, discomfort in the groin and even lumbar pain. Sometimes bilateral extrasegmen tal pain is felt posteriorly and over several segments on both sides. An acute 'thoracic' lumbago may exceptionally cause pain felt only at the sternum. This is a most misleading phenomenon, in that it is not very logical to think of a disc problem in a patient with an acute sternal ache not preceded by any posterior thoracic pain. The possibility of such reference should always be borne in mind. In posterolateral disc protrusions, the pain is felt uni laterally and is referred to one segment only. It is mainly felt posteriorly and at the side but sometimes also anteri orly. This type of protrusion usually follows a postero central displacement that has subsequently shifted more laterally. In this case, root pain is preceded by a period of extrasegmental referred dural pain. In the rare event of a primary posterolateral protrusion, the disc fragment moves directly in a posterolateral direction. From the onset pain is felt to the side, radiating segmentally anteriorly and not preceded by extrasegmental pain. Pain which increases and expands all the time is from a ' growing' disorder, usually a tumour. Older patients who are symptom free on first waking in the morning but complain of central posterior thoracic pain that starts after some hours and increases throughout the day, are likely to be suffering from posterior bulging of the whole content of an intervertebral disc as a consequence of excessive thoracic kyphosis. Pain felt at the base of the neck is sometimes the result of a problem at the first costovertebral joint, the sterno clavicular joint or a fracture of the first rib. Pain at the sternum is seldom the result of a musculo skeletal disorder. Most often it has a visceral origin. The same is true for pain felt in the abdomen: muscular lesions do exist but are rare. They usually give rise to well-localized pain.
the dura mater by a protruded disc or a tumour. In the thoracic area, it is not so simple. Many disorders other than problems of the dura may give rise to the same symptom. Deep inspiration may increase pain because of one of a number of visceral disorders or other mus culoskeletal problems. Tumours of the respiratory tract, pleurisy, lung embolism, pneumothorax, even peri carditis can all give rise to pain increased by coughing or respiration. The same may be found in non-discal musculoskeletal problems from the ribs and sternum. Fractures and contusions of the ribs, a sprained inter costal muscle and a fracture of the sternum are all in the same class. Consequently, the influence of respiration on symptoms at the thoracic level is only regarded as a dural symptom once there is clinical certainty of disc protrusion. In thoracic disc protrusions it is more usual for deep inspiration, rather than a cough, to exacerbate the symptoms. PARAESTHESIA
A protrusion of a disc in the thoracic region can produce pins and needles in two ways. First, as the result of com pression of the spinal cord, which is characterized by extrasegmental pins and needles felt in both feet and typ ically increased or provoked by flexion of the neck. Cord compression and paraesthesia can also be the result of intra- and extraspinal tumours, to intraspinal haemor rhage or to a vertebral fracture. Second, paraesthesia can be the result of a posterolateral protrusion compressing a nerve root. For example, pins and needles may be felt in the groin from compression of the T12 nerve root. In this event, the features are always localized and limited to the corresponding dermatome. Both causes are rare and when paraesthesia is present other disorders, such as neuropathy due to generalized disorders (diabetes, pernicious anaemia and multiple sclerosis), must always been considered first. ANTICOAGULANT TREATMENT AND BLEEDING DISORDERS
The use of anticoagulants is always an absolute contra indication to any manipulation of the spine, because it can lead to uncontrollable intraspinal bleeding. The same applies in congenital or acquired disorders of blood coagulation.
Is the pain influenced by coughing, sneezing or deep inspiration?
INSPECTION AND PALPATION
When a Valsalva manoeuvre or a deep breath provokes or increases the cervical or lumbar pain, it is generally interpreted as a dural symptom, from interference with
On inspection, the curvature of the thoracic spine is noted. Scoliosis and hyperkyphosis may be detected.
CHAPTER 39
SCOLIOSIS
A deformity in the frontal plane is named scoliosis. If present it is important to determine whether it is located at the lumbar or at the thoracic level. Thoracic scoliosis can often be voluntarily corrected by the patient. In this event, it is postural and has no specific pathological implications. In structural scoliosis, the deformity cannot be corrected by muscular activity. There is often also asso ciated shoulder asymmetry. In this event, the scapula at the convex side is usually more prominent and the arm of this side touches the hip but the other arm hangs further away from the body. KYPHOSIS
A hyperkyphotic thoracic spine with a flattened lumbar spine may suggest ankylosing spondylitis. An excessive low thoracic and high lumbar kyphosis can be the result of Scheuermann's disease or osteoporosis. Sometimes a localized angular kyphosis is found as the result of a collapsed vertebral body, usually due to a pathological or a traumatic fracture or resulting from adolescent osteochondrosis. It is best felt by gliding the fingers over the spinous processes in a craniocaudal direction. It is more difficult to detect at the thorax than elsewhere because of the general kyphotic shape of the thoracic spine.
FUNCTIONAL EXAMINATION
Clinical routine differs significantly according to the level of the pain (see Fig. 39.5). For a number of reasons, pain felt above the T6 level (midscapular) demands a preced ing clinical examination of the cervical spine and the shoulder girdle. First, the upper two thoracic vertebrae, anatomically belonging to the thoracic spine but clini-
Thoracic/abdominal wall lesion Examination strategy in thoracic pain.
CLINICAL EXAMINATION 601
cally part of the cervical spine, are tested in the clinical examination of the cervical spine. Second, it was demon strated previously that cervical discodural interactions often provoke extrasegmentally referred pain in the upper half of the thorax. Third, numerous lesions of the thoracic apex and the shoulder girdle although causing pain in the cranial aspect of the thorax, are only detected by a proper examination of the cervical spine and lor the shoulder girdle: a tumour of the apex of the lung involv ing the T1 nerve root is only detected by cervical tests; a neuritis of the suprascapular nerve causes pain in the supraspinatus fossa and is detected by a combined weak ness of supra- and infraspinatus muscles. A fracture of the first rib provokes upper thoracic pain but the diagno sis can be missed if the examiner proceeds immediately with the examination of the thoracic spine. For all these reasons, in patients with upper thoracic pain, a full cervical examination followed by an examination of the shoulder girdle must be done first. Only when these are negative, should a thorough examination of the thoracic spine follow. If the patient has pain below C6, a cervical or shoulder girdle problem is unlikely and attention is immediately directed to the thoracic spine. The functional examination of the thoracic spine con sists of a large set of basic tests. The examination is per formed with the patient standing, sitting and lying prone. During the procedure, dural, articular, muscular and cord signs are sought. Sometimes, when particular symptoms or signs from the basic examination warrant, the proce dure is completed by specific accessory tests. STAN DING Dural tests
It is believed that deep inspiration, neck flexion and some scapular movements may indirectly stretch the dura mater. Taking a deep breath (Fig. 39.6a). The patient is asked to take a deep breath and to state if the pain increases. A positive test is regarded as a dural sign only when, after the rest of the examination is performed, a disc lesion seems to be present. In such a case, stretching of the dura mater via the intercostal nerve roots is interfered with.
Thoracic pain
Figure 39.5
-
Flexion of the neck (Fig. 39.6b). The patient is asked to bend his head actively forward. This may increase the pain or provoke paraesthesia. In thoracic spine problems, pain during active neck flexion is basically regarded as a dural sign because flexion stretches the dura mater from above. However, pain on neck flexion as the result of impaired dural mobility does not necessarily mean a disc lesion is present. Indeed, any kind of intraspinal space-occupying
602 S ECTION EIGHT - TH E THORACIC SPIN E
(b)
(a)
(e)
lesion that interferes with the dura, such as a tumour, may provoke pain on neck flexion. A problem with one of the posterior ligaments or posterior paravertebral muscles may also cause pain on neck flexion. Sometimes a patient feels a sudden sensation on neck flexion, resembling an electrical discharge going down his back and occasionally even spreading towards both anns and legs. Sometimes it also occurs on extension of the neck. This is known as Lhermitte's sign and was pre viously regarded as pathognomonic for disorders of the cord at the cervical level. In later reports it has been sug gested that problems of the thoracic cord may cause the same sign. This can be caused by multiple sclerosis, a
Figure 39.6 Dural tests at the thoracic level: (a) taking a deep breath; (b) flexion of the neck; (c) backwards movement of the scapulae.
tumour of the cord, disc lesions, tuberculosis, spondylo sis, arachnoiditis or radiation myelopathy.6 Neck flexion may also provoke or increase pins and needles. If these are felt in one or both lower limbs, this draws attention to compression of the spinal cord at the thoracic level, which is most commonly the result of a disc lesion or a tumour. Shoulder movements: upwards, forwards and backwards.
The patient is now asked to shrug both shoulders, to bring them forwards and backwards. These tests are basically active movements of the structures of the shoulder girdle. Therefore some will be
CHAPTER 39 - CLINICAL EXAMINATION 603
positive when a disorder of one of those structures is present (see Ch. 20). However, if one or all of these movements elicits pain it is most frequently the result of a thoracic disc lesion, because they all (to a greater or lesser degree) stretch the dura mater at the thoracic level, which is elongated in a cranial direction via the Tl and T2 nerve roots (Cyriax:7 p. 202). The most sensitive test is scapular approximation (shoulders backwards, Fig. 39.6c).
the lumbar spine. Differentiation is made by the level of the pain, as indicated by the patient, and on extension pressure at the end of the examination. On flexion, extension and side flexion to both sides the range of movement is greatest in the lumbar spine, rather than the thorax. Rotation movements, in contrast, only slightly occur at the lumbar level and involve mostly the thoracic spine. The movements performed are:
Active trunk movements
•
The patient is now asked to perform six active move ments of the trunk. These involve both the thoracic and
•
•
(a)
(d) Figure 39.7
•
Anteflexion (Fig. 39.7a) Extension (Fig. 39.7b) Left side flexion (Fig. 39.7c) Right side flexion (Fig. 39.7d)
(c)
(b)
(e)
(t)
Active trunk movements: (a) anteflexion; (b) extension; (e) left side flexion; (d) right side flexion; (e) left rotation; (D right rotation.
604 SECTION EIGHT - THE THORACIC SPINE
• •
Left rotation (Fig. 39.7e) Right rotation (Fig. 39.7f)
The patient performs these movements actively. Pain and limitation are noted. In structural scoliosis the associated hump persists and is accentuated on forward bending. While performing rotations, the patient keeps his head in neutral position in relation to the shoulders, to avoid cervical rotation. Conclusions from active trunk movements. In princi ple, the six movements described so far are articular. However, because they are performed actively, they involve some contractile structures as well. Passive and resisted movements (see below) provide the key in dif ferential diagnosis between inert and contractile struc tures. After these tests, the examiner should know whether an articular pattern is present or not. The articular pattern of the thoracic spine is an equal degree of pain and limitation of both side flexions and of both rotations, together with a larger limitation of extension and little or no limitation of anteflexion (Fig. 39.8). It resembles the pattern for the cervical spine. If this is found, a disorder of the entire segment of motion such as in ankylosing spondylitis or osteoarthro sis is present. Any other combination of abnormal tests is regarded as a partial articular pattern (Fig. 39.9). Such a combina tion could be, for instance, pain on one rotation or one side flexion together with one rotation, or one side flexion and extension, or three, four or five of the six movements being positive in producing pain or limita tion. As long as abnormal tests are present in a nonFigure 39.9
Examples of partial articular patterns
symmetrical way, the pattern is regarded as being partial articular. In all types of disc lesion a partial articular pattern is expected. In the thoracic spine, a common finding is that only one out of the six articular movements is positive usually one of the rotations. Differentiation must· always be made from a facet joint lesion or a muscular lesion, in which a partial articular pattern is also found. In the latter, some of the resisted movements are more painful.
Warning
Figure 39.8
The full articular pattern.
Whe n side flexion away from the pa i nful side (Fig u re 39.10) is the o nly pai nful a nd l i mited movement th is a lways i nd icates a severe extra-articu l a r lesion such as p u l monary or a bdomi na l tumour or a s p i na l neu rofi b roma.
CHAPTER 39 - CLINICAL EXAMINATION 605
Passive tests • Passive left rotation
(Fig. 39.11a) (Fig. 39.11b)
• Passive right rotation
Figure '39.10 Pain and limitation on side flexion away from the painful (coloured) side is a warning sign for serious disorders.
SITTING
The examination is now continued by passive and resis ted rotations to both sides, with the patient sitting. In the seated position Babinski's reflex is also elicited.
The patient crosses both arms in front of the chest. The knees are held between the examiner's legs to immobilize the pelvis. The patient's trunk is now twisted towards the left and the right by the examiner. Pain, range of move ment and end-feel are noted. The normal end-feel is elastic. A hard end-feel is typical of ankylosing spondylitis or advanced arthrosis. Both an empty end-feel and muscle spasm suggest a severe disorder: neoplasm, fracture and infectious disorders. Rarely, pain is present at half range, disappearing when rotation continues. This is known as a painful arc and was regarded by Cyriax7 as pathognomOnic for a disc lesion when combined with a partial articular pattern. At the end of both passive rotations the patient is asked to bend the head actively forwards. If this move ment further increases the pain it is regarded as a dural sign if the rest of the examination suggests that a disc lesion is present. Resisted tests
In the same position as used for the passive tests isomet ric contractions are done. The patient is asked to twist the
(a) Figure 39.11
(b) Passive rotation: (a) left; (b) right. At the end of each movement the patient is asked to bend the head forwards.
606 S ECTION EIGHT - TH E THORACIC SPIN E
(b)
(a) Figure 39.12
Resisted rotation: (a) left; (b) right.
trunk to the left (Fig. 39.12a) and to the right (Fig. 39.12b), while the examiner applies counterpressure at both shoulders, so that the patient is kept immobile. Pain and weakness are noted. Because muscular lesions do occa sionally occur at this level, these tests must always be performed. The results of both resisted and passive rotations are carefully compared. In a disc lesion, passive rotations are more painful than resisted ones. Given that resisted movements are more painful, a muscular problem is most likely, unless a psychogenic problem or a rib fracture is present. In both events, accessory tests should follow (see below). Cord sign: plantar reflex
The examiner glides a relatively sharp instrument along the lateral aspect of the sole, starting at the heel and moving forwards and medially towards the big toe (Fig. 39.13). Normally the toes either do not move at all or all uniformly go into flexion. This test is pathological if the patient spreads the toes apart and the big toe moves into extension. A positive test indicates interrup tion of the descending motor fibres. If there is the slight est doubt about interference with the spinal cord, a full neurological examination of the lower limbs must be
Figure 39.13
Testing the plantar reflex.
carried out. This includes all reflexes in the lower limbs and abdomen, resisted movements of the thigh and leg musculature, control of coordination, testing for numb ness and temperature sensitivity and the straight leg raising test.
CHAPTER 39 - CLINICAL EXAMINATION 607
LYING PRONE Location of affected level by passive extension thrust
The patient lies prone and a hyperextension thrust is given over every thoracic spinous process to locate the painful level. To do this, the hand is placed obliquely, with the fifth metacarpal bone on the spinous process (Fig. 39.14). Identification of the exact level is important, because some manipulations for thoracic disc protrusions are performed specifically at the level at fault. During extension pressure, attention is also given to the type of end-feel. Normally it is elastic. Muscle spasm is a warning of more severe disorders.
ACCESSORY TESTS
To reach a diagnosis, the basic clinical examination normally suffices. In circumstances that remain unclear or when a muscular problem is suspected, accessory movements must be done.
(a)
Stretching the T1 nerve root
The patient is asked to lift the arm sideways from the hor izontal. The hand is now put in the neck by flexing the elbow (Fig. 39.15). This movement stretches the T1 nerve root via the ulnar nerve, which may provoke pain between the scapulae or down the arm when the mobility of the T1 nerve root is impaired. The test is useful for differentiating between a problem of the cervical spine and one of the
(b)
(c) Figure 39.14
Passive extension thrust.
Figure 39.15
Stretching the T1 nerve root.
608 SECTION EIGHT - THE THORACIC S PINE
(a) Figure 39.16
(b) Resisted side flexion: (a) right; (b) left.
upper thorax which interferes with the dura or the T1 nerve root: if it is painful, a thoracic problem is more likely. Resisted movements and extension of the trunk
To gain more information on a muscular lesion, the following resisted movements should be performed. Resisted side flexion (Fig. 39.16). The patient stands, with the feet slightly apart. The examiner places himself at the patient's painless side, hips against each other, and puts the arm around the farther shoulder. The patient is now asked to bend sideways away from the examiner. By holding the patient's shoulder, side flexion of the trunk is resisted.
Passive extension (Fig. 39.18c). For passive extension the patient pushes the body up off the couch by means of the arms. The pelvis must stay down on the couch. The results of extension movements are carefully com pared with each other. In a muscular lesion, active and resisted extension are painful but resisted extension is the most distressing. In a lesion of an inert structure, active
Resisted flexion (Fig. 39.17). With the patient sitting down, the examiner places one hand on the proximal part of the sternum and the other on the patient's knees. The patient tries to bend forwards against resistance exerted by the examiner. This is a test for all the flexors of the abdomen and of the hip.
Extension of the trunk. This movement is performed in three different ways. Resisted extension (Fig. 39.18a). Resisted extension is best done with the patient prone. Counterpressure is given at the proximal part of the thorax and at the posterior aspect of the knees. Active extension (Fig. 39.18b). For active extension the patient remains prone and is asked to lay both hands on the sacrum and lift the trunk off the couch actively by use of the paravertebral muscles.
Figure 39.17
Resisted flexion,
CHAPTER 39 - CLINICAL EXAMINATION 609
and passive extension are painful but the latter provokes the most pain. Testing the long thoracic nerve
The patient pushes against a wall with the arms stretched out horizontally in front (Fig. 39.19). If the medial edge of the scapula moves away from the thorax to produce a winged appearance, a disorder of the long thoracic nerve is present. Oscillation of a rib
The examiner stands on the pain-free side and places one hand distally on the thorax, with the fifth metacarpal bone exactly on the suspected rib. The other hand rests with the pisiform bone on the contralateral transverse process of the corresponding vertebra (Fig. 39.20). Oscillations are now given by the hand resting on the rib. At the same time, the other hand is used to prevent rota tion of the vertebra by pressing simultaneously on the transverse process. These oscillations influence mainly the costovertebral and costotransverse joints. When there is inflammation, pain will be provoked; when ankylosing spondylitis is present, the movement will be less elastic.
(a)
Neurological examination
A full neurological examination must be carried out when compression of the spinal cord or a neurological disorder is suspected. The following accessory tests should be performed. Beevor's sign. The patient lies supine, crosses the arms in front of the chest and is asked to raise the trunk slightly
(b)
(c) Figure 39.18 (a) resisted;
Extension of the trunk is performed in three different ways:
(b) active; (c) passive
Figure 39.19
Testing the long thoracic nerve.
6 1 0 S ECTION EIGHT - TH E THORACIC SPIN E
Table 39.1 Full neurological examination of the lower limbs Tests
Nerve root
I nspection of gait Motor tests Resisted flexion of the hip
L2-L3
Resisted extension of knee
L3
Resisted dorsiflexion of the foot
L4
Resisted extension of big toe
L4-L5
Resisted eversion of foot
L5-S1
Resisted flexion of knee
S1 -S2
Squeezing the buttocks
S1 -S2
Raising on tip toe
S1 -S2
Reflexes Patellar reflex
L3
Achilles tendon reflex
S1
Sensitivity Temperature Numbness
Oppenheim's sign. This may confirm a positive Babinski's sign. When the fingers are slid downwards along the tibia no movement of the toes should occur. In cord compres sion, the big toe extends while the others spread. However, this test is less reliable than a Babinski's sign.
Palpation
If a muscular lesion is suspected, the affected structure should be palpated. Palpation is also necessary to differentiate between a lesion of an intercostal muscle and a true rib problem. In a disc lesion, cutaneous anaesthesia must always be checked. If present in the territory of one nerve root, a posterolateral protrusion is likely; bilateral numbness suggests instead compression of the spinal cord. The clinical examination of the thoracic spine is summarized in Box 39.2. Figure 39.20 Oscillation of a rib: 1 , position of fifth metacarpal right hand; 2, position of fifth metacarpal left hand.
off the couch. The examiner pays attention to the umbili cus, which should not move during this test. Any move ment in a cranial or caudal direction or to the side may point towards a denervation of the contralateral muscles. Cremasteric reflex (in man). When the pointed end of a reflex hammer is glided over the medial aspect of the thigh, the ipsilateral half of the scrotum moves upwards via contraction of the cremaster muscle. Absence of this reflex may point towards a lesion of the spinal cord. Full neurological examination of the lower limbs.
continued in Table 39. 1 .
This is
TECHNICAL INVESTIG ATIONS
Plain radiographs are useful in confirming osseous lesions and in the evaluation of degree and development of scoliosis. During the last decades the use of computed tomog raphy (CT) in combination with myelography and mag netic resonance imaging (MRI) have greatly increased the ability to visualize accurately thoracic spine disor ders. MRI is the best way to define the specific abnor mality as well as the effect on the adjacent spinal cord. CT after myelography may be useful as well, espe cially in those patients in whom there is involvement of the posterior ligamentous and osseous structures of the thoracic spinal canal.s
CHAPTER 39
-
CLI N I CAL EXAMI NATION 6 1 1
Bo � 39.2 Summary of clinical examination of the thoracic spine H istory
Pain Wha t made the pain come on ?
I nj u ry? Bony problem Spontaneous onset? Disc lesion Arthritis Tu mour Forceful activity? M uscular lesion Where was the pain a t the beginning/where did it spread or shift to/where is it now?
I nterscapular above T6? Cervical problem Shoulder g i rd l e Thoracic lesion I nterscapular below T6? Thoracic lesion Base of the neck? Costovertebra l F i rst rib Sternoclavic u l a r Sh ifting p a i n ? Disc I ncreasing or expanding p a i n ? Tu mour Is the pain influenced by coughing, sneezing or a deep inspiration ?
Paraesthesia
M u ltisegmenta l/lower l i m bs? Cord compression Seg menta l ? Root compression Undefi ned? Other neurological d i sorder Anticoagulant treatment and bleeding disorders Inspection Standing Functional examination 3 dural tests:
Ta king a deep breath Flexion of the neck Shoulders backwards 6 active trunk movements:
Anteflexion Extension Left side flexion Right side flexion Left rotation Right rotation Sitting 2 passive tests:
Passive left rotation (+ neck flexion) Passive right rotation (+ neck flexion)
2 resisted tests:
Resisted left rotation Resisted right rotation Cord sign:
Plantar reflex Lying prone
Location of the affected level by passive extension thrusts Accessory tests
Stretching the T1 nerve root Resisted movements of the tru n k Testi n g t h e l o n g thoracic nerve Osc i l lation of a rib Neurolog ical exam i nation Pa l pation
6 1 2 S E CTION E I G HT - T H E THORACIC SPI N E
However, the superior resolution o f the available imaging methods has also made the incidental detection of asymptomatic thoracic disc abnormalities more fre quent.9 In analogy with the lumbar and the cervical spine it has become evident that the correlation between gross anatomical findings on MRI and clinical signs and symp toms detected by the clinician may be lacking. A significant proportion of the population has disc disease as depicted on imaging studies, yet many have no clini cal findings at all.1° This relative frequency of asympto matic thoracic herniated nucleus pulposus has been documented in several studies.11,12 Wood et al reviewed magnetic resonance imaging studies of the thoracic spines of 90 asymptomatic individuals to determine the prevalence of abnormal anatomical findings: 66 (73%) had positive anatomical findings at one level or more,
including herniation of a disc in 33 (37%), bulging of a disc in 48 (53%), an annular tear in 52 (58%), deformation of the spinal cord in 26 (29%) and ScheuermaIUl endplate irregularities or kyphosis in 34 (38%).13 Awwad et al retrospectively reviewed postmyelogra phy computed tomographic scans of 433 patients and identified 68 asymptomatic thoracic herniated discs. After comparing the imaging characteristics with a series of five symptomatic thoracic herniated discs, the authors were unable to identify any features that could reliably classify a herniated disc as asymptomatic or symptomatic.14 All these studies clearly demonstrate that thoracic disc herniations shown by MRI may not be related to patients' symptoms. The diagnosis 'symptomatic thoracic disc lesion' is therefore primarily a clinical one.
REFERENCES 1 . Grieve G. Modern
Vertebral COIUIIIIl.
8. Rosenbloom SA. Thoracic disc d isease and stenosis. Radiol Ciill
2. Skubic I, Kostuik J. Thoracic pain syndromes and thoracic d isc
9. Vanichkachorn JS, Vaccaro AR. Thoracic disc d i sease: diagnosis
Manual
Therapy of the
Churchill Livingstone, Edinbu rgh, 1986:408. herniation.
I n : The Adllit
Spille.
Raven
North Am 1 99 1 ;29(4) :765-775. Press, New York,
3 . Bechgaard P. Segmental thoracic pain in patients a d m i tted to a
medical department and
a coronary unit. Acta Med Scand
J Neu rol Neuros urg Psychiatr 1 966;29:530-534. 5. G roen GJ, Baljet S, Drukker
J. The innervation of the spinal d u ra
anatomy and c l i n ical i m p licati ons. Acta Neurochir
Rev Diagn lmaging 1 992;1-2 : 109-1 8 1 . 1 2 . Williams MP, Cherryman GR, Husband J E . Significance o f
thoracic disc herniation demonstrated b y M R imaging. j COli/put Assist TOl11ogr 1989;13(2):21 1-214. 13. Wood KB, Garvey TA, Gundry C, Heithoff KBJ. Magnetic reso
1 988:99:39--46. 6. Gauthier-Smith Pc. L' Hermitte's sign in subacute combined
degeneration
intervention. Phys Med Rehabil Clill North Am 1 998;9(2) :343-380. 1 1 . Martin OS, Awwad EE, Pitbnan T, Noland TW, Weaver T.
Current imaging concepts of thoracic intervertebral d isks. Crit
1 98 1;644(suppl) :87-89. 4. Edghar MA, Nundy S. Innervation of the spinal dura mater.
mater:
and treatment. j A m Acad Orthop Surg 2000;8(3):1 59-169. 10. Mink JH, Deutsch AL, Goldstein TB et al. Spinal imaging and
1 991 : 1 443-146 1 .
o f the
cord.
J Neurol
Neu ros u rg Psychiatry
1 973;36:861-863. 7. Cyriax J. Textbook of Orthopaedic Medicine, vol . 1 , Diagnosis of Soft
Tissue Lesiolls, 8th edn. S a i l liere Tind a l l, London, 1982.
nance imaging of the thoracic spine. Evaluation of asympto matic i n dividuals. J Bone joint S u rg 1 995;77A(1l) : 1 631 - - 1 638. 14. Awwad EE, Martin OS, Smith KR Jr, Baker BK. Asymptomatic
versus symptomatic herniated thoracic discs: their frequency and characteristics as detected by computed tomography after myelography. Neu ros urgery 1 991 ;28(2):180-186.
Interpretation of the clinical examination of the thoracic spine
Thoracic 'backache'
Posterocentral protrusion
Posterolateral protrusion
Thoracic 'lumbago'
Cord compression Without neurological deficit
With neurological deficit Thoracic postural pain syndrome
Interpretation of the clinical examination of thoracic pain
'Bulging' disc Anterior erosion
With possible involvement of the spinal cord
Tumours Extradural haematoma Spinal canal stenosis Fracture of vertebral body Spinal infection
No involvement of spinal cord
Fracture of spinous process Facet joint lesion Costovertebral lesion Costotransverse lesion Paget's disease Osteoporosis Spinal column deformities
i-----------------.. Lesions of the sternum Lesions of the ribs Tietze's syndrome Ribtip syndrome Postthoracotomy pain syndrome
613
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
Introduction
615
Clinical presentation 616 Symptoms and signs 616 Clinical types of thoracic disc protrusion Treatment 622 Manipulation 622 Oscillatory techniques 630 Sustained traction 630 Sinuvertebral nerve block 631 Rest in bed 631 Surgery: removal of protruded discs Prevention of recurrence 631
618
631
Disorders of the thoracic spine: disc lesions
Although the spine is anatomically part of the thoracic cage, we prefer to discuss the thoracic disorders in two main categories - spinal lesions (this chapter and Ch. 42) and lesions of the thoracic cage and abdomen (Ch. 43). Thoracic ankylosing spondylitis is discussed separately (Ch. 44). This is done to standardize the discussion of the spine throughout, in the hope that a better clinical understanding may result.
INTRODUCTION
Cervical and lumbar disc lesions are widely accepted as common causes of pain. For the thoracic spine, the situa tion is different. Although thoracic disc lesions giving rise to compression of the spinal cord are well recognized,'-5 disc protrusion resulting in pain without causing neuro logical signs are poorly documented.6 Surgeons suggest that only one in 1000 disc lesions are of thoracic origin7 although others record figures up to eight in 1000.8 The incidence of thoracic disc lesions affecting the spinal cord is about one case per million people per year3,9 usually affecting adults although cases have been reported in children as young as 12.10 The existence of minor thoracic disc lesions provoking pain in the absence of cord compression was first estab lished by Hochman who removed a disc protrusion at T8-T9 in a 67-year-old lady with continuous unilateral pain in the thorax. Neurological signs were not present. The diagnosis was established by a CT scan. Autopsy studies show thoracic disc lesions in 15-60% of all the specimens examined. A recent study documented the high prevalence of disc herniations on to magnetic resonance images of the tho racic spine in 90 asymptomatic individuals.12 Herniation of a disc was found in 33 subjects (37%), bulging of a disc in 48 (53%) and annular tears in 52 (58%).'2 The same authors studied the natural history of 48 asymptomatic thoracic herniations over a period of 26 months and could not find clinical changes: all patients remained asymptomatic during the follow-up period.13 Others reviewed the postmyelography scans of 433 asympto matic patients and could identify no fewer than 68 (16%) radiographically impressive disc protrusions. 14 615
61 6
SECTION E I GHT - T H E T H O RACIC SPINE
An unexpectedly high prevalence of thoracic disc her niation (14.5%) was also demonstrated in the thoracic spines of a group of 48 oncology patients examined with high field magnetic resonance imaging.Is However, these figures do not correspond to the real clinical situation because, as occurs in the other parts of the spine, disc lesions often remain clinically silent. We believe that symptomatic thoracic disc protrusions are far more frequent than is generally accepted and agree with Kramer,16 who estimated the frequency of tho racic disc lesions to be about 2% of all disc lesions. The low figures that have been mentioned are probably far too low, in that they only represent patients with cord compression. Thoracic disc protrusions causing only minor articular signs without neurological deficit or without signs of cord compression are unintentionally excluded because the diagnosis of a discodural interac tion is not made. These patients are often classified as suf fering from intercostal neuralgia, neuritis, cardiac neurosis or pleurodynia - diagnoses that are as unclear as the thoracic pain itself. Untreated the pain can go on for many years, causing continuing morbidity. Nevertheless, the majority of such lesions can easily be reduced in a few manipulative sessions, so fully relieving the patient's pain. Although more frequently present than commonly believed, thoracic disc protrusions are clinically far less common than those in the lumbar spine, because of the greater rigidity of the thoracic spine. This is a result partly of the stabilizing effect of the rib cage on the tho racic spine and partly of the thoracic intervertebral discs, which are thinner on account of a less voluminous nucleus pulposus.17 Therefore extension and flexion movements are of a smaller range in the thoracic spine. Minor thoracic disc lesions occur most often between T4 and T8 and seldom lower. Those with cord compres sion are usually found in the lower half of the thorax.6,18 Indeed, about 70% lie between T9 and TI2, the peak being at TIl (29%). A logical explanation for this could be that disc lesions that occur in the lower thoracic spine are much more likely to give rise to signs of cord compres sion, as a result of the critical vascular supply at this level.19
CLINICAL PRESENTATION •
�'•
•
'
'••�_.
,.:
l.:.il�
It is hypotheSized that disc degenerations and disc dis placements are of themselves painless events because the disc is almost completely without nociceptive structures. Clinical syndromes originate only when a subluxated fragment of disc tissue impinges on the sensitive dura mater or on the dural nerve root sleeve. This clinical hypothesis is extensively discussed in the lumbar section
of this book (see Ch. 50). Disc displacements (protrusions and prolapses) are either soft (nuclear) or hard (annular) and may have a posterocentral or posterolateral localization. Posterocentral protrusions compressing the dura mater may provoke multisegmental pain which is mainly referred into the posterior thorax but may also spread into the anterior chest, the abdomen or the lumbar area.20 The pain is never referred down the arm. When a posterocentral displacement increases, cord compression can result. Posterolateral protrusions interfering with the dural sleeve around the nerve root result in pain that is seg mentally referred into the corresponding dermatome. A more massive posterolateral protrusion may compress the ganglion or the nerve root fibres, resulting in motor and lor sensory disturbances in the innervation area of the root. When the Tlnerve root is compressed by a disc lesion, pain is referred to the inner side of the arm between elbow and wrist. A T2 nerve root impingement creates pain referred towards the clavicle and to the scapular spine and down the inner side of the upper arm. The cor responding dermatomes of the T3-T8 nerve roots follow the intercostal spaces, ending at the lower margin of the thoracic cage. The dermatomes of T9-TIl include a part of the abdomen, and TIl also includes part of the groin (see Fig. 39.3, p. 596). Thoracic disc protrusions may give rise to four differ ent clinical presentations: chronic thoracic backache, acute thoracic lumbago, thoracic root pain, and spinal cord compression (Cyriax:21 pp. 202-205). Each clinical pattern corresponds to a specific type of disc lesion. Besides dural and articular signs and symp toms, one must always look for elements which may indicate compression of the spinal cord.
SYMPTOMS AND SIGNS
The clinical findings in symptomatic thoracic disc dis placements are analogous to the lumbar and cervical disc syndromes. Again, both dural and articular signs and symptoms can be identified (see Ch. 52). DURAL SYMPTOMS
Increasing the intra-abdominal pressure by deep inspira tion, coughing or sneezing may aggravate the pain in all types of symptomatic disc displacements. A deep breath usually has more effect than does a cough - the opposite is true for the lumbar spine - and is the consequence 'of traction exerted on the dura mater via the intercostal nerves. This dural symptom of major importance in the
CHAPTER 41
-
DIS O R D E R S OF T H E T H O RACIC S P I N E : DISC LESIONS 61 7
lumbar spine, is less helpful in the thorax. Indeed, pain from other disorders of musculoskeletal or visceral nature may also be under the influence of respiratory movements. Therefore these symptoms are non-specific at the thoracic level and can be interpreted as only sug gesting that the dura is involved when the rest of the history and examination indicates a disc lesion. ARTICULAR SYMPTOMS
Pain in disc lesions is caused by certain positions and movements, and disappears with others. Often activities in prolonged flexion or rotation movements provoke or increase the pain. DURAL SIGNS
In dIsc lesions interfering with the normal mobility of the dura mater or of the dural nerve sleeve, movements that stretch the dura pull in harder against the protrusion and increase compression and pain. The movements regarded as dural signs are: • •
Pain on neck flexion. Pain on movements of the scapulae, most commonly on scapular approximation, which stretches the dura via the Tl and T2 nerve roots.
ARTICULAR SIGNS
A disc lesion usually affects only a part of the interverte bral joint. Therefore, certain movements cause biome chanical changes that result in forcing the protrusion against the dura. Consequently, it is to be expected that on clinical examination only some of the active move ments will increase the discodural interactions while other movements will be without effect and therefore painless. This results in a partial articular pattern, which is an absolute condition for the diagnosis of a disc pro trusion although it is not pathognomonic. Examples of non-articular patterns are illustrated in Figure 41.1. Depending on the degree of the compression, the partial articular pattern is more or less pronounced: more tests are painful and more severe pain is present. However, frequently only one movement is painful, most commonly one of the rotations. Often both articular and dural signs are present, although the latter are sometimes absent. Exceptionally, a combination of a partial articular pattern with pain on one or more resisted movements is found. In this event, the question that arises is whether there is a muscular problem or a lesion of an inert struc ture. In the latter, pain on passive movements is more
Figure 41.1
Examples of partial articular patterns.
severe, whereas in the former resisted movements are more painful. Pain and limitation on side flexion towards the pain less side as the only positive movement does not match the pattern of a disc lesion. Other disorders such as a pulmonary or abdominal tumour with invasion of the thoracoabdominal wall must be considered. An intraspinal tumour, for example a neurofibroma, is also possible (see p. 637).
Warning If p a i n and l i m itation on side flexion away from the p a i nful side is the o n l y abnormal movement (Fig. should be suspected.
41.2)
a tumour
618
SECTION EIGHT - THE THORACIC SPINE
Table 41.1 Articular and dural symptoms and signs in thoracic disc lesions
Articular
Symptoms
Signs
Particular movements or
Existence of a partial
postures increase the pain;
articular pattern
others ease Dural
Pain on deep breath
Pain on neck fiexion Pain on scapular movements
SYMPTOMS AND SIGNS OF CORD COMPRESSION
In thoracic disc lesions, careful attention must always be given to abnormal neurological elements that may indi cate compression of the spinal cord: pins and needles in both feet, disturbed coordination of lower limbs and positive Babinski's sign (see Table 41.1 and p. 202).
CLINICAL TYPES OF THORACIC DISC PROTRUSION
Symptomatic disc displacements in the thoracic spine may give rise to four different clinical syndromes: acute thoracic 'lumbago', chronic thoracic backache or 'dorsal gia', thoracic root pain and spinal cord compression (see Figs 41.3-41.5).21 Each syndrome corresponds to a specific type of disc lesion. It is obvious that, besides dural and articular signs and symptoms, elements which may indicate compression of the spinal cord must always be looked for.
Figure 41.2 Pain and limitation only on side fiexion away from the painful (coloured) side is a warning sign for serious disorders.
Figure 41.3 Thoracic disc displacement: small posterior displacement with dural contact - nuclear 'lumbago' or dorsalgia.
THORACIC BACKACHE
A small arumlar posterocentral disc displacement causes a unilateral discodural interaction. The subsequent uni lateral interscapular pain is of moderate severity and is usually brought on by prolonged activities or postures in anteflexion. The pain gets worse during or after particu lar movements or positions and wears off on rest but seldom completely disappears. In chronic thoracic back ache there is no spontaneous recovery and untreated pain can persist for many years. Because the pain is usually not severe, the articular signs are not always very impressive. However, no matter how subtle the outcome of the tests, some
Figure 41.4 compression.
Thoracic disc displacement: massive posterior displacement - cord
CHAPTER 41
-
DISORDERS OF THE THORAC I C SPINE: DISC LESIONS 61 9
Special case: self-reducing disc lesion
Figure' 41.5 Thoracic disc displacement: posterolateral displacement with radicular compression.
'asymmetry' in the clinical picture will always be present. It is for instance not unexceptional to find only one articular movement slightly positive, very often one of the rotations. This non-articular pattern, in the absence of pain on resisted movements can usually be interpreted as the outcome of a disc lesion. A further argument in favour of this diagnosis is when neck flexion increases the pain on full passive rotation of the trunk (dural sign). If both posterior and anterior thoracic pain are present, the posterior pain is often influenced by articu lar movements and the anterior pain is increased by neck flexion. Disc lesions at level T1 and T2 may give rise to diag nostic difficulties in that very little spinal mobility exists at this level and the articular movements may have no influence at all on the pain, so none is positive. The pain is often provoked only by flexion of the neck, which then suggests a cervical disc lesion. When this pattern is found, a differential diagnosis between both types of disc protrusion must be made. Stretching the Tl root and per forming all three scapular movements provides the key: they may provoke or increase the pain in a high thoracic disc lesion but usually have no influence on a cervical disc protrusion. In chronic thoracic backache there is no spontaneous recovery and, untreated, pain can persist for many years. All cases of thoracic backache from a disc protrusion, in the absence of any contraindication, should be treated by manipulations, which are usually quickly successful. If this fails, traction must be tried. If there is frequent recurrence, sclerosant infiltrations into the different liga ments and facet capsules must be given to increase spinal stability.
As the term implies, the disc undergoes spontaneous reduction. Patients who suffer from this condition usually sit for most of the day. On waking up in the morning they are symptom free but after sitting for some hours pain starts in the mid-thorax and gets progres sively worse. On lying down, the pain gradually eases off. The time needed for the pain to fully disappear depends on the degree of the displacement and is initially from 10 to 15 minutes. Later, or if the patient sits for a longer period, it may take an hour or more. Pain may be absent when prolonged sitting is not part of the daily routine - for example, at weekends. In this condition the disc gradually dehydrates as the result of the prolonged sitting position.22 Simultaneously, the imposed kyphosis pushes the whole intra-articular content of the disc posteriorly, compressing the dura mater, and resulting in thoracic backache. On lying down the effects of hyperkyphosis and gravity are largely diminished and the disc shifts spontaneously back into its original position. These patients should avoid prolonged anteflexion. Manipulative reduction is useless but sclerosant infiltrations may be helpful. ACUTE THORACIC LUMBAGO
Due to a combined flexion-rotation movement of the trunk the patient becomes suddenly immobilized, by a sharp posterior pain in the thorax, wi th the trunk fixed in flexion. The condition is similar to acute lumbago at the lumbar spine. In both, the underlying cause is a postero central disc protrusion. Pain is usually felt posteriorly in the centre of the back, radiating uni- or bilaterally around the chest. In high thoracic lesion, the pain may even reach the sternum; in low thoracic lesions, the pain is sometimes referred to the abdomen. A deep breath is very painiul and normally hurts more than a cough. Sudden onset in the absence of an injury in a middle-aged person, together with pain on deep inspi ration and on neck flexion, is very suggestive of such a disc lesion. A partial articular pattern is present in which three, four or five movements are painiul, and in severe instances all movements cause pain, but still in an asym metrical way. The symptoms and signs are thus much more pronounced than in thoracic backache. If the patient stays in bed for some days spontaneous resolution occurs over about 2 weeks. Cure can be obtained much more quickly by manipulative reduction. Exceptionally the pain can be so severe that the patient can hardly stand up or needs a great deal of time to turn around on the couch. Such patients should remain in bed until they have improved so that normal manipulations become possible. A manipulative attempt should
620
SECTION EIGHT - THE THORACIC SPINE
not be made during the initial period because it is unsupportable. Sometimes special oscillatory techniques can be tried. Recurrence may occur but the pain is not necessarily always felt at the same side. Special case: sternal lumbago
This is a rare disorder often leading to diagnostic difficulties. A high or mid-thoracic posterocentral pro trusion coming on suddenly can give rise to an agoniz ing pain felt only anteriorly over the sternum or in the epigastrium, without back pain. Differential diagnosis with an acute myocardial infarction has to be made but is not always simple. The effect of deep inspiration can be helpful: it increases the pain of a disc lesion but usually does not affect that originating from the myocardium. THORACIC ROOT PAIN
As in the cervical and lumbar spines, two types of root pain can be encountered: a primary and a secondary pos terolateral protrusion. The latter is more common. In the first type, the protrusion is from the onset deviated in a posterolateral direction; in the second, there is first a pos terocentral protrusion that later shifts laterally analogous to a lumbar disc lesion. segmental pain is felt from the start at the lateral aspect of the thorax and often radiates unilaterally to the front of the chest or the abdomen. The absence of pain in the back may lead to the discogenic origin being overlooked. In a secondary posterolateral protrusion, initially an extrasegmental posterocentral or posterior unilateral pain is present which then moves more to the side and sometimes towards the anterior thorax or abdomen - meanwhile becoming segmentally referred - a sequence of symptoms that strongly suggests a secondary posterolateral disc lesion.
• In a primary pos terolateral protrusion,
•
Both types of root compression give rise to segmental referred pain. It has a unilateral band-shaped distribution that follows the intercostal nerves. At the thoracic level a posterolateral protrusion seldom gives rise to pins and needles. If present, they follow the same segmental dis tribution as the pain. As the T12 dermatome spreads into the lower abdomen, interference with this nerve root can result in pain and occasionally pins and needles in the groin and/ or the testicles. On functional examination a partial articular pattern is usually found. Occasionally, the patient feels nothing on articular movements but flexion of the neck provokes a sharp unilateral sternal pain, sometimes accompanied by pins and needles in the same place. In that flexion of the
neck also stretches the nerve roots via the dura, one of these can be pulled further against a protrusion resulting in a sudden pain. Neurological signs are seldom encountered and, if present, are always difficult to diagnose. In that the majority of the thoracic nerve roots cannot be stretched by movements or arms or trunk, an analogue of straight leg raising does not exist. Moreover, motor defici t, except for a Tllesion, cannot be tested. The only feature that is occasionally found is numbness. When present, it is of little help in determining the exact level of the pro trusion because the dermatomes overlap. Only numb ness in the groin draws attention to a nerve root palsy T12. In rare instances, an area of hyperaestheSia is felt in the front of the chest. According to Cyriax21 a Tl root palsy is never the result of a disc protrusion but is always the outcome of some other disorder, such as superior sulcus tumour o f the lung, neurofibroma or vertebral metastases. Nevertheless, two cases of flaccid weakness of the hand from a Tl disc protrusion have been reported.23 If a neu rological deficit of T1 is present, special attention should be given to exclude the more severe disorders first, and only when this has been done should a disc lesion be considered (see pp. 637 and 656). Thoracic disc lesions compressing a nerve root do not usually resolve spontaneously. Occasionally, posterolat eral disc protrusions at Tl and T2 may heal without treat ment but the period over which this happens is not known and could be many years. Posterolateral thoracic disc protrusions which cause root pain remain reducible by manipulation, no matter how long they have existed. Where manipulation has failed or where neurological deficit is present, a sinuvertebral block should be given. COMPRESSION OF THE SPINAL CORD
The spinal cord is most vulnerable at the lower thoracic levels, between T9 and T12,23,24 because the spinal canal is at its narrowest there and the vascularization is at its most critical. It has been suggested that signs of cord compression are not always from pressure on the cord itself, but rather the result of interference with the blood supply.3-s Osteophytes narrowing the spinal canal are an extra contributing factor.2s A previous injury to the thoracic spine can also play a role in the later development of cord compression although this circumstance is rare. History
The most commonly observed chronological sequence in cord compression is pain, followed by sensory dis'tur bance, motor weakness and finally visceral dysfunction. All of these features may be present in any combination.
CHAPTER 41
Pain. Initially almost all patients complain of pain. It is never particularly severe, often has a vague band-shaped distribution, and may sometimes completely disap pear.26-29 It is usually localized in the back, although it may radiate into the pelvis or groin and down the legs. Occasionally, patients complain of subumbilical pain.] The quality varies from a constant, dull and burning pain to - exceptionally - a lancinating, cramping and spasmodic pain. Pins and needles. These are the most common symptoms. They are usually felt in one or both feet, sometimes radi ating into the legs and are often provoked or increased by flexion of the neck. Numbness. Later in the course, uni- or bilateral numb ness may set in and may be accompanied by a motor palsy. The numbness is more a diminution of the normal sensation than a complete loss of sensitivity. It oftens starts at the big toe and is accompanied by a subjective sensation of coldness.3 Weakness. Because of interference with motor function, patients often complain of difficulty on walking which sometimes presents a subjective weakness of the legs with unsteadiness or stiffness but it may truly interfere with gait so making the patient stagger or even making walking impossible. It is important to note that the patient's subjective complaint of motor weakness is not always confirmable clinically. Visceral complaints. Very often visceral complaints about urinary tract or bowel are also mentioned. Urinary symptoms may vary from difficulty in starting, to urgency, change in frequency, incontinence, incom plete emptying and even complete urinary retention. Occasionally, patients complain of impotence or of decreased sensation during intercourse. Bowel problems are of the same nature as those related to the urinary tract, with constipation quite fre quently present. Functional examination
The functional examination normally confirms what is expected already from the history. The most characteris tic signs are found on neurological examination; the articular signs are of secondary importance. Some or all of the following neurological signs may be present: • •
Disturbed coordination with spastic gait. The muscle tone is usually increased, with the affected muscles not limited to one myotome.3D Occasionally, weakness of the lower abdominal muscles can be demonstrated, when the umbilicus is seen to move as the patient attempts to sit upJ This is known as Beevor's sign.
-
• • •
• • • • •
DISORDERS OF THE THORACIC SPINE: DISC LESIONS 621
Weakness and/ or atrophy of some lower lin1b muscles. Hyperreactive patellar or Achilles tendon reflexes with ankle clonus. Occasionally, the tendon reflexes may be absent, particularly and inevitably when a flaccid type of paraplegia is present. The abdominal reflexes are often absent or diminished, most commonly in both lower quadrants. All these signs may be uni- or bilateral. Positive Babinski's and Oppenheim'S signs. Absence of the cremasteric reflex. Numbness. Limitation of straight leg raising, sometimes bilateral, has been noted.2 Occasionally a Brown-Sequard syndrome is found in cord compression.6 It is characterized by an ipsilateral flaccid segmental palsy, together with an ipsilateral spastic palsy below the lesion, with ipsilateral anaesthesia and loss of proprioception and loss of appreciation of the vibration of a tuning fork. Contralateral discrimination of pain sensation (analgesia) and thermoanaesthesia may be present and are both sited below the lesion.31,32
Although many of these tests are not included in the basic examination, they should be undertaken when the slightest suspicion of compression of the spinal cord exists. Sometimes the neurological disturbances are found to extend proximal to the territory of the level of the com pression. This may be the outcome of interference with the blood supply of the anterior spinal artery rather than compression on the cord as such.3-5 Differential diagnosis
Differentiation from other compressive disorders of the spinal cord, such as neoplasm, infection, vertebral frac ture and epidural haematoma, dissecting aneurysm and diseases of the cord (multiple sclerosis, Guillain-Barre syndrome and amyotropic lateral sclerosis) is not always easy and requires further clinical reasoning and more technical investigations. Technical investigations
The clinical description given above necessitates further imaging investigations. A plain radiograph sometimes shows a calcification in the disc that is at fa ult. 1 ,6,23,33 However, other authors, including Cyriax, consider a calcification, together with the accompanying narrowing of the intervertebral joint space to be non-specific.34 A myelogram usually indicates the level of the lesion with certainty although special projections may be needed.35 Today, magnetic resonance imaging (MRI) is the imaging method of choice in the investigation of the thoracic spinal canal.36 It provides a good-quality
622
SECTION E I G HT - T H E TH O RACIC SPINE
image over the entire length of the spine and can assess the morphology of the discs and cord. It is non-invasive, has comparable sensitivity to conventional myelography in visualizing lumbar nerve roots and allows overall assessment of the spinal canal even in the presence of cerebrospinal fluid block.37,38
Tl and T2 disc lesions will come to light in the cervical examination (rather than the thoracic examination), when a disc protrusion is present it should be treated using manipulative techniques designed for the thoracic spine. Indications and contraindications for manipulation are summarized in Box 41.1.
Treatment
The only treatment in cord compression is surgery. However, this difficult problem is best approached by microsurgical techniques, managed by a specialized surgeon.39,40 Warning S.um mary of warning si gns: these are two-fo ld. Presence of neuro logical signs. F i rst exclude: neopl astic process infectious process fracture If negative: consider d isc protrusion
(1)
(2)
Side flexion away from the painful side is the only painful and l i m ited movement: No disc lesion is present but a tumour is most l i kely
•
TREATMENT
Almost all thoracic disc protrusions can be reduced by manipulation in three to five sessions. If manipulation does not succeed after, say, three sessions, the diagnosis should be reconsidered and, if a disc lesion is confirmed, traction can be tried. Traction can also be used for tho racic postural pain syndrome and for lateral recess steno sis in the thorax (see later). Other treatments, discussed later, are sinuvertebral blocks for persistent root pain or for root pain with neurological deficit, surgery, bed rest and prevention of recurrence.
MANIPULATION
INDICATIONS
All actual and symptomatic thoracic disc protrusions in the absence of contra indications should be manipulated. Unlike the cervical and the lumbar spine, the type of onset is of less importance for treatment of the thoracic spine, since the great majority of thoracic disc protrusion is annular. Consequently, manipulations should be tried first. If these fail, and if the diagnosis of a disc lesion is confirmed, a nuclear protrusion should be considered. The time that has elapsed from the onset of the pain can also be disregarded, because thoracic disc protrusions remain reducible regardless of their duration. Although
CONTRAIN DICATIONS Relative contraindications
Disc protrusion is not present. It is obvious that in the absence of a disc protrusion manipulation is inap propriate and could even do harm by displacing a disc fragment. Self-reducing disc lesions. In self-reducing disc displace ments, no manipulative attempt must be undertaken because reduction occurs on lying down. However, measures for prevention of recurrences must be taken. A series of infiltrations with sclerosant solution is then the treatment of choice. Segmental neurological deficit. Neurological deficit indicates that the protrusion is too large to be reduced. Therefore no manipulative attempt is made if mono radicular numbness and / or motor palsy is found. Should this be present, the patient can be treated by an infiltra tion around the nerve root. Central protrusion. This occurs mainly in young patients with a large thoracic kyphosis, is nuclear in origin, posterocentrally localized and causes bilateral radiation of pain. The treatment of choice is sustained traction. Absolute contraindications
Cord compression. Signs and symptoms of compression on the spinal cord, such as positive Babinski's sign, weak ness of the lower limbs or spastic paresis, are absolute Box 41.1 Indications and contraindications for manipulation Indications A l l symptomatic disc d isplacements in the absence of contraindications
Contraindications Relative Absence of actua l symptomatic d isc displacement Self-reducing d isc lesion Monoradicular neurological deficit Absolute Signs and/or symptoms of cord compression Pati ents with b l eeding disorders Pati ents on anticoagulant treatment
CHAPTER 41
contraindications to manipulation. Such patients should be operated upon at once. Sometimes patients with cord compression are encountered who complain of pins and needles only in the legs and feet, increased or provoked by flexion of the neck. On clinical examination, further evidence of cord compression is not found. The implication is that the pro trusion interferes minimally with the cord; nevertheless, manipulations could easily increase the problem and are absolutely contraindicated. This does not apply to sus tained traction, which can be tried in cases in which the clinical features have not been present for too long. Bleeding disorders. Patients who suffer from bleeding disorders, either inherited or acquired, or who are on anticoagulants should never be subject to manipulation because this could provoke an intraspinal haematoma. If a patient on anticoagulants suffers from a disc lesion, the anticoagulants must be stopped over a period of days (should the condition for which treatment is prescribed permit) until blood coagulation has returned to normal. Manipulation can then safely be performed. TECHNIQUES
Thoracic manipulations are always performed under strong traction. Three main types of procedure are considered: extension techniques in which extension is
-
DISORDERS OF THE THORACIC SPINE: DISC LESI ONS 623
always present, sometimes together with a rotation; rota tion techniques, in which rotation is the only element and extension is not incorporated; the third type, the 'high thoracic technique', is used only in upper thoracic disc lesions. All extension manipulations of the thoracic spine are specific, i.e. they are performed only at the two vertebrae where the disc protrusion lies in between. Principle of strong traction
No one can foresee with absolute certainty the direction in which the protruded fragment will move during a manipulation. Theoretically, it could be displaced further towards the spinal cord. To avoid this and for a number of other beneficial effects (see p. 256) traction is always incorporated in thoracic manipulation. Traction is normally provided by one assistant sitting beyond the patient's head and taking either the head or the hands. Stabilization of the pelvis is either by a second assistant sitting at the patient's legs and holding the ankles or by a fixation belt around the pelvis (Fig. 41.6). Whether traction is given via the head or the arms depends on the level of the lesion and the patient's comfort. As traction on the arms opens the intervertebral joints only from T6 downwards, traction must be given via the head in disc protrusions above T6 (Fig. 41.7). Figure 41.6
Traction given by one assistant, using a
belt.
Figure 41.7 Traction is applied via the head if the lesion is situated above T6.
624
SECTION EIGHT - THE THORACIC SPINE
If traction via the arms provokes pain anywhere in the upper limb, it is replaced by traction on the head. Disc protrusion above Disc protrusion below
T6: traction via T6: traction via
the head the hands
Traction via the head is provided by putting one hand under the patient's chin and the other below the occiput, with the head and neck always kept in the neutral posi tion (Fig. 41.7). Both hands pull equally hard. Traction via the arms is achieved by the patient and assistant taking each other's wrists in their hands. Before any manipulation is done the assistant must first create traction because very often slack in a belt must be taken up and adjustment may be needed. The traction provided should always be given with maximum force in order to open the joint space as far as possible. Because maximum traction can only be ma�n tained for a few seconds, it is only given after the mamp ulator has taken up all the slack of the manoeuvre he is to perform. The different steps of the manipulation, including traction, are coordinated by the manipulator. . Although exerted with as much strength as possIble, traction is not a manipulation in itself. In other words, the assistance does not add a jerk to the pull during the manipulation but just maintains the pull maximally until the manipulation is complete.
specific in that they are performed directly on the vertebrae between which the lesion lies. Identifying the level of the lesion. The two most painful consecutive spinous processes are identified by extension pressure. The protrusion normally lie� between the�r corresponding vertebrae. If only one spmous process IS found to be tender, the disc at fault is usually the one lying just below. This being so, the extension ma �ipula tions are undertaken between the vertebra With the tender spinous process and the one immediately below. Sometimes all spinous processes are equally tender on extension pressure. It can then be useful to take two con secutive spinous processes between the fingertips one by one and to try to rotate them in the opposite direction towards each other. This is done at all levels and the two that prove most painful are indicative for the level of the lesion. From this point on, in describing the different exten sion techniques, the phrase 'two most tender spinous processes' is used. It should be understood that this always means the two most tender on extension pressure and not just on palpation for local tenderness. Some extension techniques are executed on the trans verse processes. To be able to perform these manipula tions at the right level, it is essential to have a good knowledge of the relationship between the spinous processes and their corresponding transverse processes, because this varies with the level (Fig. 41.8).
there is a difference of one level between the consecutive vertebrae, i.e. the transverse process of one vertebra lies level with the spinous process of the vertebra above. For example, the transverse process of T3 lies level with the spinous process of T2. T4-T9: there is a difference of It levels. The transverse process lies level with the interspinal line between the spinous processes of the first and the
• Tl-T4 and T9-Tl2:
Amount of force
Each manipulation must be performed with a reason able amount of force. This depends on both the manip ulator 's and patient's size and on the level of the protrusion. If a big examiner is dealing with a l�ghtly built patient, the whole of the former's strength wIll l: Ot be used, but if a lightly built manipulator has to mamp ulate a heavy man, the maximum effort may be needed to achieve good results. . Because the upper half of the thorax is the most ngld, disc protrusions at this level require a more forc�ful manipulation than for the lower half. Therefore a leSIOn below T6 can be treated with a less vigorous impulse. All manipulation must be performed using the body. The most common mistake occurs when the manipula tor uses his arms rather than his body. This leads to a loss of the slack already taken up, and results in increased amplitude of manipulation, which may be dangerous because the manipulator has no control over the force used.
•
.
T1-T4 and T9-T12
T4-T9
Extension techniques in prone position
Unless the patient is 60 years old, or more, extension tech niques are used initially. All extension manipulations are
Figure 41.8 Relationship between the level of spinous processes and their corresponding transverse processes.
CHAPTER 41
-
DISORDERS OF THE THORACIC SPINE: DISC LESI ONS 625
The 1 level difference between the spinous and transverse processes, which is present in T4-T9.
Figure 41.9
second vertebra above (Fig. 41.9). The transverse process of T8, for example, lies between the spinous processes of T6-T7, of T9 between T7-T8. Direction of rotation. This is important in manipulations that include an element of rotation. Manipulation is first undertaken in the direction of the less painful rotation. If this is only partly or completely unhelpful or makes the patient worse, rotation in the other direction follows. The direction of the rotation is always defined by the direction in which the anterior part of the upper vertebra rotates. So when the upper vertebra rotates to the left the movement is defined as a left rotation (Fig. 41.10).
Technique I: central pressure (Fig. 41.11). The patient lies prone on a low couch. The two most tender spinous processes are marked. The examiner stands to the side facing the patient and places one hand, reinforced by the other, on the lower of the two processes. Because the tho racic spinous processes cover each other like the tiles on a roof, it is logical to place the hands on the lower one in order to achieve as much movement as possible between the vertebrae. If the hand is placed on the upper vertebra, the movement is assured by the bony contact between the spinous processes; when the hand is placed on the lower vertebra, it is pushed away from the upper vertebra, resulting in increased range of motion.
.... right rotation Figure 41.10
Direction of rotation.
t-
...
left
rotation
626
SECTION EIGHT - THE THORACIC SPINE
Figure 41.11
Central pressure.
The hand makes contact with the spinous process via the fifth metacarpal bone and, to make the manoeuvre less painful, the hand is placed slightly oblique so that the hypothenar muscles lie between the bones of the hand and the patient's spine. The assistants adopt the positions already described. The manipulator leans over the patient, the shoulders vertically above the hands, elbows straight, feet far away or close to the couch, depending on the effort to be used. All the slack is taken up by use of the body weight and is maintained until the final manipulative thrust is given. The patient is now asked to fully relax by taking a deep
Figure 41.12
Unilateral pressure.
breath followed by a maximal expiration. The moment the patient starts to expire the manipulator tells the assis tants to pull. He waits until the end of expiration and, under maximal traction, the final extension thrust is given by the manipulator's body, transmitted to the patient via the arm and hands. Technique II: unilateral pressure (Fig. 41.12). This manip ulation is performed unilaterally on the transverse process. The patient lies prone and the two most painful spinous processes and their corresponding transverse processes are marked. Vertical pressure is exerted on the transverse process of the lower of the two vertebrae. The manipulator stands on the contralateral side of the patient, for a right rotation on the left. One hand, reinforced by the other, is placed with the pisiform bone on the transverse process. To make good bony contact, the paravertebral muscles are first moved to. the side. This is obtained by pushing the muscles away from the vertebra with the base of the lower hand. One assistant holds the patient's ankles, the other one grasps the head or hands. With the elbows straight, the manipulator leans over the patient and brings his body weight per pendicular over the spine, taking up all the slack. The patient is now asked to relax, to take a deep breath in and then to expire fully. The assistants are told to pull. After a couple of seconds of traction, the manipulator gives the final jerk vertically downwards. This causes a rotation and an extension movement.
CHAPTER 41
-
D I S O R D E R S OF T H E T H ORACIC SPINE: D I SC LESIONS 627
hand and the pisiform of the other are first placed just to the side of the spinous process. Both hands are now twisted into ulnar deviation so pushing the muscles further to the side and are then brought back closer to the midline but still remain on the transverse processes. With the elbows straight the manipulator leans over the patient and brings both shoulders vertically above the hands. As a result, all the slack is taken up. The assistants provide traction and the final jerk from the manipulator's body follows. Extension technique in supine position
Figure 41.13
Using crossed hands.
Technique III: using crossed hands (Fig. 41.13). Although a strong rotation element is present in this manipulation, it is still regarded as an extension technique. The patient lies prone on a low couch. The manipula tor can choose to stand on either side of the patient. The two most tender spinous processes and their correspon ding transverse processes are marked. The rotation found during the clinical examination to be the less painful is performed first. If this is without benefit, the opposite rotation is performed. One hand is put on the transverse process of one vertebra, the other hand on the transverse process of the second vertebra on the opposite side. Care should be taken to fully cross the hands. The hand closer to the manipulator is placed on the trans verse process via the pisiform bone. The other hand has contact via the base of the trapezium-first metacarpal joint. Good bony contact is essential and is achieved by first pushing the paravertebral muscles away from the spine. The trapezium-first metacarpal joint of the one
The patient lies supine just near the edge of the couch and places both hands behind the neck, the fingers covering the upper thoracic spinal processes. The elbows are placed well forwards and close together. The manipula tor stands on the right-hand side facing the patient. By grasping the patient's left shoulder in the right hand and both elbows on the left hand (Fig. 41.14a), the manipula tor flexes the patient's neck and trunk and rolls the upper body inwards (Fig. 41.14b). Then a fist is made with the middle, ring and little fingers of the right hand - thumb and index finger are left out. This fist is now brought into firm contact with the lower vertebra of the segment being manipulated - the thenar eminence against the left and the middle phalanx of the flexed middle finger against the right transverse process. In this way the spinous process of the lower vertebra lies in the groove between these two eminences (Fig. 41.14c). Now the patient is lowered back again until the manip ulator's hand is wedged between the patient and the couch. In order to achieve full control over the move ment, the patient's elbows are firmly held against the manipulator's sternum (Fig. 41.14d). Leaning well over the patient and using the weight of the trunk's, the manipulator obtains considerable separation at the inter vertebral joint. At the moment when the limit of tissue tension is felt (and the patient relaxes as fully as possible) the manipulator pushes the body forwards to apply a certain amount of overpressure. At that moment a 'click' or 'snap' is nearly always heard and felt and the result of the manipulation is then assessed.
tItI� Variations
-
• If the patient is not able to reach the upper thoracic spine with the h a n ds by reasons of stiffness or a pai nful shoulder. the techn ique may be varied by crossing the arms ful l y over the chest. The right hand clasps the l eft shoulder. the left hand the right shoulder.
• Some deg ree of rotation can be added if the thenar e m i n ence a n d the middle phalanx of the m i d d l e finger a re positioned on two consecutive transverse processes a n d not on those of the same vertebra.
628 SECT I O N E I G HT - T H E THORACIC S P I N E
(a)
(d)
(b)
(e)
(c)
Figure 41.14 Extension technique in supine position (a, b, c). Variation for upper lumbar level (d). Position for thenar and middle finger (e).
CHAPTER 41
Techniques for upper thoracic disc lesions .
Rotation techniques for upper thoracic disc lesions (Fig. 41.15). This manoeuvre is suitable only for upper thoracic disc lesions. It is best performed on a couch of medium height. The less painful rotation is done first. The patient lies prone. For a right rotation, the manip ulator stands facing the patient on the left-hand side. The right arm of the patient lies fully medially rotated on his back, the elbow flexed. One assistant exerts traction via the patient's head and also rotates it slightly to the right. In this way, the cervical spine is kept in neutral position during the whole manoeuvre. The other assistant holds both of the patient's feet. The manipulator hooks his left arm underneath the patient's furthest shoulder so that the proximal part of the lower arm can lift the patient's shoulder off the couch. The Fight hand is placed on the dorsal aspect of the ribs as high and as close to the thoracic spine as possible. The fingers of both hands are now clasped together. Both hands rest on the ribs, just lateral to the spine and not further down than mid-thorax. The manipulator now bends the trunk to the right, meanwhile pulling the patient's right shoulder off the couch via the left lower arm. The rest of the spine is held down on the couch by both hands pressing on the ribs. The assistants are asked to apply traction and the manipulator suddenly increases the side flexion. By this final movement, extension and rotation at the upper thoracic spine are increased. The rigidity of the upper thorax allows movement over only a small range.
Figure 41.15
Technique for upper thoracic disc lesions.
-
D I SO R D E R S OF T H E TH O RACIC S P I N E : DISC LESIONS 629
Longitudinal traction for upper thoracic disc lesions (Fig. 41.16). The patient stands or sits with the b �ck to the manipulator. A sitting position is preferred If the patient is taller or heavier in weight than the manip � la tor. The patient is then asked to grasp the hands behmd the neck, allowing the elbows to drop forwards. The manipulator threads the arms in front of the patient's axillae and grasps both wrists. The patient is then asked to bend the head, so allowing the elbows to drop further forwards and to lean backwards against the chest of the manipulator. The latter performs a pre liminary lift and at the moment the patient allows the trunk to sag, suddenly extends the knees. This results in a longitudinal traction and separation particular of the upper thoracic joints. A 'click' or 'snap' is felt and the result then assessed. Some degree of extension may be added to this tech nique. The manipulator achieves this by adopting a slightly modified starting position: turning the tru.nk slightly to one side allows positioning of th� lower n� s . against the spine at the level at which mampulatlOn IS required.
Warning: Beware of forcefu l ly flex i n g the neck of the patient during the upwards th rust.
Figure 41.16
Longitudinal traction for upper thoracic disc lesions.
630
S ECTI O N E I G HT - T H E TH ORACIC S P I N E
CHOICE OF MANOEUVRE
The different techniques are used in a specific sequence, depending on the patient's age, the level of the protrusion and the immediate result of the preceding manipulation. After each manoeuvre the patient is re-examined and, if improved, the same manoeuvre is repeated several times with increasing strength until the patient is com pletely relieved or until no further improvement is obtained. In the latter event, another type of manipula tion follows. If the patient does not improve or even becomes worse, the same manipulation is not carried out a second time but is immediately replaced by another. In such cases, the same type of technique but in the opposite direction is performed. If this manipulation also aggra vates the lesion, manipulation must be stopped and the diagnosis reconsidered. Improvement is indicated by pain, which is perceived over a small area and / or which becomes less severe. Another important sign is centralization of the pain: pain that first spreads far distally or laterally but becomes more centrally localized, is regarded as an improvement.41 ,42 Manipulations are stopped as soon as the pain has disappeared and the clinical examination becomes negative. A total number of five (elderly) to 10 (younger patients) manipulations are executed during one session. These can be repeated daily although for the elderly it is advisable to allow 3 or 4 days in between. It may take three to five sessions before the patient is fully recovered. A certain amount of afterpain is sometimes present. If there is a recurrence, the patient should return as soon as possible to be manipulated again. Usually the extension techniques are used first. In patients over 60 years of age, however, extension tech niques may fracture a rib and are therefore never used. The same applies if the extension pressure on the spinous processes performed at the end of the clinical examina tion is very painful. In such a case, oscillatory techniques should then be used (see below).
Box
Exte nsion techn iques should never be used in patients over age o r when there is excessive p a i n on exte nsion pressure.
FAILURE OF MANIPULATIVE REDUCTION
Ninety-five percent of the thoracic disc lesions are reduced in three to five sessions. If after three to five manipulative sessions relief of symptoms is not obtained, it should be accepted that either the diagnosis is wrong or the disc lesion is not suitable for manipulation. The latter may be the result of too large a protrusion, as shown by
Unsuccessful manipulations
Wrong diagnosis: no disc protrusion? Facet j o i nt? Tu mour? M uscu l a r lesion? Osseous lesion? Ligamentous lesion? Viscera l d isorder?
Disc protrusion confirmed Check for neurological deficit
1.
If neuro l og ica l deficit is present: - stop m a n i p u l ation - give sinuvertebral block
2.
If n o neurological deficit is present, consider nuclear protrusion: - stop m a n i p u l ation - try traction
the presence of neurological deficit or may occur when a nuclear disc lesion is present (see Box 41.2).
OSCILLATORY TECHNIQUES
Some cases respond better to oscillations. These consist of gentle high-frequency mobilizations at two to three vibrations per second. Oscillations should be given for 10-15 minutes daily and are performed either as central or as unilateral pressure to the thoracic spine.43 IN DICATIONS
There are three groups of indications: • •
Warning: 60 years of
41 .2
•
Patients who present with much discomfort but with very minor articular signs on clinical examination. Patients with acute thoracic lumbago who are in such pain that they cannot put up with normal manipulations. Oscillatory techniques can be used until the pain is reduced to a level at which normal manipulations can be started. Patients who cannot tolerate the extension or rotation techniques.
SUSTAINED TRACTION
In some patients with thoracic disc protrusion reduction by means of traction may be needed. However, traction may be technically impossible in patients suffering trom orthopnoea, asthma, hiatus hernia or who have recently undergone thoracic or abdominal surgery (see Ch. 59).44
CH APTER 41
-
D I S O R D E R S OF T H E TH ORACIC S P I N E : DISC L E S I O N S 631
INDICATIONS REST IN BED
it can be dangerous to manipulate very central protrusions, in that there is a possibility of causing compression of the spinal cord. Central protrusions are present mainly in those with a marked thoracic kyphosis, either postural or after a wedge fracture. These patients complain of central pain radiating to both sides. Failure of manipulation: patients suffering from a disc lesion in whom manjpulative attempts have failed or who have been made worse, should receive traction unless nerve root compression with neurological deficit is present. There is usually a history of a gradual onset although this is not pathognomonic in the thoracic spine for a nuclear protrusion.
• Central protrusions:
•
• SYl11ptoms of cord compression in the absence of signs:
•
patients suffering from a thoracic disc protrusion with pins and needles in both feet can undergo cautious traction if no other symptoms or signs of cord compression are present. Thoracic postural pain syndrome: these patients can be helped by daily sustained traction with increasing traction-free intervals (see p. 644).
• Disc lesions at a very kyphotic thoracic joint. • Disc lesions adjacent to a wedge fracture of a vertebral body.
(see pp. 645 and 646). (see pp. 649).
• Anterior and lateral erosion • Lateral recess s tenosis
If both manipulation and traction have failed and no indication for surgical intervention is present, the only remaining alternative is prolonged rest in bed in the hope that removing the influence of gravity on the spine may allow the protrusion to reduce spontaneously.
SURGERY: REMOVAL OF PROTRUDED DI SCS
The indications are early cord compression by a progres sive disc lesion. Laminectomies done before 1 960 were dangerous interventions with disappointing results.7,45 It was found that almost all serious complications occurred among those having midline protrusions at levels TlO-Tll.45 This is probably the outcome of the shape of the spinal canal, which is quite narrow at this level. The posterior approach used required some displacement of the cord in a very confined space, with consequent considerable risk to the blood supply. New techniques developed since 1960 are based on a transthoracic lateral approach. This seems to give better results, with less chance of disaster.1 ,7 Nevertheless, the need for surgical intervention is exceptional.
TECHNIQUE
Traction is given daily over 30-45 minutes. Thoracic discs above T9 are treated with cervical traction. For these, the rules of cervical traction should be observed (see Ch. 13). For thoracic protrusions below T9, traction is given using the lumbar technique (see Ch. 59). An intensity of 35 kg (small woman) to 70 kg (heavy, well-built man) is used. Obviously, the thoracic belt should be placed cranial to the level of the lesion. The initial traction ses sions are used as the manipulator's guide for positioning the patient and for the strength to be used. RESULTS
Improvement normally begins after six to 10 sessions, whereas full cure may require up to 20 sessions.
SINUVERTEBRAL NERVE BLOCK
In persisting root pain or in pain associated with neuro logical deficit, a sinuvertebral nerve block is the treat ment of choice. This should only be performed under radiological control.
PREVENTION OF RECURRENCE
POSTURAL PROPHYLAXIS
Reducing a thoracic disc protrusion normally does not cause much in the way of difficulties but recurrence is not uncommon and stability is often difficult to achieve. This is obviously because of the normal thoracic kypho sis which results in a posteriorly directed force acting on the disc. All the rules on prophylaxis for the lumbar spine are also applicable here. However, it is much more difficult and sometimes even impossible to carry them out. For example, it is impossible to obtain the equivalent of lumbar lordosis because even the most flexible person cannot get beyond a straight line in full extension. The most hazardous movements are those that include com bined flexion and rotation elements. Lifting a weight at the same time makes them even more dangerous. Therefore patients should avoid rotating the trunk but must turn their body around using the legs and should bend the knees to lift. Sitting for a prolonged period in a kyphotic posture must also be avoided.
632
SECTI O N E I G HT - T H E T H ORACIC S P I N E
LIGAMENTOUS SCLEROSIS
In those patients in whom the risk of recurrence is high (thoracic hyperkyphosis), or when recurrence is frequent, local reinforcement of the supra- and inter-spinal liga ments and of the capsules of the facet joints of the verte brae between which the protrusion lies, must be done. This can be achieved by infiltrating a sclerosant solution into these structures, which leads to proliferation of fibroblasts and formation of new collagen.46 The final result is increased stability of the disc fragment because the two vertebrae become less mobile. Before this proce dure is undertaken, fuJI reduction must be achieved. Occasionally, the same technique can be employed for arthritis of the facet joint or for ligamentous lesions. In these cases triamcinolone is used. The sclerosant infiltrations are given at weekly inter vals and the greatest effect is normally obtained after 3 weeks; exceptionally it may take up to 2 months. Usually, one full treatment suffices; if there is further recurrence, it can be repeated. Technique: infiltration of the interspinal and su praspinal ligaments (Fig. 41.17). A S ml syringe is filled with 3 ml of sclerosant solution and 1 ml of lidocaine (lignocaine) 2%,
Figure 41.17
Infiltration of the interspinal and supraspinal ligaments.
and a 4 cm needle is fitted to it: 2 ml of this solution are used for the interspinal and supraspinal ligaments, the rest for the facet joints. The relevant spinous processes are marked and the needle is inserted halfway in between them at the midline. At about 1 cm deep it is changed into an almost horizontal position pointing cranially and aiming at the inferior part of the upper spinous process. Once it hits the bone, 0.5 ml of the solution is infiltrated dropwise into the supraspinal ligament and the same quantity a little deeper down in the interspinal ligament. Infiltra tion is only given with the tip of the needle in bony contact. The needle is then half withdrawn and brought into a more vertical position towards the insertions of the ligaments on the upper aspect of the lower spinous process, which are infiltrated in the same way. When the supraspinal ligament is infiltrated it offers tough reSIst ance, whereas infiltration of the interspinal ligament is much easier. Technique: infiltration of the facet joint (Fig. 41.18). A 4 cm needle is used. The patient remains prone and the transverse processes corresponding to the most painful consecutive spinous processes are marked. The needle is inserted at about 1.5 cm from the midline halfway in
Figure 41.18
I nfiltration of the capsule of the facet joint.
CHAPTER 41 - D I S O R D E R S OF T H E TH ORACIC S P I N E : D I SC L E S I O N S 633
between the two transverse processes. It is thrust in ver tically downwards until it touched the articular process at about 3 cm depth. Capsular resistance to the needle tip is sought by minor repositioning of the needle. The infiltration is given mainly into the capsule with the tip of the needle always in bony contact and considerable
resistance is usually felt during the whole infiltration. This is done at both sides using 1 ml of the solution at each side. The interspinous and supraspinous ligaments and the facet joints are infiltrated at the same time, repeated three times at weekly intervals.
REFERENCES 1 . Benson M, Byrnes D. The clinical syndromes and surgical treat
22. Bruckner FE, Greco A, Leung AW. 'Benign thoracic pain' syn
ment of thoracic intervertebral disc prolapse. J Bone Joint S u rg
drome: role of magnetic resonance imaging in the detection
1975;57b(4) :471-477.
and localization of thoracic disc disease. R Soc Med 1 989;82(2):
2. Albrand 0, Corkill G. Thoracic disc herniation. Treatment and
81-83. 23. Love J, Schorn V. Thoracic-disc protrusion. JAMA 1 965;191(8):
prognosis. Spine 1979;4(1) :41-46. 3. Carson J, Gumpert J, Jefferson A. Diagnosis and treatment of thoracic intervertebral disc protrusions. j Neural Nellrosu rg
627-631 . 24. Tovi D, Strang R. Thoracic intervertebral disc protrusions. Acta ChiI' Scand 1960;41(suppl 267).
Ps:ychiatry 1971;34:68-77. 4. Bhole R, Gilmer R. Two-level thoracic disc herniation. c/in
25. Otani K, Yoshida M, Fujii E . Thoracic disc herniation: surgical treatment in 23 patients. Spine 1 988;13:1 262-1267.
OrtiJop Rei Res 1984;190:1 29-1 3 1 . 5. Shaw N . The syndrome of the prolapsed thoracic illtervertebral
26. Bohlman H, Zdeblick T. Anterior excision of herniated thoracic discs. J Bone Joint Surg 1988;70A(7) : 1 038-1047.
disc. J. Bone joint S u rg 1975;57B(4) :412. 6. Skubic JW, Kostuik JP. Thoracic pain syndromes and thoracic disc herniation. In: The Adult Spine: Principles and Practice. Raven
27. Reeves D, Brown H. Thoracic intervertebral disc protrusion with spinal cord compression. J Neurosu rg 1 968;24:28. 28. Ridenour TS, Haddad P. Hitchon Piper J, Traynelis V, Va ngilder
Press, New York, 1 99 1 : 1 443-1461 . 7. Va llo MB, Ransohoff J . Thoracic disc disease. In: The Spine, 2nd
J. Herniated thoracic disks: treatment and outcome. J Spinal Disorders 1993;6(3):218-224.
edn. Saunders, Philadelphia, 1 982-500. 8. Arce CA, Dohrmallll GJ. Herniated thoracic disks. Neural c/in
29. Ikegawa S, Nakamura K, Hoshino Y, Shiba M. Thoracic disc herniation in spondyloepiphyseal dysplasia. Acta Orthop Scand
1985;3(2):383-392. 9. Ridenour TS, Haddad P, Hitchon Piper J, Trynelis V, VanGilder J. Herniated thoracic disks: treatment and outcome. J Spinal
1993;64:105-106. 30. Hoppenfeld S. Aandoen ingen van ruggemerg en zenuwworte/s. Diagnos tiek per neu rologisch n iveau. BOrnl, Scheltema & Holkema,
Disorders 1993;6(3) :218-224. 10. MacCartee C, Griffin P, Byrd E. Ruptured calcified thoracic disc
Utrech t / Antwerp, 1984. 31. Brugger A. Die Erkrankungen des Bewegungsapparates und seines
in a child. J Bone Joint S u rg 1972;54A(6) : 1 272-1274. 1 1 . Hochman M, Pena C, Ramirez P. Calcified herniated thoracic disc diagnosed by computerized tomography. J Neu rosu rg
Nervensys tel1ls, 2nd edn. Fischer, Stuttgart, 1980;934. 32. Bannister R.
Brain 's
Clin ical Neu rology, 4th end.
Oxford
University Press, Oxford, 1973.
1980;52:722-723. 12. Wood KB, Garvey TA, Gundry C, Heithoff KB. Magnetic reso
33. Crafoord C, Hiertonn T, Lindblom K, Olsson S. Spinal cord
nance imaging of the thoracic spine. Evaluation of asympto
compression caused by a protruded thoracic disc. Report of a
matic individuals. J Bone Joint Surg 1995;77A(11): 1631-1638.
case treated with antero-lateral fenestration of the disc. Acta
13. Wood KB, Blair JM, Aepple D M et al The natural history of asymptomatic thoracic disc herniations. Spine 1 997;22:525-529.
Orthop Scand 1 959;28 34. Baker H, Love Je, Uhlein A. Roentgenologic features of pro
14. Awwad EE, Martin DS, Smith KR J l� Baker BK. Asymptomatic
truded thoracic intervertebral discs. RadiologlJ 1965;84:1059-1065.
versus symptomatic herniated thoracic disc: their frequency
35. Ransohoff J, Spencer F, Siew F, Gage L. Case reports and techni
and characteristics as detected by computed tomography after
cal notes. Trans-thoracic removal of thoracic disc. J Neurosu rg 1969;31:459-461 .
myelography. Neuros urgery 1991;28(2):180-186. 15. Williams MP, Cherryman GR, Husband JE. Significance of
36. Wallace q, Fong TC, MacRae ME. Calcified herniations of the
thoracic disc herniation demonstration by M R imaging. J Comput
thoracic disk: role of magnetic resonance imaging and com
Assist TOl11 ogr 1989;13(2) :211-214.
puted tomography in surgical plalming. Can Assoc Radial j
16. Kramer J .
In tervertebral
Disc
Diseases.
Causes,
Diagnosis,
17. Bradford
D.
Juvenile
kyphosis.
c/in
Orthop
Rel
Res
1977;128:45-55. 18. Winter R, Siebert R. Herniated thoracic disc at T1-T2 with para paresis. Spine 1993;18(6):782-784. 19. Ikegawa S, Nakamura K, Hoshino Y, Shiba M. Thoracic disc herniation in spondyloepiphyseal dysplasia. Acta Orthop Scand 1993;64(1) : 1 05-106. 20. Lyu RK, Chang HS, Tang LM, Chen ST. Thoracic disc herniation mimicking acute lumbar disc disease. Spine 1999;24(4) :416-418. 21 . Cyriax J. Textbook of Orthopaedic Medicine, vol 1 , Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982.
1992;43(1) :52-54. 37. Pui MH, Husen YA. Value of magnetic resonance myelography
Treatment and Prophylaxis. Thieme, Stuttgart, 1981 .
in the diagnosis of disc herniation and spinal stenosis. Australas Radiol 2000;44(3):281-284. 38. Francavilla TL, Powers A, Dina T, Rizzoli HV. MR imaging of thoracic disk herniations. J Comput Assist Tomogr 1987;11(6): 1062-1065. 39. Rogers MA, Crockard HA. Surgical treatment of the sympto matic herniated thoracic disk. c/in Orthop 1 994;300:70-78. 40. Dietze DD Jr, Fessler RG. Thoracic disc herniations. Neu rosurg c/in North Am 1993;4(1):75-90. 4 1 . M acKenzie R. The Lumbar Spine. Spinal Publications, Waikanae, 1972.
634
S E CTION E I G HT - T H E TH O RACIC S P I N E
42. Donelson R , Silva G , Murphy K. Centralization phenomenon:
45. Perot 1', Munro D. Transthoracic removal of midline thoracic
its usefulness in evaluating and treating referred pain. Spine
disc protrusions causing spinal cord compression. J Neurosurg
1990;15:21 1 . 43. Maitland G, Brewerton D . Vertebral Manipulation. Butterworth, London, 1977:7. 44. Grieve G. Contra-indications to spinal manjpulation and allied treatments. Physiotherapy 1989;75(8):445-453.
1969;31 : 1 63-165. 46. Troiser O. Cited in: Cyriax
JH.
Textbook of Orthopaedic Medicille,
8th edn. Baill iere Tindall, London, 1982. O. Troisier, cited by Cyriax:2l 339.
CHAPTER CONTENTS I
Introduction
Disorders of the thoracic spine: non disc lesions
635
Warning symptoms and signs Symptoms 635 Signs 636
635
Disorders and their treatment
637
Tumours of the thoracic spine 637 Extradural haematoma 641 Thoracic spine canal stenosis 641 Chest deformities 642 Fracture of a transverse process Spinal infections 648 Lateral recess stenosis
648
INTRODUCTION
649
Arthritis of the costovertebral and costotransverse joints 650 Arthritis of the thoracic facet joints Paget's disease
651
650
Non-disc lesions of the thoracic spine cover the following disorders of the thoracic spine: • • • • • • • • • •
Tumours Extradural haematoma Spinal canal stenosis Deformities of the spinal column Fracture of a transverse process Spinal infections Lateral recess stenosis Localized lesion of costovertebral and costotransverse joints Localized lesion of a facet joint Paget's disease.
Very often the signs and symptoms of the non-discal lesions of the thoracic spine resemble those in discodural disorders. Some of the lesions mentioned are serious and even life threatening. Therefore the examiner must be on guard and immediately ask for further investigation whenever there is doubt about the exact diagnosis. Warning symptoms and signs that warrant the exam iner's attention are listed here and are summarized in Box 42.1. - "':..-
_!I
1•
•..."
.U:-_'�,-. .:.-
T
WARNING SYMPTOMS AND SIGNS ...
SYMPTOMS PROGRESSIVELY INCREASING PAIN
In disc lesions the pain may increase over a short period or come and go. In expanding lesions the pain tends to increase continuously. This may occur quickly over days (extradural haematoma), weeks-months (malignant diseases) or even longer periods (benign tumours). EXPANDING PAIN
Pain that not only increases in intensity but also expands to occupy a larger area is very likely to be caused by an 635
636 SECTION EIGHT - THE THORACIC SPINE
Box 42.1 Sum mary of warning signs -
History Progressive i n creasing p a i n Expa n d i n g p a i n Cont i n u ous p a i n , not changed b y posture or activity Increasi n g postoperative thoracic backache First symptoms a n d signs i n people over 50 years of age Central p a i n ra d iating b i latera l ly a n d spread i ng a nteriorly
Examination Gross l i m itati o n of both side flexions a n d rotations Gross l i m itation of extension Pa i n and l i m itation of side f l ex i o n away from the painful side as the o n ly positive f i n d i n g Flexion with a rigid thoracic segment If one of following n e u rolog ica l signs is present: Signs of i n vo lvement of m u lt i p l e nerve roots Band-shaped a rea of n u m b ness All s i g n s of cord com p ression M uscle spasm Loca l pa ravertebral mass
lesions become less frequent with increasing age because of increasing stiffness of the spine. CENTRAL PAIN RADIATING BILATERALLY AROUND THE THORAX AND SPREADING ANTERIORLY TOWARDS THE EPIGASTRIUM2
Although a posterocentral disc protrusion may provoke this type of pain, a tumour or an extradural haematoma should always be excluded. 2
SIGNS The following may draw attention to non-discal lesions. GROSS LIMITATION OF BOTH SIDE FLEXIONS AND ROTATIONS
expanding lesion, most commonly a malignant disease or an extradural haematoma. CONTINUOUS PAIN, NOT CHANGED BY POSTURE OR ACTIVI T Y
Although this symptom is less alarming than the previ ous ones, a mechanical disorder is unlikely in the absence of variation of symptoms on movement. Nevertheless, the situation in the thoracic spine is slightly different from the rest of the spine because its rigidity sometimes results in a lack of change in pain with activity. Pain that is worse at night is seldom caused by a disc lesion, and is more suggestive of a rheumatic disorder, infection or trauma. INCREASING POSTOPERATIVE THORACIC BACKACHE
Surgery correctly indicated and performed but which is still followed by continuous pain, demands a fresh diag nostic evaluation. A clear relationship between what is found on further investigations and the patient's com plaints must be established. Local infection and a tumour must be excluded. FIRST SYMP TOMS AND SIGNS IN THE THORACIC AREA IN PATIENTS OVER 50 YEARS OF AGE
Because both intra- and extraspinal tumours occur mainly over the age of 50, symptoms that first appear beyond middle age arouse suspicion. Moreover, disc
In older subjects it is normal that these movements are diminished in range, although the limitation should not be major. In younger patients gross limitation is never normal; if present, it usually points to a non-mechanical disorder, such as ankylosing spondylitis or a tumour. GROSS LIMITATION OF EX TENSION
In an ordinary disc lesion it is usually anteflexion or one of the rotations that is most painful and limited. If active extension is severely limited and painful, attention is drawn to the possibility of a fracture of a vertebral body, an infection or a tumour. There is only one type of thoracic disc lesion in which severe limitation of active extension can occur: acute thoracic lumbago. In acute thoracic lumbago, other movements are of course also limited and / or painful. PAIN AND LIMITATION OF SIDE FLEXION AWAY FROM THE PAINFUL SIDE AS THE ONLY POSITIVE FINDING
This pattern suggests that a lesion is being stretched to such an extent that the pain becomes so severe that the movement is arrested involuntarily. This may indicate a neoplasm in the lung or abdomen, or a thoracic neurofibroma. FLEXION WITH A RIGID THORACIC SEGMENT
Absence of movement at the thoracic level indicates a dis order other than a disc lesion. Ankylosing spondylitIs is a possibility, as are advanced osteoarthrosis, fracture, tumour or a vertebral infection.
CHAPTER 42
-
DISORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
NEUROLOGICAL SIGNS
INTRASPINAL TUMOURS
' The presence of one of the following neurological signs should always put the examiner on guard.
Thoracic neurofibroma
• • •
Signs of involvement of multiple nerve roots A band-shaped area of numbness related to one or more dermatomes All signs of spinal cord involvement3-S (see pp. 620-622).
A large space-occupying process, or a large disc protru sion which cannot and may not be manipulated, is very likely and a myelogram or magnetic resonance imaging (MRI) should be ordered immediately.
MUSCLE SPASM
If one of the passive movements is stopped by an invol untary muscular contraction, a serious disorder should be expected.
LOCAL PARAVERTEBRAL MASS
A local paravertebral mass may be caused by an extraspinal invasion of a tumour.6
DISORDERS AND THEIR TREATMENT TUMOURS OF THE THORACIC SPINE Spinal neoplasms, both primary and secondary, are unusual causes of thoracolumbar pain. However, because these lesions are associated with high mortality, examiners must always be aware of the possibility of neoplastic diseases and must include them in their differential diagnosis. Malignant spinal tumours occur mainly in the middle aged and are characterized by a more or less sudden onset of the symptoms; often a minor trauma is thought to be the inciting cause and progression is swift. According to their localization (in- or outside the spinal canal) tumours can be classified as intra- or extraspinal. are sited in the spinal canal. They are further divided into intra- and extradural tumours. The former may be intra- or extramedullary. Extraspinal tumours involve the bony parts of the vertebra. Benign tumours are usually located in the posterior parts (spinous and transverse processes), malignant tumours in the vertebral body.
Pathology. This benign tumour usually originates from the dorsal root and arises from proliferating nerve fibres, fibroblasts and Schwann cells. Sensory or motor fibres may be involved.7 Some confusion exists about the termi nology: various names, such as neurofibroma, neuri noma, neurilemmoma or schwannoma have been used. Some believe that all these terms cover the same type of tumour; others distinguish some slight histological dif ferences between them. Multiple tumours in nerve fibres and the subcutaneous tissues, often accompanied . by patchy cafe au lait pigmentation, constitute the syndrome known as von Recklinghausen's disease. Neurofibroma has a slight predilection for the tho racic spine. It is equally prevalent in both sexes and has been encountered in patients from 6 to 77 years of age, though it most frequently occurs between the ages of 31 and 60.8 It is relatively common and accounts 'for approximately a quarter of all spinal tumours. The majority of neurofibromas are intradural (Fig. 42.1) and develop both proximally and distally. Extradural and mixed intra- and extradural types also occur.9 A tumour that is within the intervertebral foramen is often shaped like an hourglass or dumb-bell, one limb of which can give rise to a paravertebral extraspinal exten sion, which is sometimes palpable. Spinal neurofibromas are solitary. In a study covering 115 cases collected over 20 years, only one tumour of the spinal nerve root was found in each case.8 Eight patients had cutaneous neurofibromas and 10 had cafe au lait spots. History. Once an intradural neurofibroma starts to interfere with the surrounding dura mater or with the dural nerve sleeve, pain results. Because the tumour is growing, the symptoms also progress slowly. However, if cyst formation takes place, the occupied space increases rapidly.1o In the early stage, the diagnosis is often difficult because neurofibromas usually give rise to symptoms
• Intraspinal tumours
•
637
Figure 42.1
Intradural extramedullary neurofibroma.
638 S ECTION EIGHT - THE THORACIC SPIN E
almost identical to those of a disc lesion (Cyriax:ll p. 212; Love and Rivers12). Thoracic neurofibromas may even simulate a disc problem at the lumbar levep,12-14 The main symptom is pain, most frequently present as root pain, exceptionally as a central dura mater pain. It is increased by a deep breath or by a cough and may be present at night. Sometimes the patient prefers to sleep sitting up in a chair, a situation that is most unusual for a disc lesion. Activity or movement influences the pain only exceptionally. Pain increases slowly over months and years, a characteristic that indicates an unusual, ' slowly progressive disorder. Involvement of the sensory fibres may result in a segmental band-shaped area of numbness. The tumour may also compress the spinal cord, affecting both motor and sensory elements (see pp. 620-622). As a consequence, the patient may complain of stiffness of the legs, muscle spasms, extrasegmentally referred pins and needles, disturbed sphincter function, with loss of bowel or bladder controlY Exceptionally Brown-Sequard syndrome occurs.8 Clinical examination. Interference with the dura usually produces a clinical picture almost identical to that of an ordinary disc lesion. Neck flexion and scapular approximation are often painful. These signs, together with pain on deep inspira tion, are typical of a lesion that is interfering with the dura mater or with the dural nerve sleeve. They are not specific to a disc lesion and may occur in any space occupying lesion. Because the tumour lies outside the intervertebral joint, it does not interfere with articular movements and therefore daily activities and movements are hardly affected. Side flexion away from the painful side is some times the only painful and restricted movement and this pattern is unlikely to result from a disc lesion. All signs slowly and progressively increase. Finally, neurological signs may develop but they come on much later than in malignant tumours. They may consist of a band-shaping numbness related to one dermatome. The tumour may also affect motor fibres but segmental motor deficit is very difficult to detect. Once the tumour com presses the spinal cord, any of the signs of cord compres sion may be encountered: depression of abdominal reflexes, hyperactive patellar and Achilles tendon reflexes and sensory 10ss. 9 When a neurofibroma is suspected, the paravertebral area should always be palpated because a neurofibroma may expand extraspinally via the intervertebral foramen to give rise to a paravertebral mass. The tumour is sometimes initially mistaken for a disc protrusion because of the almost identical clinical pattern. Failure to relieve symptoms within three to five sessions
of manipulation in patients thought to have a thoracic disc lesion should automatically arouse suspicion of a neurofibroma. Warning Warning signs in neurofi broma: • Pa in: Slowly increasing pain over months, m a i nly felt at night, uninfluenced by activities. • Patient prefers to sleep sitting u p . • S i d e flexion away from pa inful s i d e is the only painful and l i m ited movement. • B a nd-shaped area of num bness rel ated to one dermatome. • P resence of p i ns and needles i n one o r both feet o r any other sign of cord compression. • Disorder m istaken as a d isc lesion, which does not respond to manipulations.
Special investigations.
There are four main approaches.
definite evidence of a tumour is found on a plain radiograph in 50% of cases. The features include an enlarged intervertebral foramen and erosion of the vertebral body or the pedicles. The tumour seldom gives rise to widening of the inter pedicular distance. Chest radiograph: this may show an abnormal soft tissue mass, extending outside the spinal canal (hour glass tumour).
• Plain radiography:
•
• Myelography, computed tomography (CT) scan and MRI:
•
accurate localization of the tumour is usually possible by these means.15 Extramedullary intradural lesions almost always cause displacement of the spindl cord or the nerve roots. Cerebrospinal fluid: in the large majority of neuro fibromas the protein level of the cerebrospinal fluid is increased.
Treatment and prognosis. Neurofibromas may undergo malignant change or produce cord compression. Therefore, they should be surgically removed. Small posteriorly or laterally sited tumours can usually be dealt with easily. Anterior neurofibromas present more problems and usually can be only partly excised.
Other intraspinal masses
These include all other infra- and extradural tumours of the spinal canal. Despite the advantage of specialized technical investigations (radiography, myelography, CT, MRI), patients with intraspinal tumours are often misdiagnosed. Clinical presentation . The primary and most univeTsal symptom is pain, which is usually felt centrally in the back and may spread bilaterally as girdle pain.2 The pain
CHA PTER 42
-
DISORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
increases progressively and is relentless, despite the patient's attempts to limit activities. In anterior compres sion of the dural sac, L'hermitte's sign is sometimes present.]6 Occasionally the pain is worst at night. Although this is classically regarded as being suggestive of a tumour, it is rather rare.1 ,12 Straining and coughing may increase the pain as may active movement, but to a lesser degree than in mechani cal disorders.1,6 The clinical pattern depends on the extent of the tumour: all tests can be completely normal or movement may be considerably limited. If the latter, anteflexion is usually involved and there is often associated muscle spasm. As a rule, in intraspinal soft tissue masses, not much is learnt from articular movements. Besides the positive articular signs, all intraspinal masses give rise sooner or later to neurological signs caused either by involvement of one or more nerve roots or by compres sion of the spinal cord (see pp. 620-622). It should be noted that a tumour is not always found where it would be expected on a clinical basis. Cases have been reported where upper thoracic tumours gave rise to pain and neurological signs in the lower limb or in the lumbar area. 1,12 Further investigations. In all instances, further investiga tion is called for. Examination of the cerebrospinal fluid may show elevated proteins, a finding strongly suggest ing a neoplasm.] The imaging techniques used to define intraspinal tumours are MRI and CT-myelography. The advantages of MRI are: ease of obtaining sagittal sections; rapid assessment of the entire thoracic spine; patient accept ability because of the absence of radiation and low inva siveness; and lack of morbidity and complications. Neoplasms that are frequently associated with skele tal metastases include tumours of the breast, prostate, lung, kidney, thyroid and colonY-2o Data from autopsy material suggest that up to 70% of patients with a primary neoplasm from one of these sources will develop pathological evidence of metastases to vertebral bodies in the thoracolumbar spine.21 Because the major ity of metastases occur in the vertebral body, they may cause anterior compression of the spinal cord, either directly by tumour growth or by a pathological fracture with retropulsion of bone and disc fragments into the spinal canal. 22 Finally compression of the cord can result from an intradural metastasis.23
EX TRASPINAL TUMOURS
Neoplasms located outside the spinal canal are called extraspinal tumours.
639
In general benign tumours are located in the posterior elements of the vertebrae and are found in patients under 30 years of age, whereas malignant tumours (both primary and metastatic) are located in the anterior com ponents of the vertebrae and are more common after the age of 50. Myelomas and metastases are the most frequent malignancies.]7 Multiple myeloma is a malignant tumour of plasma cells. Plasma cells produce immunoglobulins and anti bodies and are located throughout the bone marrow. Multiple myeloma is the most common adult primary malignancy of bone. The patients are usually in an older age group, ranging between 50 and 70. The disease leads to widespread bone destruction, abnormal immunog lobulin production and infiltration of bone marrow. Therefore a patient with multiple myeloma develops a broad range of clinical symptoms that extend beyond the orthopaedic field. Symptoms are also related to hyper calcaemia (anorexia, nausea, vomiting, kidney stones and changes in mental state), abnormal immunoglobulin concentrations (renal insufficiency and amylOidosis), haematological changes (anaemia and bleeding disor ders) and generalized weakness. Diagnosis is made on laboratory examination and radiographic evaluation. Spinal metastases are much more common than primary tumours. The prevalence increases with increas ing age. The lumbar and thoracic spines are affected in approximately 46-49% of cases, with a predilection for the thoracolumbar junction (the so-called forbidden area). Consequently signs of cord compression are often present. In other circumstances, radicular pain occurs. This is most misleading in the thoracic area, where it often mimics visceral problems. Clinical presentation. In 95% of cases, the first symptom is local neckache or local thoracic backache, which goes on to radiate. Suspicion should arise when this occurs in patients over 50 years of age complaining for the first time of backache not preceded by trauma. The pain tends to increase in intensity progressively and to involve a larger area: expanding pain. If radicular pain is present, it is usually worse at night (Borenstein and Wiesel :7 p. 309). In vertebral metastases a full articular pattern is usually present, characterized by marked painful lirnita tion on extension and symmetrical limitation of both side flexions and rotations. Muscle spasm may also be present. Local tenderness over the spinous process is found on palpation. Radicular signs or those of cord compression may occur abruptly, with full neurological features developing in 48 hours or more commonly subacutely over a week or
640 SECTION EIGHT - THE THORACIC SPINE
more. Some patients have a much slower course - neuro logical symptoms and signs progressing over 4-6 months. Tumours of T12 or L1 may compress the conus medullaris, containing the 53-55 nerve roots. This may lead to dysfunction of the urinary or anal sphincter, which is sometimes associated with saddle anaesthesia. Differential diagnosis (see Tables 42.1 and 42.2) must be careful, 1,3-6,12,24-27 because the majority of the signs
and symptoms also occur in ordinary thoracic disc lesions. It is based mainly on clinical examination, because up to 30% of the bone mass has to be lost before metastases may become visible on a radiogra phy.28 When there is the slightest possibility that there is a tumour, manipulation should never be done and further investigations such as a bone scan must be carried out.
Table 42.1 Differential diagnosis of thoracic disc protrusion and tumours Thoracic disc protrusion
Benign tumour
Malignant tumour Intraspinal
Extraspinal
Age (years)
20-50
Any age
>50
>50
Evolution
Swift or chronic (ups and downs)
Very slow
Swift
Swift
Pain At night
Shifting Better
Expanding Worse
Expanding Worse
Expanding Worse
Dural symptoms On inspiration or cough
±
+
±
±
Articular signs
Partial articular pattern
Full range, or side flexion away from painful side is the only painful and limited test
All tests normal, or limitation of anteflexion Muscle spasm
Full articular pattern Muscle spasm
Dural signs Neck flexion Scapular approximation
+
+
+
+
+
+
+
+
Neurological signs
Unusual
+
+
±
±
Palpable mass
Table 42.2 Differential diagnosis of thoracic disc protrusion and neurofibroma Neurofibroma
Thoracic disc protrusion
20-50 years
Age
Young
Pain On inspiration or cough Preferred sleeping position
Slowly increasing
Swift onset; if chronic, no increasing pain but ups and downs
+
+
Sitting up
Lying down
Articular movements
Usually negative Side flexion away from the painful side: painful and limited?
Partial articular pattern
+
+
+
+
+
Unusual
+
Unusual Unusual
Dural signs Neck flexion Scapular approximation Neurological signs Band-shaped area of numbness in one dermatome Segmental motor deficit Signs of cord compression Palpable mass
+ ±
CHAPTER 42
-
DISORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
EXTRADURAL HAEMATOMA Extradural spinal haematoma at the thoracic level can be either traumatic or nontraumatic. Spinal epidural haematoma (SEH) is an uncommon complication of severe spine injury with or without fracture of the thoracic vertebral bodies. Compression of the cord by a haematoma is also a well-known, although rare, complication of spinal surgery. 29 The reported frequency is between 1 and 6 per 1000 operations. Traumatic bleeding in the epidural space has also been reported after epidural injections and chiropractic manipulations.3o Non-traumatic extradural spinal haematoma is an uncommon condition often associated with a poor outcome. There seems to be an increase of the incidence, probably from the increased use of thrombolytic and anticoagulant therapy.31-33 Other causes of non-traumatic extradural spinal haematoma include vasculitis such as systemic lupus erythematosus (SLE), spinal arterio venous malformations and haemophilia.34,35 A spinal epidural haematoma may present acutely or subacutely over a number of days or weeks and with fluctuating symptoms. The patient usually suffers from increasing and expanding thoracic back pain, followed by progressive signs and symptoms of major neuro logical dysfunction secondary to cord compression.36 Conditions that may mimic an acute spinal haematoma include extradural abscess and extradural metastatic infiltration. It is important to make an early diagnosis because surgery may offer the best hope of restoring neurological function. MRI is the examination of choice and provides characteristic findings that allow a prompt diagnosis.37 The technique can also provide useful information about the age of the haematoma.38 Spinal epidural haematoma has always been consid ered a neurosurgical emergency. The treatment of choice is decompressive surgery as soon as possible because permanent neurological disability or death may follow if neurosurgical intervention is delayed.39,40 However, during the last decade several reports have been pub lished showing that non-operative treatment may be suc cessful in cases with minimal neurological deficits, despite cord compression revealed by MRI.41-43
THORACIC SPINAL CANAL STENOSIS This may be the outcome of either congenital deforma tion or hypertrophy of the posterior spinal elements. Most often it occurs in association with generalized rheumatological, metabolic or orthopaedic disorders,
641
such as achondroplasia, osteofluorosis, Scheuermann's disease, Paget's disease or acromegaly. It is rare in the absence of a generalized disorder.44,45 Degenerative changes in the facet joints and the intervertebral disc can diminish the volume of the spinal canal and cause cord compression.46,47 The latter is most frequently found at Tll and T12 in middle-aged people.48,49 Cli nical prese ntati o n . Patients usually complain of pseudoclaudication, characterized by pain in the lower back, buttock, thigh and in the legs, coming on during walking; sometimes standing may provoke symptoms. In addition to pain, paraesthesia may be present in one or both lower limbs. The sensation is worse on walking and improves on sitting. Numbness in the lower limbs may follow and may be associated with muscular weak ness, difficulty on walking and easy fatigue. Spastic para paresis with diminished or lost reflexes in the lower limbs, together with urinary disturbance, can be present. In rare cases, hyperreflexia is noted. Extension of the thoracic spine while upright may further compromise the cord within the narrowed canal and increase the symptoms, while improvement occurs on anteflexion. On clinical examination there may be some degree of limitation of movement in the spine, because of osteoarthritis leading to stiffness. In such a case, a capsu lar pattern is found. Arterial pulses in the lower limb are normal, which largely excludes vascular problems. Further investigations. The radiograph is often unre markable and myelography can be misleading. CT scan and MRI are usually required.44,48 Differential diagnosis.
Two differential diagnoses should
be considered: when pseudoclaudication is present differential diagnosis must be made from intermittent claudication caused by vascular abnor malities. In spinal stenosis, some patients have symp toms just on standing. In intermittent claudication the pain is brought on by walking and relieved on stand ing still; arterial pulses are usually diminished or absent. Doppler probe and arteriography may confirm the diagnosis. Disc protrusion: in spinal stenosis all postures or movements that bring the spine into anteflexion usually relieve the pain, whereas in a disc protrusion the opposite is more usual. Moreover, in a simple disc protrusion, activity of the lower limbs has no influence on the symptoms.
• Intermittent claudication:
•
Surgical intervention is necessary but established neurological features seldom regress.
Tr eat m e nt.
642 SECTION EIGHT - THE THORACIC SPINE
CHEST DEFORMITIES HYPERKYPHOSIS/PATHOLOGICAL WEDGING
The normal thoracic spine is kyphotic but if the kyphosis is beyond 40°, hyperkyphosis is present.50 The condition may occur at one or more levels and may be the result of several disorders.51 Juvenile kyphosis
Juvenile kyphosis has its clinical onset in adolescence between the ages of 14 and 18 years; for this reason the condition is sometimes known as adolescent osteo chondritis. There is a slight preponderance in females.52 It develops because of a disturbance in growth in the vertebral rim epiphysis akin to osteochondritis disse cans.53 Although the exact aetiology is unknown, it is generally believed to result from an anterior endplate lesion, through which herniations of the intervertebral disc protrude into the adjacent bone (Schmorl's nodes).54 The intervertebral disc itself becomes nar rowed, mainly anteriorly. The protrusion interferes with the growth of the vertebral ring epiphysis, which finally leads to about 5° of anterior wedging of the vertebral body. Should this occur over several levels, thoracic hyperkyphosis (with the apex normally around T7-T9) results. In this event, the condition is named Scheuermann's disease. Cli nical presentation. In adolescents the disorder usually remains painless. It usually gives rise to progressive silent hyperkyphosis, with backache present only in a minority of cases.55,56 At a later age, however, there is a predisposition to thoracic pain57 (see p. 644). On clinical examination, all movements are free except active extension, which may be limited. If hyper kyphosis is present, it does not disappear in prone position, and when a hyperextension thrust is given to the thoracic spine, stiffness is felt and slight discomfort provoked.
Wedge fracture of a vertebral body
The thoracolumbar spine is the most common site for vertebral fractures. Although they are relatively rare in autopsy series of trauma, they may occasionally be very severe and cause paraplegia.58 A fracture of a vertebral body may be the result of compression, distraction or rotation forces, often in combination and usually caused by a fall from a height, a heavy impact or a car accident. Sometimes they arise from penetrating injury. Vertebral body fracture may also result from osteo porosis or occur spontaneously in vertebral tumours and ankylosing spondylitis. All are classified as pathological fractures.59 High energy fracture . This usually arises from an axial load in combination with flexion or lateral bending. If a compression injury with a significant flexion component is the cause, a wedge-shaped deformity with consider able loss of anterior vertebral height is commonly present (Fig. 42.2), resulting in angular kyphosis. Lateral bending leads to lateral wedging. A uniformly flattened vertebral body is more indicative of a pure axial component.
Natural history. Immediately after the accident, the patient complains of bilateral girdle pain referred to the corresponding dermatome and which obliges remaining in bed. After about 2 weeks the pain diminishes progres sively; it disappears at the end of about 3 months. If damage has been done to the disc as well, a continued complaint is often the case because of segmental instabil ity. The displaced disc can be reduced by manipulation but the angular kyphosis may promote redisplacement.
Radiography. The diagnosis is mainly based on radio graphs, which are often taken for some other reason. They show narrowing of the intervertebral joint space and multiple Schmorl's nodes, giving an irregular aspect to the surface of the vertebral body. In the later stage, focal anterior wedging of the latter is seen.
This should aim to prevent further deforma tion during the growth period. If the kyphosis is still reversible, active exercises for the extensor muscles of the back should suffice. In more progressive cases, in which hyperkyphosis increases or progression of anterior wedging of the vertebrae is found, a Milwaukee brace until growth has ceased is the best advice.
Treatment.
\i�
:V··;1:�F��.
.: .... , :. j '/
I:�""
: ,,:,' ..p.�"-4.. -��.:�:��; . '�. ::
Figure 42.2 Wedge compression fracture: the middle column (posterior part of the vertebral body) remains intact.
CHAPTER 42
-
D ISORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
643
The anteflexion deformity may cause later develop ment of spinal stenosis or thoracic postural pain syn drome (see pp. 641-644).
Clinical presentation. Immediately after an injury to the spine, total immobilization is essential to prevent further displacement or damage. Thus, the patient should never be asked to perform articular movements nor should the examiner try to perform them passively. After an initial general physical examination to ascertain the site(s) of the lesion(s), a complete neurological examination follows with special emphasis on sensory loss. It should not be forgotten that other structures, such as the viscera, may also be involved. Severe muscle spasm, to splint the fracture, is present. Pain on flexion of the neck is not found but deep inspiration may influence the pain through movements of a rib. There is exquisite tender nes� on extension pressure. The absence of an increase in pain on flexion of the neck after an injury, associated with severe spontaneously present pain almost certainly excludes a disc lesion. Both supra- and interspinal ligaments around the vertebra are very tight and may become overstretched. In this event, palpation shows exquisite overlying tenderness. As these patients may continue suffering after the frac ture has healed - because of either chronic disc displace ment or ligamentous oversprain - they are often mistakenly regarded as perpetuating their chronic symp toms in a search for compensation. Radiography. Depending on the type of injury, the radiograph may show diminished anterior vertebral height, lateral wedging or a total flattened vertebra. When the loss of vertebral body height is more than 50%, differential diagnosis from a burst fracture is essen tial. In the latter, the middle column, consisting of the posterior half of the vertebral body, the posterior longitu dinal ligament and the posterior fibres of the annulus fibrosus, is disturbed, and varying degrees of retropul sion into the neutral canal takes place, provoking neuro logical signs (Fig. 42.3). Very often the posterior elements (supra- and interspinous ligaments, capsules of the facet joint and ligamentum flavum, together with the posterior arch) are also involved. A CT scan is sometimes necessary for an exact differ entiation, because plain radiography does not always reveal the full picture. These are mainly the result of osteoporosis, vertebral infections, ankylosing spondylitis and primary tumours or metastases.59 If the patient complains of severe pain after trivial injury, a pathological fracture should be suspected. The event may have been so minimal that the patient does not always mention it. The clinical presentation is the same as for other fractures of abrupt onset. Pathological fracture.
Figure 42.3 Burst fracture: the posterior half of the vertebral column is disturbed and retropulsion into the neural canal may take place.
Differential diagnosis. The differential diagnosis is with respect to the underlying cause rather than the fracture itself. Osteoporosis and neoplasm are common, tubercu losis rare. Radiography is diagnostic; CT or MRI may be helpful. •
Vertebral tumours: see earlier.
•
Vertebral infections: see later.
• Ankylosing spondylitis: •
see Chapter 44.
Osteoporotic compression fractures: osteoporosis is the
most common metabolic bone disease and leads to softening of the vertebral body by reduction of bone mass. Although if often remains silent it may be complicated by a thoracic postural pain syndrome.60,61 The cause is most frequently the imbalance between bone formation and resorption with postmenopausal or advancing age. The axial skeleton, femoral neck and pelvis are mainly affected. In the spine, it may eventually cause a biconcave vertebra from pressure by the interverte bral disc and it also predisposes to spontaneous fractures of the vertebrae. Fractures of this type are first noted in the thoracic spine62 where they usually have an anterior wedge shape. In contrast, in the lumbar spine, a transverse compression fracture is more likely, characterized by an equally diminished anterior and posterior height of the vertebral body.63 A sudden vertebral collapse causes pain, as in a high-energy fracture; if the onset is more gradual, pain is not to be expected.
Clinical presentation. Pathological fractures may occur after minor mechanical stress, such as on lifting or by sliding off a step. Symptoms may frequently be absent,
644 SECTION EIGHT - THE THORACIC SPINE
particularly in the upper thorax, where much support is provided by the rib cage. When complaints are present, midline pain over the thoracic and / or lumbar spine is characteristic; although of the mechanical type, it does not fully disappear on recumbency. Sudden fractures give rise to the same clinical pattern as in high-energy fractures, so an articular pattern is usually found. If they occur at several levels, hyper kyphosis may result. Angular kyphosis is hard to detect at the thoracic level because a normal anatomical kyphosis is already present but a more generalized round back deformity may develop. Osteoporotic fractures seldom cause acute neurologi cal problems although late features of progressive spinal stenosis from the angular kyphoSiS may occur. Spinal cord compression seldom results.60
Further examination. Uncomplicated osteoporosis may not be detectable until 30% of bone mass has been lost (Borenstein? p. 337). An early sign is accentuation of the mineral density of the endplate, apparent in sharply defined margins of the vertebral body. Diminished bone density, with shortness of horizontal trabeculae and accentuated vertical trabeculae, are characteristic. Warning The following may i n d icate a fracture. • Severe b i latera l g i rd l e p a i n after a m i nim a l i nj u ry in the a bsence of p a i n o n flexion of the neck: patho l o g i c a l fracture? • Very severe p a i n on extension pressure. • Ca psular pattern following an i njury.
In advanced osteoporosis, typical biconcave vertebral bodies (the so-called fish vertebrae; Fig. 42.4) can be seen. An osteoporotic compression fracture usually presents as anterior wedging of the vertebral body or a fracture of the endplates. Blood chemistry can differentiate all causes of second ary osteoporosis, which include malnutrition, drug intake, genetic factors, rheumatoid arthritis, immobiliza tion and malignancy. Thoracic postural pain syndrome
Cyriax regarded this pain syndrome, which affects mainly young adults and the middle aged, as being the result of a posterior displacement of the whole inter vertebral disc content, occurring mainly in patients with a marked thoracic kyphosis (Cyriax:l1 p. 210). Although dural compression by the entire disc is very likely, liga mentous overstretching of the supra- and interspinal lig aments may also be a contributing factor. Prolonged and repeated anteflexion stretches the posterior longitudinal ligament, which may become too elastic. At the same time, the kyphotic posture causes a posterior directed force on the disc. After some years, the whole disc content bulges posteriorly through the longitudinal ligament. At first this occurs only during prolonged anteflexion and ceases slowly on lying down - the phenomenon is self reducing. Later the displacement may become perma nent. Once the disc comes in contact with the dura mater, or when the posterior ligaments become severely over stretched, the patient complains of pain, which is initially temporary but later becomes permanent. The whole process depends on three elements, all of which aggravate the disorder. • • •
Figure 42.4
Advanced osteoporosis with 'fish vertebrae',
The duration of forward bending. The degree of physiological kyphosis. The load put on the disc.
Clinical presentations. The history is highly characteristic. IrUtially, the patients are well on first waking up in the morning, but pain starts after some hours of forward bending or after prolonged sitting in a kyphotic position. It is usually felt in the centre of the upper or mid-thoracic area but later may spread over the whole posterior thorax. The pain increases on carrying heavy objects or when the period of anteflexion is 'of longer duration. IrUtially, on lying down the pain disappears after some minutes, but in advanced cases it may take hours to ease off. As the condi tion develops, interscapular pain begins and increases slowly and steadily during the day, even if the patient does not bend forward. Finally pain becomes continuous day and night - the stage of anterior erosion has been reached. On clinical examination, only a few articular signs are present and they are not very pronounced. In this disor-
CHAPTER 42
- DISORDERS OF THE THORACIC SPINE: NON-DISC
645
Bone sclerosis and
--/---- Vertebral body
"'----==--'7----
LESIONS
anterior osteophytes
Bulging disk
I+------t-- Dura mater
-.-Jl--- Vertebral body
Figure 42.5
Thoracic postural pain syndrome.
der, a deep breath usually hurts at the moment the pain is maximally present. This element draws attention to a dural involvement (Fig. 42.5).
Treatment of the initial stage. Early treatment is in fact prevention: all kyphotic postures should be avoided. If this is not sufficient, ligamentous sclerosant infiltra tions over several adjacent levels around the maximum point of the kyphosis can be considered. Treatment of the advanced stage. Once a patient is used to the pain, prediction of exactly after how many hours the pain will take to come on is possible. At this stage, the advice is to lie down before severe pain starts. Besides preventive rest, daily traction can be given over 2 weeks, followed by a traction-free interval of 1 week, and with repetition for a further 2 weeks. The period without traction is progressively increased to a month, alternated with 2 weeks of traction. If this is successful, it should be continued indefinitely. Anterior erosion
This is the final stage of the postural pain syndrome and is encountered only in the elderly. Progressive increase in hyperkyphosis finally erodes the anterior portion of the disc and the anterior bony parts of the vertebrae are in contact with each other. Bone sclerosis develops and anterior osteophytes form (Fig. 42.6). Pain that previ ously ceased at night is now constantly present and is probably due to the osseous contact between the vertebrae, with subsequent local inflammation. For this reason the pain remains local. On clinical examination there is a marked thoracic kyphosis with very rigid joints. Therefore, the active
Figure 42.6 Anterior erosion: bony contact between the two vertebral bodies at the anterior side may result in bone sclerosis and pain.
articular movements no longer have much influence on the pain but passive articular movements may slightly increase the pain. Anterior osteophytes are visible on the radiograph. Treatment consists of repeated traction at intervals as the complaints demand, as for the thoracic postural pain syndrome (see earlier). Daily neck suspension can be used as an alternative. SCOLIOSIS
Scoliosis64 is defined as a lateral curvature of the spine of greater than 10°. The angle is determined by drawing lines across the upper surface of the vertebral bodies at which the curve changes direction - i.e. the vertebrae that tilt maximally into the concavity of the curve. Lines perpendicular to these are then drawn. The angle between the two perpendicular lines is Cobb's angle (Fig. 42.7). If it is greater than 10°, clinical scoliosis is present. Sometimes scoliosis is associated with an increased thoracic kyphosis (posterior convex curvature) or a diminished lumbar lordosis (anterior convex curvature). There are two types of scoliosis.5o In structural scoliosis, the deformity cannot be voluntarily corrected by the patient. It is characterized by a fixed rotation on forward bending. Some cases are congenital, others acquired. Non-structural scoliosis is frequently postural and remains under voluntary control. No fixed rotation is present on anteflexion. It is not progressive.
646 SECTION EIGHT - THE THORACIC SPINE
One curious feature of the disorder is that in childhood 90% of the curvatures are convex to the left, whereas in adolescence this is reversed.66 The condition worsens as bone growth increases and rarely changes after bone growth has stopped. However, if the angle of deformity between the lumbar and thoracic spines remains less than 60°, an effect on vital functions is not to be expected.
Figu re 42.7
Cobb's angle.
Structural scoliosis
Is the result of congenital malforma tion such as hemivertebra. It is frequently severe and may produce grotesque cosmetic deformity, reduced pulmonary function and ultimately paraplegia.
Congenital scoliosis.
Acquired scoliosis.
Is either secondary or idiopathic.
Secondary scoliosis. Has a local cause, often in associa tion with developmental disturbances. Examples are intraspinal tumours (neurofibromatosis), neuromuscu lar dysfunction, as in myopathies (muscular dystrophy), mesenchymal disorders (Marfan's syndrome), vertebral tumours, rheumatoid diseases, fractures and nerve root irritation. The pathophysiological mechanism of the thoracic malformation remains unknown in many of these. Idiopathic scoliosis. In this, an underlying disorder is not present. Ninety percent of cases are in this group, and some authors estimate the incidence as approximately 4.5% of all schoolchildren (Borenstein? pp. 1 69-1 74; Drummond65). Depending on the age of onset it is known as infantile scoliosis (0-4 years), juvenile scoliosis (4-10) and adoles cent scoliosis (over 10 to skeletal maturity). Adolescent scoliosis sometimes has adult onset when it affects females between 20 and 40 years of age. Severe adoles cent scoliosis affects girls four times more often than boys, whereas less pronounced deviations are seen equally in both sexes.65
Clinical presentation . Controversy surrounds the inci dence of thoracolumbar pain in scoliosis. Some authors contend that in the main the condition is asymptomatic and that patients with scoliosis do not suffer more from back pain than those with a normal back.67 Others main tain that the larger the scoliosis the more likely it is that pain will occur.68 Howevel� some patients initially expe rience pain at the end of the day, which stops rapidly on lying down.68 The cause may be overstretching of ligaments, overloading of the facet joints or temporal displacement of the disc. All these possibilities are compatible with a non-articular pattern on clinical exam ination. The pain is usually located at the apex of the cur vature. Progression of the deformity is usually associated with increased pain. On inspection, attention must be paid to scapular asymmetry, prominence at one side of the thorax, the dis tance between the arms and trunk and the level of the pelvis. Because a contralateral rotation occurs on side flexion, scoliosis is associated with a unilateral thoracic prominence at the convex side of the scoliosis. 50.69 Prominence of the thorax is most easily noted when the patient bends over. During functional examination, one side flexion is sometimes limited. Pain, if present, is of the mechanical type and gives rise to a partial articular pattern on clini cal examination. Advanced scoliosis may lead to a decreased vital capacity and to cardiorespiratory dysfunction.
Radiography establishes the exact location of the curvature, its degree of severity (Cobb's angle) and the stage of skeletal maturity, all of which are important for diagnosis, follow up and treatment. Skeletal maturation is judged from the ossification and closure of the vertebral ring apophyses.50 Progression is defined as an increase in Cobb's angle of at least 5° between two consecutive radiographs. Further investigations .
The higher the curvature is situated in the spine, the less favourable the outcome. Progression is possible for as long as vertebral growth continues. Prognosis.
Different types of treatment may be indi cated: observation, drugs, exercises, braces and surgery (see Box 42.2). It should be noted that there is an impor tant distinction to be made between the treatment for children and that for adults.
T reatment.
CHAPTER 42
-
D I SORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
Box 42.2 Treatment of scoliosis ,
Observation
Im mature skeleton, <20° Mature skeleton, <40° Non-prog ressive cu rves
•
Active treatment Brace
I nd ications: I m m ature skeleton, >30° Progressive cu rves of >20° Mature skeleton <40°, no severe p a i n in young a d u l t Contra i n d ications: Mature skeleton Curve >40° Th oracic l o rdosis
Sp i n a l fusion
Indications: Immature skeleton, >40° Mature skeleton, >50° Thoracic l o rdosis Fa i l u re of orthotic treatment U ncontro l l a b l e p a i n Prog ressive curve i n adu lts Structural disa b i l ities
Observation. This is undertaken in the following: • • •
All patients who have an immature skeleton, and with curve of less than 200• Curves of less than 400 in skeletally mature patients. Curves that are already thought to be non-progressive.
In all such cases, observation should be made at regular intervals to detect whether the curve pro gresses,lO Usually it is sufficient to see the patient every 6 months. In adolescents nearing the growth spurt, a check-up every 3 months is more appropriate. Exercises are of no use in this stage. Active treatment. Patients with a progressive curvature of 200 or more, or with an established curve greater than 300, and who are skeletally immature require active treat ment by either orthosis or operation. a young adult having a Cobb's angle of less than 400, in the absence of severe pain, is best treated by conservative means: non-specific anti-inflamma tory agents, facet infiltrations and physical monitor ing. A Milwaukee brace can also be considered. The main goal of the use of a brace is to prevent further progression, rather than to correct the curvature. A Milwaukee brace or plastic jacket can be used, which extends the spine by pushing it up cranially from the hips. However, a recent study of late-onset idiopathic scoliosis raises questions about the efficacy of spinal orthoses,?l Braces are contraindicated in skeletally mature patients or if the curvature is over 400 the latter usually do not respond well. A brace can not be
• Brace:
-
647
used in thoracic lordosis. When brace treatment is given, associated exercises become important in order to keep the muscles of the trunk and the abdomen in good condition. Operation: If the curve is over 400 in a skeletally immature patient, or when it is progressive or over 500 in a mature skeleton, spinal fusion is indicated to straighten and stabilize the spine,lo Other indications for operative intervention are when orthotic treat ment has failed, if pain becomes uncontrollable or when a thoracic lordosis is found.
Older adults are more likely to suffer from neutral compression. The major aim of treatment is to maintain function. With a curve under 400 this is usually possible without surgery. If there is uncontrolled pain or a pro gressive curve or structural disabilities, neurological complications or cardiorespiratory problems, surgical internal fixation is essential.8,n Non- structural scoliosis
The deformity is mainly found in adolescents and can be corrected by a voluntary effort. It is most frequently pos hlral, occasionally the result of mental disturbance. On forward bending, the patient aligns the head and spine over the pelvis so that the scoliosis disappears. The term 'compensatory scoliosis' is sometimes used. The condi tion is not of clinical importance. Scoliosis associated with inequality of limb length is usually confined to the lumbar spine.73 LATERAL EROSION
Just as hyperkyphosis may lead to thoracic postural pain syndrome and finally to anterior erosion, moderate and severe scoliosis may result in lateral erosion. The process is the same for both, but in scoliosis the entire disc of several consecutive levels shifts laterally to one side. After some years, this may lead to bony contact between the vertebral bodies at the concave side of the scoliosis (Fig. 42.8). Because the disc is displaced directly laterally, pressure on the dura mater or nerve root is not to be expected. Consequently, pain is felt only late in the development of the condition when bone sclerosis starts. The pain remains unilateral and is not increased by a deep breath. Initially, it is felt only at the end of the day and disappears at night or after a period of recumbency. Later, the pain comes on earlier in the day and disappears only after lying down for longer and longer periods. Finally, it becomes constant. Traction in the same way as for anterior erosion can be given but is often not successful. Arthrodesis is the alternative. Treatment.
648 SECTION E IGHT - THE THORACIC SPINE
in the pelvis (urinary tract, postpartum, bowel) (Borenstein and Wiesel:7 p . 249). The presence of dia betes mellitus, intravenous drug abuse, underlying chronic debilitating diseases or immunosuppression, previous infections, preceding bacteraemia and recent vertebral surgery are significantly associated with pyogenic osteomyelitis.62,76
Figure 42.8 Lateral erosion: bony contact between the two vertebral bodies at the concave side may result in bone sclerosis and pain.
FRACTURE OF A TRANSVERSE PROCESS At the thoracic level this is usually the result of a direct blow or of an extension manipulation. After the injury the patient suffers immediately from unilateral segmental pain, increased on active and resisted side flexion towards the painless side. Resisted extension is also painfu l. Spontaneous resolution of the pain occurs in about 2 weeks.
SPINAL INFECTIONS Vertebral osteomyelitis develops when an infectious organism enters the bone. A number of bacteria cause pyogenic osteomyelitis. Tuberculosis produces Pott's disease. An infection limited to the intervertebral disc is known as adult intervertebral disc space infection. In a later stage, when the infection progresses, it may also affect the vertebral body. Both osteomyelitis and disc space infections must be differentiated from discitis or intervertebral disc inflammation, which only affects children. VERTEBRAL OSTEOM YELITIS Pyogenic osteomyelitis
Since the introduction of antibiotics this disorder has changed from a disease of childhood and adolescence to one affecting mainly adults. The lumbar spine is most commonly involved.74 The most frequent organism is a Staphylococcus?5 In about 40% of patients, an extraspinal primary source of infection is found, very often sited
Clinical presentation. Although the onset may be abrupt, pyogenic osteomyelitis is most commonly insidious and progresses slowly. The pain is primarily felt locally at the site of the infection and is constantly present but often worse at night. At onset, the pain may be provoked or increased by activity and relieved in recumbency. As the condition progresses pain usually becomes more dramatic, leading to a full articular pattern with gross limitation mainly of extension, of botl1 side flexions and rotations. Rigidity and muscle spasm are also present. Gross tenderness on local pressure over the spinous processes is found. A soft tissue mass may be palpable. Chills and weight loss complete the clinical presentation. Thecal sac neurocompression by the forma tion of an epidural abscess may cause severe neurological disturbances (paraplegia or paraparesis)?7 Further investigations. The erythrocyte sedimentation rate (ESR) is constantly raised and is a good indicator of the activity of the disease.78,79 An increased white cell count is found in only half of the cases, and it seldom rises above 15 000.62,80 Spinal radiographs become positive at the earliest after 2 or 3 weeks of infection,80 when a narrowed disc space is the first sign found. This narrowing cannot be distin guished from narrowing that is the result of degenerative changes. Only later, after 1 0-12 weeks, do the adjacent endplates become more dense and eventually blurred once destructive erosion has set in. Healing is associated with osteosclerosis and leads to bony fusion across the disc space. Spongy bone erosion and rarefaction is apparent on CT scan before it is on plain radiography. However, Gallium bone scan proves to be the most valuable technique to detect early inflammatory changes and it becomes posi tive earlier than does CT scan. In a recent study gallium scanning proved to be 100% sensitive, specific and accu rate.81
The administration of antibiotics and bed rest until the ESR has returned to normal. Treatment of neurological deficit caused by epidural abscess is prompt surgical decompression, with or without fusion.82
Treatment.
Tuberculosis of the spine
Vertebral tuberculosis most frequently involves the lower thoracic and upper lumbar spines. It is always the conse-
CHAPTER 42
-
D ISORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
649
quence of haematogenous spread from a primary visceral focus (pulmonary or urinary tract) and it is the vertebral body that is involved, because the disc is avascular. However, spread to adjacent structures - discs, muscles and ligaments - may occur and a paravertebral abscess may form.
the discectomy as such. In a later stage, the vertebra may also be affected, leading to destruction of the vertebral body (see earlier - Pyogenic osteomyelitis). Treatment is bed rest and antibiotics after needle aspiration for bacteriological diagnosis.
This may be very different from a pyogenic vertebral infection. The onset is very slow and it is not unusual that many months will have elapsed before the diagnosis becomes obvious. Backache of lesser severity than in pyogenic infection is usual. Other signs and symptoms - intermittent fever, night sweat ing, weight loss and fatigue - may draw attention to tuberculosis. A localized angular bony deformity from vertebral collapse may be visible. On functional examination a full .articular pattern is found, together with severe local tenderness on extension pressure. Dural symptoms and signs are not present.
INTERVERTEBRAL DISC INFLAMMATION: DISCITIS
Clinical presentation.
Further investigations. The ESR is elevated but the white cell count may vary. Radiography of the chest and bacte riological examination of urine must always be done. On the radiograph, involvement of one vertebra is typica1.83 The most common early findings are a dimin ished disc space and osteolysis of the vertebral body Later, paravertebral granulation tissue is formed, result ing in paravertebral mass. This is usually followed by collapse of the vertebral body with formation of an angular kyphOSiS. A positive Mantoux test is not diagnostic in itself but does arouse suspicion of tuberculosis. Treatment. This comprises bed rest and administration of antituberculous drugs. Early surgical intervention with anterior debridement and grafting has been advocated to shorten the course of the disease, and it decreases the risk of neurological complications of deformity.62,83
POSTOPERATIVE DISCITIS
The most frequent cause of disc infection is posterior discectomy.8o After initial relief of the pain by surgery, the patient develops severe back pain 1-8 weeks later, often described as 'cramps pain'. Pain may radiate towards the side, the abdomen and the lower extremi ties. The typical pattern is an acute lumbago with pain aggravated by articular movements, together with marked limitation of range. Fever is usually absent, but the ESR is elevated and is used to follow the effect of the treatment. The radiograph becomes positive only after some weeks, showing at first a decreased intervertebral height, which is too pronounced and too early to be the result of
This disorder of unknown cause affects only children, most commonly between 2 and 6 years of age. Whether infection is involved remains uncertain. The lumbar spine is most usually affected. The first complaint is of back or hip pain; smaller children may just refuse to walk. On clinical examination, limited spinal movement with muscle spasm and local tenderness is found. Fever is present. Some weeks after onset, some narrowing of the inter vertebral disc space and erosion of the endplates can be seen. Although these radiographic findings are usually sufficient to establish the diagnosis of discitis, MRI is the diagnostic study of choice especially in a differential diagnosis with suspected vertebral osteomyelitis.84 Immobilization of the spine and antibiotics are the main treatment required.
LATERAL RECESS STENOSIS In some older patients, the intervertebral disc becomes completely worn out and its fragments displace posteri orly because of physiological kyphosis. As a conse quence, the intervertebral space decreases progressively and the posterior longitudinal ligament becomes rela tively long. Under the influence of the body weight it bulges posteriorly and may come in contact with the dura mater, causing central backache radiating bilaterally around the trunk, or may compress the nerve root, causing unilateral root pain (Cyriax:ll p. 211 ). This condi tion is characterized by pain that comes on immediately on standing and, unlike lumbar lateral recess stenosis, is not altered by sitting or stooping. Only when the patient lies down for 1 or 2 minutes does the pain cease, when it stops almost immediately. Because the condition occurs mainly in an elderly patient with a very stiff vertebral column, no appreciable discomfort can be provoked by articular movements. In root compression, side flexion towards the painful side is occasionally painful. Treatment.
This depends on the site of the pain.
Central pain. Daily traction can be tried. The aim is to bring as much of the disc material back into the interver tebral space, so that on load the intervertebral height
650 SECTION EIGHT - THE THORACIC SPINE
diminishes to a lesser degree and compression of the dura does not occur. If successful, it should be continued indefinitely on every other day. If traction fails arthrode sis is called for.
Unilateral root pain. If instead of central pain unilateral root pain is present, an infiltration around the nerve root should be given and can make the inflammation disap pear. If necessary, it can be repeated every 6-12 months (for technique, see Ch. 41 ).
ARTHRITIS OF THE COSTOVERTEBRAL AND COSTOTRANSVERSE JOINTS Disorders of these joints that give rise to clinical symp toms are rare, although radiology and au topsy migh t suggest the opposite. They may be affected by osteoarthrosis and ankylosing spondylitis, but very seldom by rheumatoid arthritis.85,86 Degeneration is identified mainly in the costovertebral joints of the first, eleventh and twelfth ribs, all of which have only one articular facet. It is possible that these are more vulner able to mechanical irritation by continuous rib motion, sometimes as the outcome of a mechanical injury.87 Less frequently the sixth, seventh and eight costoverte bral joints are affected, and in these it is most frequently the inferior hemifacet.88 It has been suggested that patients often have an increased thoracic kyphosis with associated scoliosis.87 Involvement of these joints gives rise to unilateral paravertebral pain radiating between the scapulae along the ribs. The pain is described as aching or burning, is usually worse in the morning and is aggravated by deep inspiration and a cough.87-89 Exceptionally, a sudden lightning pain may be present on breathing and may arrest further inspiration. Because all active movements of the trunk that have some influence on these joints will be somewhat painful, an asymmetrical pattern is encountered, together with pain on the springing test of the rib. When the first costotransverse joint is affected, the patient complains of pain unilaterally at the base of the neck. The pain is provoked by the following movements of the neck: active and passive flexion, contralateral side flexion and resisted side flexion towards the painful side. Pain may also be present on active and passive elevation of the arm and the scapula. Standard radiography, CT scan and technetium bone scans may show abnormalities of these joints. Tr eatm ent. If only one intercostal joint is affected an intra-articular injection should be given. Should this be unsuccessful, surgical excision of the joint may be considered.
The costotransverse joint is the easiest to inject. Because no clinical test is available to determine which one of the two joints - vertebral or transverse - is affected, the costotransverse joint is injected first. Local anaesthetic is used first to establish the diagnosis. If no immediate improvement results, the costovertebral joint must be at fault. Once the joint has been identified an injection of triamcinolone is given. Injection into either joint is performed with the patient in the prone lying position. Warning There is a considera b l e risk of pneu mothorax from these injections. Extreme care must be ta ken and shou l d o n l y be performed u nder rad iological contro l .
ARTHRITIS O F THE THORACIC FACET JOINTS Degeneration of thoracic facet joints most frequently affects levels C7-Tl, T3-TS and Tll_L 1.90,91 The diagno sis should be considered in those patients who complain of rather local unilateral paravertebral pain radiating only slightly towards the scapula. On clinical examina tion, dural symptoms or signs are not found. The only element is pain on one of the rotations, actively or pas sively performed. This can be either the rotation towards or away from the painful side, a situation resembling facet disorders in the cervical area. Other passive move ments are far less painful or not painful at all and resis ted rotations are pain free. Extension pressure on the spinous processes elicits pain on two consecutive processes, indicating the level of the lesion. These patients are often first mistakenly regarded as suffering from a disc lesion, because they show a partial articular pattern. After manipulation they may obtain some relief but it usually does not last longer than a few hours to a day. Therefore, if there is doubt about the diagnosis, the capsule of the affected facet joint should be infiltrated with 2 ml of lidocaine (lignocaine) 2%, which provides immediate relief in facet joint disorder. Treatment. Cure is obtained with one or two infiltrations of 1 ml of triamcinolone over 1-2 weeks.
Technique: injection of a thoracic facet joint (Fig. 41.9). The patient lies prone with the arms along the body. The two most tender spinous processes are marked and the facet joint between the corresponding vertebrae is identified. Depending on the level it lies about 1 (upper and lower thorax) to It (mid-thorax) interspinal levels higher than the lower tender spinous process.
CHAPTER 42 - DISORDERS OF THE THORACIC SPINE: NON-DISC LESIONS
Figure 42.9
Injection of a thoracic facet joint.
A syringe is filled with 1 ml of triamcinolone and a 4 cm needle is fitted. The needle is inserted vertically downwards about 1 cm from the midline. The needle is usually stopped by the lamina. It is now slightly with drawn and moved upwards or downwards until the typical capsular resistance is felt before ending at the bone. The steroid is then injected with the needle in bony contact. The patient must return after 2 weeks. If there is still some pain, the injection is repeated. If the treatment fails, a blockade with phenol solution of the medial branch of the dorsal ramus of the thoracic spinal nerve can be performed. Good results have also been reported with percutaneous radiofrequency denervation of the thoracic facet.92
PAGET'S DISEASE This focal, non-generalized osseous disorder is charac terized by thickening and deformation of the affected bone and is caused by hyperactive osteoclasts and osteoblasts, which give rise to increased bone resorption together with formation of disorganized new bone. It occurs more commonly than is generally believed and affects about 3% of all people above 40 years of age. This figure rises to about 5-10% in people over 80.93 There is a slight preponderance of males and the condition is most frequently encountered in Western Europe, Australia and New Zealand. Flat bones and the ends of the long bones are mainly affected. Most frequently involved are the spine, skull, sacrum, pelvis and femurs. About 60% of patients with Paget's disease have involvement of the lumbar spine, and 45% of the thoracic spine and sacrum. In only 15% is the cervical spine involved.94
65 1
Clinical presentation. Only about 12% of the patients affected by Paget's disease suffer from backache from the disease as such.95 It should be recognized that other dis orders, such as disc protrusions and facet joint problems, may be the basis of the pain in patients who are identified as having Paget's disease. In two-thirds the disease remains clinically asymptomatic.96,97 These cases are usually detected incidentally on a radiograph taken for some other reason or by an increased serum alkaline phosphatase level. Paget's disease usually starts in the middle aged or elderly and may give rise to local pain, local heat and deformation. The complaint is usually of a dull pain that does not increase at night. Characteristic deformities lateral bowing of the femur, anterior bowing of the tibia, increased size of the skull and decreased length of the spine - may occur. Osteoporosis and fractures from minimal trauma are often encountered and usually present in the femur and tibia, less often in the spine. The typical Paget's stature with dorsal kyphosis may be seen. Involvement of the spine occasionally results in spinal stenosis. Com p l ications. Because of multiple arteriovenous fistulae in bone, there is lowered peripheral resistance with a rise in cardiac output, which may lead to cardiac decompensation. Enlargement of the skull, with second ary compression of peripheral nerves, may result in hearing loss, tinnitus and vertigo? Pagetoid bone may convert to a highly malignant sarcoma with very poor prognosis. The probability is higher when there is polyostotic involvement. Radiology. Radiological findings depend on the stage. The initial phase is characterized by lytic bone lesions: osteoporosis circumscripta. These are rarely seen in the spine. Later, a mixed stage develops in which both demineralization and sclerosis of bone exist. The final sclerotic stage is characterized by a homogeneous increase of bone density. In the vertebrae, coarse trabeculae and a marked edge of the vertebral body ('picture frame' appearance) are present. The central portion appears decalcified. Ultimately, the bone becomes dense. When diagnostic doubt exists, bone scans must be taken. They are more sensitive than plain radiographs. laboratory. Serum calcium and phosphorus concentra tions are within normal limits, but the serum alkaline phosphatase is usually very high. Treatment. Most patients are asymptomatic and do not need any treatment. More active disease may require calcitonin or bisphosphonate to reduce the symptom but none of them is curative.
652 SECTION EIGHT - THE THORAC IC SPIN E
REFERENCES 1.
2. 3.
Epstein J, Marc J, Hyman R, Khan A, Mardayat M . Total myel
of the high thoracic and
121-1 28.
1 956;160:528-534.
Fidler M. Laminar removal and replacement: a technique for the
technique
Plasmans C , Van d e r Eycken J. Laminar removal a n d replace
1988;13(2):218-22l .
ment in combination with a spondylodesis in children with an
Roblot
P,
Alcalay
M,
Cazenave-Roblot
F,
Bontoux
D.
removal
of
epidural
tumour.
Spine
28. Emsellem H. Metastatic disease of the spine: diagnosis and
management. Sou th Med j 1 986;76:1405. pressive spinal epidural hematomas. 15 cases and a review of
Constantini S, Soffer D, Siegel T, Shalit M . Paraganglioma of the
2000;86(4) :335-345.
the
l i terature.
Rev
Chir
Orthop
Repar
Appar
Mot
30. Ruelle A, Datti R, Pisani R. Thoracic epidural hematoma after
1 989;14(6) :643-645.
spinal manipulation thera py. ]
Wells F, Thomas T, Matthewson M, Holmes A. Neurilemmoma
534-536.
of the thoracic spine. Spine 1 982;7(1) :66-70. 7.
the
Osteochondroma of the thoracic spine. Spine 1 982;7(1) :240-243. thoracic spinal cord with cerebrospinal fluid metastasis. Spine 6.
for
29. Cabana F, Pointillart V, Vital j, Senegas J. Postoperative com
2 1 5-217.
5.
cervical cord as causes. JAMA
27. Fidler M, Bongartz E. Laminar removal and replacement: a
removal of epidural tumour. Spine 1 988;13(2):218-22 1 .
intra-spinal extension of a neuroblastome. Spine 1 988;13(2): 4.
26. Scott M. Lower extremity pain stimulating sciatica, tumours
ography in the evaluation of lumbar discs. Spine 1979;4(2):
Spillal
Disord
1 999;1 2 ( 6 ) :
31 . Cohen jE, Ginsberg Hj, Emery D, Schwartz ML. Fatal sponta
Borenstein D, Wiesel S. Low Back Pain. Saunders, Philadelphia,
neous spinal epidural hematoma following thrombolysis for myocardial infarction. Surg Neural 1998;49(5):520-522.
1989. 8.
Gau tier-Smith P. Clinical aspects of spinal neurofibromas. Brain 1 967;90:359-394.
following coronary thrombolysis with
9.
CaSSidy R, Ducker T. Intradural neural tumours. In: The Adult
activator. Report of two cases. j Neurasurg 1995;83(2):350-353 .
32. Sawin PD, Traynelis Vc, Follett KA. Spinal epidural hematoma
tissue plasminogen
York,
33. Van Schaeybroeck P, Van Calenbergh F, Van De Werf F et al.
1 0 . Brugger A. Die Erkrankungen des Bewegul lgsapparates ulld seines
bolysis and anticoagulation therapy: report of three cases. Clill
Spille:
Principles
alld
Pmctice.
Raven
Press,
New
Spontaneous spinal epidural hematoma associated with throm
1 99 1 : 889-903. NerveI1systellls. Fischer, Stuttgart, 1 980.
Neural Neu ros u rg 1 998;100(4):283-287.
1 1 . Cyriax J. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bail I i ere Tindall, London, 1982.
Ignatius
P,
Marvel
J,
Cord 1 998;36(9) :658-660. 35. Leach M, Makris M, Hampton KK, Preston FE. Spinal epidural
intervertebral discs. lAMA 1 962;179:878-88l . S,
Rothman
R.
Intradural
haematoma in haemophiJia A with inhibitors - efficacy of
neurofibroma simulating lumbar-disc disease. J Bone Joint Surg
recombinant
1956;58A:1 040-1042.
1 999;5(3):209-212.
14. Shah K, Nagler W. Dumbell neurilemoma simulating lumbar disk disease. Arch Phys Med Rehabi/ 1978;59(7) :340-342. and
pathological
aspects
of
solitary
factor
VIla
concentrate.
Haemophilia
36. Daentzer D, Boker DK. Spontaneous spinal hemorrhage.
Outcome after
1 5 . Sanguinetti C, Specchia N, Gigante A, de Palma L, Greco F.
Clinical
Prasad VS, Murthy JM. Spinal
epidural haematoma in a patient with haemophilia-B. Spinal
12. Love j, Rivers M. Spinal cord tumours, simulating protruded l3. Wiesel
34. Meena AK, Jayalakshmi S,
surgical
therapy o f epidura l hematomas.
Nervenarzt 2000;71 (2) : 1 1 6-122.
spinal
37. Sklar EM, Post JM, Falcone S. MRI of acute spinal epidural
16. Ongerboer De Visser B . Het teken van Lhermitte bij thoracale
38. Lovblad KO, Baumgartner RW, Zambaz BD et al. Nontraumatic
neurofibroma. j Bone joillt Surg 1993;75 B ( 1 ) : 1 41-147. wervelaandoeningen.
Ned
Tijdschr
Geneeskd
hematomas. I COllfPllt Assist TOll1ogr 1 999;23(2) :238-243.
1 980;124(11 ) :
390-392.
epidural
hematomas.
MR
features.
Acta
Radiol
1 997;38(1):8-l3.
17. Onimus 0, Schraub S, Bertin D, Bosset J, Guidet M. Surgical 1 8 . Galasko CSB. Skeletal Metastases. Butterworths, Boston, 1 986. 19. Reith C, Reith HB, Baumgartner D, Kozuschek W, Lausberg G .
Diagnosis a n d interdisciplinary therapy of spinal cord com caused
by
spinal
metastases.
Zentmlbl
39. Alexiadou-Rudolf C, Ernestus RI, Nanassis K, Lanfermann H,
Klug N. Acute non traumatic spinal epidural hematomas. An
treatment o f vertebral metastasis. Spine 1 986;11(9):883-891 .
pression
spinal
Chir
important differential diagnosis in spinal emergencies. Spine 1998;23(16) : 1 8 1 0-1813. 40. Groen Rj, van Alphen HA. Operative treatment of spontaneous
spinal epidural hematomas: a study of the factors determining postoperative outcome. Neu rosu rgery 1996;139(3) :494-508.
1 99 1 ;116(15) :913-916. 20. Brown PD, Stafford SL, Schild SE, Martenson jA, Schiff D.
41 . Fukui MB, Swarnkar AS, Williams RL. Acute spontaneous
Metastatic spinal cord compression in patients with colorectal
spinal epidural hematomas. Am J Neuromdiol 1 999;20(7):
cancer. I Neuroonco/ 1 999;44(2) : 1 75-180.
l365-l372.
21 . Fornasier VL, Horne jG. Metastases to the vertebral column.
42. Silber SH. Complete nonsurgical resolution of a spontaneous
spinal epidural hematoma. Am ] Emerg Med 1996;14(4):391-393.
CalfCer 1 975;36:590. 22. Biyani A, Ebraheim NA, Lu J. Thoracic spine fractures in
patients older than 50 years. Clin Orthop 1 996;328: 190-193. 23. Kostuik j, Wei nstein J . Di fferential d i agnosis and surgical treat
ment of metastatic spine tumours. In: The Adult Spine: Principles
43. Serizawa Y, Ohshiro K, Tanaka K, Tamaki S, Matsuura K,
Uchihara T. Spontaneous resolution of an acute spontaneous spinal epidural hematoma with neurological deficits. In tem Med 1995;34(10) :992-994. 44. Barnett G, Hardy R, Little J, Bay j, Sypert G. Thoracic spinal
and Practice. Raven Press, New York, 1 99 1 :861-888. 24. Weinstein J . Di fferential diagnosis and surgical treatment of
primary benign and malignant neoplasms. In: The Adult Spine:
canal stenosis. ] Neu ras urg 1 987;66:338-344. 45. Govoni A. Developmental stenosis of a thoracic vertebra re;;ult
Principles and Practice. Raven Press, New York, 1 99 1 :829-860.
ing in narrowiJlg of the spinal canal. AIR 1971;112:401-404.
25. Love G, Rivers M. Intractable pain due to associated protruded
46. Milhorat TH, Kotzen RM, Anzil AP. Stenosis of central canal of
intervertebral 1962;12:60-64.
d isc
and
intraspinal
neoplasm.
Neu rology
spinal cord in man: incidence and pathological findings in 232 autopsy cases. j Neuros u rg 1994;80(4):71 6-722.
CHAPTER 42
-
D ISORDERS OF TH E THORACIC SPIN E : NON-DISC LESIONS
47. Yamamoto I, Matswnae M, Ikeda A et al. Thoracic spinal stenosis: experience with seven cases. ] Neurosurg 1988;68(1):37-40. 48. Okada K, Oka S, Tohge K, Ono K, Yonenoby K, Hosoya T. Thoracic myelopathy caused by ossification of the ligamentum flavum. Clinicopathologic study and surgical treatment. Spine
653
73. Papaioalmou T, Stokes 1, Kenwright J. Scoliosis associated with l i mb-length inequality. I Bone Joint Surg 1982;64A(1):59-63. 74. Ross P, Fleming J. Vertebral body osteomyelitis. Ciill Orthop Rei Res 1976;118:190-198.
75. Ca rragee EJ. Pyogenic vertebral osteomyelitis. J BOlle ]oillt S u rg 1 997;79A(6) :874-880.
1991;16(3) :280-287. 49. Love G, Schorn V. Thoracic-disc protrusions. JAMA 1965;191:
76. Colmenero JD, Ji menez-Mejias ME, Sanchez-Lora FJ et al. Pyogenic, tuberculous, and brucellar vertebral osteomyelitiS: a
627-631 . 50. Goldstein L , Waugh T. Classification and terminology of scolio
descriptive and comparative study of 2 1 9 cases. A lii RheulII Dis 1997;56(12):709-715.
sis. Ciin Orthop Rei Res 1973;93: 1 0-22. 51 . Guille J, Forlin E, Bowen R. Congenital kyphosis. Orthop Rev 1993:235-239. 52. Bullough P, Boachie-Adjei O. Atlas of Spinal Disease. Lippincott, Philadelphia, 1988. 53. Scheuermann H. Rontgenologic studies of the origin and devel opment of juvenile kyphosis, together with some investigations concerning the vertebral epiphyses in man and animals. Acta
77. Hadjipavlou AG, Mader JT, Necessary JT, Mu ffoletto AJ. Hematogenous pyogeniC spinal infections and their surgical management. Spine 2000;25(13):1668-1679. 78. Buchelt M, Lack W, Ku tschera H-P, Katterschafka T, Kiss H, Schneider B, Kotz R. Comparison of tubercu lous and pyogenic spondylitis. Clin Orthop Rei Res 1993;296:192-199. 79. Carragee EJ, Kim D, van der Vlugt T, Vittum D. The clinical use o f erythrocyte sedimentation
Orthop Scan 1934;5:161 .
54. Schmorl G. Ober die an den Wirbelbandscheiben vorkom
rate in
pyogenic vertebral
osteomyelitis. Spine 1997;22(18):2089-2093.
menden Ausdehnungs- und Zerreisungsvorgange und die
80. Vincent K, Benson D. Di fferential diagnosis and conservative
dadurch an ihnen und der Wirbelspongiosa hervorgerufenen
treatment of infectious diseases. In: The Adllit Spine: Prillciples and Practice. Raven Press, New York, 1991 .
Veranderungen. Verh Dtsch Pat Ges 1 927;22:50. 55. Brad ford
D.
Juvenile
kyphosis.
Clin
Orthop
Rei
Res
1977;128:45-55. 56. Segers M, Anciaux H. Pseudo-angillellze Pijnklachtell. Dienst
81. Hadjipavlou AG, Cesani-Vazquez F, Villaneuva-Meyer J et al. The effectiveness of gallium citrate Ga 67 radionudide imaging in vertebral osteomyelitis revisited. Am J Orthop 1998;27(3):179-183. 82. Arnold PM, Baek PN, Bernardi RJ,
fysische geneeskunde, Gent. 57. Murray P, Weinstein S, Spratt K. The natural history and long term follow up of Scheuermann kyphosis. I Bone Joint SlIrg
vertebral osteomy e l i t i s :
1993;2:236-248.
1997;47(6) :551-561 .
58. Willen J, Gaekwad U, Kakulas B. Burst fractures in the thoracic and lumbar spine. A c1inico-neuropathologic analysis. Spine 1 989;14(12) .
Luck EA, La rson SJ.
Surgical management of nontuberculous thoracic and lumbar report of 33 cases.
83. Fernandez M, Carrol CL, Baker osteomyelitis
in
ch i l d ren:
an
q.
S u rg Neu rol
Discitis and vertebral
1 8-year
review.
Pediatrics
2000;105(6) : 1 299-1 304.
59. Kostuik J, Huler R, Esses S, Stauffer S. Thoracolumbar spine
84. Cohen MJ, Ezekiel J, Persellin R H . Costovertebral and costo
fracture. In: The Adllit Spine: Principles alld Practice. Raven Press,
transverse joint involvement in rheumatoid arthritis. Alii Rhe/llll
New York, 199 1 .
1 978;37(5):473-475.
60. Solomon C , Chopin D, Benoist M . Spinal cord compression:
85. Benhamou C, Roux C, Tourl iere D, Gervais T, Viala J, Amor B.
an exceptional complication of spinal osteoporosis. Spine
Pseudovisceral pain referred from costovertebral arthropathies.
1988;13(2):222-224. 6 1 . Riggs B, Walmer H, Dunn W, Mazess R, Offord K, Melton L.
Spine 1993;18(6):790-795.
86. Raney F. Costovertebral-costotransverse joint complex as the
Di fferential changes in bone mineral density of pedicular and
source
axial skeleton with aging. I Ciin [nvest 1981 ;67:328.
1966;48A (7) : 1 451-1452.
porotic patient. In: The Adult Spine: Principles and Practice. Raven Press, New York, 1991 . 64. Zorab P. Respiratory tract disease chest deformities. BMI 1966;7 65. Drummond D, Rogola E, Gurr J. Spinal deformity: natural history and the role of school screening. Orth Clin North Am
410-419. Adu l t
scoliosis
and
back
pain.
Spine
68. Hall J, Nachemson A . Debate: scoliosis. Spine 1 977;2(4) :318-324. 69. Kapandji IA. The Physiology of the joints. Volume three. The Trunk Vertebral Column,
1 s t edn.
Church i l l
Livingstone,
71 . Goldberg C, Dowling F, Hall J, Emans J. A statistical comparison between natural history o f idiopathic scoliosis and brace treatment in skeleta l l y immature
loi n t
S u rg
joints. Anatomical-clinical observations in arthritis. Arthritis Rheum 1964;7(3).
88. Grant A, Keegan D. Rib pain - a neglected diagnOSiS. Irish I Med Sci (6th series) 1966;367:162-169.
Decision
Br I Surg 1935;57:412.
90. Skubic J, Kostuik J. Thoracic pain syndromes and thoracic disc Press, New York, 199 1 : 1 443-146 1 . 9 1 . Stolker RJ, Vervest AC, Groen G J . Percutaneous facet denerva tion in chronic thoracic spinal
pain. Acta Neurochir (Wien)
92. Kingma M, Leerboek Orthopedie, 5th edn. Bolm, Scheltema & Holkema, Utrecht ! Antwerp, 1 985. 93. Meunier P, Salson C, Mathieu L et al. Skeletal distribution and 1987;217:37-44. disease of bone. Clin Orthop Rei Res 1 987;217:152. 95. Kane W. Osteoporosis, osteomalacia, and Paget's disease. In:
adolescent girls.
Spine
The Adult Spine: Prillciples and Practice. Raven Press, New York,
adult
Spine
9 6 . Collins D. Paget's disease of bone: incidence a n d subclinical
199 1 .
1993;18(7) :902-908. 1979;4(6):521-525.
BOlle
94. Altman R, Brown M, Gargano G. Low back pain in Paget's
Am 1979;10(4):813-827.
J.
J
biochemical paranleters o f Paget's disease. Clin Orthop Rei Res
Edinburgh, 1974:42. 70. Bunnell W. Treatment of i d iopathic scoliosis. Orthop Ciin North
72. Kostuik
pain.
1993;122(1-2) :82-90.
1979;4(6):513-517.
the
referred
herniation. In: The Adult Spine: Principles and Practice. Raven
1979;10(4):751-759. 66. James J. The etiology of scoliosis. j Bone joint Surg 1970;52(3):
an
or
89. Shore L . On osteo-arthritis in the dorsal intervertebral joints.
May:11 55-1156.
A.
local
87. Nathan H, Weinberg H, Robin G, Aviad 1. The costovertebral
62. Macnab 1 . Backache. Williams & Wilkins, Baltimore, 1983. 63. Kostuik J. Compression fractures and surgery in the osteo
67. Nachemson
of
making
in
scoliosis.
forms. Lancet 1956;2:5 1 .
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS ,
Referred pain
6SS
Pain referred from visceral structures 655 Pain referred from musculoskeletal structures not belonging to the thoracic cage 661
Disorders of the thoracic cage and abdomen 662 Disorders of the inert structures 662 Disorders of the contractile structures 664
Disorders of the thoracic cage and abdomen
Pain in the thorax or abdomen can be the result of a local problem of either the thoracic wall or the abdominal muscles but it is often referred from a visceral structure or from another musculoskeletal source most frequently a disc protrusion. Therefore it is wise to remember the only safe approach in this area is to achieve a diagnosis by both positive confirmation of the lesion and exclusion of other possible disorders.
REFERRED PAIN
/
PAIN REFERRED FROM VISCERAL STRUCTURES
All visceral structures belonging to the thorax or abdomen may give rise to pain felt in this area (see Ch. 39). In that the discussion of these disorders is prin cipally the province of internal medicine, only major elements in the history that are helpful in differential diagnosis from m usculoskeletal disorders are men tioned here. Acute chest pain is summarized in Box 43.2 (p. 662). HEART (Fig. 43.1). Ischaemic heart disease
The innervation of the heart is derived from the C8-T4 segments. Pain is therefore not only felt in the chest but can also be referred to the ulnar side of both upper limbs, though more commonly to the left.
Heart
Figure 43.1
Referred pain in lesions of the heart.
655
656 SECTION EI GHT - THE THORACIC SPINE
It is traditionally accepted that pain felt in the chest radiating into the left arm is indicative of myocardial ischaemia, especially when the patient reports it as pressure, constriction, squeezing or tightness. However, none of these descriptions, which are usually regarded as characteristic of ischaemia, is of definitive aid in the differential diagnosis from other non-cardiogenic prob lems in the thorax. Even relief of pain after the intake of glyceryl trinitrate does not offer absolute confirmation of coronary ischaemia. For clinical diagnosis, a combi nation of several elements must be present, of which the most important is pain spreading to both arms and shoulders initiated by walking, especially after heavy meals or on cold days.1
Mitral valve prolapse
This condition usually gives rise to mild pain located in the left submammary region of the chest and sometimes also substernally. Occasionally it mimics typical angina pectoris and is sometimes accompanied by palpitations. Pericarditis
Pain that arises from the pericardium is the consequence of irritation of the parietal surface, mainly from infec tious pericarditis, seldom from a myocardial infarction or in association with uraemia. When pericarditis is the outcome of one of the latter two causes it is usually only slight. Pain is normally located at the tip of the left shoulder, in the anterior chest or in the epigastrium and the corresponding region of the back. Three different types of pain can be present. First and most obvious, but rarely encountered, is pain synchronous with the heart beat. Second is a steady, crushing substernal ache, indis tinguishable from ischaemic heart disease. Third and most common is pain caused by an associated localized pleurisy, which is sharp, usually radiates to the inter scapular area, is aggravated by coughing, breathing, swallowing and recumbency, and is alleviated by leaning forward.2
AORTA Aneurysm of the thoracic aorta
This is most frequently the result of arteriosclerosis but is rare by comparison with the same condition below the diaphragm. The majority of small aneurysms remain asymptomatic but if they expand a boring pain results, usually from displacement of other visceral structures or erosion of adjacent bone. Compression of the recur rent nerve may result in hoarseness and compression of the oesophagus in dysphagia. When acute pain and dyspnoea supervene, this usually indicates that the aneurysm has ruptured, with a likely fatal outcome.
Dissecting aneurysm of the thoracic aorta
This is an exceptional cause of chest pain, occurring mainly in hypertensive patients. The process usually starts suddenly in the ascending aorta, giving rise to severe substernal or upper abdominal pain. Radiation to the back is common and back pain may sometimes be the only feature, expanding along the area of dissection as this progresses distally. The patient often describes the pain as tearing. In most cases, it is not changed by posture or breathing. When aortic dissection involves the vessels that supply the spinal cord, neurological changes and even para plegia may result.3 PLEURA AND LUNGS
Because neither the lungs nor the visceral pleura have sensory innervation, pain is only present if the parietal pleura is involved, which may occur in inflammation or in pleural tumour. Invasion of the chest wall by a pulmonary neoplasm also provokes pain. Pain is commonly uni lateral and increased by deep inspiration and coughing. Bronchitis
This is usually painless, unless coughing causes severe irritation of the respiratory tree, which is manifested as a continuous substernal ache. Pneumonia
Although the clinical presentation of pneumonia may vary, classically the p�ient is severely ill with high fever, pleuritic pain and aAry cough. Pleurisy (pleuritis)
This is characterized by a sharp superficial and well localized pain in the chest, made worse by deep inspira tion, coughing and sneezing. Movements of the trunk which stretch the parietal pleura may increase the pain. Carcinoma of the lung
In carcinoma of lung pain is consequent upon involve ment of other structures such as the parietal pleura, the mediastinum or the chest wall. Invasion of the chest wall may cause spasm of the pectoralis major muscle, which subsequently leads to a limitation of both passive and active elevation of the arm. Superior sulcus tumour of the lung (Pancoast's tumour)
This warrants special attention because 90% of patients suffering from this disorder complain of musculosk�letal pain.4,s It is frequently mistaken for a shoulder lesion or even for thoracic outlet syndrome, an error which leads to a delay in diagnosis and treatment.6
CHAPTER 43 - DISORDERS OF THE THORACIC CAGE AND ABDOMEN
The superior pulmonary sulcus is the groove in the lung ' formed by the subclavian artery as it crosses the apex of the lung. Because most apical tumours have some relation to the sulcus, they are often called superior sulcus tumours. They frequently involve the brachial plexus and the sympathetic ganglia at the base of the neck and may destroy ribs and vertebrae. Pain around the shoulder, radiating down the arm and towards the upper and lateral aspect of the chest is usual and is often worse at night. Orthopaedic clinical examination produces an unusual pattern of clinical findings. There is often a complicated mixture of cervical, shoulder and thoracic signs. Passive and resisted movements of the cervical spine may be limited and / or painful, the result of involvement of the scaleni and sternocleidomastoid muscles. On examina tion of the shoulder girdle, a restriction of both active and passive elevation of the scapula may be present. More positive signs are detected during examination of the shoulder? Both active and passive elevations of the arm are limited because of spasm oVfue pectoralis major muscle. Passive shoulder movements may be consider ably limited in a non-capsular way. Some resisted move ments are weak. The neurological examination of the upper limb shows weakness and atrophy of the muscles on which conse quent is extension of the tumour to the lower trunks of the brachialis plexus (Fig. 43.2). The only abnormal finding during thoracic examination is pain and limitation on lateral flexion towards the unaffected side explained by putting the affected thoracic wall under stretch.
657
The clinical picture of Pancoast's tumour may be com pleted by some typical findings that are caused by an ingrowth of neurological and vascular structures at the apex of the lung.8 These include: •
•
•
Horner's syndrome: this is characterized by an ipsilateral slight ptosis of the upper lid, miosis of the pupil and enophthalmos, together with decreased sweating on the same side of the face. It is the outcome of involvement of the ascending sympathetic pathway at the stellate ganglion on the side of the tumour.9 Hoarseness: this is the result of involvement of the recurrent laryngeal nerve, which innervates the voice cords. The hoarseness is unusual and unlike that caused by local laryngeal problems. Oedema and discoloration of the arm: this occurs if the subclavian vein is obliterated by the tumour.
All the symptoms and signs mentioned (summarized in Box 43.1), either singly or in combination, call for careful clinical chest examination followed by further investigation by chest radiography or other imaging methods. Acute pneumothorax
This is characterized by a sudden dyspnoea and unilateral pain in the chest, radiating to the shoulder and arm on the affected side and often described as a tearing sensation. Breathing and activity increase the pain. If increasing tachycardia, tachypnoea and cyanosis are present, a tension pneumothorax is very likely. In this event, a large bore needle should be introduced at once into the second or third interspace at the mid clavicular line and help sought for further definitive decompression.
Box 43.1
Superior sulcus tumour of the lung
Symptoms Aggravating shoulder-arm pain (Pulmonary symptoms)
Figure 43.2 The clinical symptoms of a superior sulcus tumour of the lung are produced by local extension into the chest wall, the base of the neck and the neurovascular structures at the thoracic inlet.
Signs Cervical spine: impaired movements and positive resisted tests Shoulder girdle: impaired movement Shoulder: limited arm elevation/noncapsular pattern/weak resisted tests Upper limb: weakness and atrophy Thoracic spine: l imited side flexion away from the affected side Horner's triad: ptosis, miosis, enophthalmos Hoarseness Oedema of the arm
658 SECTION EIGHT - THE THORACIC SPINE
Pulmonary embolism
A thrombus formed in the systemic veins or in the right heart may embolize into the pulmonary arterial system. It is a rather common disorder, found in about 60% of all autopsies, but quite often clinically silent.IO Predisposing factors for pulmonary embolism are: • • • • • • • • •
Phlebothrombosis in the legs Prolonged bed rest Pel vic and lower limb fractures Pelvic or abdominal surgery Cardiac failure Pregnancy Malignant disease A hypercoagulable state Atrial fibrillation.
Symptoms and signs are mainly dependent on the extent of the lesion. A small embolus may give rise to effort dyspnoea, abnormal tiredness, syncope and occa sionally to cardiac arrhythmias. On auscultation, a few basal crackles may be heard. A medium-sized embolus may lead to pulmonary infarction, so provoking dyspnoea, sudden pleuritic pain and cough with haemoptysis. There may be tachycardia or a gallop rhythm. A loud or soft second heart sound is heard, together with some degree of pleural rub. Clinical evidence of peripheral deep venous thrombosis is often present but its absence does not exclude the diagnosis. In a massive pulmonary embolus, the patient com plains of severe central chest pain and suddenly shows features of shock with pallor and sweating. marked tachynoea and tachycardia. Syncope with a dramatically reduced cardiac output may follow. This is a medical emergency: death may follow rapidly. Pulmonary hypertension
This is often associated with valve stenosis or secondary to pulmonary disease, such as emphysema, which obstructs the pulmonary circulation. Although pain is seldom present, it may radiate into the rest of the chest and the arms. Unlike angina, it often comes on at rest and can last for hours or days. Cyanosis and dyspnoea are often encountered.2
MEDIASTINAL PROBLEMS Acute mediastinitis
This is a rare inflammation, usually the result of perfo ration of the oesophagus. The three causes are perfora tion of malignant tumour, ingestion of caustics leading to necrosis and Mallory-Weiss syndrome, in which vomit ing without appropriate relaxation of the oesophagus causes a tear of the oesophagogastric junction, often incomplete in thickness. There is very severe substernal and central dorsal pain of abrupt onset, followed by high fever and shock. Without treatment, it is rapidly fatal. Mediastinal emphysema
This is usually the consequence of a ruptured pleural bleb or a wound of the chest. Air spreads into the mediastinal tissues, giving rise to sudden or more gradual substernal pain, sometimes radiating into the neck, shoulders and interscapular area. Subcutaneous crepitus above the clavicle is pathognomonic for the condition. Mediastinal tumours
These may give rise to anterior or posterior substernal pain, which is usually steady, of mild severity and often worse at night. Radiography reveals the diagnosis. OESOPHAGUS (Fig. 43.3) Oesophageal spasm
This occurs suddenly and gives rise to substernal aching not necessarily related to the intake of food. Relief is often obtained by drinking hot water. Reflux oesophagitis
This is frequently due to a hernia of the stomach through the diaphragmatic hiatus. Pain is felt around the Xiphoid process, can be very severe and may radiate to the rest of the sternum, into the back and between the scapulae. Pyrosis or heartburn, which begins if the patient lies down immediately after meals, together with a burning sensation on eructation, are the most typical symptoms.
Oesophagus
Epidemic myalgia (pleurodynia, Bornholm disease, devi/'s grip)
Infection with coxsackie B virus can lead to very severe pain, felt over the anterior chest and abdomen. Pain is increased by movement, breathing, coughing and sneez ing. The symptom is paroxysmal, so that testing hurts one moment but not the next. There is usually accom panying fever, and symptoms persist for 3-7 days before disappearing spontaneously.
Figure 43.3
Referred pain in oesophageal lesions.
CHAPTER 43
-
DISORDERS OF THE THORACIC CAGE AND ABDOMEN
Rupture of oesophagus
659
Stomach
The symptoms are those from acute mediastinitis (see above). Malignant tumour of the oesophagus
The initial symptoms are food lodgement at the site of the tumour. Later there may be constant anterior or posterior central chest pain, unrelated to eating and mainly the result of extraoesophageal extension of the tumour. Total dysphagia may follow, and remarkable weight loss over a short period of time is an ominous sign. DIAPHRAGM (Fig. 43.4) Diaphragmatic irritation
This can be the result. of a subphrenic abscess or of air in the abdomen after laparoscopy or laparotomy. Pain arisirig from the central part of the diaphragm is referred to the base of the neck and into the shoulders, mainly in the third and fourth cervical segments. Pain originating from the peripheral part is felt more at the lower thorax and in the upper abdomen. Diaphragmatic hernia
This usually occurs due to displacement of the proximal part of the stomach as a whole when the patient is prone or head down or when intra-abdominal pressure is increased, as on straining or lifting. Pain, pyrosis and dysphagia may result. Pain usually disappears in the upright position. Hernia often causes reflux oesphagitis (see above). Subphrenic abscess
Abscesses that are truly just below the diaphragm can occur either to the right or to the left. Many so-called sub phrenic abscesses are in fact below the liver and usually follow a perforation of the gastrointestinal or biliary tract, often after surgery. Signs and symptoms are fever and upper quadrant pain, sometimes with associated shoul der pain and local tenderness along the costal margin.
Figure 43.5
Referred pain in gastric or duodenal lesions.
Dyspnoea may be associated. Persistent fever and a history of a recent intra-abdominal sepsis should arouse suspicion. STOMACH AND DUODENUM (Fig. 43.5) Gastritis
An inflammation of the superficial gastric mucosa may be the result of the intake of non-steroidal anti-inflamma tory drugs, alcohol or excessive meals. There is usually epigastric pain of short duration. Gastric or duodenal ulcer
These result in epigastric or substernal pain, often associ ated with inability to digest food. The pain usually ceases on intake of antacids or food. Other symptoms, such as nausea, vomiting, heartburn and flatulence, are atypical. In duodenal ulcer, the pain commonly comes on through the night and also occurs I-It hours after meals. A bout of symptoms over weeks or months may be followed by a similar period of relief. Pain in the back suggests a posterior ulcer that has penetrated a structure such as the pancreas. Gastric tumours
Poor general health with weight loss, nausea, anorexia and vomiting is the most frequent presentation. Dysphagia can occur, and epigastric pain is usually present but cannot be distinguished from that from gastric or duode nal ulcer, because it often responds to antacids or food.
Diaphragm
LIVER, GALLBLADDER AND BILE DUCTS (Fig. 43.6) Acute hepatitis
Figure 43.4
Referred pain in diaphragmatic lesions.
In acute hepatitis, enlargement of the liver, with subse quent stretching of the capsule, can give rise to pain felt in the right hypochondrium and upper abdomen. The development of jaundice is indicative of hepatitis and the liver is tender on palpation. It should be remembered that hepatitis B infections may be preceded in one in four cases by a polyarthritis affecting the smaller joints.
660 SECTION EIGHT - THE THORACIC SPINE
Gallbladder
Subacute or chronic pancreatitis
In a high percentage of cases, pain is referred to the back at about the T8 level. The symptoms may be the outcome of obstruction of the pancreatic duct, interstitial inflammation or infiltration by a neoplasm. Patients who suffer from these disorders often get relief in a character istic position: sitting with the trunk flexed, knees drawn up and the forearms folded around the knees to exert pressure upon it. Figure 43.6
Referred pain in lesions of the gallbladder.
SPLEEN Choledocholithiasis
This provokes spasmodic pain felt mainly in the right hypochondrium. The pain may radiate posteriorly towards the inferior angle of the right scapula (T7-T9). Cholecystitis
Pain arising from disorders of the spleen, sometimes due to splenomegaly, is felt in the left hypochondrium and is sometimes referred to the side in the lower half of the thorax (T6-nO). APPENDIX
Though traditionally described in females of 20-40 years of age, cholecystitis can occur at any age and in either sex. Localized peritoneal irritation may occur with acute abdominal pain in the right hypochondrium. Pain may radiate into the back and to the right shoulder. Sometimes nausea and vomiting are also present. On palpation, there is local tenderness over the gallbladder.
Acute appendicitis is usually the result of an obstruction of the lumen of the appendix by a faecalith. The pain starts in the centre of the abdomen, around the umbili cus and later is sited in the right iliac fossa. Nausea and vomiting are often present. There is local tenderness and guarding on palpation of the right iliac fossa, from localized peritonitis.
Liver abscess
Although liver abscesses are uncommon, they may be associated with right upper quadrant abdominal pain. General illness, varying from a very slight malaise to severe illness with septic shock, may be found. PANCREAS (Fig. 43.7) Acute pancreatitis
In acute pancreatitis the patient is usually acutely ill with central upper abdominal pain, which may radiate to the back. The clinical features of an 'acute abdomen' predominate.
Pancreas
MECHANICAL OBSTRUCTION OF HOLLOW VISCERA
Abdominal colic is the predominant symptom. Depending on the level of obstruction, it is felt around the umbilicus (small intestine) or at the level of the obstruction (colon). Distension of the splenic flexure of the colon by gas may give rise to pain in the left hypochondrium, in the precordial area and even in the left shoulder. The pain is often provoked by constipation and heavy meals. Patients usually suffer from gaseousness and aerophagy as well and are relieved by flatus or bowel movement. Ureteral obstruction provokes pain felt in the patient's side and in the lateral aspect of the abdomen. It often radiates towards the genitals.
INTRA-ABDOMINAL VASCULAR DISORDERS Aneurysm of the abdominal aorta
Figure 43.7
Referred pain in lesions of the pancreas.
This is often asymptomatic. On palpation an expansile, pulsating mass may be found. As an aneurysm expands it may give rise to pain in the abdomen or in the back. Acute rupture gives rise to very acute epigastric' pain, radiating into the back. Shock supervenes and surgical intervention is urgently needed.
CHAPTER 43 - DISORDERS OF THE THORACIC CAGE AND ABDOMEN
661
Mesenteric ischaemia
PSYCHOGENIC PROBLEMS
Mesenteric arterial occlusion sometimes comes on very suddenly, provoking catastrophic abdominal pain. In other cases, the pain is much milder and more progres sive, setting in over 2 or 3 days. Vomiting and bloody diarrhoea usually occur. Careful history for other local izations of vascular abnormalities is always necessary.
PsychogeniC problems may give rise to symptoms and signs in the thoracoabdominal area as well as in the rest of the body. Specific features are absent and the vague history without direct answers to questions, together with several clinical inconsistencies, must put the examiner on guard.
DISORDERS OF THE GENITALS (Fig. 43.8)
A torsion and rupture of an ovarian cyst gives rise to symptoms almost identical to those in acute appendicitis. In subacute torsion, the patient complains of repeated episodes of sharp abdominal pain. Each attack lasts only for a short period of time. Children and adolescents are the chief victims of tes ticular torsion. There is acute pain in the scrotum, some times radiating into the abdomen. Vomiting is often associated.
HYPERVENTILATION
Patients who suffer from hyperventilation are usually tense and anxious. They frequently complain of attacks of pins and needles in hands and feet, often associated with faintness, dizziness and precordial pain. The diagnosis is made by provoking the symptoms by asking the patient to hyperventilate.
PAIN REFERRED FROM MUSCULOSKELETAL STRUCTURES NOT BELONGING TO THE THORACIC CAGE
PARIETAL PERITONEUM Peritonitis
Irritation of the parietal peritoneum can be the result of infection (as in acute appendicitis) or to chemical irrita tion by intestinal contents (as in a perforated ulcer) and inflammatory exudate (in pancreatitis). The pain is steady and aching and is increased by any augmentation of the intra-abdominal pressure. For this reason, the patient prefers to lie still. HERPES ZOSTER
Although herpes zoster is not a visceral disorder as such, it is mentioned here because it may result in unexplained pain for a few days before the typical rash appears. The pain is persistent and burning and varies in intensity from mild to severe. The older the patient the more severe the pain. A rash, consisting of typical grouped vesicles with a unilateral segmental distribution, usually follows within 4 days.
Although some of these have already been discussed as part of the clinical examination, they are brought together here in a more schematic way to complete the account of referred pain. DISC PROTRUSIONS Cervical disc lesion Extrasegmental pain. A posterocentral cervical disc pro trusion often gives rise to extrasegmental pain referred into the thorax, most frequently felt between the scapulae above T6. When pain is present in this area, a detailed examination of the cervical spine is immediately indi cated. In a cervical disc lesion, the pain is seldom referred lower in the posterior thorax or anteriorly into the chest, but when it is, the thoracic examination remains negative except for flexion of the neck. Segmental pain. A posterolateral cervical disc lesion gives rise to segmental referred pain, which is usually absent in the thorax. However, in a C4 root compression, pain is felt just superior to clavicle and scapular spine.
Kidney-Ovary-Testicles
Thoracic disc lesion
Figure 43.8
Referred pain in ovarian or testicular lesions.
Extrasegmental referred pain. A posterocentral disc pro trusion in the thoracic spine is usually accompanied by posterior interscapular pain spreading extrasegmentally. Symptoms and/or signs of a disc protrusion are found on examination of the thoracic spine. Depending on the type, different pain patterns may result: acute thoracic lumbago, sternal lumbago, chronic thoracic pain and cord compression (see Ch. 41).
662 SECTION EIGHT - THE THORACIC SPINE
Band-shaped unilateral pain. This occurs in secondary posterolateral protrusions and is always preceded by posterior extrasegmental pain. A primary posterolateral protrusion provokes, from the onset, anterior pectoral pain in the absence of previous posterior pain. In the lower thorax, pain may be referred to the groin and even to the testicles.
Lumbar disc protrusion Posterocentral lumbar disc l esions. These may occasion ally give rise to abdominal pain, usually accompanied by posterior lumbar pain.
This can provoke pain in the groin, because their corresponding derma tomes overlap in that area. In a secondary posterolateral pro trusion the root pain is first preceded by extrasegmental lumbar pain. Root compression at L 1-L3.
NON-DISC SPINAL LESIONS
Many other types of musculoskeletal disorders of the thoracic spine may refer pain into the chest or abdomen and are discussed in Chapter 42.
Box 43.2 Summary of acute chest pain Severe chest pain of abrupt onset should arouse suspicion of: Myocardial infarction Dissecting aneurysm Pneumothorox Pulmonary embolus Rupture of the oesophagus Acute thoracic disc protrusion
DISORDERS OF THE INERT STRUCTURES LESIONS OF THE STERNUM Fracture and metastases
These give rise to well-localized sternal pain together with tenderness on palpation. A history of injury is usually obtained in the first, while a decline in general health may antedate the second. On clinical examination, all movements hurt as does deep inspiration. A radi ograph usually confirms the diagnosis. Manubriosternal arthritis
This can be the result of ankylosing spondylitis or rheumatoid arthritis.n, 12 Monoarticular steroid- sensitive arthritis is rare at this site.13 The patient complains of spontaneous pain at the angle of Louis. Local tenderness and swelling is found on palpation. In ankylosing spondylitis and rheumatoid arthritis other joints are also involved. Laboratory tests. Tests for rheumatoid disorders should be done. In monoarticular steroid-sensitive arthritis, the manubriosternal joint is the only one affected and labora tory tests are negative. Radiography. Arthritis may show erosion of the joint margin, presence of subchondral cysts, sclerosis of bone adjacent to the joint and widening or narrowing of the joint space. It may lead to total ankylosis, sometimes even to full destruction and subluxation of this joint.14 Treatment. In monoarticular steroid-sensitive arthritis, treatment consists of an intra-articular injection with 2 ml of triamcinolone, partly infiltrated into the superficial ligaments. In rheumatoid arthritis or ankyl osing spondylitis, general treatment of the disorder is undertaken.
DISORDERS OF THE STERNOCLAVICULAR JOINT
DISORDERS OF THE THORACIC CAGE AND ABDOMEN
In this book, disorders are discussed in relation to the clinical examination that is most likely to reveal them. For this reason, many structures such as the sternoclav icular joint, costocoracoid fascia and the first rib, which belong anatomically to the thoracic cage, are discussed under the shoulder girdle, the neck and the shoulder joint. Lesions of the thoracic cage commonly give rise to local pain and are often the result of a direct blow or a forceful activity during sports.
Lesions of the sternoclavicular joint are mainly character ized by local pain at the side of the manubrium or at the base of the neck. The pain is provoked by active and passive elevation of the scapula and arm. Other passive movements are only slightly painful. This combination, in the absence of any other features of a thoracic disc lesion, indicates clinical examination of the shoulder girdle (see Ch. 21). PERICHONDRITIS OF THE COSTOCHONDRAL JOINTS (TIETZE'S SYNDROME)
This may have either a sudden or a gradual onset and gives rise to spontaneous unilateral pain and swelling of
CHAPTER 43
one of the costosternal synchondroses, most frequently that 'of the second rib. In exceptional cases the manu briosternal, the xiphisternal or any other costochondral, or even the sternoclavicular joint, may be affected. It is found at all ages, even in children, and is equally prevalent in males and females.15 It is a self-limiting process often associated with a respiratory infection, although this is not always the rule. Natural history. The initial symptom is pain, which pre cedes the local swelling. Heat and erythema are absent. Usually the pain remains local, although radiation has been reported.16 The intensity of the pain ranges from mild to severe, and is increased by deep inspiration and by coughing. The local fusiform or spindle-shaped mass is exquisitely tender and over-lies the affected jointY When the Xiphisternal joint is affected, the mass and pain often increase after eating as the result of a postprandial anterior displacement of the xiphoid.J8 Local tenderness is the first symptom to disappear, usually between 10 days and 2 months. Spontaneous pain remains longer, up to several months. The swelling tends to reach a maximum size and either remains stationary or regresses slowly but seldom undergoes total regression. Recurrence may occur. Diagnosis. The diagnosis is based on the typical local swelling and tenderness, with normal radiograph. In that ultrasonographic examination of a costal cartilage is easy and quick to perform, it is the screening procedure of choice for Tietze's syndrome.1 9,20
Perichondritis usually responds well to an infiltration with steroid into the painful junction but in costochondritis recurrence is common.21,22 Treatment.
DISORDERS OF THE RIB A fractured rib
Usually the result of a direct blow to the chest. Nevertheless, fractures as a result of coughing or forceful muscular activity of the upper limb or trunk have been reported.23,24 In fracture without an obvious cause, tumour must always be considered. The patient complains of severe, well-localized pain, made worse by deep inspiration which may be arrested before reaching its peak. Every active, passive and resis ted movement of the trunk which has any effect on the fractured rib is very painful. Which particular move ments are positive depends on which rib is fractured and at which part. If the fracture lies in the neighbourhood of the origin of the pectoralis major (second to sixth ribs), resisted adduction and medial rotation of the arm are also painful. Slight movement of the fractured ends provokes sharp well-localized pain. Because a fractured
-
DISORDERS OF THE THORACIC CAGE AND ABDOMEN
663
rib is frequently accompanied by an adjacent intercostal muscle sprain, careful palpation of the muscle must follow. The pain from the fracture is felt on the rib itself, but that caused by a sprain is found in between the ribs. A radiograph confirms the diagnosis. Differential diagnosis must be made from a primary posterolateral disc protrusion in which from the onset the pain is located in the anterior thorax. In disc protrusion, local trauma is not mentioned by the patient, pain is not felt on resisted movements and moving the rib ends on either side of the site of pain is negative. Palpation is not fully reliable because exquisite local tenderness may also be found in disc lesions. Long floating rib
The tip of a long rib may strike the iliac crest on ipsilat eral side flexion and provokes a sharp momentary pain. Severe recurrent symptoms of this kind may indicate removal of the tip of the rib. The rib-tip syndrome
After an injury to the anterior chest, the anterior carti laginous tips of the eighth, ninth or tenth rib can remain detached from the bone and may subluxate inferoposte riorly.25 Contact with the intercostal nerve can give rise to pain. The patient complains of a sharp sudden pain felt at the anterior or inferior margin of the rib on local pressure, during vigorous activity or on deep breathing. Pain can spread posteriorly to the high lumbar level and may remain for some days. Often a popping sensation is felt.26 Diagnosis is based on the typical lancinating pain and the local tenderness on palpation of the tip of the rib. A click is often reproduced on palpation.27 Sometimes active abduction of the arm or ipsilateral side-flexion of the trunk provokes the pain. Treatment. This is an infiltration of a mixture of steroid and local anaesthetic around the nerve at the tip of the rib, which brings immediate and sometimes permanent relief.28, 2 9 If the pain recurs, the cartilaginous tip of the rib should be surgically removed.25
Technique: injection. The patient lies supine, with the arms elevated. The painful tip is located by palpation. The caudal edge is identified and the lesion marked. A 2.5 cm needle is fitted to a 2 ml syringe filled with 1.5 ml of triamcinolone and 0.5 ml of lidocaine (lignocaine) 2%. The needle is inserted vertically at the site of the lesion, aiming at the lower edge at the anterior aspect of the rib, and pushed in until it touches the bone. The needle is then slightly withdrawn and moved more caudally until it passes just beyond the lower edge. The infiltration is done at this point.
664 SECTION EIGHT - THE THORACIC SPINE
Post-thoracotomy pain
A significant proportion of patients who undergo thora cotomy suffer from chronic pain. It is generally not severe but a small proportion of patients may experience persistent moderately disabling pain. The reported incidence of persistent postthoracotomy pain lasting for more than 6 months is between 5 and 40%.30-32 As the pain is cutaneous, it is most probably the consequence of damage to an intercostal nerve. Patients can be treated by a nerve block around the intercostal nerve. This is tried first, with a mixture of local anaesthetic and steroid. Refractory cases require chemical rhizotomy with a 1% solution of phenol. This is usually followed by sensory loss, which is better tolerated than the pain.33 Technique: infiltration (Fig. 43.9). The patient lies prone, the arms elevated and the head resting on the hands. A cushion is placed under the chest. At about 6-7 cm from the midline, the costal angle is identified and a vertical line drawn. To interrupt the nerve before it gives off its lateral and ventral cutaneous branches it is necessary to stay just medial to the costal angle. The inferior edge of the corresponding rib is identified. Just medial to the point of transection between the vertical line and the inferior edge of the rib, a point is marked. A needle of about 3 cm is fitted to a 5 ml syringe filled with 30 mg triamcinolone acetonide and 2 ml lidocaine (lignocaine) 2%. The needle is introduced at the place marked, level with the inferior edge of the rib, and aimed cranially. In doing this, the tip must end up against the
outer aspect of the rib. Once this has occurred, the over lying skin is pulled in a caudal direction, together with the needle, until the needle has lost contact with the rib. The tip now lies just distal to the inferior edge of the rib. In this position, the needle is pushed in a further 0.20.3 mm, aspiration is performed and the injection given.34 If the anterior aspect of the rib is not precisely identified, a pneumothorax may result.34 Tumours of the rib
These may be benign, malignant, primary and secondary.35 Multiple myeloma involves the rib directly. Metastases usually derive from primary tumours of lung, kidney, thyroid and breast. The initial symptom is well-circumscribed pain, spreading and increasing in severity later as the tumour grows or when it invades other neighbouring structures such as the intercostal nerves. Pathological fractures may result. HERPES ZOSTER
This disorder usually affects only one nerve and initially pain is present in its territory. After some days the skin turns red locally, shortly followed by the appearance of grouped vesicles. The diagnosis thus becomes clear.
DISORDERS OF THE CONTRACTILE STRUCTURES MUSCLES OF THE THORACIC CAGE Sprained intercostal muscle
This is usually the result of a direct injury to the chest. It may exist alone or in association with a fracture of a rib. The patient complains of a well-localized pain, which does not radiate. Deep inspiration is painful, as are all trunk movements that stretch the affected intercostal muscle. More than one muscle can be involved, so the whole of the painful area must be carefully palpated. Differential diagnosis must be made from a fractured rib. In a sprain of the intercostal muscle, palpation is pos itive between the ribs and not on the rib itself. If the rib is also found to be tender, a fracture is most likely and a radiograph must be obtained. The lesion responds very well to a few sessions of deep transverse friction.
Treatment.
Figure 43.9
Infiltration in postthoracotomy pain syndrome.
Technique: deep friction (Fig. 43.10). The patient adopts a half-lying position and the therapist sits at the c9ntra lateral side. The tender point(s) in between the ribs are palpated and the middle finger, reinforced by the index finger are placed there. The fingers are now moved to and
CHAPTER 43
-
DISORDERS OF THE THORACIC CAGE AND ABDOMEN
665
Lesions of the latissimus dorsi
This may provoke pain in the posterior thorax, some times even at the posterior aspect of the axilla. Pain is elicited on full passive elevation of the arm, resisted adduction and medial rotation. The basic thoracic exami nation is usually negative. Treatment is either by deep transverse friction or an infiltration with procaine (see Ch. 18). Sprain of the serratus posterior inferior muscle
This may occur in athletes (Cyriax:13 p. 201). Local pain is felt dorsally in the lower thorax or upper lumbar area and is increased by ipsilateral resisted side flexion and rota tion of the trunk. Treatment is deep transverse friction. LESIONS OF THE DIAPHRAGM
Figure 43.10
Deep friction to an intercostal muscle.
fro in line with the ribs, movement obtained by a combi nation of flexion-extension at the elbow and shoulder. Every lesion should be treated each time, for about 15-20 minutes. Because this type of lesion responds very well to deep transverse friction, cure is obtained in about three to five sessions. Lesions of the pectoralis major
The localization of the pain draws attention to the thorax, which is why this disorder is included here. However, it is the examination of the shoulder which establishes the diagnosis (see Ch. 15). In a lesion of the pectoralis major, resisted adduction and internal rotation of the arm are painful. The patient is asked to press both hands against each other with the arms stretched out horizontally in front of the body, which Is even more painful. The lesion usually lies in the muscle belly at the infra clavicular portion or at the lateroinferior part of the muscle, almost in the axilla. This disorder must be differentiated from a fractured rib, which may give rise to pain on the same shoulder tests. Fracture is associated with pain on deep inspira tion and on coughing, as well as with some movements of the trunk. Palpation of the tender spot, with and without contraction of the pectoralis muscle, can be compared. More pain on contraction suggests a problem in the muscle, more pain with the muscles relaxed suggests that the cause is in a rib or the intercostal muscles. Treatment is deep friction or an infiltration with procaine (see Ch. 18).
A severe blow on the chest can be transmitted to the diaphragm, causing a sprain. Pain is felt on respiration, and is not provoked or altered by movements of the trunk. In this condition, all movements of the trunk should be tested while the breath is fully held, because otherwise the patient may give false-positive responses related to respiration and not to the tests as such. When the central fibrous portion of the diaphragm is affected, pain is referred to the tip of the shoulder, whereas a lesion at the insertion at the ribs provokes more local pain at the lower margin of the thoracic cage. The peripheral costal insertion can be treated by deep transverse friction.
Treatment.
Technique: friction (Fig. 43.11). The patient adopts a ha]£ lying position and fully relaxes the abdominal muscles. The therapist sits at the patient's painful side. The lesion is palpated at the inner side of the lower ribs. The finger tips of three or four fingers are hooked under them. Friction is obtained by a movement parallel to the rib, meanwhile applying anterior pressure against its posterior aspect. LESIONS OF THE ABDOMINAL MUSCLES
Pain in the abdomen is usually the result of a visceral disorder. Exceptionally it arises from a musculoskeletal lesion, most frequently a thoracic or lumbar disc problem giving rise to segmental or extrasegmental referred pain. Local muscular problems of the abdominal wall may also occur. They are usually encountered in athletes, very often soccer players. Pain is usually under the influence of movement and local pressure, sometimes of lifting and coughing. When this type of lesion is sus pected, resisted flexion and rotations of the trunk must
666 SECTION EIGHT - THE THORACIC SPINE
Figure 43. 1 1
Deep friction t o the peripheral costal insertion o f the diaphragm.
Figure 43.12
be checked. Active extension or active contralateral side flexion of the trunk can also be painful as the muscle is stretched. If, after a complete examination, the differen tial diagnosis between a visceral and a muscular problem remains unclear, palpation with the abdominal muscles relaxed is compared with palpation with the muscles in contraction. Greater pain on palpation with the muscles relaxed points towards a visceral problem, the opposite to a lesion of the abdominal muscles (Cyriax:13 p. 219; Ramboer and Verhamme26). Lesions of the rectus abdominis muscle
These are usually located in the most distal 4 cm of the muscle belly, just above the pubic symphYSiS. The patient complains of local suprapubic pain during activity. Pain is found on resisted anteflexion of the trunk and on active trunk extension. Bringing the patient's ipsilat eral arm upwards and backwards during active exten sion of the trunk increases the pain because of further stretching of the rectus muscle. Differential diagnosis
The differential diagnosis includes lesions of the rectus femoris or the psoas muscles and osteitis pubis (see p. 1035). In the former two, the pain lies more laterally and is also provoked by resisted flexion of the hip which provides the diagnostic key. In osteitis pubis the pain is at the pubic symphysis and is also provoked by resisted adduction of the hips. The fact that the pain is reproduced during the examination of both lower extremities should help in the differentiation.36,37 An infiltration of 10-20 ml 0.5% procaine is normally curative.26 Deep friction is also effective.
Treatment.
Injection of a lesion of the rectus abdominus muscle.
Technique: injection (Fig. 43.12). A 4 cm needle is fitted to a 10-20 ml syringe filled with 0.5% procaine. The patient is put in the half-lying position, keeping the abdominal muscles well relaxed. The tender part of the muscle is taken between thumb and index finger and the needle thrust in obliquely in a caudal direction. Special care must be taken not to push the needle in too deeply. With several withdrawals and reinsertions the procaine is infiltrated. The patient is reassessed 1 week later. If full cure has not been achieved, a second infiltration is given. Three infiltrations may be necessary. Technique: deep friction (Fig. 43.13) The patient is put in the half-lying position with the abdomen well relaxed. The therapist sits at the painless side and places two or three fingers on the tender spot. Counterpressure is taken with the thumb. Friction is a to-and-fro movement by flexion-extension of the elbow. The oblique muscles
A sprain of one of the oblique muscles gives rise to pain in the anterolateral part of the abdomen. Pain is provoked or increased by resisted rotation of the trunk: pain on resisted rotation away from the painful side signifies a lesion of the external oblique muscle; pain on resisted rotation towards the painful side originates from the internal oblique muscle. Stretching the affected fibres also hurts. Consequently active extension of the trunk or active side flexion towards the painless side is also likely to be painful� The lesion can lie either at the costal origin or in the muscle belly. In the former, palpation should be done at
CHAPTER 43 - DISORDERS OF THE THORACIC CAGE AND ABDOMEN
667
Figure 43.13 Deep friction to a lesion of the rectus abdominus muscle.
the inferoposterior margin of the ribs, with the finger pressing against the internal aspect of the rib for the inter nal oblique muscle or against the external aspect for the external oblique muscle. lesion at the origin of the external oblique muscle or in the muscle belly is treated by deep trans verse friction. The origin at the ribs of the internal oblique muscle can be treated only by deep friction, using the same technique as for the costal origin of the diaphragm (see above).
Treatment. A
Technique: deep friction to the muscle belly (Fig. 43.14). The patient is put in a half-lying position with the therapist sitting at the side opposite to the lesion. The tips of two or three fingers are placed on the painful area. Friction is given by a flexion-extension movement at the elbow, transverse to the direction of the fibres i.e. in the direction contralateral shoulder-ipsilateral hip. Each session takes about 15 minutes. Cure is normally obtained in about 10-15 sessions.
Figure 43.14 Deep friction to the muscle belly of the external oblique.
668 SECTION EIGHT - THE THORACIC SPINE
REFERENCES 1 . Master A. The spectrum of anginal and noncardiac chest pain. lAMA 1964;187:894-899. 2. Rawlings M. Differential diagnosis of painful chest. Geriatrics 1963;Feb:139-150. 3. Erb B, Tullis I. Dissecting aneurysm of the aorta. Circulation 1 960;22:315. 4. Spengler D, Kirsh M, Kaufer H, Arbor A . Orthopaedic aspects
and early d i agnosis of superior sulcus tumour of lung (Pancoast). I Bone loint Surg 1 973;55A(8) : 1645-1650. 5. Brown C. Compressive, invasive referred pain to the shoulder. Clin Orthop Rei Res 1983;173:55-62. 6. Bisbinas I, Langkamer VG. Pitfalls and delay in the diagnosis of Pancoast tumour presenting in orthopaedic units. Ann R Coli Slirg EngI 1 999;81(5):291-295. 7. Demaziere A, Wiley AM. Primary chest wall tumor appearing as frozen shoulder. Review and case presentations. ] Rheumatol 1991 ;18(6):911-914. 8. Dartevelle P, Macchiarini P. Surgical management of superior sulcus tumors. Oncologist 1999;4(5) :398-407. 9. Johnson DE, Goldberg M. Management of carcinoma of the
superior pulmonary sulcus. Oncology 1997;11(6):781-785. P, Clark M. Clin ical Medicine, 3rd edn. Bailliere Tindall, London, 1 994:607. Grosbois B, Pawlotsky Y, Chales G, Meadeb J, Carsin M, Louboutin J. Etude cliruque et radiologique de l'articulation manubriosternale. Rev Rhum 1981 ;48:495. Sebes J, Salazar J. The manubriosternal joint in rheumatoid disease. Am J Rheul7latoI 1983;140 : 1 1 7. Cyriax J. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesiolls, 8th edn. Bailliere Tindall, London, 1982. Goei The HS. The Clinical Spectrum of Chronic Inflammatory Back Pain in Hospital Referred Patients. Rijksuniversiteit Leiden Drukkerij Schrijen-Lippertz BV, Voerendaal, 1987. Kayser H. Tietze's syndrome: a review of the literature. Am J
10. Kumar 11.
12. 13. 14.
15.
Med 1956;21 :982-989. 16. DLiben W. Das Tietzesyndrom und seine differentialdiagnost ische Bedeutung. Dtsch Med Wochenschr 1 952;77:872-875.
E, Rhim HR, Reddy A, Karten 1, Taranta A. Costochondritis. A prospective analysis in an emergency department setting. Arch Inter Med 1994;154(21):2466-2469. 18. Jelenko C. Tietze's syndrome at the xiphisternal joint. South Med
1 7. Disla
1 1 974;67:81 8-820.
19. Kamel M, Kotob H. Ultrasonographic assessment of local steroid
injection in Tietze's syndrome. Br I Rheul11atoI 1997;36(5):547-550. 20. Choi YW, 1m JG, Song CS, Lee JS. Sonography of the costal car tilage: normal anatomy and preliminary clinical application. I Clin Ultrasound 1 995;23(4) :243-250. 2 1 . Gray R, Gottlieb N. Intra-articular corticosteroids. An updated assessment. Clin Orthop Rei Res 1983;177:236-263. 22. Dunlop R. Tietze revisited. Clin Orthop Rei Res 1969;62:223-225. 23. Mitchell J. Cough fracture. BM] 1 951;2: 1492-1493. 24. Lageze P, Torante R, Riffat G. Fracture de cote par la toux. Lyon Mid 1953;188:489-491 . 25. McBeath A, Keene J . The rib-tip syndrome. J Bone Joint Surg 1975;57A(6):795-797. 26. Ramboer C, Verhamme M. Abdominale Wandpijn. Tijdschr Geneeskd 1 993;49(7):445-449. 27. Scott EM, Scott BB. Painful rib syndrome - a review of 76 cases. Gut 1993;34(7) : 1006-1008. 28. Barki J, Blanc P, Michel J et al. Painful rib syndrome (or Cyriax syn drome). Study of 100 patients. Presse Med 1996;25(21):973-976. 29. den Dunnen WF, Verbeek Pc, Karsch AM. Abdominal pain due to nerve compression. Ned Tijdschr Geneeskd 1999;143(11):576-578. 30. Marin I, Lepresle C, Mechet MA, Debesse B. Postoperative pain
after thoracotomy. A study of 116 patients. Rev Mal Respir 1991;8(2):213-218. 31. Kalso E, Perttunen K, Kaasinen S. Pain after thoracic surgery. Acta Anaesthesiol Scand 1992;36(1):96-100. 32. Perttunen K, Tasmuth T, Kalso E. Chronic pain after thoracic surgery: a follow-up study. Acta Anaesthesiol Scand 1999;43(5) :563-567. 33. Skubic J, Kostuik J. Thoracic pain syndromes and thoracic disc herniation. In: The Adult Spine. Prillciples and Practice. Raven Press, New York, 1 99 1 : 1443-1 461 . 34. Jenkner F . Nervenblockaden auf pharlllakologischelll U lld allf elekfrischelll Weg. 3rd edn. Springer, Vienna, 1980:33. 35. Marcove R. Chondrosarcoma: diagnosis and treatment. Orthop Clin North AI11 1977;8(4) : 1 443-1461 . 36. Fricker PA, Taunton JE, Ammann W. Osteitis pubis ill athletes. Infection, inflammation or injury? Sports Med 1991 ;12(4): 266-279. 37. Briggs RC, Kolbjornsen PH, Southall RC. Osteitis pubis, Tc-99m MDP, and professional hockey players. elill Nuci "Med 1992;17(11):861-863.
CHAPTER CONTENTS Cl inical findings
669
Ankylosing spondylitis Ankylosing spondylitis ligament 670 Ankylosing spondylitis Ankylosing spondylitis Ankylosing spondylitis
of the thoracic spine 669 of the anterior longitudinal of the thoracic facet joints 670 of the costovertebral joints 670 of the manubriosternal joint 670
Ankylosing spondylitis of the thorax
Further investigations 670 Laboratory tests 670 Radiography 670 Treatment
670
About 0.1% of the total population has ankylosing spondylitis (AS). It affects mainly the attachment of liga ments to the axial skeleton. Solitary involvement of tho racic spine and cage is seldom encountered because this is normally part of a generalized ankylosing spondylitis. Only 2-5% of all patients have chest pain as an initial symptom.1,2 The condition usually starts in the sacroiliac joints and extends upwards to the spine, often first to the thoraco lumbar junction, later to the lumbar, thoracic and cervical spines. Although involvement of the sacroiliac joints may remain silent, spinal localization of ankylosing spondyli tis without sacroiliitis is very rare.3
CLINICAL FINDINGS ANKYLOSING SPONDYLITIS OF THE THORACIC SPINE Patients complain of a chronic stiff back, especially early in the morning and easing with activity. Periods of wors ening of pain and stiffness come on spontaneously and are not provoked by activity or exercise. During the pain free periods, the patient is effectively normal. Only slight radiation to the sides is present. Because several levels are usually involved and little referred pain is present, the pain is distributed in the vertical axis. All these are important differences from disc lesions, in which pain is usually referred horizontally, is worse during daytime and is brought on by activity. The findings on inspection depend on the duration of the disorder. Initially, a rigid lumbar segment is present, which later becomes flat, together with a slight accentu ation of the thoracic kyphOSiS. This develops further to a thoracic hyperkyphosis with hyperextension of the upper cervical spine and flexion of the hip.4 Chest expansion may be diminished. On functional examination, a clear capsular pattern is present with an equal amount of pain and limitation of both side flexions and rotations, more pain and limita tion on extension and only slight discomfort on flexion. The end-feel on rotation and extension is typically hard. The range of rotation has a significant negative correla669
670 SECTION EIGHT - THE THORACIC SPINE
tion with the duration of the disease.s Pain provoked by pressure on the spinous processes is usually much more severe than in an ordinary disc lesion.6 At a later stage, the vertebrae are much more vulnerable to fractures, because of loss of normal capsular and ligamentous elasticity.
ANKYLOSING SPONDYLITIS OF THE MANUBRIOSTERNAL JOINT This joint is affected in 50% of all cases.12 Forced inspira tion may be painful. Palpation reveals a precise area of local tenderness together with swelling of the ligaments.
The capsular pattern with hard end-feel, chronic pro longed morning stiffness and pain with periods of spon taneous exacerbations, together with other localizations
FURTHER INVES TIGATIONS
of the same disorder, all in young patients (mainly 18-30 years), strongly indicates AS. A radiographic examination should be done at once and must always include the sacroiliac joints.
ANKYLOSING SPONDYLITIS OF THE ANTERIOR LONGITUDINAL LIGAMENT
LABORATORY TESTS The erythrocyte sedimentation rate may be elevated in active disease. A mild anaemia may be present. HLA
B27, although not diagnostic as such, is present in over 90% of cases, whereas in a normal population it is only found in 8%.6
Involvement of the anterior longitudinal ligament gives rise to pain felt only at the sternum or in the epigastrium, without central dorsal pain. The pain has the same char acteristics as in other localizations of AS at the thoracic spine.
ANKYLOSING SPONDYLITIS OF THE THORACIC FACET JOINTS The apophysial joints are usually involved, together with the intervertebral joints. The former are mainly responsi ble for bilateral paravertebral pain. Ankylosing spondyli
RADIOGRAPHY Sacroiliac joint Early confirmation of AS is based mainly on radiography of the sacroiliac joints. Initially, this shows loss of outline and pseudowidening. Later, subchondral sclerosis and joint bridges may develop, ultimately with total fusion of the joint.
Spinal changes •
tis may lead to total fusion of the facet joints.
'Squaring': erosion of the superior and inferior anterior rim and ligamentous ossification make the vertebrae square; this is best seen in a lateral view.
ANKYLOSING SPONDYLITIS OF THE COSTOVERTEBRAL JOINTS Costovertebral and costotransverse joints are often
•
'Bamboo'spine: later, because of ossification of the outer fibres of the intervertebral discs and spmal ligaments, the characteristic 'bamboo' spine develops. Osteoporosis may also be found in late stages.
affected in ankylosing spondylitis. Computed tomogra phy (CT) scans usually show the classical lesions: ero
Manubriosternal joint
sions, sclerosis, joint widening and bridging.7 It is
The earliest information that can be gained on AS is
accepted that these changes provide the anatomical basis
sometimes a radiograph of the manubriosternal joint.
for the understanding of the thoracic pain in ankylosing
Normally, the joint surfaces of the manubriosternal joint
spondylitis patients.8 Although the pain is usually rather
are flat. In AS they may become biconcave.
dull, it may sometimes be severe, even mimicking renal colic.9 Chest expansion is diminished. Therefore chest expansion should always be assessed when AS is sus
TREATMENT
pected. It is measured level with the nipples. Normal dif ference between inspiration and expiration is at least
The aim of treatment is to keep pain and stiffness under
7 cm. Less than 4 cm is regarded as abnormal.10
control, to maintain mobility and a straight spine and as
Surprisingly enough, reduced chest expansion seldom
satisfactory a respiratory excursion as possible.
interferes with normal lung and heart function, because
The basic treatment is administration of anti-inflamma
of normal diaphragmatic mobility.11 If it does chronic cor
tory drugs and a daily exercise programme. Exercises,
pulmonale is to be expected, with shortness of breath.
sports and swimming are strongly recommended.
The latter may also be the result of upper lobe fibrosis from involvement of the lung by AS.
Significant involvement of the costovertebral joints 'may affect their mobility, and care should be taken to prevent
CHAPTER 41
-
ANKYLOSING SPONDYLITIS OF THE THORAX 671
this. Deep breathing should be practised regularly and can
increase joint movement on inspiration and expiration
be assisted by a therapist. Mobilization exercises to
must also be performed.
REFERENCES l.
Borenstein D, Wiesel S. Low Back Pain. Saunders, Philadelphia,
thoracic
1989:179.
1992;39(1):15-17.
2.
Macnab I. Backache. Williams & Wilkins, Baltimore 1983:70.
3:
Cheatum D. Ankylosing spondylitis without sacro-iliitis in a
8.
Veys E, Mielants H, Verbruggen G. Reumatologie. Omega
Pascual E, Castellano ]A, Lopez E. Costovertebral joint
Benhamou C, Roux C, Tourliere D, Gervais T, Viala
L
10.
Veys E, Mielants H, Verbruggen G. Reumatologie. Omega
11.
Zorab P. Respiratory tract disease. Chest deformities. BMf
12.
Goei The HS. The Clinical Spectrum of Chronic InJlallllnatory Back
Editions, Ghent, 1985.
880-883.
Cyriax]. Textbook of Orthopaedic Medicine, vol. 1, Diagnosis of Tissue
Reumatizalll
arthropathies. Spine 1993;18(6):790-795.
Viitanen]. Thoracolumbar rotation in ankylosing spondylitis.
Soft
spondylitis.
Arnor B. Pseudovisceral pain referred from costovertebral
A new noninvasive measurement method. Spine 1993;18(7): 6.
ankylosing
J RheumatoI1992;31(6):413-415. 9.
Editions, Ghent, 1985:447. 5.
in
changes in ankylosing spondylitis with thoracic pain. Br
woman without the HLA-B27 antigen. J Rheumatol 1976; 3:420. 4.
spine
Lesions,
8th edn.
Bailliere Tindall,
London,
1982:214. 7. Jelcic A, Jajic 1, Furst Z. Radiologic changes in the costoverte
bral and costotransverse joints and functional changes in the
1966:7 May:1135-1156. Pain in Hospital Referred Patients.
Rijksuniversiteit Leiden
Drukkerij Schrijen-Lippertz BV, Voerendaal, 1987.
THIS PAGE INTENTIONALLY LEFT BLANK
SECTION NINE
The temporomandibular joint SECTION CONTENTS 45. Applied anatomy of the temporomandibular joint Bones 675 Joint capsule and ligaments 675 Intra-articular meniscus 676 Nociceptive innervation 676 Muscles and tendons 676 Biomechanical aspects 677 Nerves and blood vessels 678
675
46. Clinical examination of the temporomandibular joint Pain 679 History 680 Inspection 681 Functional examination 681 Palpation 684 Technical investigations 684
679
47. Interpretation of the clinical examination of the temporomandibular joint 48. Disorders of the temporomandibular joint 689 Disorders of the inert structures 689 Internal derangement 691 Arthrosis 692 Luxation of the condyle 694 Synovial disorders 694 Disorders of the contractile structures 695 Myalgia 695 Muscular trismus 696 Abscess in the pterygoid muscle 696
684
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
Bones
675
Joint capsule and ligaments Intra-articular meniscus
676
Nociceptive innervation
676
Muscles and tendons
675
Applied anatomy of the temporomandibular joint
676
677 Forward movement of the mandible 677 Opening and closing the mouth 677 Grinding movements 677
Biomechanical aspects
Nerves and blood vessels
678
The temporomandibular joint (TMJ) is sited at the base of the skull and formed by parts of the mandible and the temporal bone, separated by an intra-articular meniscus. It is a synovial joint capable of both hinge (rotation) and sliding (translatory) movements. Like other synovial joints, it may be affected by internal derangement, inflamma tory arthritis, arthrosis, and muscular disorders.
BONES
The mandible has a horizontal part (the body) and a vertical part (the ramus). They meet at the mandibular angle. The cranial end of the ramus has two processes: anteriorly the coronoid process and posteriorly the condylar process, which has a head on top and a distinct neck below. The squamous portion of the temporal bone contains the articular surface with a concave articular fossa posteriorly and a convex articular tubercle anteri orly. The articular surface is about three times as large as that of the mandibular head and is covered with fibro cartilage which continues anteriorly into the articular tubercle, the posterior aspect of which is the most important part of the joint. From the temporal bone develops a zygomatic process which, together with the temporal process of the zygomatic bone, forms the zygomatic arch (Fig. 45.1). The midline fusion of the left and right mandibular bodies provides a connection between the two temporo mandibular joints, so that movement in one joint always influences the opposite one.
JOINT CAPSULE AND LIGAMENTS
The joint capsule is wide and loose on the upper aspect around the mandibular fossa. Distally, it diminishes in a funnel shaped manner to become attached to the mandibular neck (Fig. 45.2). Its laxity prevents rupture even after dislocation. Laterally and medially, a local reinforcement of the joint c�psule is found. The lateral collateral ligament courses from the zygomatic arch obliquely downwards 675
676 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
\
-'-------:-"....=-...,..,"---'.-"-- 5 --"'7'L-----6
5
2 Figure 45.2 The joint capsule and the intra-articular meniscus: 1, condylar process; 2, mandible; 3 meniscus; 4, joint capsule; 5, articular fossa; 6, articular tubercle.
6
4
Figurer 45.1 Osseous structures of the temporomandibular joint: 1, mandibular head (condylar process); 2, neck of mandibule; 3, ramus; 4, body; 5, coronoid process; 6, mandibular angle; 7, zygomatic arch.
surface to the anterior portion of the condyle. The meniscus always follows the movement of the condyle: when the mandibular head glides anteriorly on opening the mouth, the meniscus moves anteriorly; when it moves back on closing, so does the meniscus.
NOCICEPTIVE INNERVATION
and backwards towards the posterior rim of the mandibular neck, lateral to the outer aspect of the capsule. At its posterior aspect, it is in close relation to the joint capsule and prevents the joint from opening widely. Medially, the joint capsule is locally reinforced by the medial collateral ligament. There are also two extracapsular ligaments: the sphenomandibular (between the spine of the sphenOid bone and the lingula of the mandible) and the stylomandibular (from the styloid process of the temporal bone to the mandibular angle).
The articular cartilage, the synovial tissues and the central portion of the disc do not contain any pain receptors and therefore cannot give rise to pain. All other capsular and intra-articular structures do possess nociceptors; the meniscus has them mainly at the poste rior edge, less on its anterior portion. They are chiefly activated by high mechanical stresses and by acute or chronic inflammation.
MUSCLES AND TENDONS INTRA-ARTICULAR MENIS CUS
The intra-articular meniscus, or disc (Fig. 45.2), is attached along its entire circumference to the capsule. It compensates for the discongruent articular bony sur faces and contributes to the stability of the joint. The meniscus divides the joint into an upper and a lower compartment, each fully separated from the other (see Hodges, 1990, in bibliography). The upper compartment is a sliding joint, the lower a hinge. Because the menis cus is malleable, it fills the whole joint space in any posi tion of the condyle. Its anterior aspect is connected to the lateral pterygoid muscle. Posteriorly, the condyle is attached to the meniscus by loose connective tissue - the bilaminar zone - which is also fused to the posterior capsule. The superior surface of the meniscus relates to the middle third of the articular tubercle, the inferior
The most important contractile structures are the mas seter, temporal and pterygoid muscles (Fig. 45.3). The masseter muscle originates at the lower edge (superficial part) and deep aspect of the zygomatic arch and at the temporal fascia (deep part). Both parts course superficially from the mandibular ramus towards the angle, where they have broad insertions into the tuber osity. Contraction of the masseter closes the mouth. The origin of the temporalis muscle is in the temporal fossa and at the temporal fascia. It stays deep to the zygomatic arch and inserts into the coronoid process of the mandible. It also closes the mouth. The medial pterygoid originates in the pterygoid fossa at the base of skull and inserts into the deep aspect of the mandibular angle at the pterygoid tuberosity. It acts synergistically with the masseter and temporalis muscles.
CHAPTER 45 - APPLIED ANATOMY OF THE TEMPOROMANDIBULAR JOINT 677
2 Figure 45.3
5
Muscles of the temporomandibular joint: 1, temporalis; 2, masseter; 3, joint capsule; 4, lateral pterygoid; 5, medial pterygoid,
The lateral pterygoid muscle lies on the deep aspect of the mandibular neck. It has two heads: one originat ing at the major wing of the sphenoid bone, the other at the lateral aspect of the pterygoid process. The two heads course laterally and posteriorly, join each other and insert into the pterygoid fovea of the mandibular condyle, the joint capsule and the meniscus. Because the muscle courses in an anteromedial to posterolateral direction, bilateral simultaneous action of both lateral pterygoids pulls the mandibular condyles anteriorly, which opens the mouth. Unilateral contraction provokes a contralateral deviation of the chin. The medial and lateral pterygoid muscles are too deep to be palpated. The suprahyoid muscles - digastric and stylohyoid and the muscles of the floor of the mouth - mylohyoid and geniohyoid - only take part in opening of the mouth when the effect of gravity is excluded, for example lying down. They are of little clinical importance.
BIOMECHANICAL ASPECTS
mandible is pulled backwards on closing by the posterior fibres of the temporalis muscle.
OPENING AND CLOSING THE MOUTH
Because the TMJ contains a meniscus, two independent movements are possible: a rotation or hinge movement and a translatory glide. From the onset of opening to the midpoint, the mandibular head rotates on the undersur face of the intra-articular meniscus because of the effect of gravity and the action of the muscles of the floor of the mouth. At the same time, the collateral ligaments are taut. On further movement, condyle and meniscus glide together anteriorly and slightly caudally on the articular tubercle because of contraction of the lateral pterygoid. No further rotation occurs once the anterior translatory movement has begun. If for some reason the anterior movement of the mandibular head on opening is not possible on one side, the chin deviates to the ipsilateral side. The mouth is closed by contraction of the temporalis, masseter and medial pterygoid muscles.
The mandible allows three types of movement. GRINDING MOVEMENTS FORWARD MOVEMENT OF THE MANDIBLE
The lateral pterygoid muscle pulls the mandible forwards (anterior translatory movement). During this process the mandible moves slightly downwards because the condyle is pressed down on the articular tubercle. The
The mandible rotates around a vertical axis through the contralateral mandibular head by a unilateral contraction of the lateral pterygoid muscle. This is followed by a con traction of the posterior fibres of the temporal muscle, which repositions the head of the condyle. When this occurs on alternate sides, a typical grinding movement
678 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
results. If at the same time the other masticatory muscles contract, food can be crushed.
2 ---1----1+'1 3---1----\
NERVES AND BLOOD VESSELS
Between the tragus and the mandibular condyle lie the superficial temporal artery and veins. The superficial temporal artery is the continuation of the external carotid artery and the veins course towards the internal jugular vein. Deep to the neck of the mandible passes the maxil lary artery, a branch of the external carotid. The auriculotemporal nerve, a branch of the mandi bular nerve, which again originates from the trigeminal nerve (V), is just posterior to the blood vessels, which it follows cranially. The upper branch of the facial nerve (VII) passes superficially to the blood vessels at the level of the mandibular neck and runs horizontally for wards before breaking up into several terminal branches (Fig. 45.4).
4 Figure 45.4 Nerves and blood vessels around the temporomandibular joint: 1, superficial temporal vein; 2, superficial temporal artery; 3, auriculotemporal nerve; 4, upper branch of facial nerve.
BIBLIOGRAPHY Fautrez J. Leiddrnad bij de Studie vall de Stelselmatige Olltleedkullde vall de mens, vol l. Uitgevers Desoer, Luik, 1967. Gerritsen B, Heerkens Y. Anatomie in vivo van het Bewegingsapparaat. Bunge, Utrecht, 1986.
Hodges JM.
Managing temporomandibular
joint
syndrome.
Laryngoscope 1990;100:60-66. McMinn R, Hutchings R. Atlas of HUl1lal1 Anatomy, 2nd edn. Wolfe, London, 1993. Sobotta
J,
Becher H. Atlas der Allatomie des MellscileH, vols 1 and 3.
Urban & Schwarzenberg, Munich, 1967.
CHAPTER CONTENTS Pai n
679
Pain referred from the temporomandibular joint 679 Pain referred to the temporomandibular joint area 680
History
680
Inspection
Clinical examination of temporomandibular joint
681
Functional examination
681
Active movements 681 Resisted movements 682
Palpation
The most characteristic symptoms of disorders of the
684
Technical investigations
684
temporomandibular joint (TMJ) are orofacial pain, noises in the joint, limitation of movement - mouth opening - or a combination
of these.
Limitation
may present suddenly as locking or may be slowly progressive.
PAIN Pain in the TMJ area usually has a local cause and is seldom referred to any distance. The patient should also be asked about the influence of chewing, yawning, swallowing or talking. If pain is present on one of these, a disorder of the TMJ is most likely. Some disorders of the cervical spine (see Section 2) and the parotid gland may exceptionally also provoke pain on swallowing. A clear description of the type of pain should always be sought. A sharp severe pain tends to suggest an arthro genic problem, a diffuse ache of less intensity points more to a muscular disorder. A painful click may be the consequence of subluxa tion of the intra-articular meniscus. Pain coming on spontaneously and progressively increasing over some weeks is often the result of arthritis. Continuous dull pain felt in the area of the masticatory muscles and usually worse at the end of the day may indicate myalgia.
PAIN REFERRED FROM THE TEMPOROMANDIBULAR JOINT Pain of the TMJ structures may arise from the masticatory muscles or from the joint itself. The main inert structures that can give rise to pain are the intracapsular tissues located posterior to the condyle: the posterior part of the meniscus, the meniscus attachments to the capsule, the capsule and the retromeniscal fat pad.1 Pain is often accompanied by headache, earache or pain in the post auricular area. Pain arising from the TMJ sometimes refers to the maxilla. 679
680 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
PAIN REFERRED TO THE
Non-neurological disorders
TEMPOROMANDIBULAR JOINT AREA
Otitis media, otitis externa and parotitis. These all give
Occasionally pain is referred from the neck. When there
rise to pain in the TMJ area. Pain usually remains local
is doubt, a preliminary examination of the neck must be performed. Other structures may give rise to painful conditions in the TMJ area and can be divided in neurological and non neurological disorders.
and increases on pressure on the tragus (otitis) or parotid gland (parotitis epidemica). These conditions mainly affect children and are usually accompanied by fever. Paranasal sinusitis. This results in a constant, knocking
pain usually felt around the orbits, sometimes radiating towards the cheek and into the teeth.
Neurological disorders
Infection of the teeth and dental abscess. Tooth infec
Atypical facial neuralgia. This can be uni- or bilateral
tions are followed by pain in the cheek on percussion
and is of unknown origin. It usually causes a burning sensation, pins and needles, and continuous pain, in cycles of severity: it may occur after dental procedures. Trigeminal nerve neuritis. This may be encountered in
patients of 45-60 years of age. It affects females more often than males and the right side more frequently than the left. The patients complain of unilateral shooting pain, from the ear towards the temporal area and the maxilla, sometimes even in the forehead and towards
which is provoked or increased by eating sugary food. An abscess gives rise to local swelling of the gingiva. Cluster headache (Horton's neuralgia). This predomi
nantly affects males, is unilaterally localized, and is associated with increased lachrymation, rhinitis and ipsilateral facial redness. Attacks of severe headache in or around the eyes, usually unilaterally, come on within
5-10 minutes and last from about 45 minutes to a few hours. Attacks occur in clusters.6
the pharynx. The cause of the pain may be so obscure
Temporal arteritis. This is one of the manifestations of a
that unnecessary dental extraction takes place. Pain is
giant-cell arteritis, an autoimmune process? It is usually
seldom accompanied by diminished sensitivity but
seen unilaterally in males over 50 years of age and is
characteristic trigger points are often found. Stimulation
frequently associated with polymyalgia rheumatica. It is
of these, even sometimes by light touch, results in pain
characterized by a knocking pain around the temporal
felt elsewhere, which is followed by a refractory period
vessels. The skin overlying the artery is red, swollen and
of up to 30 seconds during which stimulation does not
warm. The erythrocyte sedimentation rate is raised.
lead to new pain. The pain attacks seldom last longer than a few seconds. They may recur at irregular inter vals, sometimes on a daily, weekly or even a monthly basis. They are isolated or come on in clusters.2 Herpes zosteroticus infection. This can give rise to
dysaesthesia preceding the characteristic vesicles. No
leaking cerebral aneurysm. It has an explosive onset of
headache, nausea and vomiting, together with photopho bia and stiffness of the neck. Aneurysm at the level of the posterior communicating artery may be followed by pain in the first division of the trigeminal nerve. It is the com monest cause of so-called ophthalmoplegic migraine.s
true trigger points are present. About 15% of all periph eral facial palsies is caused by this virus.3
HISTORY
Idiopathic peripheral facial palsy (Bell's palsy). This is a
disorder of the facial nerve, probably the result of a cranial neuritis.4,s It mainly affects patients between 20 and 50 years of
Questions are asked about the onset of pain, its nature, localization, intensity and duration. The examiner should discover which factors increase or relieve pain.
age. It is seldom painful although at the onset some pain around the ear may be felt. It gives rise to a palsy of the facial muscles, characterized by lowering of the ipsilat eral side of the mouth. It may also cause diminished pain
As well as taking a history of pain, a number of other aspects should be discussed with the patient. •
sensibility, changes in taste, diminished lachrymation
and condyle is disturbed, giving rise to a click on
and increased salivation. Peripheral neuropathy. This is usually the result of
diabetes, long-standing temporal arteritis or Raynaud's
Does the joint click? In an anterior subluxating meniscus, the normal relation between meniscus opening the mouth.
•
Is movement limited, either in range or by locking? If there is a diminished range of opening of the mouth,
syndrome. It usually leads to a burning sensation and
did the limitation come on suddenly or was it more
loss of sensibility on lips, cornea or conjunctivae.
progressive? If 'sudden' locking is mentioned, can the
CHAPTER 46 - CLINICAL EXAMINATION 681
patient still open or close the mouth? Inability to
lead to adaptation in the TMJ. Problems with the joint can
open suggests meniscus displacement, which is
cause changes in dental occlusion.
usually unilateral, and in which at least 1 cm of mouth opening is always retained. If closing is impossible, a luxation of the mandibular condyle is most likely. Excessive limitation coming on rapidly may be the result of hysteria or of tetanus; mouth opening is impossible in these circumstances. A
•
The influence of all five active movements on pain, range
outcome of arthrosis of the TMJ.
of movement, deviation, abnormal sounds and crepitus
Is there crepitus? Crepitus is the result of
are noted.
advanced changes in the joint. It may be present in osteoarthrosis.
Does the patient suffer from clenching or grinding? This occurs mainly at night in stressed people. The patient may not be aware of it, relatives may have to be asked.
•
Is there tinnitus, vertigo or a hearing problem? Vertigo may result from differences in vestibular impulses as a result of TMJ problems. Other symptoms, such as mild deafness, a sensation of fullness in the ear and tinnitus, may also be present.
•
ACTIVE MOVEMENTS
limitation of slow development is usually the
movement across an irregular surface because of
•
FUNCTIONAL EXAMINATION
Have there been changes in sensibility? These can indicate peripheral neuropathy. It frequently affects the lips, cornea and conjunctivae. In atypical facial neuralgia, severe diminished facial sensibility is often found. Trigeminal neuritis is seldom accompanied by disturbed sensibility.
Active opening of the mouth (Fig.
46.1). Because it is
difficult to measure the range of motion of the TMJ in degrees, the interincisal distance at maximum opening is used. It is about 36-38 mm in adults but may vary between 30 and 67 mm, depending on sex and age.no12 A practical and quick way of checking range of motion is to ask the patient to insert the knuckles in between the front teeth (Fig. 46.2). Active closing of the mouth. The patient is asked to close
the mouth (Fig. 46.3). Active deviation of the mandible to the left and right
(Fig. 46.4). When the mandible deviates to the side it rotates around a vertical axis through the ipsilateral mandibular ramus. The contralateral mandibular head moves anteriorly at the same time. Active forward protrusion of the chin (Fig.
INSPECTION On inspection, attention must be paid to local swelling,
geniohyoid and digastric muscle. When it is disturbed, this is usually the consequence of an inert problem.
deformation, deviation of the chin and teeth wear. Swelling may be the result of a bacterial or an inflammatory arthritis (frequently rheumatoid, seldom due to psoriasis or gout) or in childrenlO may be caused by an inflammation of the parotid gland. In Bell's palsy, there is lowering of the ipsilateral side of the mouth and a smoothing out of wrinkles. Severe inflammatory disorders of the TMJ area during childhood may result in asymmetrical development of the lower face because of disturbance of the growth centre in the mandible. Advanced arthrosis may lead to asymmetry of face and head and to narrowing of the external auditory canal. Synovitis usually causes an ipsilateral deviation when the mouth is opened and a contralateral deviation when closed.9 Abnormal wear and tear of the teeth may be a sign of bruxism or grinding. Malocclusion and missing teeth may result in a TMJ problem. A bilateral relationship between the teeth and TMJs exists. Changes in the dental relationship, as in malocclusion and missing teeth, may
46.5). This is
performed by the lateral and medial pterygoid, masseter,
Figure 46.1
Active opening of the mouth.
682 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
Figure 46.2
Figure 46.3
Checking the range of motion.
Figure 46.4
Active deviation of the mandible.
Figure 46.5
Active forward protrusion of the chin.
Active closing of the mouth.
RESISTED MOVEMENTS Resisted opening of the mouth (Fig.
46.6). The examiner
places one hand underneath the patient's chin, the other on the vertex. With the mouth open about 1 cm, the patient is now asked to open further while the examiner provides strong resistance, so preventing any movement. The strength of the lateral pterygoid is tested by this manoeuvre.
CHAPTER 46
-
CLINICAL EXAMINATION 683
(a) Figure 46.6
Resisted opening of the mouth.
Resisted closing of the mouth (Fig.
46.7). A rubber pad
about 1 em thick is put between the teeth. The patient is asked to bite as hard as possible. This is a test for all the muscles that close the mouth: masseter, temporal and medial pterygoid. Resisted deviation of the mandible to the left and right
(Fig. 46.8). The examiner puts one hand on the left side of
(b) Figure 46.8
Resisted deviation of the mandible (a) to the left; (b) to the right.
the patient's chin and holds the head stable by placing the other hand against the right temporal area. The patient is now asked to deviate the chin to the left against the resistance offered by the examiner's hand. The test is
Figure 46.7
repeated to the opposite side. This movement tests the Resisted closing of the mouth.
contralateral lateral pterygoid.
684 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
(a)
(b)
Figure 46.9
Palpation of the temporomandibular joint: (a) anterior to the tragus; (b) in the external auditory meatus.
Further palpation is done to elicit local tenderness of
PALPATION
some masticatory muscles, the joint capsule and bone
The joint is palpated during active opening and closing
palpated on opening the mouth and on clenching the
and during active deviation to the left and right. On opening, the TMJ is palpated with the finger below the zygomatic bone just anterior to the condyle or, as for
around the tooth sockets. The masseter muscle can be teeth. Palpation of the temporal muscle is performed on clenching the teeth.
closing, with the tip of the finger placed either just ante rior to the tragus (Fig. 46.9a) behind the condyle or in the external auditory meatus (Fig. 46.9b), exerting some ante
TECHNICAL INVESTIGATIONS
rior directed pressure against the posterior aspect of the joint. The examiner normally feels a depression on opening. If a severe effusion is present, a bulge may be palpated. Attention must be paid to abnormal sounds and crepitus and to the anteroposterior gliding move ment of the condyle. The coronoid process can be palpated on opening and closing the mouth when the fingers are placed just below the zygomatic arch. The process is felt through the masseter muscle.
The erythrocyte sedimentation rate is frequently elevated in systemic diseases and infections. Plain radiography does not provide much information except for evidence of arthrosis.13 A CT scan can deter mine more accurately the position and condition of the
meniscus and the joint. 14,IS
In recent years, magnetic resonance imaging has been increasingly used to investigate temporomandibular dis orders, for example internal derangement.l6-IB
REFERENCES 1. Rocabado M. Arthrokinematics of the temporomandibular
joint. Dental C!ill North Am 1983;27(3):573-594. 2. Fromm CH, Terrence CF, Maroon
Je.
Trigeminal neuralgia:
3. Adour KK. Current concepts in neurology: diagnosis and man
agement of facial paralysis. New Engl J Med 1982;307:348--a51. 4. Adour KK, Wingerd
J.
Idiopathic facial paralysis (Bell's palsy):
current concepts regarding etiology and pathogenesis. Arch
factor affecting severity and outcome in 446 patients. Neurology
New·oI1984;41:1204-1207.
1974;24:1112-1116.
CHAPTER 46 - CLINICAL EXAMINATION 685
5. Adour KK, Byl FM, Hilsinger RL Jr, Kahn ZM, Sheldon MI. The
13. Hansson LG, Hansson T, Petersson A. A comparison between
true nature of Bell's palsy: analysis of 1000 consecutive patients.
clinical and radiological findings in 259 temporomandibular
Laryngoscope 1978;88:787-801.
joint patients. J Prosthetic Dentistry 1983;50:89-94.
6. Kudrow L. Cluster Headache: Mech anisms and Management.
Oxford University Press, London, 1980. 7. Mumenthaler M. Giant-cell arteritis: cranial arteritis, poly
myalgia rheumatica. J NeuroI1978;218:219-236. 8. Mumenthaler M (ed) Circulatory disturbances and hemorrhages
of the brain. Ill: Neurology, 3rd edn. T hieme, New York, 1990:93. 9. Hodges JM. Managing temporomandibular joint syndrome. Laryngoscope 1990;100:60-66. 10. De Bant L, Stegenga B, Boering G. Kaakgewrichtsstoornissen.
Deel I, Gedachtenontwikkeling en c1assificatie. Ned Tijd Tandheelkd 1989;96:496-500. 11. Mezitis M, Rallis G, Zachariades N. The normal range of mouth
opening. J Oral Maxillofac Surg 1989;47:1028-1029. 12. Claes J. Het temporomandibulair pijndysfunctiesyndroom in otorhinolaryngologie. Acta OtorhinolaryngoI1981;35(2):170-183.
14. Helms CA, Morrish RB, Kircos LT, Katzberg RW, Dolwick MF.
Computed tomography of mandibular
joint.
the meniscus of the temporo
Preliminary
observations.
Radiology
1982;145:719-722. 15. Raustia AM, Phytinen J, Virtanen KK. Examination of the tem
poromandibular joint by direct sagittal computed tomography. Clin RadioI1985;36:291-296. 16. Kircos LT, Ortendahl DA, Mark AS, Arakawa M. Magnetic res
onance imaging of the TMJ disc in asymptomatic volunteers. J Oral Maxillofac Surg 1987;45:397-401. 17. Schellhas KY. Imaging of the temporomandibular joint. Oral Maxillofac Surg Clin North Am 1989;1:13-26. 18. Eberhard D, Bantleon HP, Steger W. Functional magnetic reso
nance imaging of temporomandibular joint disorders. Eur J Orthodon 2000;22(5):489-497.
THIS PAGE INTENTIONALLY LEFT BLANK
I�terpretation of the clinical examination of the temporomandibular joint I-----...� Monoarticular steroid-sensitive arthritis Rheumatoid-type arthritis Septic arthritis Sympathetic arthritis Arthritis due to loss of molar teeth Arthrosis
Interpretation of the clinical examination of the temporomandibular joint
Internal derangement other than the capsule
Contactile structures
I-----...� Reciprocal clicking Fixed dislocation of the meniscus Luxation of the condyle
1----- Muscular lesions
E
Reciprocal clicking Subluxations Dislocations
687
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Di S-orders of the inert structures Internal derangement 690 Arthrosis 691 Luxation of the condyle 693 Synovial disorders 693
689
Disorders of the contractile structures 694 Myalgia 694 Muscular trismus 696 Abscess in the pterygoid muscle 696
Disorders of the temporomandibular joint
A great number of people (60-70%) have some problem with the temporomandibular joint (TMJ) but most are asymptomatic. About 25% of this group has symptoms that can be attributed to the TMJ.1,2 Of this group only 5% will get treatment and these patients are mostly women they
outnumber
male
patients
by
at
least
4:1.3
Temporomandibular disorders occur at any age but most often in young adults.4,5 Pain the temporomandibular area is the most common complaint and is easily related to a lesion of the TMJ.6 However, the exact cause of TMJ problems is often difficult to determine because several disorders may be present at the same time and combined muscular and inert tissue disorders are not uncommon. As a conse quence, it may be necessary to treat both joint and muscle. Conservative treatment is still the most effective management for more than 80% of patients.s There are several major causes of TMJ problems:9 •
A single major injury, even if it has been only a light blow to the mandible, or extreme stretching of the TMJ can permanently injure the joint and ligaments.lO
•
Repetitive microtraumas, such as clenching, grinding or atypical chewing for a prolonged period of time, may damage the joint and then lead to muscular problems.
•
Monoarticular arthritis and inflammatory polyarthritis, such as rheumatoid arthritis, but seldom psoriatic arthritis, may affect the joint.11
•
Abnormal biomechanical loading as a result of structural changes of the teeth may also be harmful. However, this should not be overestimated as a cause of TMJ problems.12 Disorders
of
the
temporomandibular
joint
are
summarized in Table 48.1 (p. 690).
DISORDERS OF THE INERT STRUCTURES The most common disorders of the inert structures are internal derangement and arthritis. The former may be present in hypermobile joints or may affect a normal joint, so leading to hypomobility. 689
690 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
INTERNAL DERANGEMENT Internal derangement is usually the result of lack of coor dination between the meniscus and the condyle, in which the meniscus displaces anteriorly and the condyle pos terosuperiorly. Acute or chronic repetitive injury may be the cause. Acute injury, such as whiplash, traumatic tooth extraction or intubation during anaesthesia, may displace the condyle posteriorly, so stretching the posterior attach
sliding posteriorly to the posterior band of the meniscus so that the meniscus is displaced anteriorly. In addition to repetitive clicking, there is often a stiff feeling and a short period of pain after the joint has been immobile for a while. On clinical examination, opening of the mouth is slightly decreased and provokes a small deviation of the chin to the affected side because the condyle cannot move fully anteriorly.
ments of the meniscus. Repetitive microtraumas occur
Treatment
ring over a longer period, as a result of loss of posterior
Treatment aims to fully restore the normal range of
teeth or interference with the incisors, may provoke a posteriorly directed force on the jaw, which again dis places the mandibular head posteriorly. Initial! y, this process is characterized by reciprocal clicking, later by temporary or continuous locking. Finally, osteoarthrosis may result. Each stage of internal derangement may give rise to painful chronic irritation of the synovium, with resulting arthritis.
motion, mainly the lost anterior translatory glide. The technique used is called 'joint liberation'13 and consists of passive movements applied in all directions in order to realign the shortened fibres of the capsule. All the tech niques can be performed under steady pull or, if pain is excessive, with small vibrations. Each manoeuvre is per formed over about 20-30 seconds and repeated several times. The whole procedure takes about 15 minutes. Technique: distraction. The patient sits on a chair with
the therapist facing the painless side and stabilizing the
RECIPROCAL CLICKING Clinically there is a 'click', usually most noticeable on opening the mouth and less so on closing. A click implies that the TMJ, which is normally a friction-free joint, is functioning abnormally. With the mouth closed, the meniscus lies too far anteriorly in relation to the condyle (Fig. 48.1). On opening, the click occurs when the condyle moves anteriorly and snaps beneath the meniscus and its posterior attachments to fall into its normal position. The opening click implies a reduction of the meniscus. Clicks may occur early, intermediate or late in relation to the range of opening of the mouth. Early clicks indicate a small degree of anterior displacement; clicking more towards full opening indicates that the displacement is greater, as a result of progressive stretching of the poste rior attachments. A closing click does not occur unless there is a preceding opening one. The click is present just before the mouth is closed and is the result of the condyle
patient's head with the ipsilateral hand. The other thumb, protected by a rubber pad, is placed on the molar teeth and the fingers pass round the mandibular body. Downward pressure is applied to the molar teeth, which distracts the joint surfaces, allowing repositioning of the meniscus on the condyle. Technique: distraction with anterior glide. In the same
position, the tip of the index finger of the manipulating hand
is
hooked
around
the
mandibular
angle.
Downward pressure and anterior pull are applied. This restores the anterior translatory glide which has been lost because of capsular retraction or because of the anteriorly displaced meniscus. Technique: combined distraction,
anterior glide and
lateral stretch. The mandible is additionally pulled to
the side, towards the therapist, thus realigning the fibres in all three planes of space. Technique: lateral glide without distraction. The posi
tion and fixation of the patient is the same as for previous techniques. The hand grasps the mandible around the angle and pulls it towards the therapist, restoring lateral joint movement. Home exercise programme. The patient is shown how to
perform self-mobilizing techniques on opening, on forward movement and on lateral excursions of the mandible. The muscles of mastication should be gently stretched to their full length. Coordination can be increa;ed by practising hinge-type movement of the jaw and then Figure 48.1
Anterior displacement of the disc.
making specific lateral movements without protrusion.
CHAPTER 48
-
DISORDERS OF TEMPOROMANDIBULAR JOINT 691
Jaw movements must be limited to the click-free range and dlewing on the side that provokes any noise must be avoided. If significant painful clicking is associated with a pos sible meniscus displacement, a repositioning occlusal splint can be useful. It is used only if a small change in the position of the mandible stops the click on opening and closing of the mouth. It should initially be worn
24 hours a day for 8-10 weeks, except while eating. Once the clinical symptoms have diminished, use of the appliance is progressively decreased, although a part-time repositioning appliance is needed.9,14 Resisted muscular exercises on opening, forward movement and lateral deviation may be used in association.I5
FIXED DISLOCATION OF THE MENISCUS Progression of the disorder may finally lead, via momen tary self-reducing dislocations, to a permanent luxation of the meniscus. From time to time the joint becomes
Figure 48.2
Manipulative reduction of a dislocated disc.
I suddenly locked, with the meniscus lodged anterior to the condyle. With a dislocated meniscus, clinical examination shows a reduced range of opening of the mouth. Because of loss of anterior translatory glide, only rota tion is possible. In such a condition the patient can always open the mouth by at least 1 cm but often not any wider. Full closure remains possible and is painless. The chin deviates to the ipsilateral side and deviation to the contra-lateral side is painful.
Treatment Manipulative reduction. Manipulative treatment aims to restore the normal relationship between the meniscus
translatory glide. On clinical examination, excessive movements are found together with clicking. Treatment consists mainly of stabilizing the joint and avoiding excessive anterior translatory gliding of the condyle by controlling the rotation in the joint. To do this, the patient is instructed to put and to keep the distal third of the tongue flat against the palate during opening, which limits opening to rotation movement only and reduces the tendency to anterior sliding. This method of opening should also be performed when chewing and protects the joint from further wear and tear.
and the joint surfaces.
48.2). The patient lies on a high couch. The manipulator stands at the patient's opposite side and
Technique (Fig.
puts one thumb, protected by a thick pad, on the molar teeth of the affected side. The other hand is put around the patient's head and holds it steady. Caudal pressure is now applied to the molar teeth and swift translatory movements of the patient's mandible are performed, three or four times. During the manoeuvre, the reduction click is felt.16 Manipulative reduction usually succeeds in one session.
ARTHROSIS Arthrosis of the TMJ may be the final stage of internal derangement or is sometimes due to bruxism or missing molar teeth. In primary osteoarthrosis, no apparent cause is present.17 The outcome of progressive change in internal derangement is shortening and fibrosis of the meniscus condyle attachments, and occasionally perforation or total rupture of the meniscus. Paradoxically if the latter occurs, there is only a small limitation or even complete freedom of movement so that subjectively the patient is
PROBLEMS ARISING BECAUSE OF
better although radiography clearly shows the degener
HYPERMOBILITY
noise.
ative changes. The click changes to a more grinding
Hypermobile joints may also give rise to reciprocal click
Patients with arthrosis are usually over 40 and it
ing, subluxations and dislocations because of excessive
remains uniIateraP8 Usually, it does not give rise to signifi-
692 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
cant inflammation or swelling, or to severe pain or limita tion of movement. Only when the capsule is inflamed does it cause pain, in which case it is often present in any part of the range of movement. Crepitus is frequently found; lim itation of opening of the mouth and of contralateral devia tion of the chin may be present. On opening, the chin deviates to the affected side. Palpation of the back of the condyle is usually tender. Pain and stiffness increase during the day. A radiograph shows flattening of the anterior slope of the condyle and the posterior slope of the articular tuber cle, with loss of joint space and formation of osteophytes. The complaints usually diminish progressively over
2-3 years with little painless residual disability. However, about one in five patients still has pain after 2 years.19 Ankylosis is uncommon.
Treatment Treatment should be directed towards the cause: dental correction is performed and clenching and grinding is stopped. Symptoms may be relieved by deep friction to the joint capsule followed by forced movements.15 A intra-articular injection with steroid should be given if stretching alone is insufficient. The results are better than forced movements and friction alone. If intra-articular injection is without effect, or when ankylosis appears imminent, capsular stretching should be performed. If either intra-articular injections or capsular stretching have failed, arthroplasty may be indicated. Because open surgery can be followed by formation of fibrotic adhe sions in the joint, so limiting the normal range of move ment, or cause malocclusion, surgical treatment must
Figure 48.3
Deep friction to the temporomandibular joint capsule.
A 2.5 cm needle is fitted to a syringe containing 1 ml triamcinolone acetonide. The needle is thrust in almost vertically and penetrates the joint space about 1 cm deep to the skin. The full amount of fluid is injected provided there is no resistance. If resistance occurs, the needle must lie either in the articular cartilage, the meniscus or under the periosteum. Injection into cartilage must be avoided because of the risk of further damage. The needle is slightly withdrawn and its tip relocated. The patient is reviewed after a week. Usually, one to two injections suffice.
only exceptionally be recommended. Technique: deep
friction (Fig.
48.3). For friction the
patient lies on a couch, painful side up. The therapist sits behind the patient and places the index of the ipsilateral hand, reinforced by the middle finger, in front of the joint line. This is easily palpable, just cranial to the mandibular head, on opening and closing the mouth. The other hand stabilizes the head on the skull. The index finger is now pulled backwards while pressure is applied. Friction is given for about 20 minutes, three times a week. Technique:
intra-articular
injection (Fig.
48.4). The
patient lies with the affected side up. The posterior aspect of the mandibular condyle is palpated, anterior to the tragus and below the zygomatic bone. The space to be injected lies just posterior to the condyle and is located with the patient's mouth wide open, moving the condyle as far anteriorly as possible. The injection should be given into the inferior compartment of the joint, beneath the meniscus.
Figure 48.4
Intra-articular injection of the temporomandibular joint.
CHAPTER 48
-
DISORDERS OF TEMPOROMANDIBULAR JOINT 693
LUXATION OF THE CONDYLE In luxation, both condyle and meniscus lie in front of the articular tubercle (Fig. 48.5). It is usually bilateral and is encountered most frequently in hypermobile joints. The onset is often a result of yawning or excessive laughing with the mouth wide open. The patient is suddenly unable to close the mouth. If closing is tried passively, there is an elastic recoil. Sometimes the dislocation is temporary and can be reduced by the patient. In other cases, manual reduction is needed.
Treatment Treatment is by manipulative reduction. Technique:
manipulative
reduction (Fig.
48.6). The
patient sits in a chair. The manipulator stands at the front, puts both thumbs on the molar teeth and grasps the mandible with the fingers. Caudal pressure is now
Figure 48.6
Manipulative reduction of luxation of the condyle.
applied with the thumbs and simultaneously the chin is pulled in the cranial direction so as to close the mouth.20
SYNOVIAL DISORDERS
Opening the mouth becomes progressively painful and limited and may lead to inability to take solid food.
Arthritis of the TMJ is clinically characterized by pain on movement, crepitus and tenderness over the joint.
On mouth opening the chin deviates towards the affected side but at rest in the closed position it deviates towards
Sometimes progressive limitation of opening of the mouth
the other side. The disorder may persist for months.
follows but the joint is only exceptionally ankylosed.
Because the lateral pterygoid muscle is attached to the anterior part of the joint capsule, in a severe case resisted
MONOARTICULAR STEROID-SENSITIVE ARTHRITIS15 For no apparent reason, a patient may develop progres sive pain in one of the TMJs without other joints being affected.
opening of the mouth may also be painful.18 Pain and stiffness are worse in the morning and improve after movement. Technical investigations for inflammatory disorders, such as radiography and labora tory tests, are negative.
Treatment An intra-articular injection with steroid is usually effec tive and may be repeated after 1 week (see above).
INFLAMMATORY POLYARTHRITIC DISEASES Juvenile rheumatoid arthritis, ankylosing spondylitis and rheumatoid arthritis sometimes involve the TMJs. They affect the synovium and may subsequently lead to destruction of bone. The clinical findings are the same as for monoarticular steroid-sensitive arthritis. The fact that other joints are affected, together with radiograph findings and laboratory tests positive for rheumatological disorders, reveal the exact nature of the condition. Psoriatic arthritis, gout and lupus erythematosus are Figure 48.5
Luxation of the condyle.
very rare and seldom give rise to bone destruction. There
694 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
is no separate treatment for the TMJ; the joint is included in measures against the underlying disorder.
INFECTIONS Infections of the TMJ are rare and are usually the result of an adjacent infection of the external auditory canal, the parotid gland or the middle ear. Inflammation may some times occur in viral diseases such as infectious mono nucleosis, measles and mumps.18 Gonococcal infection has been reported. The patient may be severely ill and complains of tem poromandibular pain and limitation of mouth opening, with deviation towards the ipsilateral side. Bacterial infection of the TMJ requires hospitalization and, after
DISORDERS OF THE CONTRACTILE STRUCTURES Muscular disorders are usually the consequence of bruxism or clenching, which is commonly an uncon scious way of coping with the stress of daily life and is seen more often in patients who are more subject to anxiety and depression than are members of the average population.22 In addition to muscular pain, tooth wear, alveolar tenderness, mobility of the anterior teeth, pain and morning jaw stiffness are usually found. The pain is elicited on maximum resisted isometric contraction.
culture of aspirated pus,21 is treated by antibiotics.
SYMPATHETIC ARTHRITIS An abscess in the neighbourhood of a TMJ may provoke a 'sympathetic' arthritis.15 Causes are peritonsillar abscess, pericoronitis of a partially erupted wisdom tooth or molar extraction. There is progressively increasing difficulty in opening the mouth, usually starting, if the cause is dental, 1-2 days after an intervention. Pain is found on all movements, and the bone at the base of the tooth is tender on palpation. Spontaneous cure is usual in 2-3 weeks after molar extraction. If active treatment is necessary, it should be directed to the underlying disorder and not to the arthritis as such.
ARTHRITIS DUE TO LOSS OF MOLAR TEETH Patients lacking all molar teeth (unilaterally or bilater ally) sometimes develop unilateral arthritis which may occur at either side in relation to the missing molar teeth. Molar teeth normally have a distance-maintaining effect in apposition between the mandible and maxilla. Should this be lost, excessive upward pressure by the mandibu lar condyle on the temporal fossa occurs, which may lead to arthritis. This can also occur as a result of treating patients, who have missing molars, by cervical traction. Patients complain of a continuous deep burning pain in the temporomandibular area, not necessarily influenced by eating. On examination pain is found at the extreme of all movements and slight limitation of opening may be present. Treatment consists of dental correction of the distance between mandible and maxilla. When cervical traction has to be given, a splint of sufficient thickness to divert the strain to the posterior part of the mandible should be used (Cyriax:15 his p. 1 99).
MYALGIA Myalgia is described as a dull aching pain felt continu ously in the area of the masticatory muscles and it may affect any of these.23 Cold weather may precipitate the symptom which, although present at all times, is usually worse at the end of the day, sometimes also disturbing the patient's sleep. Resisted closing of the mouth is painful, as is maximum active opening, which stretches the muscles. The muscles are usually very tender, and firm palpable bands within them are often present. The differential diagnosis includes temporal arteritis, which can also lead to myalgic pain. Redness and swelling over the artery are characteristic of arteritis.
Treatment Primary therapy is a full-arch occlusal stabilization appliance. This involves the construction of a flat occlusal surface that is adjusted to have multiple tooth contact in a habitual comfortable jaw closure posi tion.9,24 Initially it is worn continuously, except on eating, for 6-8 weeks and is adjusted several times to establish a comfortable jaw position. As the symptoms decrease, the amount of daytime wear of the appliance is progressively reduced. In musculoskeletal pain from bruxism or tooth clenching the patient must break the habit. Advice is given to reduce all physical and mentally stressful activ ities during treatment. Muscle relaxants or anti-anxiety drugs can be useful. Hard or chewy foods are avoided. Application of moist heat to the temporal and masseter
muscles for 20 minutes, three or more times a day can
be helpful.
CHAPTER 48
-
DISORDERS OF TEMPOROMANDIBULAR JOINT 695
Table 48.1 Summary of disorders of the temporomandibular joint Disorder
Symptoms
Signs
Treatment
Mainly on opening
Opening slightly diminished
Stretching capsule and
Temporary locking
Chin deviation to ipsilateral side
ligaments
Disorders of the inert structures Internal derangement Reciprocal clicking
Stiff feeling Fixed dislocation of meniscus
Repositioning splint
Sudden locking
Opening strongly limited
Manipulation
Chin deviates to ipsilateral side Pain on deviation to contralateral side Arthrosis
Grinding sound I
I Crepitus
Luxation of condyle
Cannot close mouth
Pain at all tests and during the whole
Spontaneous cure
of each movement
Stop clenching
Crepitus
Dental correction
Opening limited
Friction to joint capsule
Contralateral deviation limited
Intra-articular injection
On opening: chin deviates to ipsilateral side
Forced stretching
Back of condyle tender on palpation
Arthroplasty
Closing of mouth limited
Manipulative reduction
Elastic recoil on passive closing Synovial disorders Monoarticular steroid-sensitive
Crepitation
Opening painful and limited
arthritis
Pain
Ipsilateral deviation on opening
Stiffness
Contralateral deviation when closed
Intra-articular injection
Resisted opening: pain Infiammatory polyarthritic
As in monoarticular steroid-sensitive
As in monoarticular steroid-sensitive
General treatment of
diseases
arthritis
arthritis
underlying disorder
Infections
Pain
Severely ill
Hospitalization
Opening painfully limited and
Aspiration
ipsilateral deviation
Antibiotics
Sympathetic arthritis
Pain
Opening slightly diminished
Spontaneous cure
Pain on all movements
Antibiotics
Tenderness on palpation Abscess Arthritis from loss of molar teeth
Continuous pain
Opening slightly decreased
Dental correction
Pain at extreme of all movements Disorders of the contractile structures Myalgia
Muscular trismus
Dull aching, continuous pain
Pain on resisted closing and on maximal
Stabilization appliance
worse in cold weather
active opening
Stop bruxism or tooth
and at end of day
Painful bands
clenching
Vague pain
T remor of jaw
Solve underlying problem
Incoordination on movement Diminished opening Abscess in pterygoid muscles
Pain on chewing
Opening diminished
Antibiotics
Pain on clenching
Drainage
Resisted contralateral deviation painful Fever
696 SECTION NINE - THE TEMPOROMANDIBULAR JOINT
Warning
MUSCULAR TRISMUS
When trismus is present, tetanus should not be forgotten.
Pathological muscular stimulation or inhibition may limit the opening of the mouth but only very rarely affect closing. Limitation is often the result of attempt ing to avoid pain. Trismus can be the outcome of a
Painless stiffness coming on abruptly at the TMJ, and causing complete inability to open the mouth, may be an early sign of the condition. In this event, both joints are usually affected.
chronic pain problem or of a recent local event (injury or surgery). When movement is attempted, there is often tremor of the jaw and incoordination. Treatment consists of solving
ABSCESS IN THE PTERYGOID MUSCLE
the underlying problem. Hysterical trismus is characterized by a total loss of
An anaesthetic injection for dental work may be followed
ability to open the mouth. A vague pain, which extends
some days later by an abscess. The cheek begins to hurt
over the whole of the head and face, is usually
and feels stiff. The patient complains of problems on
described. Very often these patients also hold the neck
opening the mouth and has pain on chewing.
extremely still. Because it is very difficult to examine
Clinical examination reveals a loss of range of mouth
the TMJ in an unwilling patient, it is better to proceed
opening, together with pain on clenching. Resisted
with caution: multiple positive findings and inconsis
deviation towards the painless side also hurts.
tencies should warn the examiner of a severe disorder or hysteria.
Signs of infection including pyrexia should be sought. Treatment is with antibiotics and drainage.
REFERENCES 1. Salonen L, Hellden L. Prevalence of signs and symptoms of dys function in the masticatory system: an epidemiological study in an adult Swedish population. J Craniomandib Disord (J Orofac
Pain) 1990;4:241-250. Assessment
joint. Dent Ciin North Am 1983;27(3):573-594. 14. De Laat A. F unctionele behandeling van kaakgewrichts klachten. Tijd Geneeskd 1986;42(11):753-757.
2. McNeill C (ed) Temporomandibular Disorders - Guidelines for
Classification,
13. Rocabado M. Arthrokinematics of the temporomandibular
and
2nd
Management,
edn.
Quintessence Books, Chicago, 1993.
15. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, Diagllosis of
Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:117. 16. Cyriax JH. Textbook of Orthopaedic Medicine, vol II, Treatment by
3. Dworkin SF, Huggins KH, Le Resche LR et al. Epidemiology of signs and symptoms in temporomandibular disorders. 1. Clinical signs in cases and controls. J Am Dent Assoc 1990;120:273-281. 4. Greene CS, Marbach JJ. Epidemiologic studies of mandibular dysfunction: a critical review. J Prosthet Dent 1982;48:184-190. 5. Dimitroulis G. Temporomandibular disorders: a clinical update.
BMJ 1998;317:190-194. 6. Ohrbach R, Gale EN. Pressure pain thresholds, clinical assess ment and differential diagnosis: reliability and validity in
Manipulation, Massage and Injection, 11th edn. Bailliere Tindall, London, 1984. 17. De Bont L, Stegenga G, Boering G. Kaakgewrichtsstoornissen. Deel I, Gedachtenontwikkeling en classificatie. Ned Tijd Tandheelkd 1989;96:496-500. 18. Hodges JM. Managing temporomandibular joint syndr· ome. Laryngoscope 1990;100:60-66. 19. Toller P. Osteoarthrosis of the mandibular condyle. Br Dent J 1973;20:223-231. 20. Steenks H. Welke niet-chirurgische behandelingsstrategie kan worden gekozen bij een 'closed lock' van het kaakgewricht.
patients with myogenic pain. Pain 1989;39:157-169. 7. Dworkin S, Le Resche L, De Rouen T, Von Korff M. Assessing
Respons 1990;3:1-2.
clinical signs of temporomandibular disorders: reliability of
21. Friedman M, Weisber J, Agus B. Diagnosis and treatment of
clinical examiners. ] Prosthet Dent 1990;63(5):574-579.
inflammation of the temporomandibular joint. Sem Arthritis Rheum 1982;12(1):44-51. 22. Thomas L, Tiber N, Schireson S. The effects of anxiety and frus tration on muscular tension related to the temporomandibular
8. Dimitroulis G, Gremillion
HA,
Dolwick MF,
Walter
JH.
Temporomandibular disorders. 2. Non-surgical treatment. Aust
Dent J 1995;40:372-376. 9. Clark G. Diagnosis and treatment of painful temporomandibu lar disorders. Dent Ciin North Am 1987;31(4):645---674. 10. Ryan
DE.
Temporomandibular
disorders.
Curl'
Opin
1993;5:209-218. 11. Veys E, Mielants H, Verbruggen G. Reumatologie. Omega Editions, Ghent, 1985:169. 12. Greene C, Marbach J. Epidemiologic studies of mandibular dys function: a critical review. J Prosthet Dent 1982;48(2).
joint syndrome. Oral Surg 1973;Nov:763-768. 23. Ernest E,
Martinez M,
Rydzewski D,
Salter
E.
Photo
micrographic evidence of insertion tendinosis: the etiologic factor
in
pain
for
temporal
tendinitis.
J
Prosthet
Dent
1991;65(1):127-131. 24. Clark GT, Adler RC A critical evaluation of occlusal therapy. Occlusal adjustment procedures. J Am Dent Assoc 1985;110: 743-750.
'
SECTION TEN
The lumbar spine
SECTION CONTENTS 49. Introduction to the lumbar spine
50. Applied anatomy of the lumbar spine
703
Human posture 703 Vertebrae 704 Intervertebral discs 705 Facet joints 710 Ligaments 711 Muscles and fasciae 713 Spinal canal 714 Dura mater 714 Nerve roots 716 Epidural space 721 Innervation 721
57.
Mechanical disorders of the lumbar spine: differential diagnosis 847
58. Non-mechanical disorders of the lumbar spine Introduction 851 Warning signs in backache and sciatica 851
736
Disorders Spondylolisthesis 855 Osseous disorders 857 Rheumatological disorders 861 Infections 863 Intraspinal lesions 864 Pain referred to the back 867
743 746
59. Treatment of the lumbar spine
53. The ligamentous concept
775 Introduction 775 Mechanism of ligamentous pain Postural syndrome 776 Posterior dysfunction syndrome
775 779
54. The stenotic concept 787 Introduction 787 Spinal stenosis 788 Lateral recess stenosis 791 55. Clinical examination of the lumbar spine
History 799 Introduction 799 Routine of history taking Inspection 802
833
837 Definitions 837 Anatomy 838 Classification of lumbar instability 839 Instability and the clinical concept of mechanical lesions of the lumbar spine 840 Diagnosis of lumbar instability 841 Treatment of lumbar instability 842
Relationship between degeneration and symptoms 739
Hypothesis 743 Clinical syndromes Lumbago 746 Backache 757 Sciatica 757
812
56. Lumbar instability
51. Ageing of the lumbar spine 729 Introduction 729 Ageing of the disc 730 Disc displacements 731 Ageing of the surrounding tissues Radiological changes 738
52. The dural concept
Functional examination Palpation 830 Accessory tests 831 Local anaesthesia 832 Technical investigations
699
802
799
873 Introduction 873 Manipulation 875 Traction 893 Alternative procedures for reducing nuclear protrusions 901 Injections 903 Epidural local anaesthesia 903 Nerve root blocks 914 Injection of ligaments 918 Prevention of lumbar spine disorders 921 Spinal surgery 928 Surgery for discodural or discoradicular interactions 928 Surgery for spinal stenosis and lateral recess stenosis 930 Lumbar arthrodesis 931
851
THIS PAGE INTENTIONALLY LEFT BLANK
Introduction to the lumbar spine
There is much confusion about the meaning of commonly used words such as backache, sciatica and lumbago. In this book they are defined as follows: pain in the lower back, central, unilateral or bilateral with or without radiation to the gluteal region and iliac crest. Lumbago: acute and severe 'backache', causing twinges on attempted movement together with some degree of fixation and/ or trunk deviation. The pain reference is wider and sometimes involves the legs in an extrasegmental distribution. Sciatica: pain in the leg, radiating segmentally to L4, LS, 51 and 52. Pain felt along the anterior aspect of thigh, as a result of L3 root compression, is not true 'sciatica' although patients may describe it as sciatica.
• Backache:
•
•
During recent decades, syndromes related to the lower back have been identified by many epidemiologi cal studies. As a result, the incidence of low back pain, and its socioeconomic impact, are well known.] Low back pain is so common that only a minority of individ uals escape it. Eighty percent of the general population will at some time suffer from low back pain and 20% are suffering at any given time.2,3 A recent study estimates the I-month prevalence of low back pain to be 39%.4 Knepel reported that in general practice every tenth patient had back complaints.slt has been suggested that an increase in the incidence of low back disability throughout Western society has taken place between the 19S0s and 1970s.6 Backache and sciatica have also become an increasing problem in industrialized countries: back disorders account for between 1 and 2% of all working days lose-ll and account for 12.S% of all sickness absence daysY It is the most common cause of disability among younger adults in the United States.13 The number of lost working days per year because of low back pain is 1400 per 1000 workers in the USA,14 and 2600 per 1000 workers in some British factories.1S,]6 Svensson and Andersson found a direct association between the occurrence of low back pain and frequent lifting, and Biering-Sbrensen found that a worker was three times more susceptible to low back pain injury if exposed to 699
700 SECTION TEN - THE LUMBAR SPINE
manual handling tasks.17 Several studies also suggest an increased risk of low back pain in drivers of tractors, trucks and buses.18,19 The cost of treatment of and compensation for low back syndromes is enormous and increases every year. In 1976, in the USA, the total cost of spinal disorders was approximately $14 billion. By 1983, this had risen to $20 billion2o and some analyses have estimated the bill has already risen to more than $50 billion.21 Backache and sciatica are complaints rather than specific diagnoses. Although most of such symptoms stem directly or indirectly from lesions of the interverte bral discs, it is widely accepted that low back pain spans a group of disorders with varying causes. As much as 80% of all cases of low back syndromes relate to the lumbar intervertebral disc; the posterior support structures (facets, ligaments, laminae and fasciae) are directly responsible for less than 20% of cases of back disorders.22 The evidence for this statement is derived from anatomical and imaging studies, but Cyriax23 came to the same conclusion almost 50 years ago, purely on careful clinical observations: 'In my experience lumbar disc lesions are responsible for more continuing - yet avoidable - annoyance, frustration, semi-invalidism, general misery and bad temper than any other tissue in the body. In our view, lumbar disc lesions are responsible for well over 90% of all organic symptoms attributable to the back.' It is remarkable that, in disorders that affect both indi viduals and society so much, there is so little agreement about possible pathogenesis and pathological entities. Despite the advanced technology available for diagnosis and treatment, the number of patients suffering from backache and sciatica continues to increase.24 It has even been suggested by both the lay press and professionals that the epidemic increase in disability is partly caused by unnecessary technical investigations and too much surgical treatment.25 The main reason for ineffective diagnosis and treat ment is that patients are submitted to technical investi gations and tests before careful clinical assessment has been made. A basic knowledge of anatomy, histology and behaviour of the tissues involved is necessary to be able to understand a patient's complaints and to inter pret the signs found during the clinical examination. These skills are not widely taught nowadays. Students are trained in interpretations of discograms, myelo grams and magnetic resonance images (MRI), but they do not learn how to take a history and make a clinical examination effectively or how to interpret the clinical picture that emerges from the findings, how this can be translated into a diagnosis and what is the natural history of the detected disorder.
As for other parts of the body, the information gained from the history and physical examination is the first and most important requisite for correct diagnosis. If the clin ical assessment is properly done, technical investigations add little information and scarcely improve the precision of diagnosis. If clinical assessment is omitted, the results of radiographs, myelograms, discograms, computed tomography (CT) scans and MRI will pose more ques tions than they solve, simply because these investiga tions, although very sensitive, are not sufficiently specific to guarantee that the detected lesions are indeed the source of the pain. Indeed CT investigations have a false positive rate of 15.5% and a false-negative rate of 40%; MRI has false-positive rate of 13.2% and a false-negative rate of 35.7%.26 These rates are far too high for imaging alone to be decisive in the diagnosis of an individual patient's problem. In spite of this, many surgeons base their decision to carry out surgery solely on the outcome of these investigations . With a good understanding of the applied anatomy and a clear inSight into the way that tissues behave, it is possible to translate the symptoms and signs found during clinical assessment into a deduction about the anatomical changes that have taken place in a patient's back. The true art of clinical, investigation is to put all the clinical information together and examine the typical patterns that constitute the clinical syndromes. There are in fact only a few symptom patterns and patients' descriptions are frequently strikingly similar. The dura mater is the most important pathway by which an intervertebral disc produces pain. It is the link between the macroscopic changes at the posterior aspect of the intervertebral joint and the symptoms: backache or lumbago result when the dural sac is compressed; sciatica occurs when the dural investment around the spinal nerve is pinched. This'dural concept', in which both disc and dura have a particular role, accounts for most of the low back syndromes, and is discussed in the chapter on the dural concept (Ch. 52). Changes in the disc can also have consequences for the posterior support structures and result in other signs and different findings. We discuss these in the chapter on the ligamentous concept (Ch. 53). Increasing degeneration of the spine usually remains painless and in fact is a normal event which does not signify any particular disease. Sometimes increasing degeneration can account for acquired stenosis of the vertebral canal or the lateral recess. The resulting symp toms and signs are discussed in the chapter on the stenotic concept (Ch. 54). There are also a number of pain syndromes not related to mechanical problems, such as spondylolisthesis, irlfec tious and rheumatological diseases and diseases of the
CHAPTER 49
osseous structures. These are discussed in the chapter on non�mechanical spinal disorders (Ch. 58). The treatment administered for lumbago, backache and sciatica depends on the diagnosis, i.e. on the data obtained during history taking and clinical examina tion. A'standard' treatment for backache does not exist; treatment depends on the underlying disorder causing the symptoms. For example, if there is a small posterior displacement of the intervertebral disc, impinging on the dura mater, attempts are made to shift the protruded fragment back into place, either by manipulation or by
-
INTRODUCTION 701
traction, depending on the history of onset. If the pro trusion is unstable, and the patient has a history of recurrent back trouble, strong prophylactic measures against further disc displacements should be taken and therefore the patient attends a 'back school'. If pro phylaxis proves impossible, epidural local anaesthesia or ramus posterior block can be used to diminish the symptoms. If the pain is caused by a sprained posterior ligament or an inflamed facet joint, local scler osing injections or infiltrations with triamcinolone should be used.
REFERENCES 1. Office of Health Economics: Back Pain. London, 1985. 2. Valkenburg HA, Haanen HCM. The epidemiology of low back pain. In: White AA, Gordon SL (eds) Idiopathic Low Back Pain. Mosby, St Louis, 1982.
3. Biering-Sorensen F. A prospective study of low back pain in
14. Snook SH. Low back pain in industry. In: W hite AA, Gordon SL (eds) Idiopathic Low Back Pain. Mosby, St Louis, 1982.
15. Berm RT, Wood PHN. Pain in the back: an attempt to estimate the size of the problem. Rheumat Rehabi/1975;14:121.
16. Svensson HO, Andersson GBJ. Low back pain in forty to forty
general population. 1. Occurrence, recurrence and aetiology.
seven year old men: working history and work environment
ScandJ Rehabil Med 1983;15:71.
factors. Spine 1983;8:272-276.
4. Papgeorgiou AC, Croft PR, Ferry S, Jayson MIV, Silman AJ. Estimating the prevalence of low back pain in the general pop ulation. Spine 1995;20:1889-1894.
5. Knepel H. Bedeutung und Haufigkeit bandscheiben-bedingter Erkrankungen. Med Diss Dusseldorf 1977.
6. Waddell G. A new clinical model for the treatment of low-back pain. Spine 1987;12:632-644.
7. Horal J. The clinical appearance of low back disorders in the city of Gothenberg, Sweden: comparisons of incapacitated probands with matched controls. Acta Orthop Scand 1969;118(suppl).
8. Gibson ES, Martin RH, Terry CWo Incidence of low back pain and pre-placement X-ray screening. ] Occup Med 1980;22:515-519.
9. Svensson HO, Andersson GBJ. Low-back pain in 40-47 year old-men:
frequency of occurrence and impact on medical
services. Scand J Rehabil Med 1982:14:47-53.
10. Spitzer WO et at. Scientific approach to the assessment and
17. Biering-Sorensen F. Risk of back trouble in individual diseases occupations in Denmark. Ergonomics 1985;28:51.
18. Seidel H, Heide R. Long-term effects of whole body vibration: a critical survey of the literature. lnt Arch Occup Environ Health
1986;58:1-26. 19. Kelsey JL, Hardy RJ. Driving of motor vehicles as a risk factor for acute herniated lumbar intervertebral disc. AII1 J Epidemiol
1975;102:63-73. 20. Genant HK.
and costs of low back pain. Orthop Gin North Am 1991;22:
263-271. 22. Frymoyer JW, Gordon SL. American Academy of Orthopaedic Surgeons Symposium, New Perspectives on Low Back Pain.
Quebec Task Force on Spinal Disorders. Spine 1987;12(suppl 7).
February 1989.
Quebec. ] Occup Med 1987;29:670-674.
12. Andersson GBl. Epidemiologic aspects on low-back pain in industry. Spine 1981;6:53.
13. Kelsey JL, Mundt DJ, Golden AL. Epidemiology of low back
1984: Perspectives in Radiology,
Education Foundation, San Francisco, 1983.
American
occupational back pain: a study of 2500 cases representative of
Update
21. Frymoyer IW, Cats-Baril WL. An overview of the incidence
management of activity-related spinal disorders. Report of the
11. Abenhaim L, Suissa S. Importance and economic burden of
Spine
Orthopaedic Surgery and Neurosurgery. Radiology Research and
Academy
of
Orthopaedic
Surgeons,
Chicago.
23. Cyriax JH. Disc Lesions. Cassell, London, 1953. 24. Report of the Commission on the evaluation of pain. Soc Security Bull 1987;50(l). 25. Nachemson A. Work for all. For those with low back as well. Gin Orthop 1983;179:77-85. 26. Jackson RP, Cain IE , Jacobs RR, Coopper BR, McManus GE. The
pain. In: Jayson MIV (ed). The Lumbar Spine and Back Pain, 4th
neuroradiographic diagnosis of lumbar herniated
edn. Churchill Livingstone, Edinburgh; 1992:537-549.
pulposus: II. Spine 1989;14:1362-1367.
nucleus
THIS PAGE INTENTIONALLY LEFT BLANK
Applied anatomy of the lumbar spine
CHAPTER CONTENTS
703
Human posture Vertebrae
704
Intervertebral discs 705 Functions of the disc 706 Behaviour of the disc 706 Facet joints Ligaments
710 711
Muscles and fasciae Spinal canal Dura mater
713
714
Dural mobility 715 Dural sensitivity 716 Nerve roots 716 Definition 716 Boundaries 716
717
Anatomy Epidural space Innervation
HUMAN POSTURE
714
721
721
Sinuvertebral nerve 721 Posterior primary ramus 722
The human spine is a self-supporting construction of skeleton, cartilage, ligaments and muscles. Erect there are four sagittal curves, which are the result of man's evolu tion from quadruped to biped. This evolution began in Africa 3 million years ago with Homo australo-pithecus, which had a pelvis strong enough to support an erect posture. After a further 1.5 million years, the definite erect posture had been adopted Homo erectus.J The four curves resulted: cervical lordosis, thoracic kyphosis, lumbar lordosis and sacrococcygeal kyphosis. This S form seems to be a compromise between the static and the dynamic qualities of the spind theoretical considera tions suggest that the S form is the shape an elastic bar adopts when it is subjected to axial compression.3 The phylogenetic evolution from the large thoraco lumbar kyphotic spine of a quadruped into two kyphotic and lordotic curves is also reflected in the spine's ontogeny. In intrauterine life and during the first 5 months after birth, the spinal curves are absent and there is only one slight kyphosis of the whole spine. At 13 months the lumbar spine is straight, at 3 years some lumbar lordosis is present and by 8 years the lumbar spine has attained its normal adult posture (Fig. 50.1).4 -
Figure 50.1
Development of the lumbar lordosis. 703
704 SECTION TEN - THE L U M BAR SPI N E
A s a result o f the lumbar lordosis, the intervertebral space is larger in front than behind, which has some con sequences for the intervertebral disc. It is clear that axial pressure exerted on the disc in a lordotic spine will result in a forwards strain on the disc, whereas increased axial pressure during trunk flexion will force the disc back wards. A backwards shift of the disc is a most undesir able event because nerve roots and dura mater emerge at the posterior aspect of the vertebral column. Indeed, these very sensitive structures lie at the weakest and most unprotected part of the column, and good posture, rather than ligamentous device, protects them against a posterior or posterolateral shift of the disc. Maintaining the normal physiological lordosis is therefore important in the prophylaxis of low back syndromes. The development of the erect posture is recent and it seems that, apart from the compensatory lordosis, not much in the way of structural adaptation has taken place. Comparative anatomical evidence suggests that the spine has evolved as a hanging structure between the anterior and the posterior part of the body. However, during development from quadruped to biped, the function of the spine had to alter completely (see Table 50.1); this has serious consequences. In an upright position, the spine is submitted to axial load, which probably leads to the premature disc degenera tion from which humans are apt to suffer. In the upright position, the lumbar spine has to resist flexion, whereas the quadruped spine has to resist extension because it is structurally undesirable for a 'bridge' to sag in the middle. The change to an upright position, however, has not yet been followed by anatomical adaptation, and the human spine has an anatomy that more readily with stands extension than flexion: the anterior part of the annulus fibrosus is stronger and thicker than the poste rior, and the anterior longitudinal ligament is almost twice as thick and broad as the posterior.s Conclusion: the s p i n e was o r i g i n a l l y designed as a horizon tal, s l ightly kyphotic and hang i n g structure, strong i n resist ance to extension. Once the erect posture was achieved, the s p i n e became s u b m itted to axial and flexion stresses. S l i g ht lordosis prevents l u m bar d iscs from shift i n g backwards and keeps them away from pai n f u l and vital structures, such as d u ra and nerve roots.
VERTEBRAE
Embryologically, the lower half of a vertebra and the upper half of the one below it originate from the same segment. Between them is the disc, which is partly a remnant of the notochord.
Table 50.1 Comparison of the quadruped and biped lumbar spines Quadruped
Biped
Structure
Horizontal
Vertical
Load
Horizontal
Axial
Curve
Slight kyphosis
Lordosis
Strength
Against extension
Against flexion
Strong structures
Anterior
(Posterior?)
Each vertebral body is more or less a cylinder with a thin cortical shell which surrounds can cellous bone. From L1 to L5 the posterior aspect changes from slightly concave to slightly convex, and the diam eter of the cylinder increases gradually because of the increasing loads each body has to carry. At the upper and lower surfaces, two distinct areas can be seen: each is a peripheral ring of compact bone - surrounding and slightly above the level of the flat and rough central zone - which originates from the apophysis and fuses with the vertebral body at the age of about 16. The central zone - the bony endplate - shows many perfora tions, through which blood vessels can reach the disc. A layer of cartilage covers this central zone, which is limited by the peripheral ring. This is the cartilaginous endplate, forming the transition between the cortical bone and the rest of the intervertebral disc. A sagittal cut through the vertebral body shows the endplates to be slightly concave, which consequently gives the disc a convex form.6 Vertebral bodies.
Pedicles. The two pedicles originate posteriorly and attach to the cranial half of the body. Together with the broad and flat lamina, they form the vertebral arch. From L1 to L5, the pedicles become shorter and broader and are more lateral. This narrows the anteroposterior diameter and widens the transverse diameter of the ver tebral canal from above downwards. Together with the increasing convexity of the posterior aspect of the verte bral body, these changes in the position of the pedicles alter the shape of the normal bony spinal canal from an ellipse at Ll to a triangle at L3 and more or less a trefoil at L5 (Fig. 50.2). Laminae. Each lamina is flat and broad, blending in cen trally with the similarly configured spinal process, which projects directly backwards from the lamina. The two transverse processes project laterally and slightly dor sally from the pediculolaminar junction. The superior and inferior articular processes originate directly from the lamina. The part of the lamina between the superior and infe rior articular processes is called the 'pars interlaminaris'. It runs obliquely from the lateral border of the lamina to its upper medial border. This portion of the lamina is sub-
CHAPTER 50 - APPLIE D ANATOMY 705
. . .I·· ��_.
I
"
\:.'; .'
.
.
.. .
. __ . . .
.
. .
I
L1,
L5
L3
L3 and L5 from above, showing the changes in the diameters of the spinal canal.
jected to considerable bending forces as it lies at the junction between the vertically oriented lamina and the horizontally oriented pedicle. This 'interlaminar part' will therefore be susceptible to fatigue fractures or stress fractures (spondylolysis) (see p. 855).7
INTERVERTEBRAL DISCS
Two adjacent vertebral bodies are linked by an interverte bral disc. Together with the corresponding facet joints, they form the 'functional unit of JW1ghans' (see Fig. 50.3).8 The disc consists of an annulus fibrosus, a nucleus pul posus and two cartilaginous endplates. The distinction between annulus and nucleus can only be made in youth, because the consistency of the disc becomes more uniform in the elderly. For this reason, nuclear disc pro trusions are rare after the age of 70. From a clinical point of view, it is important to consider the disc as one integrated unit, the normal function of which depends largely on the integrity of all the elements. That means that damage to one component will react adversely to the others.
Figure 50.3
..:�.
.
L1
Figure 50.2
"-'-'"
Lateral view of two vertebrae: the 'functional unit'.
An upper and a lower cartiLaginous endpLate (each about 0.6 to 1 mm thick) cover the area of the ver tebral body, encircled by the peripheral apophyseal ring already described. The endplate covers the nucleus pul posus in its entirety; peripherally it fails to cover the entire extent of the annulus fibrosus.9 The collagen fibrils of the inner lamellae of the annulus enter the endplate and merge with it, resulting in all aspects of the nucleus being enclosed by a fibrous capsule.lO The endplate permits diffusion and provides the main source of nutrition for the disc.ll, 1 2 Up to the age of 8 years, the cartilaginous endplates are penetrated by blood vessels which pass into the peripheral layers of nucleus and annulus. Thereafter, the disc's nutrition is achieved by diffusion through the endplate. The hyaline endplate is also the last part of the disc to wear through during severe disc degeneration.13 Endplates.
This is made up of 15-25 concentric fibrocartilaginous sheets or 'lamellae' (Fig. 50.4), each formed by parallel fibres, rW1ning obliquely with a 30° angle between the vertebral bodies.14 Because the fibres of two consecutive layers are oriented in opposite directions, they cross each other at an angle of approximately 120°.15 This arrangement of the annular fibres gives the normal disc great strength against shearing and rotational stresses16 whereas angular movements remain perfectly possible.I 7,18 The outermost layer is attached to the verte bral body by mingling with the periosteal fibrils (fibres of Sharpey). The outer two-thirds of the annulus fibrosus is attached firmly to the apophyseal ring and the inner third merges with the cartilaginous endplate (Fig. 50.5). Annulus fibrosus.
Nucleus pulposus. This consists of a gelatinous sub stance, made of a meshwork of collagen fibrils sus pended in a mucoprotein base which contains mucopolysaccharides and water.19 As age advances, the amount of mucopolysaccharides diminishes, as does
706 SEGION TEN - THE L U M BAR SPINE
3
5
Figure 50.5 The intervertebral disc: 1, nucleus; 2, annulus; 3, cartilaginous endplate; 4, anterior longitudinal ligament; 5, posterior longitudinal ligamenl.
More recent studies have demonstrated mechano receptors to be present in the outer two or three lamellae of the human intervertebral disc and the anterior longi tudinal ligament.25 Although the presence of substance P generally accepted as an important nociceptive neurotransmitter - has so far not been demonstrated in human intervertebral discs26 other neuropeptides have.27 The exact relationship between the existence of small nerve endings in the outer layers of the disc and back pain therefore still remains controversial. The lack of blood supply to the intervertebral disc has been shown by rnicroangiographic studies.28 There is some vascularization of the vertebral borders of the disc in children but by the age of 8 years all cartilaginous pen etration by blood vessels has disappeared. Vascular buds in the bony endplate remain during adulthood as a vas cular bed under the cartilaginous endplate, and diffusion from these through the endplates remains the main nutri tional pathway for the disc during adult life,29,3o although some nutrition via contact with the intimate anterior and posterior longitudinal ligaments is also possible.31. The disc is thus the largest non-vascular structure in the body, which causes difficulties in healing and regeneration after damage. -
Figure 50.4
Lamellar construction of the annulus fibrosus,
that of the water they bind. A young nucleus is 85% water, whereas it is only 65% water in the elderly.2o These biological changes are mirrored in the macro scopic aspects of the nucleus. In the second and third decade the nucleus is clear, firm and gelatinous but subsequently it becomes drier and more friable. In the elderly, the nucleus has the appearance of thickened cream cheese: dry, brownish and friable. At birth the nucleus pulposus occupies the centre of the intervertebral space. In that the anterior part of the verte bral body grows faster than the posterior part, the nucleus comes to lie more posteriorly. Consequently, the anterior part of the arumlus will have thicker and stronger fibres,21 which means that the annulus gives better protection against anterior than posterior displacements of the nucleus, which is disadvantageous with respect to the contiguous nerve roots and dura. Cartilage is devoid of nerves and it has been conven tional to draw the same conclusions about the disc. However, over the last decades, there has been much research on the possibility that there is some innervation. The presence of free nerve endings has been demon strated as far as one-third of the way into cadaveric annuli fibrosi,22 and as far as half way into annuli fibrosi obtained during posterior fusion operations.23 Other research has shown a few nervous elements in the periphery of the annulus fibrosus.24
FUNCTIONS OF THE DISC
The primary function of the disc is to join the vertebrae and allow movement between them. The other func tions are typical of the erect spine: a shock absorber; a load distributor; and a separator of the posterior facets to maintain the size of the intervertebral foramen.
BEHAVIOUR OF THE DISC The disc as an osmotic system The main structural components of the intervertebral disc are collagen, proteoglycans (PC) and water. The water is
CHAPTER 50
not free but is bound by the PCS32 which, because of their pronounced osmotic properties, maintain the hydration and turgor of the disc. The proportion of the three con stituents varies across the disc. Fluid and PC concentra tions are highest in the nucleus and lowest in the annulus, whereas the reverse is true for collagen. Proteoglycans are complex chemical structures, exist ing as monomer subunits and aggregates. The former are made up of a central protein molecule with an attached long-chain glucosaminoglycan; the latter consist of monomers, attached to a long hyaluronic acid filament (see p. 36). The synthesis of PCs is performed by the car tilage cells and is a continuous process, demanding a well-balanced metabolism.33 For its nutrition, the disc, devoid as it is of any penetrating vascular structure, depends entirely on diffusion through the central portion of the endplates and the outer annulus.u Consequently, the disc is vulnerable and changes in its composition are inevitable as age advances. Although the total collagen content remains fairly constant during adult life,34 the PC concentration falls.35,36 The result is that the osmotic properties and the turgor of the disc will also decline as age advances (see p. 730).37 Proteoglycans play a key role in the osmotic system of the intervertebral joint, which incorporates the nucleus, annulus and cartilaginous endplates and also the can cellous bone of the vertebrae. Two compartments nucleus and paravertebral tissues - are separated by the semipermeable barrier formed by the cartilaginous end plate and the annulus fibrosus, which permits the trans port of small molecules only: water, ions and substances of low molecular weight. Diffusion tests with dye demonstrate that only substances with a molecular weight under 400 can pass the disc tissue barrier.38 The PCs of the inner compartment take up water, until the hydrostatic pressure that results is in balance with the physical tension that arises from the tensile forces of the annulus and the loads applied by muscles, ligaments and gravity (see Fig. 50.6). At this point, there is no net fluid loss or gain. If the external stress is increased, say by an increase in load, the balance will be disturbed and fluid is expressed from the nucleus (Fig. 50.7a). This loss of fluid has two consequences: tensile stress in the collagen network falls and the concentration of the PCs in the nucleus and thus the osmotic pressure rises. In other words, loss of fluid increases the internal swelling pressure, until the latter has risen to the physical stress and a new balance is achieved.4o The reverse happens when the external load decreases: the internal osmotic pressure is momen tarily higher than the external load and fluid is attracted (Fig. 50.7b). The concentration of the PCs and the swelling pressure decrease until external and internal pressures again reach an equilibrium.
-
APPLIED ANATOMY 707
C o n c l u s i o n : the f l u i d content of the d i sc i s not an i nt r i n s i c property of the t i ss u e but depends o n c h a n g es i n the extern a l load. F l u i d flow is ca used by press u re changes o n t h e d i sc: i n creased l o a d c a u ses f l u i d to be exp e l l e d, whereas low pressure a l l ows PGs i n t h e d isc to suck i n flu i d from t h e s u rrou n d i n g tissues.41
Influence of the external load on hydration of the disc Using diffusion techniques with dye and with radioactive substances, Kramer was able to show that in normal non-degenerated discs there is an extravasation of fluid when a load of more than 80 kPa is applied. Absorption takes place when the load is lower than 80 kPa.42 From 1966 on, Nachemson and co-workers demon strated the relationship between body posture and intradiscal pressure by intravital recordings.43-48 They demonstrated that the pressure in an L3 disc of a healthy individual, weighing 70 kg, is 30 kPa in a supine lying position. Standing and walking around sets up a pressure between 70 and 85 kPa, whereas sitting raises the pressure to 100 kPa and slightly bending forwards
Load + tensile stress
Internal swelling stress
Metabolite and fluid exchange
Figure 50.6
Kramer.39
The intervertebral disc as an osmotic system, as described by
708 SECTION TEN - THE LU M BAR S P I N E
These findings suggest the dehydration-hydration point, found by Kramer to be around the standing and walking position (see Fig. 50.8). The supine position causes a hydration of the disc, whereas sitting, bending or lifting squeezes fluid out of the disc. Since the transport processes in the disc depend largely on fluid flow, continuous change in intradiscal pressure could be of utmost importance for the nutrition of the disc.sO Load and de-load acts as a pump, and transports water and metabolites from and to the inter vertebral disc.s1 In order to protect discs against early degeneration, it is therefore important to keep the intradiscal pressure as low as possible during daily activ ities. This can be achieved by adopting a slight lordosis at the lumbar spine which protects the disc against exces sive pressure. Also regular changes in position continu ously alter the intradiscal pressure, so causing a nutritional fluid flow to and from the disc. The prophyl actic measures derived from these findings will be dis cussed in the section on back schools (see p. 921).
(a)
Dehydration
�
(b)
Hydration
Figure 50.7 (a) Increase in external stress causes dehydration of the nucleus; (b) decrease in external stress causes hydration of the nucleus.
to 120 kPa. Lifting a 20 kg object with a bent back and straight legs increases the intradiscal pressure to a surprising 340 kPa.
�
:::J (/) (/) Q)
n:
80 kPa Figure 50.8
Intradiscal pressure is related to position49
Biomechanical properties of the disc The fibroelastic annulus provides the disc with hydraulic properties and gives resistance to tensile forces. Retained by this fibroelastic mesh, the nucleus pulposus acts like a fluid-filled balloon. During load it distributes the axial pressure equally over the cartilage plates and the annulus fibrosus (Fig. 50.9). The annular fibres are under constant and slight stretch, because of
CHAPTER 50 - APPL I E D ANATOMY 709
P
2
3
Figure 50.10 Figure 50.9 During an axial and symmetrical load, the nucleus pulposus distributes the force to all sides and therefore perpendicularly on the stretched annular fibres. P, load; 1 , endplates; 2, nucleus; 3, annular fibres.
the turgor of the nucleus. McNab52 compares the annulus with a coiled spring that pulls the vertebral bodies together against the turgor of the nucleus. If the load is axial and symmetrical, the nucleus pulposus dis tributes the force to all sides and therefore perpendicu larly on the stretched annular fibres. In this position the disc is very strong and, during high compressive loads, outwards herniation of the nucleus is not seen but there is collapse of the cartilaginous endplates.53 Asymmetrical loading, however, simultaneously involves tension, compression and shear stresses at dif ferent locations in the disc. Bending results in a tensile stress on the convex and a compressive stress on the concave side: that under tension stretches, while that under compression bulges.5 4 Tensile stresses on the convex side are increased by the migration of the nucleus. During such asymmetrical loading, the nucleus pulposus is pushed away from the area of compression, following the simple mathematical parallelogram of forces (Fig. 50.10). This means that in bending forwards the nucleus will move posteriorly, and therefore greater stress will fall on the posterior annular fibres, which are already subjected to a strong tensile stress. The posterior migration of the nucleus pulposus in bending has been demonstrated experimentally by putting a metal pin in the nucleus pulposus.55 On contin-
Asymmetrical loading.
uous forward bending, the nucleus migrated backwards with a speed of 0.6 mm/ min during the first 3 minutes and this continued very slowly during the next hour. After relief of bending, the nucleus only very slowly regained its original position. These findings have been confirmed by discography56 and by MRI studiesY Biomechanical studies, conducted in vitro, have also demonstrated that the normal nucleus moves posteriorly in kyphosis and anteriorly in lordosis.58-tiO The weak zone of the disc. Several anatomical, biochem ical and biomechanical properties make the posterior aspect of the disc the most critical and vulnerable part of the whole intervertebral joint. • •
•
•
The posterior annular fibres are sparser and thinner than the anterior. Because the area available for diffusion is smaller posteriorly than anteriorly, the posterior part of the nuclear-annular boundary receives less nutrition and again the posterior part of the disc is the most strained part.61 The posterior longitudinal ligament affords only weak reinforcement, whereas the anterior fibres are strengthened by the powerful anterior longitudinal ligament. Because of the special mechanical arrangements of the annular fibres, the tangential tensile strain on the posterior annular fibres is four to five times the applied external load.62
7 1 0 SECTION TEN - THE L U M BAR SPINE
All these elements explain the predominance of the posterior part of the disc in the development of weaken ing, radiating ruptures and posterior nuclear displace ments. This is unfortunate, because most nociceptive tissues responsible for backache and sciatica (nerve roots and dura mater) emerge just beyond the posterior aspect of the disc. In order to prevent early degeneration and internal derangement, the erect body has developed only one ade quate defence system, namely a slightly lordotic lumbar posture. Cyriax was the first clinician to point out the importance of the lumbar lordosis. Long before bio mechanical experiments, such as those of Nachemson, and purely on clinical findings, he demonstrated the impor tance of correct poshlre in the avoidance of backache and sciatica.63 This is the physiological lumbar lordosis, which diminishes the intradiscal pressures and protects the disc against backwards displacements of the nucleus pulpo sus. 'Keep your back hollow' is still the best advice against recurrent discogenic backache, even more so in recent decades, because of the more sedentary jobs many people have. A sitting position not only increases the intradiscal pressure but also forces the lumbar spine into kyphosis by a backwards inclination of the sitting pelvis.64 Increased sedentary work is probably one of the reasons for the rising rate of lumbar syndromes.
FACET JOINTS
The joints between the lower and upper articular processes are called zygapophyseal joints, apophyseal joints or 'facet' joints. They are true synovial joints, com prised of cartilaginous articular surfaces, synovial fluid, synovial tissue and a joint capsule (Fig. 50.11). The supe rior articular surface is slightly concave and faces medi ally and posteriorly. The convex inferior articular surface points laterally and slightly anteriorly. In general, there is a change from a relatively sagittal orientation at Ll-L3, to a more coronal orientation at L5 and Sl (Fig. 50.12).65 ,66 Unlike the disc, the facet joints normally do not bear weight and during normal loads they are not subjected to compression stain.62 In degenerative fragmentation of the disc, however, intervertebral height diminishes and the articular surfaces are subjected to abnormal loading, setting up spondylarthrosis.67 The main function of the facet joints is to guide lumbar movements and keep the vertebrae in line during flexion-extension and lateral flexion. Because of the more sagittal slope of the articular surfaces, very little rotation takes place at the four upper lumbar levels. More distally, at the lumbosacral level, the joint line has a more coronal plane, which makes rota tional movements potentially possible but these are limited by the iliolumbar ligaments (see p. 712).68 The
Anterior
3
Posterior
Figure 50.11 Lateral view of facet joint with the capsule partly removed. 1, Inferior articular process; 2, superior articular process; 3, superior capsule; 4, inferior capsule; 5 part of posterior capsule (rest has been removed).
total range of rotation in the lumbar spine is therefore very limited although not completely zero.69 The capsule of the joints is well developed and thick and elastic at the dorsal, superior and inferior aspects. At rest, the fibres run slightly diagonally from lateral-caudal to medial-cranial. In that the articular excursion is about 0.5 cm at each level, the capsule must have a considerable laxity to follow the points of insertion during flexion. It therefore possesses capsular recesses of varying size, at the superior and inferior poles of the joint which gives the joint the appearance of a dumb-bell during arthro graphiC examinations.?o In extension the posterior capsule can become pinched between the apex of the inferior facet and the lamina below. In order to prevent this, some fibres of the multifidus blend with the posterior capsular fibres and keep the capsule taut?] The ventral aspect of the capsule is an extension of the ligamentum flavum. It is very thin72 and may rupture during intra-articular injections.73 Small intra-articular 'menisci' in the facet joints have been described by several authors.74-76 These are either small connective tissue rims that fill the space left by the curved margins of the articular cartilages or fibroadipose meniscoid structures which project from the inner surface of the superior and inferior capsular pouches.77 Others have identified small pads of fat, covered by a synoyial fringe at the upper and lower poles of the capsule?8-80 Stretching of the capsule during flexion makes them dis appear. Some believe that these fibro-adipose enlarge-
CHAPTER 50 - APPL I E D ANATO MY 711
---I111�"''''' 11 II!iiI!� '''''II�-IIII!!!''!!'
L4-L5
Ti+I'III't-- 3
2
L4-L5
Figure 50.1 3 Anterior longitudinal (1) and supra- and interspinous ligaments (2 and 3, respectively).
(/f.\,:>?!:;,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 <
1 . Washburn SL. The evolution of man. Sci Am 1978;239:146. 2. Lippert H. Probleme der Statik und Dynamik von Wirbelsaule
und Riickenmark. In: Trostdorf E, Stender H (eds) Wirbelsiiule und Nervensyslem. Thieme, Stuttgart, 1 970.
q. On the form of the human spine and some aspects of its mechanical behaviour. Acta Orthop Belg 1969;35:584. Kapandji IA. I' Anatomie fonctionelle du rachis lombosacree. Acta Orthop Be/g 1969;34:543. Thaczuk H. Tensile properties of human longitudinal l igaments. Acta Orthop Scand 1968;115(suppl). Hall LT, Esses SI, Noble PC, Kamaric E . Morphology of the lumbar vertebral end plates. Spine 1998;23:1517-1523. Troup JDG. The etiology of spondylosis. Orthop Clin North Am
3. Snijders 4. 5. 6. 7.
1977;8:57-64.
27. Ashton IK, Roberts S, Jaffray DC, Polak JM, E isenstein SM.
Neuropeptides in the human intervertebral disc. j Orthop Res 1994;12:1 86-192. 28. Hassler O. Human intervertebral disc. Acta Orthop Scand 1 970;40:765. 29. Ogata K, Whiteside LA. N utritional pathways of the interverte
bral disc. An experimental study using hydrogen washout tech nique. Spine 1981;6:211-216. 30. Urban JPG, Holm S, Maroudas S. Diffusion of small solutes into the intervertebral disc: an in vivo study. Biorheology 1978;15: 203-221 . 3 1 . Maroudas A. Nachemson A, Stockwell R, Urban J . In vitro studies of nutrition of intervertebral disc. Society for Back Pain Research, London, 1973.
8. Farfan HF. Mechanical Disorders of the Low Back. Lea & Febiger,
32. Mankin HJ, Thrasher AZ. Water content and binding in normal
Philadelphia, 1973. 9. Roberts S, Menage J, Urban PG. Biochemical and structural
and osteoarthrotic human cartilage. J Bone Joint Surg 1 975;57A: 76-80. 33. Jayson MIV, Barks JS. Structural changes in the intervertebral disc. A n n Rheum Dis 1 973;32: 10-15. 34. Brickley-Parson D, Glimcher M. Is the chemistry of collagen in the intervertebral disc an expression of Wol ff's law: a study of the human lumbar spine. Spine 1984;9:148-163.
properties of the cartilage end-plate and its relation to the inter vertebral discs. Spine 1989;14:1 66-174. 10. Taylor JR. The development and adult structure of lumbar inter vertebral discs. J Man Med 1990;5:43-47. 1 1 . Nachemson A, Lewin T, Maroudas A. Freeman MAR. Tn vitro diffusion of dye through the end plates and the annulus fibrosus of human lumbar intervertebral discs. Acta Orthop Scand 1970;41:589-607. 12. Roberts S, Menage J, Urban JPG. Biomechanical and structural
properties of the cartilage end-plate and its relation to the inter vertebral disc. Spine 1989;14:1 66-174. 13. Vernon-Roberts B. Ageing Lumbar Spine. Lecture to the Society of
Back Pain Research, 1975. 14. Joplin RJ. Intervertebral disc. Surg Gynecol Obstet 1935;61:59 1 . 1 5 . Markolf KL, Morris J M . The structural components of the inter
vertebral disc. j Bone Joint Surg 1974;56A:675-687. 16. Krismer M, Haid C, Rabl W. The contribution of anulus fibers to
torque resistance. Spine 1 996;21 :2551-2557.
17. Galante J. Tensile properties of the lumbar annulus fibrosus. Acta Orthop Scand 1967;100(suppJ). 18. Marchand F, Ahmed AM. Investigation of the laminate struc
ture of lumbar disc anulus fibrosus. Spine 1990;15:402-410. 19. Eyre DR. Biochemistry of the intervertebral disc. In: Hall DA, Jackson DS (eds) International Reviews of Connective Tissue Research. Academic Press, New York, 1979. 20. Naylor A . Intervertebral disc prolapse and degeneration. The biomechanical and biophysical approach. Spine 1976;1:108. 21 . Inoue H, Takeda T. Three-dimensional observation of the colla
gen frame-work of the lumbar intervertebral disc. Acta Orthop Scand 1975;46:946-956. 22. Bogduk N, Tynan W, Wilson AS. The innervation of the human lumbar intervertebral discs. j Anat 1981;132:39-56. 23. Yoshizawa H, O' Brien JP, Smith WT, Trumper M. The neuro
pathology of intervertebral discs removed for low-back pain. J PathoI 1980;132:95-104.
24. Konttinen Y, Gronblad M, Antti-Poika I et a/. Neuro-immuno
histochemical analysis of peridiscal nociceptive neural elements
Spine 1990;15:383-386. 25. Roberts S, Eisenstein SM, Menage J, Evans H, Ashton K.
Mechanoreceptors in intervertebral discs; morphology, distri bution and neuropeptides. Spine 1995;20:2645-2651 . 26. Kordala 0, Gronblad M , Liesi P, Karahurju E . Immuno histochemical demonstration of nociceptors in the ligamentous sh'uctures of the lumbar spine. Spine 1985;10:156-157.
35. Adam P, Muir H. Qualitative changes with age of proteoglycans
of human lumbar discs. A n n Rheum Dis 1976;35:289-295. 36. Johnstone B, Bayliss MT. The large proteoglycans of the human
intervertebral disc. Spine 1 995;20:674-684. 37. Lyons G, Eisenstein SM, Sweet MBE. Biochemical changes
in intervertebral disc degeneration. Biochem Biophys Acta 1981;673:443-453. 38. Kramer J. Biomechanische Veranderungen im lumbalen Bewegungssegment. In: Die Wirbelsiiule in Forsch ung lind Praxis. Chapter 58, Von H Junghanns. Hippokrates, Stuttgart, 1 973. 39. Kramer J. Bandscheibenbedingte Erkrankungen. Thieme, Stuttgart, 1978. 40. Adams M, H u tton We. The effect of posture on the fluid
content of the lumbar intervertebral disc. Spine 1983;8:665-671 . 4 1 . Urban JPG, McMullin JF. Swelling pressure of the lumbar inter
vertebral discs: influence of age, spinal level, composition and degeneration. Spine 1988;13: 1 79-187. 42. Kramer J. Biochemie der Zwischenwirbelscheiben. Wirbelsiiule Forsch Prax 1 974;59:10. 43. Nachemson A . Lumbar intradiscal pressure. Acta Orthop Scand
1 960;43(su ppJ). 44. Nachemson A. The influence of spinal movements on the
lumbar intradiscal pressure and on the tensile stresses in the anulus fibrosus. Acta Orthop Scand 1963;33 : 1 83. 45. Nachemson A, Morris J. In vivo measurements of intradiscal pressure; discometry, a method for the determination of pres sure in the lower lumbar discs. J Bone joint S u rg 1964;46A: I 077. 46. Nachemson A. The load on lumbar discs in d ifferent positions
of the body. Clin Orthop 1966;45:107. A, E l fstrom G. In travital
47. N achemson
Dynamic
Pressure
Measurements in Lumbar Discs. A Study of Common Movements, Maneuvers and Exercises. Almquist & Wiksell, Stockholm, 1 970.
48. Nachemson A. The lumbar spine, an orthopaedic challenge. Spine 1976;1:59. 49. N achemson A. Towards a better understanding of low-back
pain: a review of the mechanics of the lumbar spine. Rheumatol RehabiI 1 975;14: 1 29. 50. Holm S, Nachemson A. Variations in the nutrition of the canine
intervertebral disc induced by motion. Spine 1 983;8:866-874.
726 SECTI ON TEN - THE L U M BAR SPI N E
5 1 . Holm S , Urban JPG. The intervertebral disc: factors contribut
78. Engel R. Bogduk N. The menisci of the lumbar zygaphophy
ing to its nutrition and matrix turnover. In: Helminen HJ (ed) Joint Loading. Wright, Bristol, 1987. 52. McNab 1 . Backache. Williams & Wilkins, Baltimore, 1983.
79. Taylor JR, Twomey LT. Age changes in lumbar zygapophyseal
53. Hirsch C. The reaction of intervertebral discs to compression
forces. J Bone Joint Surg 1955;37 A:1188-1 191 . 54. White A,
Panjabi M. Clinical Biomechanics of the Spine. Lippincott, Philadelphia, 1978:1-18, 328-344, 502-504. 55. Vogel G. Experimental Untersuchungen zur Mobilitat des Nucleus Pulposus in Lumbalen Bandscheiben. Medical Dissertation, Du sseldorf, 1977. 56. Shah JS, Hampson WA, Jayson MIV. The distribution of surface strain in the cadaveric lumbar spine. J Bone Joint S u rg 1978;608:246-251 . 57. Beattie PF, Brooks WM, Rothstein JM et al. Effect of lordosis on
seal joints. J Anat 1982;135:795. joints. Observations on structures and function. Spine 1986;11 :739-745. 80. Hodley LA. Anatomico-Roen tgenographic Studies of the Spine Thomas, Springfield, 1964. 8 1 . Kos J, Wol f J. Les menisques intervertebraux et leur role dans les blocage vertebraux. Ann Med Phys 1 972;15:203-218. 82. Giles LGF, Taylor JR. Inter-articular synovial protrusions. Bull Hosp Joint Dis 1982;42:248-255. 83. Bogduk N, Jull G. The theoretical pathology of acute locked
back: a basis for manipulative therapy. Man Med 1985;1: 78-82. 84. Bogduk N, Wilson AS, Tynan W. The human lumbar dorsal
the position of the nucleus pulposus in supine subjects. Spine 1994;19:2096-2102. 58. Krag MH, Seroussi RE, Wilder DG, Pope M H . Internal dis placement distribution from in vitro loading of human thoracic and lumbar spinal motion segments: experimental results and theoretical predictions. Spille 1987;12:1 001-1007. 59. Schnebel BE, Simmons JW, Chowning J, Davidson R. A digitiz ing technique for the study of movements of intradiscal dye in
87. Ramsey RH. The anatomy of the ligamenta flava. Clin Orthop
response to flexion and extension of the lumbar spine. Spine 1988;13:309-312.
88. Olszewski AD, Yaszemski MJ, White AA. The anatomy of the
60. Serrousi RE, Krag MH, Muller DL, Pope MH. Internal defor
mations of intact and denucleated human lumbar discs sub jected to compression, flexion and extension loads. J Orthop Res 61 . 62. 63. 64. 65.
] 989;7:1 22-1 3 1 . Belytschko T, Kulak RF, Schultz A , Galante J. Finite element stress analysis of an intervertebral disc. J Biomech 1974;7:277-285. Nachemson A. Some mechanical properties of the lumbar intervertebral disc. Bull Hosp Joint Dis 1962;23: 130. Cyriax JH. Disc Lesions. Cassell, London, 1953. Cyriax JH. The Slipped Disc. Scribner, London, 1980. Schneck CD. The anatomy of lumbar spondylosis. Clin Orthop
66. Ebraheim NA, Lu J, Hao Y, Biyani A, Yeasting RA. Anatomic
considerations of the lumbar isthmus. Spine 1997;22:941-945.
67. Groher W. Diagnostik und konservative Behandlung der
Lumbosakralarthrose. Orthop Prax 1 977;8:564. 68. Chow D, Luk K, Leong J, WOO C. Torsional stability of the lumbosacral junction. Significance of the iliolumbar ligament. Spine 1989;14(6) :611-615. 69. McFadden KD, Taylor JR. Axial rotation in the lumbar spine, and gaping of the zygapophyseal joints. Spine 1990;15:295-299. A.
Verhalten
lumbar longitudinal ligaments: Correlatice MR and anatomic study. Radiology 1989;171:197-205. 86. Hukins DWL. Disc structure and function. In Gosh P (ed) TIle Biology of the In tervertebral Disc, vol 1 . CRC Press, Boca Raton, 1988:1-37. 1966;44:129-140.
human lumbar ligamentum flavum; new observations and their surgical importance. Spine 1996;21:2307-2312. 89. Yahia LH, Garron S, Strykowski H, Rivard CH. Ultrastructure
of the human interspinous ligament and ligamentum flavum. Spine 1990;15:262-268. 90. Heylings DJA. Supraspinous and interspinous ligaments of the human lumbar spine. J Anat 1978;125:127. 91. Dickley JF, Bednar DA, Dumas GA. New insight into the
mechanics of the lumbar interspinous ligament. Spine 1996;21: 2720-2727. 92. Hukins DWL, Kirby MC, Sikoryn TA, Aspden RM, Cox AJ.
Comparison of structure, mechanical properties and functions
Rei Res 1985;193:20-37.
70. Kaschner
rami J Anat 1982;134:389-397. 85. Grenier N, Gressel JF, Vital JM et al. Normal and disrupted
der
Wirbelgelenkkapsel
of lumbar spinal ligaments. Spine 1990;15:787-795. 93. Adams MA, Hutton WC, Stott JRR. The resistance to flexion of
the lumbar intervertebral joint. Spine 1980;5:245. 94. Tesh KM, Shaw Dunn J, Evans JH. The abdominal muscles and
vertebral stabili ty. Spine 1 987;12:501-508. 95. Pearcy MJ, Tibrewal SB. Lumbar intervertebral disc and ' liga
ment deformations measured in vivo. Clin Orthop Rei Res 1984;191:281-286. 96. Leong JCY, Luk KDK, Chow DHK, Woo Cw. The biomechani
bei
cal functions of the iliolumbar ligament in maintaining stabil
Stel lungsanderungen im lumbalen Bewegunssegment. Med Diss, Dusseldorf, 1976.
ity of the lumbosacral junction. Spine 1987;12:669-674. 97. Luk KDK, Leong JCY. The iliolumbar ligament: a study of its anatomy, development and clinical significance. J Bone Joint
71. Lewin T. Osteoarthritis in lumbar synovial joints. Acta Orthop Scnnd 1966;supp1.73. 72. Yong-Hing K, Reilly J, Kirkaldy-Willis WHo The ligamentum
flavum. Spine 1976;'1:226-234.
73. Moran R. O'Connell D, Walsh MG. The diagnostic value of
facet joint injections. Spine 1988;13: 1 407-1410. 74. Tondury G. Beitrag zur Kermhlis der kleinen Wirbelgelenken.
Z Anat En twGesch 1940;110:568. 75. Emminger E . Die Gelenkdisci a n der Wirbelsaule (eine
mogliche Erklarung wirbelsaulenabhangiger Schmerz zustande). Hefte Unfal/heilk 1955;48:142. 76. Dorr WR. Ober die Anatomie des Wirbelgelenke. Arch Orthop Unfal/chir 1985;50:222. 77. Bogduk N, Engel R . The menisci of the lumbar zygapophyseal
joints. A review of their anatomy and clinical significance. Spine 1984;9:454-460.
Surg 1986;68B: 197-200. 98. Hanson P, Solesson B. The anatomy of the iliolumbar ligament. A rch Phys Med Rehab 1994;75:1 245-1246. 99. Basadonna P-T, Gasparini D, Rucco V. Iliolumbar ligament
insertions; in vivo anatomic study. Spille 1996;21:231 3-2316.
100. Mitchell GA. The l umbosacral junction. J Bone Join! Surg 1934;16:233-254. 1 0 1 . Yamamoto I, Panjabi MM, Oxland TR, Crisco JJ. The role of the
iliolumbar ligament in the lumbosacral junction.
Spine
190;15:1138-1141 . 102. Hasue M, Fujiwara M, Kikuchi S. A new method of quantita
tive measurement of abdominal and back muscle strellgth, Spine 1980;5:1 53-148. 103. Bogduk N. A reappraisal of the anatomy of the human erector spinae. J Ana! 1980;131:525-540.
CHAPTER 50 - APPLI E D ANATOMY 727
1 04. Bogduk N, Macintosh JE. The applied anatomy of the thoraco
Lumbar fascia. Spi/le 1984;9:1 64-170.
1 28. Smyth MJ, Wright V. Sciatica and the intervertebral d isc. An
experimental study. 1 Bone 10inl Surg 1 959;40A : 1 401-1418.
105. Vleeming
A, Pool-Goudzwaard A, Stoeckaert R, van Wingerden J-p, Snijders e. The posterior layer of the thoraco
1 29. Walton IN. (ed) Brain 's Diseases of the Nervous Systelll, 8th edn.
lumbar fascia. Spine 1995;20:753-758. 106. de Berail A. Exploration radiologique du rachis lombaire
1 30. Guyer RD, Collier RR, Ohnmeiss DD et al. Extraosseous spinal
normal et son application au syndrome du canal lombaire etroit. Thesis of Medicine 1 976: 1 76. 107. Duby P. Contribution a l'etude anatomique du cul-de-sac dural. Implications en medecine osteopsyhique. Ann Med Osteop 1985;1(1):9-14. 108. Hofmann M. Die Befestigung der Dura mater im Wirbelkanal. Arch Anal Physio (Anat Abt) 1899;403. 1 09. Parkin IG, Harrison GR. The topographical anatomy of the
lumbar epidural space. J Anal 1 985;141 :21 1-217. 110. Scapinelli R. Anatomical and radiological studies on the
lu mbosacral meningovertebral ligaments of humans. J Spinal Disord 1990;3:6-15. 111 . Posner T, White AA, Edwards WT, Hayes We. A biomechani
cal analysis of the clinical stability of the lumbar and lumbo6acral spine. Spine 1982;7:374-389. 1 1 2. Tencer AF, Allen BL, Ferguson RL. A biomechanical study of thoraco-lumbar spine fractures with bone in the canal. Part III: Mechanical properties of the dura and its tethering ligaments. Spille 1985;10(8):741-747. 113. Hollinstead WHo Analomy for Slirgeons, Vol 3: The Back and Limbs, Harper & Row, New York, 1969. 114. Wiltse LL, Fonseca AS, Amster J el al. Relationship of the dura,
Hofmann's ligaments, Batson's plexus and a fibrovascular membrane lying on the posterior surface of the vertebral bodies and attaching to the deep layer of the posterior longi tudinal ligament. Spine 1993;18:1 030-1043. 115. Nowickj BH, Haughton VM. Neural foraminal ligaments of the lumbar spine: appearance at CT and NMR imaging. Radiology 1992;183:257-264. 116. O'Connell JEA. The clinical signs of meningeal irritation. Brain 1946;69:9-2 1 . 1 1 7. Breig A. Adverse Mechanical Tension i n the Cenlral Nervous Syslem. Amqvist and Wiksell, Stockholm, 1 978. 118. Reid JD. Effects of flexion-extension movements of the head
and the spine upon the spinal core and nerve roots. / Neurosurg Psychialry 1 960;23:214-221 . 119. Adams C, Logue V. Studies in cervical spondylotic myelopathy.
120. 121 . 122. 123.
1. Movement of the cervical roots, dura and cord and their rela tion to the course of extra thecal roots. Brain 1971;94:557-568. Bourret P, Louis R. Analomie du Systeme Nerveux Central, 2nd end. Expansion Scientifique Franc;aise, Paris, 1974. Louis R. Dynamique vertebro-radiculaire et vertebro-medul laire. Anal Ciin 1981;3: 1-1 1 . Decker R . La mobilite d e la moelle epiniere a l'interieur du canal vertebral. Ann Radiol (Paris) 1 961;83:883-888. Klein P, Burnotte J. Contibution a I'etude biommecanique de l a moelle epiniere e t ses enveloppes. A n n Med Osteopath
1 985;1(3). 124. Goddard MD, Reid JD. Movements induced by straight-leg raiSing in the lumbo-sacral roots, nerves and plexus, and in the
intrapelvic section of the sciatic nerve. 1 Neurol Neurosurg Psychiatry 1 965;28:12-18. 125. Martins AN. Dynamics of the cerebrospinal fluid and the spinal dura mater. J Neurol Neurosurg PsychialnJ 1972;35:468-473. 126. Cyriax JH. Lumbago: the mechanism of dural pain. Lancet 1945;ii:427. 127. EI Mahdi MA, Latif FYA, Janko M. The spinal nerve root inner
vation, and a new concept of the clirticopathological interrela tions in back pain and sciatica. Neurochirurgia 1981;24:137-1 4 1 .
Oxford University Press, Oxford, 1977:407-408. lesions mimicking disc disease. Spine 1988;13:228-231 . 1 3 1 . Cuatico W, Parker Je. Further investigations o n spinal
meningeal nerves and their role in pain production. Acla Nell rochir 1989;101 : 1 26-128.
132. Pedersen HE, Conrad FJ, Blunck MD, Gartner E. The anatomy
of lumbosacral posterior rami. and meningeal branches of spinal nerves (sinu-vertebral nerves) with an experimental study of their functions. J Bone 10inl S u rg 1 956;38A(2):377. 133. Stilwell DL. The nerve supply of the vertebral column and its
associated structures in the monkey. Anat Red 1956;125(2): 1 39-162. 134. Jackson He, Winkelmann RK, Bickel WHo Nerve endings in
the human lumbar spinal column and related structures. J BOlle Joint Surg 1966;48A:1272-1 281 . 135. Edgar MA, Nundy S . Innervation o f the spinal dura mater. / Neurol Neurosurg Psychiatry 1966;29:530-534. 136. Edgar MA, Ghadially JA. Innervation of the lumbar spine. Ciin Orlhop Rei Res 1976;115:35-4 1 . 137. Ahmed
M , Bjurholm A , Kreicbergs A , Schultzberg M . Neuropeptide Y, tyrosine hydroxylase a n d vasoactive intes
tinal polypeptide - immunoreactive nerve fibers in the verte bral bodies, discs, dura mater and spinal ligaments of the rat lumbar spine. Spine 1993;18:268-273. 138. Kallakari S, Cavanaugh JM,
Blagoev De. An imm uno histochemical study of innervation of lumbar spinal dura and
longitudinal ligaments. Spine 1 998;23:403-4 1 1 . 139. Groen GJ, Baljet B , Drukker J. The innervation of the spinal
dura mater: anatomy and clinical implications. Acla Neurochir (Wien) 1 988;92:39-46. 140. Groen GJ, Baljet B, Drukker J. Nerves and nerve plexuses of the human vertebral column. Am / Anal 1 990;188:289-296.
1 4 1 . Pertuiset B. Compression extra-durale et extra-medullaire. Rev Prat 1966;XVI(19):2605-2612. 142. Buchheit F, Maitrot D, Middleton L, Gusmao S. Narrow radic
ular canal. In: Wackenheim A, Babin E (eds) The Narrow LlIlllbar Canal. Springer, Berlin, 1980. 143. Bose, K, Balasubramaniam P. Nerve root canals of the lumbar
spine. Spine 1984;9: 1 6. 144. Ciric I, Mikhael MA, Tarkington JA, Vick NA. The lateral recess syndrome. / Neurosurg 1980;53:433. 145. Weinstein PR. The application of anatomy and pathophysiol ogy in the management of l u mbar spine disease. Clill Neurosllrg 1980;27:517. 146. Crock HV. Normal and pathological anatomy of the lumbar spinal nerve root canals. J Bone /oinl Surg 1981;63B:487. 147. Neirdre A, MacNab 1. Anomalies of the lu mbosacral nerve
roots. Spine 1983;8:294-299. 148. Kadish LJ, Simmons EH. Anomalies of the lumbosacral nerve
roots. / Bone Joint Surg 1984;66B:411-416. 149. Dorwart RH, Vogler JB, Helms CA. Spinal stenosis. Radiol Ciill North Am 1 983;21:20 1 .
150. Brieg A. Biomechanics of the lu mbosacral nerve roots. Acta Radiol (Oiagn) (Stockh) 1963;1: 1 1 4 1 . 1 5 1 . Forestier J . Le trou d e conjugaison vertebral e t I'espace
epidural. Etude Analomique el Clinique. These Paris, 1922. 152. Spencer DL, Irwin GS, Miller JA. Anatomy and significance of
fixation of the lumbosacral nerve roots in sciatica. Spine 1983;8(6) :672-679. 153. Sunderland S. Meningeal neural relations in the intervertebral
foramen. J Neurosurg 1974;40:756-763.
728 SECTION TEN - T H E LU M BAR SPINE
154. Falconer MA, McGeorge M, Begg C A . Observations on the
163. Parkin IG, Harrison GR. The topographical anatomy of the
cause and the mechanism of symptom production in sciatica and low back pain. J Neurol Neurosurg Psychiatnj 1 948;11:13-26.
164. Batson Ov. The function of the vertebral veins and their role in
155. Charnley J. Orthopaedic signs in the diagnosis of disc protru
sion. Lancet 1951;i:186-1 92. 156. Estridge MN, Rouhe SA, Johnson NG. The femoral stretching
test. J Neurosurg 1982;57:813-817. 157. Breig A, Troup J . Biomechanical considerations in the straight leg-raising test. Cadaveric and clinical studies of the effect of medial hip rotation. Spine 1 979;4:242-250. 158. Cyriax J H . The Slipped Disc, 2nd edn. Gower Press, Epping, 1975:44. 159. Lindahl O. Hyperalgesia of the lumbar nerve roots in sciatica. Acta Orthop Scand 1 966;37:367. 160. Murphy RW. Nerve roots and spinal nerves in degenerative
lumbar epidural space. J Anat 1995;141:211-217. the spread of metastasis. Ann Surg 1940;112:138. 165. Cyriax JH. Textbook of Orthopaedic Medicine, vol 1, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:358.
166. Luschka H. Die nerven des Menschlichen Wirbelkanales. Verlag
der H. Lapschen Buchhandlung P.Y. 1850;4850:8: 1 . 167. Wiberg G. Back pain i n relation to the nerve supply of the
intervertebral disc. Acta Orthop Scand 1 948-50;214: 18-19. 168. Lazorthes G, Poulhes J, Espagno J. Etude sur les nerfs sinu
vertebraux lombaires. Le nerf de Roofe, existe-t-il? Compt Rend Assoc Anat 1 948;34: Reunion; 317. 169. Bradley KC. The anatomy of backache. Aust NZ J Surg 1 974;44:227-232.
disc disease. Clin Orthop 1977;129:46. 161 . Inman VT, Saunders JB. The clinico-anatomical aspects of the
1 70. Sunderland S. Nerves and Nerve Inju ries, 2nd edn. Churchill
lumbo-sacral region. Radiology 1 942;38:669. 162. O'Connell JEA. Sciatica and the mechanism of the production on the clinical synd rome in protrusions of the lumbar inter vertebral discs. Br J Surg 1943;30:315.
1 7 1 . Bogduk N. The innervation of the lumbar spine. Spine
Livingstone, Edinburgh, 1 978. 1985;8:286-293. 1 72. Bogduk N, Wilson AS, Tynan W. The human lumbar dorsal
rami. J Anat 1982;134:383-397.
Ageing of the lumbar spine
CHAPTER CONTENTS I';troduction
729
Ageing of the disc
•
730
Mechanism 730 Structural changes Disc displacements
731
731
Posterior displacements 733 Posterolateral displacement 734 Anterior displacement in adolescents 735 Anterior displacement in the elderly 735 Vertical displacement 735 Circular displacement 736 Ageing of the surrounding tissues
INTRODUCTION
736
Effects on the ligaments 736 Effects on the facet joints 736 Effects on the spinal canal and intervertebral foramen 737 �adiological changes
738
Relationship between degeneration and symptoms
739
The human spine functions in a reverse way from that for which it was originally developed: instead of a hanging bridge connecting the anterior to the posterior limbs, it has become a vertical column, fundamentally changing the biomechanics and imposing larger loads on the lower lumbar discs. The upright posture in man has been blamed for a long time as the main cause for the development of early disc degeneration: 'interverte bral disc disease is the price we pay for the gift of the erect posture'.1 Disc degeneration in animals is very unusuaJ.2 Also localized bulging and Schmorl's nodules have never been observed in quadrupeds.3 However, a quadruped forced to live in an erect position quickly develops structural changes in the annulus fibrosus and nucleus pulposus.4-6 Large disc herniations at the lumbosacral level also occur in 25% of bipedal rats? It seems obvious therefore, that the upright position and the consequent increase in static loading of the disc8 are the main causes of the early and progressive development of degeneration in the human lumbar spine. Degenerative changes in the intervertebral discs are so common that they can be regarded as normal and physi ological processes. Therefore we do not use the term intervertebral disc ' disease' but prefer to speak of inter vertebral disc ageing'. Degeneration of the lumbar discs starts very early in life. Clear microscopic signs of degeneration have been demonstrated in a 4-year-old.9 Several reports of prolapsed discs in children and adolescents show that major disc degeneration appears at or before pubertylO-I4 and it has been maintained that after the age of 30 years there is no lumbar disc which does not show some degenerative changes. IS There seems to be no way to escape this degeneration because it affects all, whatever their weight, physical build or athleticism.I 6 I
729
730 SECTION TEN - THE LUMBAR SPINE
AGEING OF THE DISC MECHANISM
Both the erect posture, which imposes heavier mechanical stresses on the spine, and the decreased regenerative capacity of the disc make it very vulnerable. As has been described (see Ch. 50), the disc depends for its nutrition on diffusion through the endplates and annulus, which can only take place as an outcome of change in intradiscal pressure within a physical range (Fig. 51.1). Consequently, both excessive forces, and immobilization will have deleterious effects on disc tissueF A modern lifestyle for example, in which a sitting position is the rule, puts continuous increased pressure on the disc; which is then constantly kept low in water content, which prevents transport of nutrients. As the cells are undernourished the fibrils and ground substance become damaged and their chemical composition changes.1s Enzymatic depoly merization of collagen and mucopolysaccharide causes a decrease in weight and content that results in a decrease of oncotic pressure, which leads to further loss of water.19 !he drying out of the disc is the most characteristic sign of mtervertebral degeneration. The loss of hydrostatic pres-
Pre
�
Hydration
_.
rn
ure
80 kPa
-.
+-.. Figure 51.1
sure in an ageing disc is also reflected in the changing of the daily variations in body height: in adolescence the dif ference in body height between morning and night is 2%, but this drops to 0.2% in adults.2o The mature disc is thus permanently dried out and lacks the osmotic elasticity of the young disc. Loss of water-binding capacity is also responsible for the decrease of disc turgor and the loss of endurance. The disc does not sustain the normal loads and the hydra tion-dehydration curve shifts in the direction of further dehydration (Fig. 51.2). A vicious cycle of further degen eration, further decrease in molecular weight and further fall in water-binding capacity is set up (Fig. 51.3).2 1 The permeability of the vertebral endplates also decreases with advancing age and disc degeneration.22 The early stage of the changes in vertebral bone structure can be seen on MRI.23 Vertebral endplate sclerosis, which accompanies advanced disc degeneration, later becomes radiographically visible.24 Another consequence of the decrease of oncotic pres sure is loss of disc height and narrowing of the interver tebral space, which in turn influences the function of the facet joints and the anatomical relationships of the inter vertebral foramina.
Dehydration -..
t ..
Hydration-dehydration changes with load and consequently with activity and posture.
-+
CHAPTER 51
-¢�
Dehydration
Hydration
60
80
Figure 51.2 . Loss of water-binding capacity leads to loss of endurance; the disc cannot sustain normal loads and the hydration-dehydration curve shifts further in the direction of dehydration.
STRUCTURAL CHANGES
As the nucleus pulposus dries out, it becomes less able to exert fluid pressure. The annulus is no longer under con stant tension in relation to the nucleus. A greater share of vertical load is therefore borne by the annular fibres, which are subjected to bulk deformations and shear strains.25 Consequently the greater stresses lead to tears in the am1Ular fibres,26 occurring first in the weakest part of the disc. The posterior boundary zone between nucleus and am1ulus is the first to be exposed to nutrient deficiency.27 The area between annulus and nucleus posteriorly is also particularly under mechanical strain.28 This part of the annulus will therefore be the first to wear through, so that small radial fissures appear.29 ,30 Further softening and loosening of annular tissue leads to expansion of these fissures and the formation of cavities and cysts, which are radiographically seen as air pockets.31 Nuclear displace ments through these fissures will lead to a further decrease of disc height. As a result, the intervertebral joint becomes unstable and is subjected to more bulk deformation and more shear strain. Ruptures permit further migration of the disc material in the direction of
-
AGEING OF THE LUMBAR SPINE 731
least resistance (mostly backwards). The result is intradiscal displacements, bulging beyond the vertebral borders and disc prolapses (see Ch. 52). Ageing of the disc also involves structural changes in the endplate. Between the ages of 20 and 65, the end plate becomes thinner and cell death occurs in the superficial layer of the cartilage.32 The vascular channels in the subchondral bone of the endplate are gradually occluded, finally leading to complete endplate sclerosis. In that the endplate plays an important role in the nutri tion of the disc, changes in it will contribute to further degeneration of the whole intervertebral disc. Also, the strength of the vertebral endplate decreases with age which renders it more liable to (micro )fractures. Microscopic defects may be followed by invasion of the disc by young blood vessels and connective tissue cells.33 The latter undergo metaplasia into cartilage cells and granulation tissue and adult connective tissue also forms.34 This 'invading' connective tissue can spread out into the disc, create zones of decreased resistance and cause more weakness and instability. It has even been hypothesized that this 'new' proliferative tissue takes part in disc herniations.3 5 The macroscopic degeneration of the disc was divided into four grades by Friberg and Hirsch36 and later by Nachemson.37 This scheme for assessing the gross mor phological changes in the lumbar intervertebral discs has recently been improved by Thompson et al38 who con sider five morphological grades (Table 51.1 and Fig. 51.4). Macroscopic grades of disc degeneration have been correlated with age, sex and spinal level for 600 lumbar in:ervertebral discs from 273 cadavers in a review by . MIller et al.39 TheIr conclusion was that by the age of 50 years 97% of all lumbar discs exhibit degeneration and that the L3-L4 and L4-L5 levels usually contain the n:os� . severely degenerated discs. They also reported slgmficantly more degeneration in males than in females, a�d suggested this was because of the greater compres S10n load on and the longer avascular nutritional pathway of the disc in men. These figures establish that disc degeneration is a normal age-dependent pathophysiological process: it therefore cannot be regarded as a 'disease' but is a normal biological event from which no one will escape.
DISC DISPLACEMENTS
Figure 51.3
Vicious cycle of disc degeneration.
Fissures in the annulus fibrosus will inevitably lead to changes in the biomechanical behaviour of nucleus and annulus, which can then result in intradiscal nuclear displacements, protrusions and prolapses (Fig. 51.5). The disc tissue itself is virtually insensitive, so that displacements are painless, except when they irritate
732 SECTION TEN - THE LUMBAR SPINE
Table 51.1 Description of the morphologic grades Grade
III
Nucleus
Annulus
Endplate
Vertebral body
Bulging gel
Discrete fibrous lamellae
Hyaline, uniformly thick
Margins rounded
White fibrous tissue
Mucinous material between
Thickness irregular
Margins pointed
peripherally
lamellae
Consolidated fibrous tissue
Extensive mucinous infiltration; loss
Focal defects in cartilage
IV
Horizontal clefts parallel to
Focal disruptions
endplate
Early chondrophytes or osteophytes at margins
of annular-nuclear demarcation Fibrocartilage extending from
Osteophytes less than 2 mm
subchondral bone; irregularity and focal sclerosis in subchondral bone
V
Clefts extend through nucleus
Diffuse sclerosis
Osteophytes greater than 2 mm
and annulus
Reproduced with pernission from Thompson et aP8
other and more sensitive tissues, such as the dura or nerve root sleeves. Therefore not only is the size of the displacement of importance but also its position in the canal and the degree of irritation of sensitive tissues. Because imaging techniques (CT, disco gram, CT discogram and MRI) can only detect the size and the localization of the bulges, and not always their effect on surrounding tissues, many more disc displacements are
detected during imaging than actually cause symp toms.40,41 More than 50% of asymptomatic patients over 40 years of age have either alterations in or displacements of disc.4 1 Single or multilevel disc bulging is visible on the MRIs of between 28 and 85% of the adult population who do not have activity-limiting low back pain.4 2-4 S Cyriax46 listed five different directions in which discal tissue can move: posterior, posterolateral, anterior,
Figure 51.4 The appearance of typical disc of each grade. From Thompson et a(38, with permission.
CHAPTER 51 - AGEING OF THE LUMBAR SPINE 733
(c)
(b)
(a)
Figure 51.5 Disc displacement: (a) displaced tissue within the disc; (b) bulging of the intervertebral disc without perforation of the annlus fibrosus; (c) herniation of intervertebral disc tissue through the annulus fibrosus into the spinal canal (prolapse).
vertical and circular. Each type of displacement occurs during a specific period in the degeneration of the disc. Posterior and posterolateral displacements are typical in the thirci, fourth and fifth decades. Anterior displace ment resulting in osteochondrosis is a disorder of teenagers, whereas anterior displacement in combina tion with a disc resorption is a lesion of the elderly and is seldom seen below the age of 50. POSTERIOR DISPLACEMENTS
The posterior boundary zone between the annulus and the nucleus is the first part to develop areas of degenera tive change and fissures (see p. 731). In sitting and forward bending, the disc is asymmetrically loaded, with a compression strain anteriorly and a tensile stress dor sally. Because of the increase of intradiscal pressure, the nucleus pulposus is pushed dorsally and applies more stress to the weakened posterior fibres which are already subjected to the strong tensile stress imposed by the flexion. 47
(a)
(b)
Posterior migration of disc tissue beyond the posterior limits of the intervertebral joint space causes tension on the posterior longitudinal ligament. Irritation of liga ment, dura mater and the Hofmann complex combine to produce backache (Fig. 51.6a). The patient's history usually suggests the type and localization of the dis placement and the degree of dural irritation: progres sively increasing backache usually stems from a nuclear displacement. A sudden shift indicates that the material that has moved is of harder, annular consistency. If the bulge irritates the dura centrally, the pain is central, prob ably with some bilateral gluteal radiation. If it lies more to one side, unilateral pain and pain in one buttock result. In a large posterior displacement, the dura mater is much more irritated; the clinical picture that results is an attack of acute lumbago (Fig. 51.6b). In a cartilaginous displacement the patient states that bending, lifting or standing after having sat for a while, results in acute and severe pain. Alternatively, the pain and disability have come on gradually, some hours after a period of stooping or sitting, which suggests protrusion of part of the
(c)
Figure 51.6 Posterior disc displacement in (a) backache; (b) acute lumbago; (c) massive posterior protrusion (84 or cauda equina syndrome).
734 SECTION TEN - THE LUMBAR SPINE
nucleus. In both events a constant ache is experienced which forces a pain-avoiding position, usually in flexion and / or lateral deviation. The pain is agonizing and radi ates to one or both legs in an extra-segmental way. Dural symptoms (pain on coughing and sneezing) are positive, as are dural signs (limited straight leg raising and lumbar pain on full neck flexion), indicating that the dura is under constant and severe stress. In backache and lumbago, the posterior displacement puts the posterior longitudinal ligament under tension, which causes counterpressure on the bulge. This explains why acute lumbago usually ceases after a lapse of time, especially when the intradiscal pressure is reduced by lying down and avoiding sitting or bending. Alternatively, the tension in the ligament may be increased mechanically by manipulation or traction, which may push the sublux ated fragment away from the pain-sensitive structures. A massive posterior protrusion may cause a rupture of the posterior longitudinal ligament. The entire cauda equina will then be compressed against the anterior aspect of the two laminae. This not only squeezes the nerve roots on both sides but also causes compression and atrophy of the centrally localized S3 and S4 roots, with disturbance of bladder and rectal function (the S4 syndrome or cauda equina syndrome48) (Fig. 51.6c).
have passed off to be replaced by pain in the limb. According to the severity of irritation, which is deter mined not only by the degree and consistency of the bulge but also by the tightness of the 'tethering ligaments', the size of spinal canal and the degree of inflammatory response, the symptoms and signs are related to impair ment of mobility of the dural sleeve (pain and limitation of straight leg raising) alone, or interference with conduc tion (paraesthesia, numbness and motor deficit). Primary posterolateral protrusion. Here the pain usually begins in the calf and the posterior thigh; the absence of previous backache indicates that the dura has not been previously compressed. This condition usually affects young adults (aged 18-35 years). The signs are radicular, with pain and paraesthesia in the affected dermatome and limitation of straight leg raising. Signs of impaired conduction at the affected root are exceptional. It is surprising to find that low back syndromes (lumbago, backache, sciatica) are age related,49,so whereas the incidence of fissures, ruptures and degen eration of the disc increases linearly during the whole of life. The extensive pressure within the nucleus pulposus is higher in individuals between 30 and 50 years of age
POSTEROLATERAL DISPLACEMENT
1.0
Root pain results from pressure of the prolapsed or pro truded disc against the dural sleeve of the nerve root and the subsequent irritation of the latter (Fig. 51.7). This may be primary or secondary.
0.5
Secondary posterolateral protrusion. This is more common. The root pain starts after the patient has suf fered a number of attacks of lumbago or backache. After the most recent attack, the counterpressure exerted by the posterior longitudinal ligament has not resulted in the usual reduction of the bulge but rather in a lateral shift which impinges on the nerve root. The back pain will
o 80 60 40 20 OJ
:;
U (fJ til OJ
"OE >,!::
U l:l c c OJ>, ::J (fJ D"u OJ (fJ
li:=-o
o
10
20
30
40
50
60
70
80
Age (years)
Figure 51.7
Posterolateral disc displacement.
Figure 51.8 The relationship of age to acute disc syndromes. From Kramer J. Intervertebral Disc Diseases, Causes, Diagnosis, Treatment and Prophylaxis, 1981, Thieme, Stuttgart, with permission.
CHAPTER 51
than in the elderly (Fig. 51.8).51 The conclusion is that posterior displacement of the disc will be more likely to appear when an increased intradiscal pressure coincides with some damage to the posterior annular fibres. In other words, the combination of intradiscal pressure and lowered resistance of the annulus fibrosus is the main biomechanical factor contributing to protru sion-prolapse. When the expansive forces of the nucleus pulposus decrease and, because of the loss of water, the disc gradually deflates, the tendency to displacement becomes less. Other factors protecting the ageing disc against displacements are increasing stiffness of the pos terior ligaments, which limit spinal mobility, and the formation of osteophytes, which distribute the load over a larger area.
ANTERIOR DISPLACEMENT IN A DOLESCENTS
Because of its high oncotic and hydrostatic pressure, the young disc sometimes invades the vertebral endplates. This occurs particularly in the regions where the end plates have low resistance against increased anterior loading.52, 53 The nucleus pulposus may then move for wards between the cartilaginous endplate and the bone of the vertebral body, causing injury to the growth zone of the vertebra (Fig. 51.9). The result is a developmental deformity of the anterior part of the vertebra. During the course of this, protrusion may separate a small triangle of bone at the anterior corner of the vertebral body (limbus vertebra).54 If the osteochondrosis involves several consecutive vertebrae, a kyphotic deformity results (Scheuermann's disease).55 Such deformities occur only during the period of spinal growth and are asymptomatic. Care must there fore be taken not to overemphasize the significance of incidental radiological findings.
-
AGEING OF THE LUMBAR SPINE 735
ANTERIOR DISPLACEMENT IN THE ELDERLY
Tears at the anterior and anterolateral part of the disc lead to both anterior and anterolateral herniation. Anterior displacement of the disc causes dissection of the anterior longitudinal l igament from its bony attachments, which stimulates bony outgrowths along the anterior and anterolateral aspects of the vertebral body. These first appear in a horizontal direction and then vertically, fol lowing the course of the anterior longitudinal ligament (see p. 711). In advanced cases, the whole disc is dis placed anteriorly. On a lateral radiograph this can be seen as two 'beaks', containing the disc, while the interverte bral space is so narrowed that the vertebral bodies come to lie in apposition.56 Cyriax called this situation the 'mushroom' phenomenon, because of the characteristic appearance of the osteophytes, surrounding a 'mush room' - the anteriorly displaced disc (Fig. 51.10).57 The formation of the protrusion itself is completely painless but the gross narrowing of the intervertebral space, the folding of the posterior longitudinal ligament and the enlarged arthrotic posterior joints can cause considerable narrowing of the spinal canal and the lateral recess, which may result in compression of dura or nerve root when the spine is subjected to an axial load. VERTICAL DISPLACEMENT
There are two types of vertical displacement: Schmorl's node and biconvex disc. A herniation of the nucleus through the cartilaginous endplate is known as Schmorl's nodes (Fig. 51.11),58 although it was first described by von Luschka in 1858.59
·f;'".
\',:.':
\�>{
Figure 51.9
Intravertebral herniation in adolescence,
.• Figure 51.10 Anterior displacement in the elderly: the 'mushroom' phenomenon,
736 SECTION TEN - THE LUMBAR SPINE
Figure 51.11
Vertical displacement: Schmorl's nodes.
After the nuclear material has invaded the cancellous bone, a reactive osseous shell forms, visible on a radiograph from the age of 17 and which does not alter over the years. The disorder is very common at the lower thoracic and upper lumbar levels. Schmorl reported an incidence of 13% on radiographic examination of an adult and asymptomatic population but postmortem studies reported nodes in more than 75% of ordinary individuals.6o Biconvex discs appear as the result of traumatic or degenerative changes in the cartilaginous or bony end plates. Osteoporosis or osteomalacia causes a weakening of the bone and the disc becomes ballooned between two adjacent and slightly collapsed vertebrae.61 CIRCULAR DISPLACEMENT
As a result of degeneration, weakening and drying out, the disc may bulge out all the way round the joint. The outwards pressure pulls on the ligaments and lifts the periosteum off the bone. Formation of osteophytes at the anterior and lateral aspects of the vertebra results. These bony outcrops encircle the damaged disc. Mechanically, the presence of osteophytes is beneficial because they increase the weight-bearing surface and decrease the load per unit area.62 They also decrease mobility. Both effects augment the stability of the joint.
The first sign of degeneration and instability of the disc is the formation of small traction spurs63 which project horizontally to about 2 mm above and below the verte bral body (Fig. 51.12a). Their formation is explained as follows: decrease in turgor in the disc and the increasing anteroposterior instability which results, cause the outer most fibres of the annulus, firmly attached to the under surface of the epiphyseal ring, to exert traction on the periosteum. A horizontal lifting of the periosteum results in the formation of traction spurs. Spo ndylitic spurs or claw spurs are formed as the result of subperiosteal ossification at the anterior and anterolat eral aspect of the vertebrae (Fig. 51.12b). A softened and dehydrated disc bulges easily under the influence of external load and lifts the longitudinal ligament and the periosteum from the vertebral margin. Osseous reaction takes place, provoking the formation of new bone in a beak-like protuberance.64 This process can be viewed as if the vertebral body is trying to expand its articular surface area. By distributing axial loads over a wider area, the vertebral body lessens the stress applied to the annulus fibrosus during weight bearing. EFFECTS ON THE FACET JOINTS
The disc and facet joints form a 'three-joint complex'. Degenerative changes affecting the disc are followed by increasing changes in the posterior joints. Arthrosis of a facet joint is thus always secondary to changes in mechanical load, induced by disc degeneration.65,66 Initially, alterations in the height and volume of the disc result in positional changes of the facet joints. Axial compression on a degenerated and narrowed disc causes subluxation of the posterior joints: they move telescopically in relation to each other and slide past the normal range of movement, sometimes to such a degree that the tip of the inferior articular facet impinges on the adjacent lamina.
(a)
AGEING OF THE SURROUNDING TISSUES EFFECTS ON THE LIGAMENTS
The adjacent vertebral endplates develop poorly demar cated sclerotic densities, probably as the result of changed load distribution on the disc.29 However, the most commonly observed radiographical manifestation of disc degeneration is osteophyte formation in the vertebral bodies.
Figure 51.12
Traction spur (a) and spondylitic spur (b).
(b)
CHAPTER 51
A height reduction in the functional unit results in chaRges in the orientation of capsular fibres: they become stretched during axial loading, which gives the capsule a load-bearing function in the upright posi tion.67 The apophyseal joints resist about 16% of the intervertebral compressive forces in the erect standing posture if the disc is thinned.68 Another consequence of disc degeneration is that flexion-extension movement in the functional unit becomes disturbed. In a normal disc with adequate turgor, the instantaneous axis of rotation remains more or less in the region of the nucleus. In full flexion, it moves immediately anterior to the nucleus and in full extension it lies posterior to it.69 In a normal joint, the vertebral bodies thus rock over the nucleus and the facet joints serve only to guide the movement. When disc degenera tion is present, the axis of movement becomes irregular and· completely unpredictable: sliding and anteroposte rior movements, or tilting of the upper vertebra during flexion, become possible. Alternatively, the axis of rota tion remains constant in position through or behind the posterior joints?O Then the facet joints not only guide and steady motion but are also subjected to a rocking move ment, which results in compression of the articular surfaces and distraction of the capsule (Fig. 51.13). These abnormal stresses cause laxity of the facet joints and the posterior ligaments. Together with the increasing laxity of the disc, the final result is instability of the func tional unit, which in turn favours the development of internal derangement at the intervertebral disc.71 This instability of the three-joint complex most commonly appears during a particular period in the cycle of degen-
-
AGEING OF THE LUMBAR SPINE 737
eration, which normally falls between the third and fifth decade, when backache is most likely to occur.49 At the posterior (zygapophyseal) joints, the repeated pressure results in erosion and thinning of the cartilage. Where cartilage is lost, fibrofatty intra-articular inclu sions may increase in size to fill the space vacated by the cartilage.72 Other regions may exhibit swelling with subsequent formation of subperiosteal osteophytes and periarticular fibrosis.73 Osteoarthrotic changes in the apophyseal joints finally result in gross enlargements of both inferior and superior facets, giving them a bulbous aspect. All these degenerative changes cause a substantial decrease in motion of the facet joints and, together with the stabilizing changes in the disc, they provide, at the end of the degeneration cycle, the ultimate stabilization of the functional unit. EFFECTS ON THE SPINAL CANAL AND INTERVERTEBRAL FORAMEN
Because of the change in pressure and volume of the lumbar disc, the position of the intervertebral joints changes so that the articular processes override each other. As the vertebral bodies approach each other and because of the inclination of the joint surfaces, the upper vertebra moves backwards (retrospondylolisthesis) to the intervertebral foramen (Fig. 51.14). With increasing approximation of the vertebrae, both the ligamentum flavum and the posterior longitudinal ligament may buckle, so further narrowing the lumbar canaP4 Further, hypertrophied and bulbous arthrotic apophy seal joints commonly project into the intervertebral foramina, where they may add to compression on the dural sac and nerve rootS.65 2
Figure 51.13
In a normal functional unit the vertebral bodies roll over the nucleus and the facet joints only guide the movement (a). When disc degeneration is present, the facet joints are subject to rocking movements, resulting in compression and distraction (b).
Figure 51.14 Effects on the spinal canal and the lateral recess. 1, The vertebral bodies approach; 2, owing to the inclination of the joint surfaces, the upper vertebra is displaced backwards and produces a retrospondylolisthesis; 3, the posterior longitudinal ligament buckles; 4, the facet joints become hypertrophied and develop a bulbous aspect.
738 SECTION TEN - THE LUMBAR SPINE
j- .j
Anterior wall .... ). .....1
Fibrotic degeneration of the nucleus Concentric tears Radial tears Traction spurs Cysts Posterior displacements: Bulging Protrusion Prolapse
Fissures and cavities Marked height decrease Circular and anterior displacements Gross osteophytosis Disc resorption
....j
Stabilization
Spondylosis
Figure 51.15
Spondylarthrosis
Natural history of d ege neration of the lumbar spine.
The natural history of degeneration of the lumbar spine is summarized in Figure 51.15.
Alterations of adjacent vertebral bodies frequently accompany disc degeneration. Increased and poorly demarcated bone density of the adjoining vertebral end plates is clearly visible on plain radiographs and is often referred to as 'discitis'. Two types of osteophyte are commonly seen. Traction spurs which project horizontally from the corner of the vertebral body are located about 5 mm from the vertebral margin (see Fig. 51. 12a). They are believed to be caused by degenerative disc disease, allowing abnormal motion between the vertebrae. Traction spurs are there fore thought to be associated with segmental instability. Claw osteo phytes are larger and arise from the margin of the vertebral body. These bone formations are thought to be a response to increased mechanical loading which arises in deficient discs (see p. 736). The radiological signs of degeneration in the apophy seal joints include joint space narrowing, sclerosis of the subchondral bone and osteophyte formation. Increasing narrowing of the intervertebral space also provokes some subluxation of the zygapophyseal joints. On a lateral view, the tip of the superior articular facet is then seen to extend more than a few millimetres beyond the posteroinferior border of the vertebral body above?8 Further damage to the posterior joints results in retrolis thesis. Oblique projections of the lumbar spine can detect more malalignment of the articular surfaces and the onset of arthrotic deformity. The end result of disc degeneration is radiologically characterized by an almost complete loss of disc, which is now represented only by a thin intervertebral space between the dense and sclerotic vertebral end plates. 79 Gross beak-like osteophytes are seen at the anterior aspect of the vertebrae. The intervertebral foramen is narrowed, the facet joints are subluxated and enlarged, and retrolisthesis may be visible (see Table 51.2).
RADIOLOGICAL CHANGES The direct radiological signs of disc degeneration include disc space narrowing, gas within the disc space, vertebral sclerosis and osteophytes. Radiological signs of apophyseal joint degeneration are the same as seen in other degenerative joint diseases elsewhere in the body (joint space narrowing, sclerosis, osteophytosis and subluxation). An ageing disc loses height because of a loss of water and altered biomechanics. Consequently, narrowing of the intervertebral disc space is the first radiographic sign of lumbar degeneration. The presence of air pockets, located in discrete cavities within the nucleus is evidence of long-standing disc degeneration?5 The mechanism by which the gas is pro duced has been ascribed to a vacuum phenomenon?6,77
Table 51.2 Radiological changes in apophyseal and intervertebral joints Apophyseal joint
Intervertebral joint
Early
Joint space narrowing
Intervertebral disc space
changes
Beginning subluxation
narrowing Traction spurs Beginning endplate sclerosis
Late
Joint space narrowing
Considerable disc space
changes
Subchondral sclerosis
narrowing
Osteophyte formation
Air pockets (vacuum
Enlargement of articular
phenomenon)
facets
Endplate sclerosis
Joint subluxation
Claw osteophytes Retrolisthesis
CHAPTER 51 - AGEING OF THE LUMBAR SPINE 739
RELATIONSHIP BETWEEN DEGENERATION AND SYMPTOMS Although disc degenera tion and its radiographic appearances progressively increases with age, it cannot be too strongly emphasized that low back pain and dis ability do not. It is well known that backache peaks in the middle working years of life (40 years),80-83 which establishes that disc degeneration as such does not produce symptoms per se. It is therefore unwise to rely on radiographic appearances for the diagnosis of lumbar disorders. It has been shown repeatedly in con trolled studies that there is absolutely no relationship between clinical symptoms and the radiographic changes of degeneration.8 4-91 To take but one example, a prospective study on 536 patients by Sanders et at com pared the radiological findings of patients with back ache and disablement (/1 = 270) with those of an asymptomatic control group ( n = 266): there was not the slightes� radiographic difference between the two. Their conclusion was that radiography afforded little or no help in the diagnosis of mechanical lumbar disorders9 2 and remains a very poor method to indicate past, present or future low back pain.93 In contrast, the practitioner must constantly be aware of the problems that can be induced by the interpretation the clinician, the radiologist or the patient places on a
radiograph. The results of radiographic examinations should never be given to the patient as a diagnosis. Since there is no evidence that there is a correlation between the radiographic appearances and the actual complaints, it is vital to be extremely careful in discussing the results of radiology with the patient. Telling the patient that the back shows 'a marked degree of arthrosis' may to the patient mean incurability, and may conjure up a picture of a hopelessly crumbling spine. The radiograph, instead of helping the patient, will increase the disability. Many patients become depressed when they hear that the back is 'worn out'. Symptoms are produced by a more complex pathway than simple and uncomplicated arthrosis. Making a specific diagnosis, and designing a specific treatment is only possible if symptoms and signs are meticulously assessed. The interpretation of the data obtained is based on the knowledge of the mechanical behaviour of the tissues involved and the mechanism of pain production. In this way, it is possible to classify activity-related spinal disorders under three major concepts: the dural, the liga mentous and the stenotic (Chs 52-54). These three appear in a specific age group, have a certain correlation with the natural ageing of the lumbar spine and are clinically dis tinct. Classification of a particular patient's backache into one of these types thus depends on the information obtained from the history and clinical examination, and not on the interpretation of radiographs.
REFERENCES 1. Reishauer F.
Ulltersuc/llIl1gel7 iiber den lUl1lbalell lind cervikalen Wirbelbandscheibenvorfall. Thieme, Stuttgart, 1949.
2. Hansen H-J. Comparative views on the pathology of disc degeneration in animals. Lab Invest 1959;8:1242-1265. 3. Exner G. Die Halswirbelsiiule. Thieme, Stuttgart, 1959. 4. Ushikubo S. Study of intervertebral disc herniation in bipedal rats Shikoku. Acta Med 1959;15:1759-1780. 5. Yamada K. The dynamics of experimental posture: experimen tal study of intervertebral disc herniation in bipedal animals. 1 962;25:20-3 1 .
Ciill Orthop
6. Wassilev W, Dimova R . D e r Einfluss der mechanischen Faktoren auf die Struktur der Zwischenwirbelscheiben. Arch
11. O'Connel l JE. Intervertebral disc protrusi ons in children and adolescents. Br J Surg 1960;47:611 . 12. da Silva U, Beyeler F, M umenthaler M, Robert F, Vassella F. Die l u mbale Diskushernie im K indesa l te r. Ther Ul11sch 1977;34:405. 13. Blaauw G, Schaafsma J, Blaau w-Van Dishoeck M. Prolaps van de lumbale tussenwervelschijf bij kinderen en adolescenten. Ned Tijdschr Geneeskd 1981;125(35):1404-1407. 14. Erkintalo MO, Salminen JJ, A l anen AM, Pa ajanen H EK, Kormano MJ. Development of degenerative changes in the lumbar intervertebral disk: results of a prospective MR imaging study in adolescents with and without low back pain. Radiology
Orthop Ullfall-Cilir 1970;68:273. 7. Cassidy JD, Yong-Hing K, Kirkaldy Willis WH, Wilkinson AA.
1 995;196:529-533. 15. Schmorl G, Junghans H .
A study on the effect of bipedism and upright posture on the lumbosacral spine and paravertebral muscles of the Wistar rat. Spine 1988;13(3):301-308. 8. Lotz Ie, Colliou OK, Chin JR, Duncan NA, Liebenberg E . Compression-induced degeneration of the intervertebral disc:
5th edn. Thieme, Stuttga rt, 1968. 16. Jochheim K, Lowe F, Ri. i tt A. Lumbaler Bandscheibenvorfall. Springer, Berlin, 1961. 17. Holm S, Nachemson A. Nutritional change in the canine intervertebral d isc after spinal fusion. Clin Ortilop 1 982;169: 243-258.
an ill vivo mouse model and finite-element study. Spine 1998;23:2493-2502. 9. Tondury G. Der Wirbelsau lenrheumatismus. In: Rheumatis111us
ill Forsc/lllllg lind Praxis.
Chapter IV, W. Belart Huber, Bern,
J968:115. 10. Key JA. Intervertebral disc lesions in children and adolescence. J Balle Joint SlIrg 1 950;32:97.
Die Gesunde lind die kranke Wirbelsiiule
in Rontgenbild lind Klinik,
18. Buckwater JA. Spine update. Aging and degeneration of the human intervertebral disc. Spine 1995;20:1307-1314. 19. Jolmstone B, Bayliss MT. The late proteoglycans of the human interverteb r a l disc. Changes in their biosynthesis and structure with age, topography, and pathol ogy. Spine 1 995;20: 674-684.
740 S ECTION T EN - TH E LUMBAR SPIN E
20.
Koller W, Miihlhaus S, Meier W, Hartmann F. Biomechanical
appearances in both symptomatic and control population.
properties of human intervertebral discs subjected to axial dynamic compression: influence of age and degeneration.
1993;18:1801-1 811 .
] Biolllech 1986;19:807-816. 21 . Kramer J . Bandscheibenbedingte Erkrallkungen. Thieme, Stuttgart, 1978. 22. Sobel DF, Zyroff J, Thorne RP. Diskogenic vertebral sclerosis: MR imaging. j Comp Assist Tomogr 1987;11:855-858. 23. Modic MT, Steinberg PM, Ross JS et at. Degenerative disc
45.
Boos N, Rieder R, Schade V. The diagnostic accuracy of mag netic resonance imaging, work place perception, and psycho social factors in identifying symptomatic disc herniations. Spine
46.
Cyriax JH.
47.
McNally DS, Adams MA, Goodship AE. Can intervertebral
disease: assessment o f changes in vertebral body marrow with MR imaging. Radiology 1988;166:193-199.
24.
Bernick S, Cailliet R. Vertebral end-plate changes with aging of human vertebrae.
25. 26. 27. 28.
Farfan HF. Mechanical Philadelphia, 1973.
Disorders of the Low Back.
Lea & Febiger,
Maroudas A, Stockwell RA, Nachemson A, Urban J. Factors involved in the nutrition of the human intervertebral d isc; cellu larity and diffusion of glucose in vitro. j Anat 1975;120:113-130. Belytschko T, Kulak, RF, Schultz A, Galante J . Finite element stress analysis of an intervertebral disc.
29. 30. 31. 32.
human vertebrae.
33.
48.
Spine 1982;7:97-102.
Ritchie JHW, Fahrni WHo Age changes in lumbar intervertebral discs? Canad j Surg 1970;13:65.
by disc mechanisms?
Spine
Kostuik JP, Harrington, J, Alexander D, Rand W, Evans D. Cauda equina synd rome and lumbar disc herniation. ] Bone
joint Surg 1986;68A:386-391 . 49.
Kelsey J , White A A . Epi demiology and impact o f low back pain.
Spine 1980;6:133-142. 50.
Rowe
ML.
Low
back
pain
in
industry.
, Occup Med
1969;11:161-169.
52.
Kramer J . Biomechanische Veranderungen im lumbale Bewegungssegment. In: Junghanns H (ed) Die Wirbelsaule in Forschung und Praxis, Chapter 58. Hippokra tes, Stuttgart, 1973. Mau H. Verschaubung und dorsolaterale Versteifung im
53.
Lumbosakralabschnitt. Z Orthop 1974;112:785. Resnick D, Niwayama G. Intervertebral disc herniations; carti
51.
Vernon-Roberts B. Pathology of degenerative spondylosis. In: Jayson M (ed) The LlImbar Spine and Back Pain. Pitman Medical, Lond on, 1985:55-76. Shirazi-Adl A. Strain in fibers of a l u mbar disc. Analysis of the role of lifting in producing disc prolapse. Spine 1989;414:96-103. Knu tsson F. The instability associated with disc degeneration in the lumbar spine. Acta Radiol (Stockh) 1944;25:593. Bernick S, Cailliet R. Vertebral end-plate changes with aging of
prolapse be predicted
1993;18: 1525-1530.
] Biomech 1974;7:
277-285.
1995;20(24):2613-2625. Textbook of Orthopaedic Medicine, Vol 1, Diagnosis of Soft Tissue Lesions, 8th edn. Baill iere Tindall, London, 1982.
d isc
Spine 1982;7:97-102.
Acarpglu ER, Iatridis Je, Setton LA et at. Degeneration and aging a ffect the tensile behaviour of human lumbar annulus fibrosus. Spine 1995;20:2690-2701 .
Spine
laginous (Schmorl's nodes).
Radiology 1978;126:57-65.
54.
Ghelman B, Freiberger RH. The limbus vertebra: an anterior disc herniation demonstrated by discography. Am ] ROlltgenol
55.
Scheuermann H. Kyphosis dorsalis juvenilis. Z
1976;127:854. Orthop Chir
1921;41:305. 56.
Crock HV. A reappraisal of intervertebral disc lesions.
Med ,
Aust 1970;1:983-989. 57. 58.
Cyriax JH. Treatment of lumbar disc lesions. BM! 1950;ii:1343. Schmorl G. Uber Verlagerungen von Bandscheibengewebe und ihre Folgen. Arch Klin ChiI' 1932;172:240.
34.
Bernick S, Cailliet R. Vertebral end-plate changes with aging of
59.
Von Luschka H. Die Reimer, Berlin, 1858.
35.
human vertebrae. Spine 1982;7:97-102. Lipson SJ. Metaplastic proliferative fibrocartilage as an alterna
60.
H ilton Re, Ball J, Benn RT. Vertebral end-plate lesions (Schmorl's nodes). Ann Rheum Dis 1976;35: 127.
1988;13:1055-1060.
61.
Friberg S, Hirsch e. Anatomical and clinical studies on lumbar disc degeneration. Acta Orthop Scand 1949;419:222-242. Nachemson AL. Lumbar intervertebral pressure: experimental
62.
Vernon-Roberts B, Price CJ. Healing trabecular micro-fractures in the bodies of lumbar vertebrae. Ann Rheulll Dis 1973;32:406-412. Frymoyer JW, Moskowitz RW. Spinal degeneration, pathogene sis and medical management. In: Frymoyer JW (ed) The Adult Spine. Raven Press, New York, 1991 :629. MacNab 1. The traction spur: an indication of segmental insta bility. j Bone Joint Surg 1971;53A:891. Collins DH. The Pathology of Articular and Spillal Diseases. Edward Arnold, London, 1949. Vernon-Roberts B, Pirie CJ. Degenerative changes in the
tive
36. 37.
concept
to
herniated
studies on post-mortem material.
i n tervertebral
disc.
Spine
Acta Orthop Scand 1960;(suppl
43):42-43. 38.
Thompson JP, Pearce RH, Schechter MT
et al.
Preliminary eval
uation of a scheme for grading the gross morphology of the human intervertebral disc.
39. 40. 41.
63. 64.
Spine 1990;15:411-415.
Miller JA, Schmatz C, Schultz AB. Lumbar disc degeneration: correlation with age, sex, and spine level in 600 a utopsy speci mens. Spine 1988;13:1 73-178.
65.
Hi tselberger WE, Witten RM. Abnormal myelograms in asymp tomatic patients. ] Neurosurg 1968;28:204-206. Wiesel SW, Tsourmas N, FeHer HL, Citrin CM, Patronas N. A study of computer-assisted tomography: I. The incidence of positive CT scans in an asymptomatic group of patients. Spine
66.
intervertebral discs of the lumbar spine and their sequelae.
Rheul11atol Rehabi/ 1977;16:13-21 . 67.
1984;9:549-551. 42. 43.
Boden SD, Davis DO, Dina TS, Patronas NJ, Wiesel SW. Abnormal magnetic-resonance scans of the l umbar spine in asymptomatic subjects. ! Bone joint Surg 1990;72A:403-408. Jensen M, Brandt-Zawadzki M, Obuchowski N. Magnetic reso
N Engl j Med 1994;331:67-73. Buirski G, Silberstein M. The symptomatic l umbar disc in patients with low-back pain: magnetic resonance imaging
Butler D, Trafimow JH, Anderson GBJ, McNeill TW. Discs degenerate before facets. Spine 1990;15: 111-113. Hedtmann A, Steffen R, Methfessel J, Kolditz D, Kramer J, Thois . Measurements of human lumbar spine ligaments d uring loaded and unloaded motion. Spine 1989;14(2) :
1 75-185. 68.
Adams MA, Hutton We. The effect of posture on the role of the apophyseal joints in resisting intervertebral compressive forces.
] Bone Joint Surg 1980;62B:358-362. 69.
Adams MH, Hu tton We, Stott JRR. The resistance to flexion of the lumbar intervertebral joint. Spine 1980;5:245.
70.
Gianturco e. A Rontgen analysis of the motion of the lower lumbar vertebrae in normal individuals and in patients with low back pain. AJR 1944;52:261-268.
nance imaging of the lumbar spine in people without back pain.
44.
Halbgelenke des menschlichen Korpers.
C HAPTER 51
-
71 .
Kirkaldy-Willis WH, Wedge JH, Young H i ng K, Reilly J .
representativeness
1982;29:289-299.
72.
P9thology and pathogenesis of lumbar spondylOSiS a n d steno sis. Spine 1978;3:319. Twomey LT, Taylor JR. Age changes in the lumbar articular
73.
triad. Aust J Physio 1985;31:106-112. Taylor JR, Twomey LT. Age changes in lumbar zygapophyseal
74.
75. 76.
joints. Spine 1986;11:739-745. Vernon-Roberts B. The pathology and interrelation of interverte bral disc lesions, osteoarthrosis of the apophyseal joint, lumbar spondylosis and low back pain. In: Jayson MIV (ed) The Lumbar Spine alld Back Pain, 2nd edn. Pitman Press, Bath, 1985. Armstrong J. Lu mbar Disc Lesions. Williams & Wilkins, Baltimore, 1965. Edeiken J, Pitt MJ. The radiological diagnosis of disc disease symposi um on disease of the intervertebral disc.
84.
78.
vacuulll I U lllbar disc. AlR 1977;128:1056-1057. Macnab 1. Disc degeneration and low back pain.
79. 80.
C rock HV. Isolated lumbar disc resorption as a cause of nerve root canal stenosis. Ciin Orthop 1976;115:109. Cochrane Report. Working Group on Back Pain. HMSO, London, Horal J. The clinical appearance of low back pain disorders in the city of Gothenborg, Sweden. Acta Orthop Scand
83.
Bieri ng-Sorensen F. Low back trouble in a general population of 30- 40- 50- and 60-year-old men and women: study design,
Bill/
Splithoff CA. Lumbosacral junction: Rontgenographic compari
lAMA 1953;152:
La Rocca H, MacNab 1. Value of pre-employment radiographic Can Med Assoc assessment of the lumbar spine.
j 1969;101:383-388. 87.
Wiltse LL. The effect of the common anomalies of the lumbar spine upon disc degeneration and low back pain. Ort//Op Ciin
North AII1 1971;2:569-582. 88.
Magora A, Schwartz A. Relation between the low back pain syndrome and X-ray findings. Scand 1 Rehabi/ Med ] 976;8:
89.
Torgeson WD, Dotler WE. Comparative rontgenographic study of the asymptomatic and symptomatic lumbar spine. 1 Bone
115-125. joint Surg 1976;58A:850-853. 90. 91.
Park WM. The place of the radiology in the investigation of low back pain. Ciin Rheum Dis 1980;6:93-132. Wiesel SW, Bernini P, Rothman RH. Diagnostic studies in eval uating disease and aging i n the lumbar spine. In: The Agillg
Lumbar Spine.
Saunders, Philadelphia,
1982:
Chapter
2.
92.
Sanders H WA et al. Klinische betekenis van degeneratieve afwijkingen van de l u mbale wervelkolom en consequenties van het aantonen ervan. Ned Tijdschr Geneeskd 1983;127:
93.
Glover JR. Prevention of back pain. In: Jayson MIV (ed)
j Occup Med 1969;11:
161-169.
Med
86.
1969;118(suppl):1-109. 82. Rowe ML. Low back pain i n industry.
Dan
Fullenlove TM, Williams AJ. Comparative rontgen findings in symptomatic and asymptomatic backs. lAMA 1 957;168:572-574.
1979. 81.
results.
85.
Ciin Orthop
1986;208:3-14.
basic
1610-1613.
North AII1 1971;2:405. Ford LT, Gilula LA, Murphy WA, Gado M . Analysis of gas i n
and
son of patients with and without backache.
Orthop Ciin
77.
AGEING OF THE LUMBAR SPINE 741
1 374-1385. Lumbar Spine and Back Pain, Wells, 1 976:Chapter 3.
The
1 st edn. Pitman Medical, Tunbridge
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
,
Hypothesis 743 Clinical evidence for the insensibility of the disc 743 Clinical evidence for the sensibility of the dura mater 743 T he mechanism of dural pain is dual 744 The dural concept in the natural history of the ageing disc 745
The dural concept
Clinical syndromes 746 Lumbago 746 History 746
Clinical examination 748 Natural history 749 Treatment 749 Backache 751 Mechanism 751 History 751 Clinical examination 752 Natural history of discodural backache Particular types of backache 754 Treatment 755 . Sciatica 757 Mechanism 757 History 760 Clinical examination 762 Natural history 765 Treatment 769
HYPOTHESIS
754
The dural concept was first defined by James Cyriax in 1945. 1 His hypothesis was that lumbago and backache originate when a subluxated fragment of disc tissue impinges on the sensitive dura mater. This concept lumbar pain may be of dural origin - is based on two premises: • •
Disc degeneration and disc displacements are of themselves painless events. The dura mater is sensitive and translates deforma tions of the posterior border of the disc into pain.
CLINICAL EVIDENCE FOR THE INSENSIBILITY OF THE DISC The most important evidence for the fi rst premise (insensibility of the disc) is the poor correlation between obvious disc lesions and lumbar pain: •
•
•
•
Data obtained from postmortem studies show the existence of large, symptomless disc protrusions in almost 40% of the cadavers.2 Several controlled studies have failed to show a relationship between radiological changes seen in disc degeneration and the existence of clinical syndromes. 3-5 Myelograms in asymptomatic patients show defects in 37% of cases6 and the incidence of asymptomatic disc herniations demonstrated by CT in subjects over 40 years of age is more than 50% .7 Recent MRI studies8-11 have demonstrated anew the high incidence of disc degeneration and displacement in an asymptomatic group of patients.
These observations permit the conclusion tha t degenerated or displ aced disc tissue is not itself the source of lumbar pain, which only appears when other, more sensitive structures are involved.
CLINICAL EVIDENCE FOR THE SENSIBILITY OF THE DURA MATER The second premise was deduced from the clinical obser vations of the natural course of backache and sciatica. 743
744 SECTION TEN - THE LUMBAR SPINE
One of the most striking clinical features to support the pain-mediating role of the dura is the chronological evo lution from backache to sciatica. Almost every instance of sciatica starts with a period of central or unilateral back ache but once leg pain supervenes the backache usually disappears. Since the work by Mixter and Barr,12 it has been widely accepted that most radicular pain is caused by a disc protrusion compressing the dural investment around the nerve root and, if this is so, it is logical to argue that the earlier backache was brought about by the same disc lesion. If sciatica is referred pain from the dural sleeve, by analogy the prior backache must have origi nated from the dura mater. Sciatic pain is thus only the final stage of a progression. A small posterior protrusion, bulging out of the intervertebral joint, lifts the posterior longitudinal ligament, touches the dura mater and causes backache. Kept under control by the posterior ligament, the bulge can recede, resulting in spontaneous recovery, or stay unaltered, causing chronic backache. If it increases, however, the cow1terpressure exerted by the stretched posterior longitudinal ligament pushes it later al ly. No longer subject to any resistance, it immediately swells and compresses the nerve root. At the same time, pressure against the dural tube is released and backache ceases (see p. 757). Another proof of the role of the dura in lumbar pain syndromes is the effect of diagnostic local anaesthesia. A weak solution of procaine, induced via the sacral hiatus into the epidural space, and thus forced between the dural tube and the boundaries of the neural canal, causes contact anaesthesia of the dura mater (see p. 903). Because procaine 0 .5% is too weak to penetrate the liga ments or the dural membrane, it acts as a surface anaes thetic, thus only desensitizing the structures with which it comes into contact. If the patient had backache before the injection, and anaesthesia affords temporary relief of symptoms and signs, the dura is most likely to be the source of pain. In all cases of acute lumbago and in most cases of acute or recurrent backache, epidural local anaesthesia immediately abates the pain, thus strongly suggesting a dural origin. During the last decades, numerous neuroanatomical stud ies have shown that the ventral half of the dura mater is supplied by small branches of the sinu vertebral nerve . l 3, 14 Immunohistochemical studies further demonstrate a significant number of free nerve endings in the dura that contain substance P, calcitonin gene-related pep tides and other neurotransmi tters contributing to nociception. 1 5, 1 6
dura or the dural sleeves of the nerve roots. These pain sensitive structures translate the anatomical changes into back pain or root pain, respectively (Fig. 52. 1 ). However, recent anatomical and biochemical studies have slightly changed this original concept: Al though earlier anatomical studies demonstrated the disc to be totally deprived of innervation,17 more recent research could detect sparse nerve fibres and free nerve endings in the three outer lamellae of the annulus fibrosus, 1 8-20 penetrating to a maximum depth of 0.9 mm into the annulus. This means that, except at the surface, a normal intervertebral disc remains almost without innervation.
• The outer border of the disc is innervated.
• Dura mater attachments exist between the anterior part
of the dura and the posterior longitudinal lignment
•
(Fig. 52.2). Recent anatomical and MRI studies have demonstrated that the dura mater is not totally disconnected from the vertebral column but attached to the posterior longitud inal ligament by connective tissue, consisting of ventral and lateral fibrous bands.2 1-24 Although these ligaments are sufficient to allow for displacement of the du ral sac during movement, they could act to place traction on the dural sac in the event of nuclear bulge or herniation.25 Pain is not only mechanical: inflammatory mechanisms are also involved . Apart from being
THE MECHANISM O F DURAL PAIN I S DUAL The original concept was guite simple: a sub luxated (but of itself painless) component of the d isc impinges on the
Figure 52.1
Interaction between displaced disc tissue and the dura mater.
CHAPTER 52 - THE DURAL CONCEPT 745
This hypothesis has important clinical consequences. Because the mechanism is dual, the symptoms and the physical signs are also dual. Therefore both 'discal' (artic ular) signs and symptoms and 'dural' signs and symp toms should be looked for during history taking and functional examination. •
•
Dura mater attachments: 1, vertebra; 2, dura mater; 3, nerve root; posterior longitudinal ligament; 5, lateral expansion of posterior longitudinal ligament; 6, intervertebral disc; 7, dural ligaments. Small arrow: sinuvertebral nerve, anterior to the nerve root (3). Figure 52.2
Articular signs and symptoms are those that are related to the mechanical behaviou r of the disc: certain postures and movements create biomechanical changes, which force the protrusion against the dura mater. Dural signs and symptoms are those that are related to the increase of dural irritation: traction exerted from a distance (straight leg raising and neck flexion) pulls on the inflamed dura or, via the du ral ligaments, on the posterior longitudinal ligament or outer annular rim. Also a sudden increase in spinal fluid pressure pushes the dura against the protrusion (painful coughing and sneezing).
The duality is also important in drawing up a thera peutic strategy. The first measure is to attempt to alleviate the pain by removing the subluxated disc from contact with the dura, which can be achieved by manipulation or traction. If this fails, attempts can be made to desensitize the dura by epidural local anaesthesia.
4,
THE DURAL CONCEPT IN THE NATURAL HISTORY OF THE AGEING DISC
stimulated mechanically, nociceptors in dura mater may also be activated chemically. An increasing number of experimental studies suggest that disc lesions and / or displacements may induce sufficient chemical changes to irritate the dura mater and to elicit dural pain .26-31 Although these new anatomical and histochemical developments have improved the understanding of the discodural relation, the original (Cyriax) concept has not changed. From a clinical point of view, the mech anism of discodural interactions is still that of a conflict between an inert and mostly painless structure (nucleus and ilmer part of the annulus) and a pain-sensitive duroligamentous complex (outermost rim of annulus, posterior longitudinal ligament, dura mater and dural ligaments) all innervated by the sinuvertebral nerves. Discodural pain therefore has a multisegmental behav iour with a broad reference that involves multiple der rnatomes and crosses the midline. The interaction is not just a mechanical impingement of discal tissue on the dura mater but also involves inflammatory reactions of the pain-sensitive tissue.
One of the factors involved i n the du ral concept is a sub luxated portion of the disc and so the biomechanical conditions to allow such a displacemen t must be present. First, there must be some degeneration of the disc, leading to weakness of the annular fibres and to radiating fissures. These changes are present very early in the degeneration cycle and, because of a number of biomechanical and biochemical reasons, occur most fre quently at the rear side of the disc. Second, repeated wear and tear, together with shearing forces and slight decrease of d isc height, creates some ligamentous laxity which results in an instability of the whole 'motion segment'. Third, through enzymatic depolymerization of macromolecules in the disc, the oncotic pressure tem porarily rises. 32 This means that du ring a particu lar period of life (between the ages of 20 and 50 years), the osmotic pressure within the nucleus pul po sus increases. Raised intradiscal pressure together with increased segmental laxity is the perfect foundation for disc dis placement. A kyphosis imposed on such a predisposed intervertebral j oint not only increases the i ntradiscal pressure but also tends to shift disc material backwards
746 SECTION TEN - THE LUMBAR SPINE
in the direction of the convexity.33 The intensity of the contact between disc and dura determines whether lu mbago or backache will resu lt. When the protrusion is more posterolateral, the dural investment and the content of the nerve root rather than the d ural tube are compressed, with the symptomatic outcome of root pain. Fu rther degeneration of the disc resul ts i n its , defl ation' and a decline of intradiscal p ressure. Decrease in disc height leads to reactive changes at the intervertebral joint and at the posterior structures, which sti ffen and stabilize the segment and so diminish the tendency for disc displacements du ring the later stages of ageing of the spine (Fig. 52.3).
Con cl u si o n : acute l u mb ar clin ical syn d romes of d u ral o r i g i n occu r d u ri n g a specific period of l i fe. Th i s h as been estab l i shed by epidem i o l o g i cal stud i e s, w h i ch pl ace the peak i n ci d e n ce between the ages of 30 and 60 years.34,35
Fibrotic degeneration of the nucleus Concentric tears Radial tears Traction spurs Cysts Posterior displacements: Bulging Protrusion Prolapse
Hypermobility Compassion and distraction Joint subluxation
Fissures and cavities Marked height decrease Circular and anterior displacements Gross osteophytosis Disc resorption
Subperiosteal osteophytes Enlargement of facets
Spondylosis
Spondylarthrosis
F i gu re 52.3 Position of discodural interactions in the degeneration of the lumbar spine.
CLINICAL SYNDROMES LUMBAGO
The most striking example of a discodural interaction is acute lumbago - a sudden attack of severe and incapaci tating backache, with obvious limitation of movement together with gross dural signs and symptoms, summa rized in Box 52.1 (p. 744).
HISTORY The history is typical and depends largely on the com position of the protruded disc tissue: annular, nuclear or combined . Annular lumbago
The patient states that, during some trivial activity, a sudden 'snap' was felt and agonizing pain in the back immediately followed . Very often this acute event has occurred during a simple movement: coming up after bending, rising from a chair or picking up a light object. Initially, the pain is central and spreads bilaterally over the lower lumbar area and the buttocks. Later, it often tends to radiate more and more unilaterally. Although centralized in the lumbar and I or gluteal area, it spreads to the groin and abdomen, downwards to one or both legs as far as the ankles, or upwards in the trunk as far as the inferior aspect of the scapulae (Fig. 52.4). Differential diagnosis from radicular pain must be made if the ache spreads to one leg only. In such a 'pseudoradicular' dural pain, the distribution is vague, covers several derma tomes and never spreads into the feet. The lumbar or gluteal component also remains more pronounced than the vague and poorly localized referred pain in the limb. A typical statement in acute lumbago is that the pain is aggravated by sitting and bending forwards, the latter even being impossible. Also, changing from sitting to standing or raising the trunk after lying down for some time is extremely painful and often takes considerable time. The most characteristic sensations in acute lumbago are sharp twinges. For fear of these, lumbar movements are executed very cautiously and in 'slow motion'. The spine is held in the position of least pain by reflex spasm of the trunk muscles and every attempt to straighten the back is associated with severe twinges; the patient walks with the trunk largely immobile, leaning forwards or sideways, keeping the hips and knees slightly bent. Coughing and sneezing are extremely painful and some patients find that even taking a deep breath increases their pain.
CHAPTER 52
-
THE DURAL CONCEPT 747
posterior longitudinal ligament against the dura mater (Fig. 52.5a). It is obvious that a history of sudden pain, immediately followed by a ' locking' in flexion indicates some internal derangement, just as a sudden pain in the knee, followed by inability to straighten it, indicates a subluxation of a meniscus. The dural extrasegrnental ref erence of the pain, together with pain on coughing and sneezing, implicates the dura mater and therefore excludes locking of the posterior facet joints. In displace ment at the back of the intervertebral joint, the lumbar spine is held in flexion because extension squeezes the protrusion, which in turn increases the painful pressure on the dura. In order to keep the protrusion away from the dura and as immobile as possible, the patient adopts a flexed position. Muscle spasm prevents any further movement at the lumbar spine. Nuclear lumbago
Figure 52.4
Possible reference of dural pain caused by an L5 protrusion.
Usually, the patient retires to bed, which is probably the only place where more or less freedom from pain can be assured. Characteristically the ' psoas position' is adopted: supine, with hips and knees flexed to 90°. The pain eases gradually and in most cases all symptoms have gone after a few days or weeks. An attack of acute annular lumbago is caused by pos terior subluxation of part of the annular rim, pressing the
(a)
Figure 52.5
(a) Annual and (b) nuclear lumbago.
The pain, although equally incapacitating, does not appear suddenly but gradually increases over the course of a number of hours or days. Alternatively, after heavy work involving much stooping and lifting or sitting for an unusual length of time in an uncomfortable position, slight backache is felt but is initially regarded as trivial. However, by the next morning the backache is sufficiently severe to make getting out of bed impossible. The pain radiates in a way typical of dural involvement (Fig. 52.4). The patient is immobilized in flexion or side flexion and every attempt to straighten the back is fol lowed by an agonizing twinge in the lumbar area and the buttocks. Sometimes even simple neck flexion is impossi ble or coughing or sneezing creates a twinge. As in an attack of annular lumbago, the patient has to go to bed to
(b)
748 SECTION TEN - THE LUMBAR SPINE
cope with the pain. As a rule the pain eases after a few days or weeks. In gradually increasing lumbago, the protrusion pre sumably consists of soft and pulpy nuclear material, oozing slowly backwards. This typically happens during the maintenance of a kyphotic posture (sitting, bending or lifting). The displaced nuclear material gradually presses more and more against the outermost layers of the annulus and the posterior longitudinal ligament and makes them protrude (Fig. 52.5b). This provokes dural irritation, resulting in the typical dural pain in lumbar area, buttocks and limbs. Mixed lumbago
Sometimes there is a sudden attack of acute low back pain, increasing slowly during the following few hours or days. This indicates that the protrusion is probably mixed, consisting of an annular crack, with some pulpy material oozing backwards between its edges. The distinction between an annular and a nuclear pro trusion is extremely important, for both treatment and prophylaxis. A hard fragment reacts very well to ma nipulation, a soft protrusion is more difficult to reduce. In the maintenance of reduction and in prophylaxis a patient with a history of recurrent annular protrusions has to be constantly on guard during specific movements (bending and lifting) but a nuclear protrusion only re appears after prolonged loading of a joint in flexion.
the right. This curious phenomenon is explained by the dura slipping to one or other side of a midline protrusion. Spinal movements
There is gross but unequal degree of limitation in the four directions (the partial articular pattern) which indicates that part of the joint is more affected . Extension. As a rule, extension is considerably limited (Fig. 52.6) on account of the posterior displacement of the disc causing a block at the back of the joint. Side flexion. In one direction side flexion is considerably more limited than it is in the other and is usually associ ated with visible lateral deviation on inspection. If side flexion towards the pain is more limited, manipulation seems to be less effective but, if pain is felt more on the side away from which the patient bends, manipulative reduction usually succeeds. ' Alternatively there is a gross painful arc when the trunk passes the vertical, on swinging from one side to the other. Both side flexion are then painless at the end of range. This phenomenon indicates a central bulge at the fourth lumbar level and corresponds with the alternating deviation seen on inspection.
During clinical examination the following are important.
Flexion. This is extremely painful in cases of acute lumbago and is usually the last movement to become free after a manipulative session. Sometimes devia tion during flexion will appear, despite an absence of lateral deviation in the standing position. In contrast, a lateral tilt in the upright position sometimes disappears during the flexion.
Inspection
Dural tests
CLINICAL EXAMINATION
Deviation towards flexion is noted and the sacro-spinalis muscles are seen and felt to be in contraction to maintain the adaptive posture. Because the flexed position places the upper trunk in front of the centre of gravity, the muscles contract to prevent further forward toppling. Lumbago is not caused by muscle spasm - as was main tained by some authorities for many years36 - but is the result of a disorder at the posterior aspect of the inter vertebral joint. When gross lateral deviation is present, a lesion at the fourth or third lumbar level should be suspected. Because of the stabilizing effect of the iliolumbar ligaments, fifth lumbar protrusions very seldom result in gross lateral deviation. Further, alternating deviation is pathognomonic for central protrusions at the fourth lumbar level. At one moment, the patient is deviated to the left, but after performing some lumbar movement, then deviates to
Neck flexion. In lumbago, neck flexion often hurts in the lower back, which proves the involvement of the dura mater in the origin of the pain3? (see p. 715). Straight leg raising (SlR). We have discussed evidence that SLR is a dural sign (see p. 715) and, just as neck flexion stretches the dura from above, so SLR stretches it from below. A lesion resulting in such a gross discodural interaction as acute lumbago, therefore must influence SLR. Acute lumbago with a full and painless SLR should make the clinician reluctant to accept the diagnosis of a displaced disc. If the acute pain in the back is so severe that the patient calU10t move out of bed, but dural symp toms and signs - including a positive SLR - are absent, gross bony lesions such as osteomyelitis or metastases should be considered (see p. 852). ' Lumbago usually causes bilateral limitation of SLR: because the bulge and the dura mater both lie centrally,
CHAPTER 52
-
THE DURAL CONCEPT 749
Tests for conduction
Neither muscle weakness nor cutaneous analgesia is present i n cases of an acute lumbago. Because protrusion is more or less central, nerve roots are not involved. Care should be taken however not to miss a compression of the fourth sacral root. Because i t lies centrally, partly pro tected by the posterior longitudinal ligament, a central protrusion can endanger i t, especially if the protrusion overstretches the ligament. Physical findings are non existent and the diagnosis is made entirely on the history. If pain deep in the sacral area, pain and paraesthesia in the penis, vagina or rechlm, numbness in the saddle area or problems with continence are mentioned, damage to the fourth sacral root should be considered and the patient immediately referred for further assessment. 39 A fourth sacral lesion occurs at a level proximal to the pos terior ganglion and permanent interference with bladder function can resul t if decompression is not carried out.40 Therefore its onset, however slight, is an indication for laminectomy. Cyriax41 (his p. 286) recommends operation even when, after the attack of lumbago bladder function is returning, because there is no guarantee that lasting incontinence may not follow the next attack.
NATURAL HISTORY
Figure 52.6 Two examples of gross partial articular patterns. Upper: gross limitation of flexion and left side flexion, slight limitation of extension, normal right side flexion. Lower: gross limitation of flexion, slight limitation of extension and left side flexion.
raising both legs pulls on the dura equally. In unilateral lumbago there will often be more limitation of SLR on the painful side. Occasionally this may be reversed, when the crossed SLR phenomenon is present (see p. 823). The degree of limitation of SLR is an indication of the intensity of the discodural interaction.38 I n hyperacute lumbago, any attempt to move the straight leg upwards results in considerable pain, whereas in a more moderate lumbago the SLR is limited at 45-60°. During recovery, when the reduction is almost complete, SLR will prob ably only be painful at the end of range or show a painful arc at mid-range. The progress of SLR is therefore a very sensitive clinical index in following the position of the protrusion during manipulation.
With, without or despite treatment, most cases of acute lumbago spontaneously and completely recover wi thin 2-6 weeks ( Dixon;42 Choler, cited by Nachemson;43 Spitzer44). The tension in the posterior longitudinal liga ment exerts counterpressure on the bulge, which moves gradually anteriorly, until compression of the dura mater ceases and symptoms disappear. However, in that cartilage has little tendency to reun ite, a fragment that has moved backwards once will sooner or later move again, which implies that although complete recovery after an attack of acute lumbago is the rule, recurrences are to be anticipated.45 Sometimes, however, a disc protrusion will not recede completely and chronic backache results. Although the patient largely recovers and most of the symptoms dis appear, a continuous lumbar ache remains, especially during or after particular movements or in particular positions. Alternatively, the lumbago disappears but there is simultaneous onset of root pain. As has already been dis cussed (see p. 734), the protrusion has moved from the centre to one side.
TREATMENT Most cases of acute lumbago recover without treatment. MacNab put it well when he remarked that 'The physician
750 SECTION TEN - THE LUMBAR SPINE
must constantly remind himself that even if he elected to treat the patient by rubbing peanut butter on each buttock, in the balance of probabilities, the patient would get well fairly quickly' .46 However, keeping the intradiscal pressure as low as possible will of course ease symptoms and hasten the reduction of the bulge. It is therefore wise to adopt from time to time the supine lying position with the knees and the hips flexed to a right angle,47 which decreases the load on the disc to about 30 kPa48 (the 'psoas position'; Fig. 52.7). It is also wise to avoid movements and positions that cause high intradiscal pressures, such as sitting or bending (Nachemson.49 p. 708). Standard textbooks al most u nanimously recommend bed rest as the fi rst l i ne of treatment for acute lumbago.50,51 However, it has never been proven that complete and continuous bed rest decreases the time of recovery. In a comparative trial, statistically significant differences between bed rest, early mobilization and no treatment have not been found, although results tended to favou r early mobilization.52 Others have reported little di fference between mobilization and rest53 and 2 days in bed was found even better than 7 days or, put the other way around, 7 days in bed was more ha rmful than 2 days.54 Therefore bed rest is only neces sary if bed is the only place where the patient is comfortable. If, after a couple of days walking around withou t a considerable i ncrease i n pain i s possible, such a regime should be followed. Fu rthermore, a patient shou ld never be forced to stay in bed against his or her will . Annular lumbago
If acute lumbago is of the annular type there is a good chance of early and complete reduction in the course of one or two manipulative sessions and, instead of await ing spontaneous recovery over 2 or more weeks, the patient can return to work from the second or third day.
lateral deviation away from the painful side. A good alternative then is a sustained manual stretching tech nique. Positioning the patient in increasing but stil l comfortable lordosis (McKenzie technique) is another alternative in treating acute nuclear lumbago. The effec tiveness of this method has been proven in a prospective randomized triaP5 Although effective in chronic nuclear backache, where the dural symptoms are much more mild, traction should never be used in acute nuclear lumbago. Experience shows that if traction is applied on a patient who men tions the presence of 'twinges', considerable worsening of the condition for several days may be expected. The reason for this is not completely understood. Presumably the size of the bulge increases when the hydrostatic and osmotic conditions within the disc change during traction (see p. 708). Hyperacute lumbago
If the lumbago is really hyperacute, which means that the dural symptoms are so intense that repeated and agonizing twinges force the patient to lie motionless, any attempt at manipulative reduction is unthinkable. It is obvious that manipulation cannot be done when the patient can hardly move or when it takes him some minute to roll from a prone- to supine-lying position on the examination couch. In these cases, the only alterna tive to several weeks of bed rest is epidu ral local anaes thesia, which affords immediate and complete relief of symptoms over 1 or 2 hours. Curiously enough, and although the anaesthesia only works for 2 hours, there is lasting relief from the next day on. Probably the injec-
Box 52.1 Summary of lumbago Definition:
a sudden attack of severe and in capaci tati ng backache, caused by a l arge posterior shift of d i sc material, with d u ral con tact
Acute onset:
ann u l ar
Slow onset:
n u clear
Nuclear lumbago
In nuclear types of acute lumbago, classical tive reduction usually fails. A slow onset of toms usually i ndicates that the protrusion is be pushed back. Manipulation is also apt
Figure 52.7 The 'psoas position'.
manipula the symp too soft to to fail in
Articular
D ural
Sym p to m s
Twinges Pain on sitti n g ! bend ing
E xtraseg mental pain Pain on coughing! sneezing
Sig n s
Deviation: forwards sideaways Gross partial arti cu l ar pattern
Pain on neck flexion Li m i ted straight leg raising
Treatmen t
Man i p u l ation Mobil izations Rel ative rest
Epid ural i n jectio ns
CHAPTER 52 - THE DURAL CONCEPT 751
tion has some long-term effect on the inflamed dura, rendering it less sensitive. The immobilizing twinges having been abolished, the patient is then capable of getting up and travelling for manipulative reduction of the resi dual displacement. This combination of epidural local anaesthesia and manipulation is rapidly successful in nearly all cases of hyperacute lumbago.56
BACKACHE
About 80% of all cases of low back pain relate directly to the intervertebral discS.57 Discodural backache presents a typical complex of symptoms and signs, both articular and dural . The mechanism of pain and dysfunction is exactly the same as described in lumbago, but the signs and .symptoms are less acute because the discodural interaction is more moderate.
MECHANISM In a predisposed and slightly degenerated disc a small posterior displacement occurs when the biomechanical factors are favourable: increased load in a flexed spine shifts the disc material backwards (towards the convex ity). Contact with the dura mater then creates the pain. If the displaced disc material is nuclear, the onset of the symptoms will be slow; if it is annular the pain will appear suddenly. Because, in contrast to lumbago, the protrusion is rather small, the dura will not be stimulated continuously and therefore dural irritation remains mod erate: the twinges and gross deviation typical of lumbago are absent. Sometimes dural contact occurs during par ticular movements of the spine only when an increase in load pushes the bulge in the direction of the dural tube. The protrusion may not be large enough to interfere with the dura when the latter is moved forwards during neck flexion or straight leg raising and therefore dural signs are not present. This explains why in moderate backache there can be articular signs only, even though the mecha nism of pain is that of a discodural interaction.
HISTORY The pain is usually located in the back, unilaterally or centrally, at the sacral region or in one buttock. Because the pain is of dural origin, it can spread to the iliac crest, the trochanteric area and the groin, although seldom beyond the gluteal folds. Occasionally it may be vaguely situated in the posterior or anterior aspect of the thigh. Depending on which part of the dura is irritated, the pain is central or unilateral or shifts in location. 58 Shifting pain is a common history and indicates that the lesion has
moved from one side of the intervertebral joint to the other. Shifting pain in the back is one of the most charac teristic phenomena in discodural backache. An alternat ing ache in the buttock, however, suggests sacroiliac arthritis rather than a disc problem (see Ch. 61). The localization of pain not only varies according to the site of compression of the dural tube but is also deter mined by the intensity of the stimulation. One of the rules of referred pain is that the stronger the stimulus, the further the pain will be referred. This has some practical bearings when it comes to evaluation of therapy: when the pain has originally been located in a buttock but, during a manipulative session, tends towards the centre and becomes paravertebral, this implies that the pain stimulus has been reduced and discodural contact is now less pronounced than it was. 'Centralization' of the pain is thus a good predictor of successful outcome.59 The reverse change - pain moving more and more distally indicates that the situation has worsened. The onset of the complaints is very important from a clinical point of view but cannot always be recalled. Especially in long-standing cases, the patient may have difficulty in remembering if the symptoms appeared suddenly - as would occur with an annular lesion - or if disability was progressive - a nuclear displacement. In an annular protrusion, the patient m ay describe a sudden sensation of something giving way in the back, which may have been accompanied by an audible click or ' thud' in the lower back, associated with a twinge of pain. From that moment the back has ached during par ticu lar positions and movements. They typical history of a nuclear protrusion is that the initial symptoms were slight, with little disability, the patient easily being able to continue normal activities, with probably only minor backache. The same evening, however, after sitting to eat, read or relax, considerably increased discomfort will have been felt and the following day worsening will have become apparent from the momen t an attempt was made to rise from bed. Relation between posture/movement and pain. In minor disc lesions, the ache probably depends entirely on the level of exertion. Any work involving stooping or lifting or sitting for too long is followed by pain, which may however be almost or completely absent at rest. In more advanced instances, particular positions are very painful or even impossible. It is obvious that contact will increase in positions and activities that increase intra discal pressure and thus discodural contact. Bending forwards and lifting results in higher pressure than standing erect. To most patients with backache, walking around is more comfortable than sitting, because the latter imposes more load on the disc.6o Sitting without support causes yet more load and consequently more pain than does sitting with a reclined back rest.49
752 SECTION TEN - THE LUMBAR SPINE
The pain is influenced not only by position but also by particular movements. It is striking that in backache caused by disc problems one of the most consistent com plaints is a temporary increase in pain when the patient changes position. The aggravation of pain on standing after sitting for some time or the momentary increase in pain on sitting after walking is typical of a discodural interaction. Turning in bed and putting on footwear in the morning is often mentioned as associated with an increase in pain. Dural symptoms, such as pain on cough ing and sneezing, are often present. A paradoxical symptom complex is sometimes encountered. The dynamics of the disc, described above (see p. 708), suggest that intradiscal pressure should decrease and any bulge become less prominent when the patient lies down. Yet some patients have more pain during and after bed rest, wake during the night and have to get out of bed before dawn. The explanation is probably an increase in swelling when the external load diminishes. Diurnal changes in disc hydration and pressure have been demonstrated both in vitro61 and in ViVO.62,63 A small posterior bulge that becomes more hydrated swells to increase dural contact. An increase i n discodural contact in the morning h a s been demon strated by comparing the range of SLR after recumbency and after 2 hours erect, when an increase of 10% or more took place in 70% of patients.64 The characteristics of discodural pain are summarized in Box 52.2.
CLINICAL EXAMINATION Inspection
Lateral deviation or flexion deformity is present only in more marked cases of backache. As in lumbago, the lateral tilt may be either away from or towards the painful side. Some protective muscle spasm may be seen or felt. In mild examples, inspection reveals nothing special, nor does the patient mention any pain in the neutral position. Spinal movements
A partial articular pattern is present on the four active movements. The degree of l imitation is unequal in
Box 52.2 Characteristics of pain in discodural conflicts • • • •
D ural reference D ural sym ptoms: on cou g hi n g , sneezi ng and pressing Shifting pai n Pain i n creases d u ring sitting/be n d i n g and when position changes • (Pai n worse i n the morn i ng)
different directions (Fig. 52.8); if there is no limitation, some movements are painful at their extremes and some not. All these findings are typical of internal derange ment - some movements increase the annu lar or nuclear bulge, so increasing the dural contact, while others reduce it. Extension. This is painful in the centre of the lumbosacral area and, if the protrusion lies centrally, is also limited. Sometimes the lumbar spine is seen to shift slightly later ally during extension. Side flexion. Usually this is unequally limited (Fig. 52.8a). Alternatively there is pain at the end of one side flexion only, the other being full range and painless. If side flexion away from the pain is the more difficult to achieve, manipulative reduction will almost certainly succeed, but in the reverse situation quick and lasting relief by manipulation is more uncertain. Sometimes there is a painful arc (Fig. 52.8d): momentary pain is experienced on moving the trunk from one side to the other. The arc may be quite extensive and is only overcome with considerable effort. Therefore the patient should be encouraged to continue movement and not stop the moment pain is felt, otherwise the presence of an arc could be missed. Sometimes both side flexions are full and painless. This does not eliminate a disc protrusion but probably indicates that it is too small and too centrally localized to come in contact with the dura during side flexions. Only extension or flexion will then influence the pain and asymmetry is probably only shown by some momentary deviation, a painful arc during flexion or unilateral localization. Forward bending. As in acute lumbago, forward bending is usually the most painful and limited movement, because it not only acts on the intervertebral joint but also drags the dura forwards in the direction of the protru sion. During flexion the trunk may deviate, although in the upright position it was straight. The reverse may also happen: a lateral tilt in the erect position is lost during flexion. Sometimes the deviation is momentary: the spine shifts away from, then back towards, the midline as the movement proceeds. There may also be an alternating deviation: one way in forward flexion and the other way when the direction of movement is reversed . Deviations, whether in the upright or in the flexed position or alternating, are all defensive mechanisms to avoid pain: the dura mater has to be held to one or the other side of the projection. Therefore the clinical finding of deviation, of whatever type, strongly suggests a disc protrusion. , It is also possible for flexion to be of full range and only painful at the extreme. Or pain is only provoked when, at the end of range, active neck flexion is added .
CHAPTER 52
( a)
THE DURAL CONCEPT 753
( b)
(d)
(c)
Figure 52.B
-
Example of partial articular patterns. The lower figures are in association with a painful arc: (c) during fiexion; (d) during side fiexion.
Painful arc. Frequently, a painful arc is encountered, with a transient pain somewhere at mid-range (Fig. 52.8c,d). Alternatively, slight deviation may be seen at the mid point of flexion. Careful observation is needed to detect this visible arc of which the patient is usually unaware. A painful arc during flexion can be associated with a partial articular pattern but it can also be an isolated finding. It always means that a small fragment of disc tissue impinges momentarily against the dura mater. At the beginning of the flexion, increase in both intradiscal pres sure and convexity of the posterior aspect of the interver tebral joint provoke disco dural contact (Fig. 52.9). Flexion beyond the horizontal imposes more distraction than compression on the intervertebral joint. The backwards pressure on the disc then decreases and is replaced by a more centripetal force on the disc, which is supported by
the tightening of the posterior longitudinal ligament. The small posterior displacement is then removed from contact with the dura and pain ceases. Dural signs
Any hindrance to the normal mobility of the dura leads to a limitation of SLR or to pain during neck flexion. This is the normal finding in acute lumbago. In discodural backache SLR may be painful or limited but, should this not be the case, the disc cannot be automatically elimi nated as a cause of symptoms. Especially in mild exam ples, the displacement can be small and the impact of the bulge on the dura not continuous. In a supine-lying posi tion the protrusion may not be large enough to cause interference with dural mobility, and so SLR remains negative. Contact between disc and dura then only
754 SECTION TEN - THE LUMBAR SPINE
( a)
(b)
(c)
�
Figure 52.9
Painful arc: (a) erect position, (b) 3D· of flexion, (c) 60· of flexion.
originates when a momentary increase of the intradiscal pressure moves the disc backwards, which happens during forward flexion while standing. I n the course of manipulative treatment it is a common finding that SLR becomes negative before reduction is complete. Lumbar movements, tested while the patient stands, then still provoke pain because, in the erect position, the joint is subjected to axial pressure, which causes increased posterior bulging of the disc. Root signs
In uncomplicated backache there are no root signs.
NATURAL HISTORY OF DISCODURAL BACKACHE It is extremely difficult to predict the natural history and therefore unwise to tell the patient that backache will very soon abate. Although it is true that most episodes are self-limiting,65 the disability often becomes chronic. An acute bout shows some tendency to spontaneous cure66 as does acute lumbago, but chronic backache does not and patients may have suffered for years from chronic or recurrent lower lumbar pain.67,68 There is an increasingly unfavourable outlook in terms of return to work as the duration of symptoms increases: 6 months after an episode, the likelihood of ever returning to work is 50%; by 1 year the figure is 20%; and at 2 years the probability approaches zero.69 Often backache becomes intermittent, with repeated recurrences following an acute episode.7o A large number of patients also experience a continuous or intermittent minor ache without chronic disablement or continuous
work loss.71, 72 Although daily activities may be possible, prolonged sitting or, say, digging in the garden may cause considerable increase of pain. Permanent relief occurs only in the very long term, when stabilization in the 'motion segment' develops (see Ch. 51).
PARTICULAR TYPES OF BACKACHE Bruised dura
Sometimes a patient complains of a constant ache in the back which is unaltered by any position or movement. The onset is as an attack of acute lumbago. As is usual, resolution occurred within 2 weeks, except for persistent constant backache over months or years. Coughing and sneezing may aggravate the pain but other movements definitely do not, although there may be increased pain during the night or in the morning. Clinical examination reveals absolutely nothing: there is a full range of spinal movements and dural signs are absent. A possible explanation for this type of backache is a 'bruising' of the dura mater?3 The acute lumbago has induced an inflammation of the dura mater. Although the disc displacement has receded after some time, the dura has remained inflamed, which results in continuous pain. Obviously this type of backache - chronic pain unaltered by posture or exertion and with a negative clinical exam ination - can also exist as the result of pain referred to the back from other (visceral) structures. When a bruised dura is suspected, an epidural }njec tion with procaine 0.5% is indicated. A positive diagnos tic response not only settles the differential diagnostic question but is also the treatment, because about half of
CHAPTER 52 - THE DURAL CONCEPT 755
those with backache attributed to a bruised dura are permanently cured by one injection. Nocturnal or morning backache
Backache may be confined to night time. The patient can do everything normally undertaken during the day, without the slightest discomfort, but every morning is woken in the early hours because of increasing and severe backache which forces rising from bed. The pain quickly eases, and once upright for, say, half an hour, the disability has totally disappeared. A pain-free d ay follows, in spite of the level of exertion. Alternatively, unbearable backache after 2 hours of sleep forces the suf ferer out of bed. The pain abates quickly and resumption of sleep is possible. During the day there is not the slightest discomfort, even on heavy work. Clinical examination during the day is negative: there is a full range of movement, and dural signs are absent. This nocturnal backache often occurs in middle-aged people. It is best explained by increase in intradiscal oncotic pressure at an early stage of degeneration. When the external load is diminished in the horizontal position, considerable increase in the water content takes place. Expansion forces the disc against the pain sensitive dura. Resumption of the u pright position raises the hydrostatic pressure, water is extruded and the disc deflates, which alleviates the tension on the dura mater so that pain disappears. Because the pain is of dural origin, epidural injection is the treatment of choice and succeeds in about 70%. Should the injection fail, ligamentous sclerosis, in order to stabilize the lower lumbar segments, is used.
TREATMENT Before specific treatment is given, some questions must be answered: • Is the backache caused by an activity-related spinal disorder ? •
If this is the case, is the disorder a discodural interaction or not ?
When there is a clear combination of both articu lar and dural symptoms and signs, the answer is obvious. In moderate disco dural backache, however, when the patient presents with articular signs only, it may be more difficult to make a certain diagnosis of internal derange ment. However, a partial articular pattern always indi cates a disc lesion, except in a few cases (see Ch. 58). A deviation, whether in the upright position or in flexion, signifies a protrusion. Also the presence of a painful arc, whether during side or forwards flexion, is the sign of a small posterior bulge. The therapeutic approach to discodural backache differs from patient to patient and depends largely on the data obtained from history and clinical examination. Although most cases of backache are caused by an impingement of a subluxated disc against the dura mater, the size, structure, position, level and stability of the bulge differ considerably. Treatment therefore must be selective. A single definitive treatment for discodural low back pain does not exist. If a subluxated fragment of disc is believed to be the cause of the pain, further questions should be posed: • What is the level of the lesion and what is the size and
composition of the bulge? Is the subluxated fragment an acute and occasional event, or has the patient recurrent attacks of backache ? How long does the disability last? Does the pain disappear completely between bou ts or is there a continuous ache ? • What is the degree ofpain and how much is the dura inflamed ? • What attitude does the patient have towards the problem ? • Does the patient want to get better ? Is there any compensation claim or does the patient show clear evidence of psychological disorder ? (see Section 16).
•
Nuclear self-reducing disc
Sometimes the history obtained is the converse of that described in the previous section. Waking is comfort ably pain free and exertion does not cause symptoms. Backache starts after some hours upright, increases slowly as the day goes on, being worst in the evening, and varies in intensity according to activities. Lying down abolishes the pain, which has completely gone by the next morning. Clinical examination in the morning is negative with a full range of movement and absence of dural signs. By the evening a partial articular pattern and pain on SLR are present. Clearly there has been protrusion of nuclear material as the result of axial loading of the spine. Recumbency during the night then results in spontaneous reduction. Because this history indicates a reducible but unsta ble disc protrusion, the treatment should be directed to stabilization of the intervertebral joint. This can be achieved by sclerosing injections, which usually give good results.
If there is proof of a disc lesion and the patient is well motivated, conservative treatment consists of: • • •
Reduction of the displacement Maintenance of reduction Desensitization of the dura (in acute or gross inflammation of the dura, it is sometimes better to desensitize it in order to abate the pain instead of trying to move the disc back into place).
Reduction
Reduction is achieved by manipulation or traction. When a slight displacement of disc tissue is believed to be
756 SECTION TEN - THE LUMBAR SPINE
responsible for the symptoms, the obvious treatment is to restore its anatomical position. If the displacement is annular, the treatment of choice is manipulative reduction. A nuclear displacement is an indication for sustained traction. Although the two tech niques are to some extent interchangeable, some protru sions prove irreducible by traction, yet reducible by manipulation and vice versa. It is obvious that a protru sion composed of hard annular material will respond better to manipulation but that a soft nuclear bulge requires traction. Cyriax said:41 'You can hit a nail with a hammer, but treacle must be sucked'. If sufficient data on the onset of the complaints cannot be obtained and the choice of treatment is in doubt, manipulation should be tried first. If it fails, the patient should attend for traction from the next day on. If considerable improvement is achieved by manipulation but, despite further attempts, a residual displacement cannot be reduced, traction should be substituted so as to complete the process. Manipulation. The indication for manipulation is a poste rior annular displacement. Signs that favour the use of manipulation are a small painful arc or a small lateral deviation during flexion. Reduction is usually easy to achieve in patients whose pain is greatest when they bend away from the painful side. The chance of success of manual reduction is also greater in elderly patients. The manipulation techniques used in this book tighten the posterior longitudinal ligament and create room at the posterior aspect of the joint. The increased distance between the two vertebral borders gives the fragment space to move and the force exerted by the posterior ligament pushes it back in place. Displacements at the third and fourth levels respond best to rotatory manoeuvres, whereas at the fifth level extension manoeuvres are u sually more effective. Rotatory manoeuvres are also chosen if deviation of any kind exists. Elderly patients tolerate prone extension techniques better than rotational techniques. The simple and easy-to-learn manipulation measures are usually speedily effective. Overall, acute backache is relieved by one session of manipulation in between 46 and 57% of patients.74, 75 As a rule, small annular dis placements are cured by one single manipulative session. In larger protrusions, two to four sessions may be requ ired. When the patient presents with a marked lateral deviation, up to four manipulation sessions are sometimes needed. Manipulation is successful after a small number of session or not at all. Hence, if the patient does not almost immediately and lastingly improve, it is unwise to continue treatment and daily traction should be used instead. Young patients tolerate daily manipulation when repeated sessions are required. In the elderly, however, it
is wise to manipulate on alternate days, for fear of increasing ligamentous pain. Sustained d aily traction . The indication for traction is a patient under 60 years old, who describes a slow onset of pain in the back. Patients with a discodural conflict, where the consistency of the protrusion is uncertain, and who do not immediately improve after manipulation, should also be treated with daily traction. Experience also teaches that, when trunk side flexion towards the painful side increases the pain, traction will succeed better than manipulation. The intention of traction is to create a negative pres sure in the disc76 and to tauten the posterior longitudinal ligament, which exerts a centripetal force on the nuclear materiaP7 This results in a gradual reduction of the bulge and a release from the dura mater. Maintenance of reduction
Once the displacement is reduced and the patient asymp tomatic, the question of specific prophylaxis arises. If the history is that of a nuclear protrusion, the patient should be careful about posture, especially during pro longed sitting or bending. To maintain the spine in slight lordosis is beneficial and helps to prevent posterior bulging of nuclear material. Occasional attacks of annular low back pain, say once a year, can be managed by a good manipulator, pro vided one is available. More frequent recurrences call for attention to active prevention. The necessity for low ering the intradiscal pressure and keeping the back hollow during daily activities should be explained during 'back school' sessions, where the patient is instructed in sitting, standing, bending and lifting. However, the back school is prophylactic not thera peutic, and patients should never attend before ' they are completely asymptomatic. Strengthening the muscles of the trunk does not increase the stability of the disc. Back muscles do not directly control the intervertebral content and in conse quence stability will not depend upon their strength but upon the position in which they keep the body. Exercise and strengthening of the abdominal and sacrospinalis muscles are therefore futile and may make backache worse because intradiscal pressure increases significantly with prone-lying extension exercises78 and sit-up and curl-up exercises.79,8o In recurrent backache, where the disc is unstable and the patient suffers repeated attacks despite maintaining good posture, sclerosing injections should be given to the posterior ligaments. The purpose is to induce an inflammation at the inter- and supra-spinous liga ments, the posterior capsule of the facet joints and the deep aspect of the lumbar fascia, at the fourth and fifth lumbar
CHAPTER 52 - THE DURAL CONCEPT 757
levels. In response to the inflammation, fibrous tissue and tissue contracture in the injected ligaments occurs. Permanent shortening of the injected structures then decreases the mobility and increases the stability of the intervertebral joint. About 80% of patients treated by sclerosing injections benefit. Another indication for these stabilizing injections is nuclear self-reducing disc protrusion, for which no other treatment is effective. They are also indicated when nocturnal or morning back ache does not respond to epidural local anaesthesia. Epidural injection
In discodural interactions in which the inflammation of the dura is more important than the actual disc protru sion, the treatment of choice is epidural injection of a local anaesthetic. This is, for instance, the case in noctur nal backache, where a discal swelling only intermittently presses against the dura. Also when backache is brought about by a 'bruised dura', epidural local anaesthesia is used. When backache is clearly the result of a low lumbar disc displacement but proves refractory to both manipu lation and traction, the next step is epidural injection. If it is impossible to correct the discal bulge, it is logical to try to desensitize the dural tube. Definition, symptoms, signs and treatment of disco dural backache are summarized in Box 52.3.
SCIATICA
Since Mixter and Bar published their classic paper in 1934,12 it has been generally acknowledged that lateral disc displacements are the main source of radicular pain. Pressure of the protruded disc against the nerve root causes mechanical nerve fibre deformation and changes in the nerve root circulation, which result in pain and functional changes.
MECHANISM A posterior disc displacement (Fig. 52. lOa) usually remains more or less under the physical influence of the posterior longitudinal ligament. The resistance of the ligament keeps the bulge in place or tends to push the protrusion forwards again, as happens during the spontaneous or manipulative reduction of a disc in acute lumbago: the pressure exerted by the ligament is higher than the intradiscal pressure and moves the bulge gradu ally forwards. Sometimes, however, when intradiscal pressure remains high, the displaced tissue is pushed more and more laterally towards the posterolateral edge of the disc - a zone of lesser resistance (Fig. 52. l 0b).81, 82 Moved
Box 52.3 Summary of discodural backache Definition Backache, sometimes with dural reference in buttocks or legs, which is caused by a posterior shift of disc material constantly or intermittently pressing against the d u ra mater
Symptoms Acute, chro n i c or recurrent Onset i n d i cates the type of protrusion: a n n u lar protrusion Acute onset: n u clear protrusion Slow and gradual onset: Acute onset, with slow worse n i n g : m i xed protrusion Pain is u n i l ateral, central, bi lateral or alternating (extrasegmenta l pai n reference i n buttocks and legs is possible) Pa i n is in creased by particu lar movements: as a rule sitting, com i n g u p r i g ht after sitting, a n d getting out of bed are the most painful D u ra l symptoms may be present Particu lar types of backa che Continuous pain, 'bru ised d u ra'? Noctu rnal/morning backa che Self-red ucing disc Signs
Arti cu lar Partial a rticu l a r pattern Deviation: in u p r i g ht position, in flexion or a lternating Momentary deviation during flexion Pai nful arc D u ral (not always present) Neck flexion? Positive stra i g ht leg raising Pa inful arc during stra i g ht leg ra ising Treatment
M a n ipu lation A n n u l a r lesions Sma l l n u clear lesions Traction N u clear lesions D isc lesions u n a ltered after m a n ipu lation Epidural i n jections Intractable backa che Nocturnal and morning backa che Bruised d u ra Back school: only as a prophylactic measure Sclerosing i njections Recurrent d iscodural conflict Self-reducing n u clear protrusions Nocturnal and morning backa che
laterally, and freed from the counterpressure of the strong central part of the posterior longitudinal liga ment, the bulge enlarges, lifts or ruptures the lateral ligamentous expansion and herniates into the lateral compartment of the epidural space where it compresses
758 S E CTION T E N - T H E L U M BAR S P I N E
Figure 52. 1 0
Mechanisms of sciatica (see text for detail).
the nerve root. This is the typical development of a sec ondary posterolateral protrusion leading to a classical attack of sciatica. For a good understanding of the clinical picture, it is important to remember that the severity of the symptoms depends not only on the mass of protruded disc mate rial83 but also on other factors (Fig. 52.11). Among these, the distension within the mass - in other words the soft ness or hardness of the bulge - plays an important role. 84, 85 Furthermore, the relative fixation of the root to the bony elements of the intervertebral foramen can determine the degree of traction upon it.86, 87 Finally the degree of inflammation of the nerve is a significant element in producing symptoms.88 There can be a direct chemical injury to the nerve root,89-93 or extra- and intra-
neural swelling,94, 95 with further compression.96 Many experts have emphasized that pain is provoked mainly when the nerve root is the site of a chronic irritation,97-99 and experimental confirmation of this has been obtained by inflating Fogarthy balloon catheters, placed around the roots, which produce sciatica only if the pressure is maintained long enough to set up an inflammatory reac tion.lOO During operations using progressive local anaes thesia, sciatica can be produced only by direct pressure or stretch on an inflamed nerve root, whereas pressure on a normal root is painless.58 It should thus be clear that the severity of sciatic symptoms and signs is a function of the magnitude of the mass, the intensity of the discoradicular contact and the inflammatory responses around the nerve roOt. 1 01 For 2
3 Figure 52.1 1
the nerve root.
Factors in the production of symptoms and signs in sciatica: 1, in hardness; 2, size of the bulge; 3, relative fixation of the nerve root; 4, inflammation of
CHAPTER 52 - T H E D U RAL CO N C E PT 759
all these reasons, sciatica is not simply the existence of a bulge; demonstrable on CT. Judging the severity of the sciatica therefore depends only on the data obtained from history and clinical examination. Technical investi gations usually add little information. Symptoms and signs, the consequence of the involve ment of the nerve root in the pathological changes, are articular, dural and nervous. Nerve root sleeve and nerve root fibres give rise to two different sets of clinical findings: dural and parenchymal. T he dural sleeve
Symptom : segmental pain . The dural investment is first to be compressed and inflamed and causes the appear ance of radicular pain. Unlike extrasegmental pain from pressure on the dura, pain stemming from the dural root sleeve follows exactly the rules of segmentally referred pain102 (see Ch. 1 ). However, an inexperienced examiner may sometimes find it difficult to differentiate segmen tal radicular pain from extrasegmental dural pain. The following features may then be of value. First, dural pain is never felt beyond the ankle, whereas radicular pain of L4, L5, Sl and S2 usually spreads to the foot and the toes. Second, dural pain is not restricted to precise dermatomes of which the patient can give an accurate description but is felt vaguely over a large area. The patient will therefore be more imprecise in describing the area. Sign: alterations in mobility. The dural sheath of the nerve root moves in relation to the neighbouring struc hues. In that the course of the nerve root is downwards and slightly anterior and the nerve root is loosely bound to the pedicle below by the lateral root ligament, it will be caught against the posterolateral aspect of the disc when downward traction is exerted103 (Fig. 52. 1 2). During SLR, the L4, L5, Sl and S2 roots undergo a downward and anterior excursion of 2-4 mm at the level of the intervertebral foramen104 (see p. 719). It is obvious that, in large posterolateral disc protrusions, the mobility of these roots is impaired and SLR painfully limited. Sometimes a painful arc rather than limitation is observed: pain appears during the movement but disap pears when the leg is raised higher - an indication of a small projection, which the nerve catches against and then slips over. 10S Such a momentary pain is an encour aging sign for conservative treatment. The third lumbar root continues into the femoral nerve, which remains relaxed during SLR. Therefore lack of pain with this manoeuvre is not an indication that the L3 root is intact. A better test is knee flexion in the prone position.1 06 There are no clinical tests for the mobility of the S3 and S4 roots.
Figure 52.12
The nerve root drags anteriorly on the disc bulge.
T he parenchyma
Mechanical factors are mainly responsible for intraneural blood flow and formation of intraneural oedema, which in turn causes structural damage to the nerve fibres. It has also been suggested that breakdown products from the degenerating nucleus pulposus may leak through the root and induce a 'chemical radiculitis' 88,107 and that autoimmune mechanisms play a role in the inflammatory tissue reactions seen around degenerating discs. 1 08, 1 09 The details of disturbances in nerve tissue during discoradic ular interaction are not yet fully u nderstood; however, their clinical consequences and functional changes are clear. no On the one hand, hyperexcitability of the fibres results in paraesthesia111 and muscle fasciculations.ll2 On the other hand, there is loss of nerve function - muscle weakness, sensory deficit and reflex changes. Sym ptom: paraesthesia. Pins and needles only appear as the result of hyperexcitability of nervous tissue. They are therefore pathognomonic for peripheral nerve lesions. In nerve root compression they are strictly limited to the . respective dermatome and occupy an area at its distal extremity. As a rule, paraesthesiae tend to disappear when numbness begins - hypereXCitability ceases when pressure has induced a sensory deficit (see Ch. 2). Sig ns: sensory deficit. motor deficit and reflex changes. Sensory and motor deficit are not always easy to detect, and the two limbs should be carefully compared. Motor deficit usually remains moderate and most patients are unaware of loss of function. Nevertheless, weakness has important therapeutic and prognostic consequences and it must be sought in each muscle group. On account of the obliquity of the nerve roots and the fact that the sensory and motor rootlets have separate courses within the dural sleeve, it is possible for one
760 SECTI O N TEN - T H E L U M BAR S P I N E
protrusion to compress one root, half of a root, two roots or the halves of two consecutive roots (see Fig. 52. 16). This is particularly so in a lesion at the fifth lumbar level, where the same protrusion compresses the motor rootlet of L5 and the 51 sensory fibres. The root signs in discoradicular interactions (see Fig. 52. 1 7) are as follows (see reference 113 and Cyriax:41 pp. 283-286): • • •
•
•
•
•
• •
L 1 : cutaneous analgesia at, and just below the inner half of the inguinal ligament. L2: cutaneous analgesia from the groin to the patella, and weakness of the psoas muscle. L3: cutaneous analgesia over the anterior aspect of the leg, from the patella to the ankles, weakness of the psoas and quadriceps muscles and a sluggish or absent knee jerk. L4: cutaneous analgesia over the outer ankle, dorsum and inner aspect of the foot and big toe, and wea k tibialis anterior and extensor hallucis muscles. L5: cutaneous analgesia over the outer leg, the dorsum of the foot and the inner three toes, weak extensor hallucis and peroneal muscles; the ankle jerk may be absent or sluggish. 5 1 : cutaneous analgesia of the posterolateral aspect of the leg, behind the lateral ankle, the lateral aspect of the foot and the two outer toes; the peronei, calf ham strings and gluteus medius muscles may be weak; the ankle jerk is sluggish. 52: cutaneous analgesia of the dorsum of the leg and the heel, and weakness of the calf, hamstrings and gluteus medius muscles. 53: cutaneous analgesia at the inner aspect of the thigh; no muscle weakness. 54: numbness of the saddle area and dysfunction of bladder and rectum.
HISTORY Secondary posterolateral protrusion
This is 'classical sciatica'. The patient is usually between 20 and 50 years of age. A number of attacks of backache or lumbago have taken place. Again a sudden or increas ing backache occurs, which tends to become unilateral. Then the pain shifts towards one aspect of the limb, where it occupies one particular dermatome; as a rule the backache ceases when pain in the limb begins. The exact localization of the pain is of considerable help in diagnosis. Pain at the groin and the front of the thigh may indicate a second or third nerve root compression. When anterior pain spreads down towards the ankles, the third nerve root is at fault. Pain at the lateral aspect of the leg and crossing the dorsum of the foot is caused by a fourth or fifth disc lesion. The differentiation between these is not always easy. If the big toe only is affected both
roots may be responsible but if in addition the second and third toes hurt the lesion of the fifth lumbar root. Pain at the lateral aspect of the leg and foot, reaching the two outer toes, indicates a first sacral lesion, whereas a second sacral root pain occupies the dorsal aspect of the thigh, ca 1£ and heel. After a while, and in addition to the increasing root pain, the patient will report paraesthesia at the distal aspect of the respective dermatome. Pins and needles not only indicate that nerve fibres are being compressed, which immediately excludes other, non-radicular sources for the segmental pain, but also provide a better pointer to which nerve root is at fault. Later, the patient will mention numbness and weakness of the leg or foot. As weakness increases to a maximum, the pain ceases - the root has atrophied. The symptoms caused by a posterolateral disc displace ment have a striking similarity. 114 The history is vital in the diagnosis of sciatica and is probably the most important diagnostic technique. The onset and the development of symptoms, their relation to posture and exertion, the exact localization of the pain and the presence of paraes thesia and numbness are extremely important features in diagnosis and decision making for both treatment and prophylaxis. The pain often increases on sitting, and eases in recumbency, especially when the patient adopts the 'psoas position' - supine, with the hips and knees flexed (see Fig. 52.7). In severe instances, however, when the continuous pressure has induced a considerable inflammation of the dural sheath, the pain may be con tinuous, sometimes with increase at night. As a rule standing is better than sitting but sometimes walking can be difficult, especially if nerve root mobility is impaired in such a way that moving the affected leg forwards during the swing phase drags on the sciatic nerve. The patient then walks with an adaptive gait. In lesions cif the third lumbar root, the pain increases on standing or reclining and eases only in sitting, because the latter is the only position which relaxes the tension on the femoral nerve and the third lumbar root. These patients often prefer to sleep sitting. In discoradicular interactions the symptoms are usually worse in the morning, probably as a result of the increased swelling pressure in the disc. (Kramer:32 pp. 1 7-21). In an active patient, the pain decreases somewhat around midday and increases again by the evening. Coughing and sneezing may cause pain in the gluteal area or in the limb. Sym ptom sequence. The progression from central bulge to posterolateral protrusion, with pressure on the nerve root sleeve and subsequently the nerve root fibres, is reflected in the sequence of symptoms. Initial backaehe is followed by radicular pain, then paraesthesia, sensory and motor deficits. As the last two increase, the nerve root sheath becomes insensitive and sciatic pain abates. A
CHAPTER 52
large protrusion which causes nerve atrophy may produce complete loss of function: the patient may then be spontaneously and subjectively better but anatomi cally worse. However, most patients recover from the palsy without lasting loss of power, especially if only one root is paretic. For diagnostic, therapeutic and prognostic reasons it is very important to differentiate between radicular pain and dural pain in the limb. In acute lumbago or severe backache, this is usually not very difficult, since the referred pain in the leg is not as severe as the lumbar or gluteal pain itself. Also when the patient presents with a clearly outlined and severe ache in the leg, it is easy to recognize the segmental pain of root compression. However when, as happens occasionally, only referred dural pain is present, to distinguish this from segmental pain can be more difficult. The typical example is pain in the groin, which can stem from dural reference, segmen tal reference from LI-L2 or segmental reference from T12. Also pain in the buttocks sometimes causes diagnostic problems: in one or both buttocks it is usually of dural origin, especially if the pain is restricted to the upper buttock and is not as severe as the back pain. Pain in one lower buttock is only rarely dural and more often a segmental reference from S2. Although the sequence of symptoms as set out above is always present in primary posterolateral protrusions it is not always as typical as described. Pre-existing backache may never have occurred but backache and sciatica have originated almost simultaneously. Careful enquiry, however, may show that 2 days or so before the onset of the sciatic pain there had been vague sacral aching after prolonged sitting or difficulties on bending. Alternatively, acute backache may have almost immedi ately changed into leg ache. The short or slight period of backache will not be mentioned unless specifically enquired for. Sometimes the pain in the back does not disappear when the root pain comes on and this is par ticularly so in elderly patients. In these cases the symp toms can go on indefinitely, which is not the case i n 'classical sciatica'. Especially when the back aches more than the limb, this type of sciatica shows little tendency to spontaneous cure.
-
THE D U RAL CO N C E PT 761
but seldom spreads to the foot. Very occasionally the onset is with numbness in the heel, l ater spreading to an ache in the calf and thigh. The moment the patient stands up the pain di sappears. Previous backache has not occurred and the patient usually does not associate the pain in the calf or knee with a disorder in the back; however, a cough or sneeze hurts in the leg. The ache gets slowly worse over a period of months, du ring which it spreads upwards to the posterior aspect of the thigh. By the time the pain has reached the buttock, it may be constant except in bed. The diagnosis of a primary origin of the posterolateral protrusion is important with respect to treatment. Because a primary posterolateral protrusion is always nuclear, manipulations do not influence the symptoms. 'Bruised' dural sleeve
Sometimes the root pain is constant, unaltered by posture or exertion. Usually the patient has a history of a typical discoradicular pain from which recovery has been largely complete. However, the pain failed to dis appear completely and is now more or less constant, although less than before. Alternatively, the patient may have had a discectomy, which improved his condition considerably but not to the point of cure. Sometimes the pain is bilateral, which strongly suggests spondylo listhesis. Clinical examination reveals nothing but a full range of movement. A possible explanation for this unusual pain synd rome is probably a persisting i nflammation of the root sleeve, resulting from a past disc lesion that has undergone spontaneous reduction or has been surgically removed. Although there is no more dis cal contact, the sleeve remains irritated. 83 Epidural injection with local anaesthesia is necessary to determine the diagnosis and often abolishes the pain permanently. Differential diagnosis
Sciatica has not only to be differentiated from dural extrasegmental pain i n the limb (see earlier) but also from segmental pain not caused by discodural interactions. These disorders will be discussed in detail in a separate chapter, but a few salient points are listed here:
Primary posterolateral protrusion
•
In this type of discoradicular interaction, the pain is radicular from the beginning and there has been no pre vious backache. The lesion is nuclear and only affects young patients between the ages of 18 and 35 years. The protrusion is usually at the L5-S1 joint, where it com presses the SI root. The history is typical. A young patient states that a calf aches when sitting is prolonged. Alternatively, the pain may be at the lateral side of the knee and the leg
•
Sciatica in the elderly is more often caused by a lateral recess stenosis and, especially if the pain appears during standing or walking, the existence of a narrow radicular canal should be suspected1l6 (see Ch. 54). B ilateral sciatica i s seldom caused by one disc lesion, unless there is a massive protrusion of the disc with rupture of the posterior longitudinal ligarnent. Evidence for an S4 lesion will also be present (see above). Another, although uncommon, possibility is
762 S E CTI O N T E N - T H E L U M BAR S P I N E
•
•
the presence o f two posterolateral protrusions, one a t L5 and another at L 4 o n the other side. Alternatively, one d isc has developed two posterolateral disc protrusions, one at each side of the posterior longitudinal ligament. In bilateral sciatica in younger patients, spondylolisthesis should be considered; in elderly patients spinal or lateral recess stenosis. Alternating sciatica is rarely caused by a disc lesion but suggests the sacroiliac arthritis of an early ankylosing spondylitis. Increasing backache together with worsening sciatica indicates serious disorder, especially if the pain does not vary with exertion but steadily gets worse, irrespective of posture or exertion (see eh. 58).
CLINICAL EXAMINATION Inspection
A lateral pelvic tilt or a deviation may be present. As in lumbago, the deviation can be towards or away from the painful side, depending on the position of the protrusion. If the latter occurs lateral to the nerve root, there is a lateral shift towards the painless side, which reduces contact with the root (Fig. 52.13). If the protrusion is located at the 'axilla' between the dura and dural sleeve of the root, the spine is deviated towards the painful side in an attempt to decrease the pressure on the root. It is rare to see patients with sciatica adopting the flexed posture so common in acute lumbago. Extension is not possible and every attempt to straighten the back is followed by severe pain at the back of the leg. This form of sciatica is very difficult to treat conservatively and most patients end up with a discectomy. In compression of the L3 root, the patient may adopt a specific posture: slight flexion of the trunk and flexion of the hip. Patients with acute hip lesions position them-
Figure 52.13
selves similarly and a clinical distinction between the two must be made. Spinal movements
In sciatica, as in lumbago or backache, articular signs indicating a partial blocking of the joint may be present. It should be remembered, however, that flexion is not only an articular sign but also a test of the mobility of the root and, except in L3 lesions, is usually limited because of increasing pain in the limb. The classical pattern in sci atica, the consequence of disc lesions, is thus a severe and increasing leg ache during flexion, together with pain felt in the lower back or upper buttock during one or two of the other lumbar movements. If there is a discoradicular contact only, and the dural tube remains untouched during lumbar movements, the pain will be felt in the limb only on flexion. This is typically the case in a primary posterolateral protrusion, where flexion is the only painful and limited movement. Sometimes an increasing lateral tilt is seen during flexion. Again the deviation can be towards or away from the painful side, depending on the position of the protrusion. I f side flexion or extension hurts in the leg instead of at the lumbar or gluteal area, manipul ation nearly always fails, especially if the patient is less than 60 years old (Fig. 52.14). A full and painless range of flexion does not imply the absence of a disc lesion - it is possible for even a large protrusion not to cause limitation of flexion. In L3 com pressions, for instance, the nerve is relaxed during flexion and therefore this movement can be painless. Also in severe compression, in which root atrophy has devel oped, flexion is again of full range and painless. The patient has lost the pain and the lumbar movements have returned to their normal degree but the considerable
Common patterns in sciatica. Arrows within the circle indicate pain in the back/buttock. Arrows outside the circle symbolize pain in the leg.
CHAPTER 5 2 - THE D U RAL C O N C E PT 763
Figure 52.14
Unfavourable patterns in sciatica.
weakness of some muscles is evidence of the gross posterolateral disc lesion. •
Root tests
Testing the mobility of the root. Straight leg raising examines the mobility of the nerve root sleeves of L4 and S2, whereas prone-lying knee flexion tests that of the L3 root. It is important to remember that each nerve root is incompletely fixed by a l igamentous band, running from the sheath of the nerve root to the inferior pedicle of the respective foramen87, 117, 1 1 8 . During SLR, the sciatic nerve is pulled downwards and the root dragged forwards. Because of its fixation, the nerve root cannot slip away and it is caught against any space occupying lesion at the front of the cana1. 86 In contrast, compression of the nerve root from above or from behind does not result in a decrease in root mobil ity. The anterior and relatively fixed position of the root protects it from a posterior compression when SLR is performed. This observation is extremely important in the differential d iagnosis of radicular pain. Lateral recess stenosis or hypertrophy of the facets causes com pression from behind (posterior wall lesions) and does not influence the mobility of the root. Thus, SLR (or femoral stretch) specifically tests the mobility between the nerve root and the posterior aspect of the inter vertebral joint (anterior wall). However, limitation of nerve root mobility is not pathognomonic of a disc lesion: 119,120 •
Any space-occupying lesion at the anterior aspect of the nerve root canal which interferes with the anterior aspect of the nerve root will cause the same clinical feature. Such, for instance, is the case in neuromas
•
and tumours, which cause as much limitation of SLR as do d isc lesions. Lesions in the buttock can also produce significant limitation of SLR. The combination of a limitation of SLR with serious limitation of flexion of the hip immediately draws attention to such lesions (see Section 12). Lesions of the hamstrings and sacroiliac joints also cause pain at the extreme of SLR, as the result of direct tension being exerted on tender structures.
On the other hand, full and painless SLR does not exclude a disc lesion: 1 21 , 122 •
•
• •
Lesions at LI, L2 and L3 are not detected by SLR because the sciatic nerve does not directly pull on the roots of these levels. However, the L3 root can be subject to some traction at the extreme of SLR, because of the downward pull on the dura mater, exerted from the nerve roots below. Small posterolateral protrusions are sometimes not large enough to impinge on the dural sleeve during mobilization of the roots in the supine position. In contrast, trunk flexion with the patient erect can provoke pain in the leg because the joint is now compressed by the body weight and the bulge is squeezed in the direction of the root. There is not therefore any inconsistency in a patient being unable to bend fully forwards and yet having a full and painless SLR. In root atrophy, SLR is also of full range and painless. When sciatica causes gross limitation of extension of the trunk, SLR is also often of full range and painless although at laminectomy a large disc protrusion may be seen. These cases of sciatica are resistant to conser vative treatment. It has been suggested that the nerve
764 S E CTION T E N - T H E LU M BAR S P I N E
degree of the discoradicular interaction; therapeutic because signs of interference with conduction mean that an attempt at reduction is no longer indicated. Clinical examination of the conduction of the nerve roots must be thorough. Because the lesion is often incomplete, most of the patients are unaware of any loss of power or sensitivity, except when complete root atrophy is present. Because of the oblique course of the nerve roots, a disc lesion can compress one single root or two consecutive roots. It is also possible for compression to affect just the upper part of the root and cause sensory deficit, whereas pressure from below will result in motor palsy. A large protrusion can compress two consecutive roots, or the motor fibres of one root and the sensory part of the root below (see Fig. 52.16). A fourth-fifth root compression, resulting in a permanent drop foot can result from a large protrusion at the fourth level. A fifth-first sacral com pression can occur at the fifth level. Combined third-fourth palsies are extremely rare, and seem to occur only in congenital anomalies of the nerve rootS.124, 1 25 Also triple palsies are not possible in single disc lesions. Because L2 disc lesions are extremely rare, an L2 palsy (psoas) always suggests a non-discogenic lesion. Also, bilateral palsies are scarcely ever caused by disc lesions, hence neoplasm should be suspected when there is bilateral weakness. Serious lesions should also be suspected if total loss of power is present, for it is unusual for a disc lesion to cause a complete palsy. The power of all the key muscles is tested and alter ations in skin sensitivity are sought. The latter are sub jective and may at times be very difficult to assess. It is also vital to test identical areas in both limbs, at the same time or consecutively. Sometimes, in severe sciatica, the affected leg is found to be colder than the other. Attention may be drawn to this by the patients and confirmation obtained during the clinical examination or by thennography. 126-1 28 In our
root emerges here a l ittle higher up in the foramen and therefore is not affected during SLR or bending. For these reasons it must never be assumed that a disc lesion cannot be present simply because SLR is full range and painless. Tests for dural mobility must always be interpreted in the context of other clinical findings and SLR as an isolated test has no diagnostic significance. However, a painful arc during SLR is pathognomonic of a disc lesion and also indicates that the lesion is so small that the nerve root is only temporarily intercepted. A painful arc is an encouraging sign that manipulative reduction will be successful. Sometimes SLR on the painless side causes pain in the other limb and sometimes may even be limited. This phe nomenon - crossed straight leg raising - is encountered more frequently at the L4-L5 level,123 and indicates axil lary protrusion: the downwards movement of the dura mater drags the medial aspect of the root against the pro trusion (see Fig. 52.15). When neurological deficit is not present, the degree of restriction of SLR is proportional to the pressure exerted on the nerve root. The course over time of SLR is then the best objective criterion by which the development of sci atica can be fol lowed . However, this situation changes when conduction becomes impaired and then the degree of interference with thi s affords the best measure of the size of protrusion.41 Testing root conduction. Once the compression of nerve fibres is such that it causes deformation, neurological deficit becomes clinically detectable. From this stage onwards, the magnitude of the protrusion is no longer determined by the limitation of root mobility but is reflected in the degree of deficit. Sensory and motor con duction and reflex changes must be carefully tested, since the existence of neurological deficit has both diagnostic and therapeutic value: diagnostic because it indicates pressure to the nerve root(s), and is a standard for the
( a)
Figure 52.1 5
( b)
Straight leg raising: (a) unilateral limitation; (b) bilateral limitation; (C) crossed limitation.
(e)
CHAPTER 52 - THE D U RAL CO N C E PT 765
Figur� 52. 1 6 Compression of the root at the same level two halves of two roots (3) and the whole of two roots (4).
( 1), the root below (2),
experience, a cold limb only occurs in combination with neurologica I defici t. Ankle and knee jerks sometimes disappear earlier than the muscle power or skin sensitivity (Fig. 52. 1 7). Loss of ankle jerk is permanent in about half of the cases, whereas the knee jerk recovers more often. It is a curious phenomenon that both ankle jerks occasionally disappear during a unilateral sciatica. Bilateral loss of ankle jerk should therefore not be a reason for concern.
NATURAL HISTORY In discoradicular interactions, spontaneous recovery from root pain is the rule. Although low back pain can continue for years, sciatica usually has a natural history of spontaneous improvement, even if there is clinical evi dence of weakness or radiological evidence of disc extru sion. However, during recent decades the belief that a herniating disc should be treated operatively has been generally accepted: especially if the signs and symptoms have not improved after a few weeks of bed rest, and if the diagnosis is confirmed by a positive CT, surgical intervention is recommended.l21 This opinion is not supported by prospective long-term studies, however, which show equally good or better results after conser vative treatment. Two studies have found no difference between the final results of surgical and non-surgical therapy after 7 and 20 years of observa tion, 129, 130 and a third study found the same after 4 and 10 years of obser vation, 131 These views have been confirmed by the most recent study, which found that conservative treatment has as good a result as the operative approach after 1 year of follow Up.1 32 A 92% rate of return to work has been found in a group treated conservatively, even
though 60% had had muscle weakness and 26% an extruded disc fragment documented on CT scan.1 33 These figures compare favourably with recent surgical studies, where the rate of return to work has been between 75 and 85% . 134,135 As a rule, root pain takes 6-12 months to recover at the L4 and L5 levels, but at the L3 level it is usually faster. The process seems to start from the moment that the protrusion has moved laterally beyond the edge of the posterior longitudinal l igamen t. It is a striking clini cal fact that chronic backache can go on for ever but that once it has changed into localized root pain the evolu tion to spontaneous recovery has started. The prognosis of spontaneous recovery from root pain is related to the date of onset. If backache or gluteal pain continues unchanged - which indicates that the bulge is sti ll in dural contact - spontaneous relief cannot be expected. Also, in elderly patients, spontaneous recovery from root pain commonly does not occur, probably as the result of combination with lateral recess stenosis. In bilateral root pain, spontaneous recovery does not often take place and symptoms can continue unchanged for many years. The different mechanisms that result in spontaneous recovery in sciatica, enumerated by Cyriax,4 1 (his pp. 233-234) are spontaneous reduction, erosion of the pos teroinferior aspect of the vertebral body, disc shrinkage and root atrophy. The more important mechanisms are disc shrinkage and root atrophy. Spontaneous reduction of the bulge
This accounts for most of the recoveries in lumbago and acute backache but does not play an important part in the natural history of sciatica. Because the bulge lies lateral to the ligament, there is not very much centripetal force and the protrusion has no tendency to return forwards. For the same reason, manipulative treatment in sciatica is not as successful as in lumbago or backache. Erosion of the posteroinferior aspect of the vertebral body
As described by Young, this is probably not a very impor tant mechanism in recovery from sciatica. 1 36 However, there have also been recent reports of disc herniation eroding bone and thus effectively creating more space and less pressure, 137-140 It is considered likely that the defect is caused by a purely mechanical effect. 139, 140 Disc shrinkage
The protrusion slowly shrivels away in the course of some weeks or months, and this probably accounts for the slow and progressive spontaneous recovery from an uncomplicated sciatica without neurological deficit.1 41, 142 CT studies have demonstrated that a high proportion
766 SECTI O N TEN - T H E L U M BAR SPI N E
Nerve fibres
Sheath
Signs
Symptom
Sign
Symptom
Pain
Mobility
Paraesthesia
Motor deficit
Sensory deficit
Reflex disturbances
L1
None
None
None
I nner half inguinal ligament
None
L2
None ( femoral stretch)
Root
Psoas
I
None
I� L3
Femoral stretch
Psoas quadriceps
SLR
Tibialis anterior, Extensor haliucis longus
Knee jerk
)1
L4
n L5
SLR
Extensor hallucis longus, Peronei , Gluteus medius
I
Knee jerk
Ankle jerk
CHAPTER 52 - T H E D U RA L CO N C E PT 767
Nerve fibres
Sheath Symptom
Sign
Symptom
Pain
Mobility
Paraesthesia
Root
S1
Motor deficit
,11
SLR
�
(
S4
Figure 52.17
I
I
Reflex disturbances
Ankle jerk
n
n
S3
Sensory deficit
Peronei, Calf muscles, Hamstrings, Gluteal muscles
SLR
S2
I
Signs
Calf muscles, Hamstrings, Gluteal muscles
Ankle jerk
None
None
None
None
None
None
Perineum
Sphincters
Perineum
None
Radicular signs and symptoms in sciatica.
768 S E CTION TEN - T H E L U M BAR S P I N E
of intervertebral disc herniations have the potential to resolve spontaneously. The largest herniations appear to be the most likely to undergo a significant decrease in size. The presence of large herniations and / or disc extrusions should therefore not be considered as indica tions for su rgery. 1 43- 1 46 Recent MRI reports confirmed a spontaneous regression of herniations. The more degenerate the disc and the larger the initial herniation, the more the size of the herniated fragment decreased.l47-l49 There seems also to be a higher inci dence of diminution of lateral hernias, compared to central hernias150 and the further the herniated nucleus pulposus migrated, the more rapid decrease in size could be observed.l5l The precise mechanism i s not totally understood, but a plausible explanation could be that the dissolution of disc material is accelerated when the latter enlarges and becomes deprived of the nutrient influence of the end plates and the posterior longitudinal ligament. 1 52,1 5 3 Loss of water content then deflates the protrusion, which decreases the pressure on the nerve root. Additionally, cellular infiltration of the epidural space promotes phagocytosis 1 54, 155 of the offendi ng nuclear material, which is transformed into scar tissue.156 La ter on, inflammation 96 and resultant venous congestion157 decrease, which in turn further reduces pressure on the root. The spontaneous shrinkage of the protruded mate rial is probably comparable with the disc shrinkage induced by chemonucleolysis (see p. 929). 1 58, 159 Root atrophy
As ischaemic root atrophy becomes complete, the pain abates quickly and the patient experiences symptomatic improvement. It is obvious that this situation does not represent a neurophysiological recovery - initially the patient is anatomically worse. Recovery from the palsy may take 6-18 months. The clinical picture is as follows. The patient, who suffers from sciatica, suddenly experiences an increase in pain . After a certain length of time (hours to days), the pain ceases and the skin in the respective dermatome becomes numb. From this time, there may be some weak ness in the foot or the leg. Examination shows full range of SLR but a complete root dysfunction, both motor and sensory. In root atrophy, there seems to be a relationship between the degree of pain relief and the neurological deficit: the more marked the neurological weakness, the quicker the pain d isappears. Neurophysiological recovery is usually slow and not always complete - the atrophy may lead to some slight permanent weakness if two consecutive roots are paretic. A large posterolateral protrusion at the fourth level, for instance, compressing both L4 and L5, may occasionally result in a permanent
drop foot. In general, however, and when only one nerve root is involved, complete return of strength within 1 year is the rule. The spontaneous recovery of neurologi cal deficit has been studied in monoradicular weakness: in all cases, full recovery was complete in an average of 7 months; when there was multiradicular weakness, only 13% recovered fully.l6o One of the present authors re examined 42 patients with a monoradicular deficit due to a discoradicular interaction, 1-4 years after they had recovered from their sciatic pain; all were completely rehabilitated and muscular weakness could not be detected. Some cutaneous analgesia may be permanent, for instance the outer side of the foot stays numb after an SI palsy, or the dorsum of the foot after an L4 root palsy. Some permanent sensory dysfunction remains in about 35% of patients after 10 years.l30 In about half, the ankle jerk will not recover but the knee jerk usually does. The speed of recovery from neurological deficits is very variable and difficult to predict. Usually, a nerve root recovers slowly over 6-1 2 months, but it can recover with inexplicable rapi dity, sometimes within 2-4 weeks and before the pain has ceased completely. This cannot be explained by a simple regrowth of the axons - as regrowth of nerve is at a rate of about 1 .5 mm a day - and it has been suggested that there might be a peripheral reinnervation of the muscle from intact nerve endings.162,1 63 It is important to remember that myelograms1l7 and CT can remain positive for up to 15 months after the pain has disappeared. The same phenomenon has been reported after successful treatment with chymopa pain. l 64 It is therefore unwise to rely on the CT for evalu ation of the course of sciatica and again the clinical facts are more important than the radiological appearances. Because most of the patients are unaware of loss of motor function, the statement that there is 'some loss of power' must immediately be followed by explanation and reassurance. Too many operations are done because there is slight weakness and the patient has been told that there is a risk of persistent lameness. To date, there is no evidence that surgically treated patients recover more quickly or better from a neurological deficit than do those treated conservatively. Slight or moderate weakness is therefore not an indication for operation. However, if there is evidence of an incipient drop foot or the third and fourth sacral roots are threatened, surgery should be rec ommended immediately. Once there has been a spontaneous recovery from sci atica, whether by erosion, shrinkage or atrophy, there is no likelihood of recurrence of sciatica at the same level. All the mechanisms of spontaneous cure seem to encourage some stabilization at the joint and therefore recurrence is not the rule. This does not imply that there might not be
CHAPTER 52
some chronic or recurrent backache, because of a fresh lesiGn at another level or other mechanisms (ligamentous laxity, and posterior wall problems - see Ch. 53). Also, the development of sciatica at another level remains possible. However, and as a rule, patients who have recovered without surgical treatment do not need to take more care than others. They can therefore continue their normal lifestyle and perform any sports they used to do before the episode. This contrasts strongly with the attitude to be taken to those who have had a laminectomy. The ten dency to recurrence then prohibits heavy work, and even with care a constant or intermittent ache may make them aware of their back. Seventy percent of operated patients still complain of backache and 45% of sciatica 4-1 7 years after the intervention and 37% are still undergoing some form of treatment. The incidence of re-operation ranges from 1 7_20%.1 65-168 The decision to intervene surgically should therefore not be taken lightly and not until all pos sible non-operative management, including epidural local anaesthesia, has been tried. Even in an ' unrelenting' case, with tolerable root pain, the patient should be made aware of the chance of spontaneous recovery and encour aged to wait at least 8-1 2 months before opting for oper ation. With such a conservative approach, very few patients will need an operation. Our personal experience is that such an attitude is appropriate, provided pain remains reasonably controlled.
TREATMENT The possibility of spontaneous resolution must influence any evaluation of treatment. Placebo treatment can be effective, as for instance in randomized trials in which a placebo for chymopapain injection gave relief in 42-60%.169-1 72 Apart from awaiting a spontaneous cure or referring the patient for surgical treatment, there are two different strategies for solving discoradicular problems. The first is reduction of the protrusion. If it is not too large, not too laterally placed and not too long standing, a trial of reduction should always be undertaken. If reduction is not possible, attention should be given to the second component of the interaction - the nerve root. A caudal epidural injection should then be given in an attempt to reduce some of the inflammatory reactions. Should this injection fail, nerve root infiltration can be tried. As for the treatment of discodural interactions, there is not a clear-cut overall treatment for sciatica (Fig. 52.18). As the anatomical basis of sciatica differs completely from one patient to another, treatment will always be chosen in relation to the symptoms and signs: 'Sciatica has many faces, and treatment should always be selec tive' (James Cyriax).
- THE
D U RAL CO N C E PT 769
Repositioning the disc by manipulation or traction
A few patients with sciatic pain can be treated by manip ulation or traction. Only those protrusions that are not too large, or too long standing, will have a reasonable chance of quick improvement with traction or manipula tion, i.e. patients with recent root pain (less than 6 months' duration) and without neurological deficit. There are, however, a few exceptions. In elderly patients (over the age of 60), there is no time limit for manipula tion, especially in those who still have low back pain after the appearance of the sciatica. Also, in recurrent sciatica, where the history indicates the motor deficit to stem from a previous attack, the present bout can some times be alleviated quickly by manipulation. The choice between manipulation and traction is made on the data obtained from the history and clinical exami nation. If these indicate a soft nuclear displacement, trac tion should be applied. If the features point towards a hard annular protrusion, manipulation should be under taken. In elderly patients traction is of no use and in young patients suffering from primary posterolateral protrusions manipulation will always fail . If neither the patient's age nor symptoms indicate the consistency of the displacement, manipulative reduction should be undertaken first. If there is immediate improvement, such treatment can be continued. If there is no response, traction is substituted. Only 30% of patients suffering from sciatica can be treated successfully by manipulation or traction, which means that for the majority another strategy must be considered. Epidural local anaesthesia If impaired conduction (motor or sensory) or increasing noc turnal pain shows the discodural contact is intense,
attempted manipulative reduction will almost certainly
�I�:I' �/ 2 Figure 52.18
Impact of the different therapies for discodural conflict: 2, nerve root infiltration; 3, epidural local anaesthetic.
1, repositioning;
770 S E CTI O N TEN - T H E L U M BAR S P I N E
fail . The disorder should be treated by epidural anaesthe sia. Thi s also appl ies to laterally situated protrusions. Because the protrusion has moved lateral to the posterior longitudinal ligament, the ligament no longer pushes on the displaced bulge during manipulation or traction. Therefore if there is root pain only, manual reduction will almost certainly fai l. I n contrast, the more backache accompanies the sciatica, the greater the chance of relief by reduction. If root pain is long standing, an attempt at manipulative reduction will always fail. It is generally agreed that after 6 months of radicular pain, attempts at manipulative reduction are in vain. Epidural local anaesthesia is also the treatment of choice in sciatica that is recovering: the patient is sympto matically over the worst and leg pain has largely sub sided with bed rest. Root pain without physical signs, the 'bruised ' root, is also treated by epidural injection. The injection initially given for diagnostic purposes often also permanently abolishes the pain. The mechanism of caudal epidural injection is still a matter of discussion. Probably the fluid has some hydro static effects - epidu ral injections with 50% of 0.5% pro caine produces a hydrostatic pressure that removes the du ral tube and the nerve roots from the bulge. 1 73 The effect is not just temporary but continues during the next few weeks. Another explanation for the results obtained after procaine injections in sciatica is that they might influence the chemical mediators of infl ammation. Procaine seems to produce better results than lidocaine (lignocaine) perhaps because of the higher pH of pro caine (6.5), which may have an influence on the chemical radiculi tis. 88, 1 74 Nerve root infiltrations
Nerve root infiltration is an alternative way to deal with the painful inflammation caused by a d iscoradicular interaction and is used when the induction of epidural local anaesthesia has been unsuccessful. If signs and symptoms are unaltered 1 or 2 weeks after the epidural
injection the next approach to the problem is to intro duce 20 mg of triamcinolone around the affected nerve root. The main d ifficulty, however, is to decide at what level to inject, especially in the case of a fifth lumbar root pain, where the protrusion can lie at either the fourth or the fifth level. I n general, elderly patients respond better to nerve root infiltrations than to epidural local anaesthesia. Also lesions of the second or third lumbar nerve root are treated preferentially by a local nerve block, because epidurals seem only to have moderate effect.175 Discoradicular sciatica is summarized in Box 52.4.
Box 52.4 Summary of discoradicular sciatica Definition Leg pain. radiating segmentally and caused by a postero lateral sh ift of d i sc material. compressing against the nerve root
Symptoms Onset: primary posterolateral or secondary posterolateral Segmental pain Segmental paraesthesia Weakness/sensory d i sturbances
Signs Partial articular pattern I mpaired m o b i l ity of the nerve root (SLR and L3 stretch) Sensory deficit Motor deficit Reflex changes
Spontaneous development Spontaneous reduction E rosion Shrinkage (absorption) Root atrophy
Treatment Reposition (man i pu l ation/traction) Desensitization (ep i d u ral i njection/nerve root block) Awaiting spontaneous recovery Surgery
REFERENCES 1 . Cyriax J H . Lumbago: the mechanism of dural pain. Lancet 2. MacRae DL. Asymptomatic intervertebral disc protrusion. Actal
I
Bone
loillt Surg 1 976;58A:850. 4. Wi ltse LL. The effect of the common anomalies of the lumbar spine u pon disc degeneration and low back pain. Orthop Ciin North Alii 1 971;2:569-582.
6. H itselberger WE, Whi tten RM. Abnormal myelograms i n asymptomatic patients. ] Neurosurg 1 968;28:204.
Radio/ 1 956;46:9. 3. Torgerson W, Dotter WE. Comparative rontgenographic study of the asymptomatic and symptomatic lumbar spine.
5. Waddell G. A new clinical model for the treatment of low-back pain. Spine 1987;12:632-644.
1 945;ii:427.
7. Wiesel SW, Tsourmas N, FeHer 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 1 984;9:549-551 . 8. Powell MC, Wilson M , Szypryt P, Symonds EM. Prevalence of lumbar disc degeneration observed by magnetic resonance in symptomless women. Lancet 1986;Dec 13:1 366-1367.
CHAPTER 52 - T H E D U RAL CO N C E PT 771
9. Boden SD, Davis DO, Dina TS, Patronas MJ, Wiesel Sw.
28. Kayama Satoru, KOlmo S, Olmarker K, Yabuki S, Kikuchi S.
A];mormal magnetic resonance scans of the l u mbar spine in
Incision of the annulus fibrosus induces nerve root morpho
asymptomatic subjects. J Bone Joint S u rg 1990;72:403-408.
logic, vascular and functional changes. Spine 1 996;22:2539-2543.
10. Jensen M, Brandt-Zawadzki M, Obuchowski N et al. Magnetic resonance imaging of the lumbar spine in people without back pain. N Ellgl J Med 1994;331:67-73.
29. Takahashi H, Suguro T, Okazima Y et al.
I n flammatory
cytokines i n the herniated disc of the lumbar spine. Spine 1996;21 :218-224.
1 1 . Boos N, Rieder R, Schade V. The diagnostic accuracy of mag
30. Chen CC, Cavanaugh JM, Ozaktay AC et al. Effects of phospho
netic resonance imaging, work place perception, and psycho
lipase A2 on lumbar nerve root structure and function. Spine
social factors in identifying symptomatic disc herniations. Spine
1997;22:1 057-1064.
1 995;20(24):261 3-2625.
31 . Nygaard OP, Mellgren 51, Osterud B. The inflammatory proper
12. Mixter WJ, Barr J5, Ruptures of the intervertebral disc, with involvement of the spinal canal. N Eng J Med 1934;211 :210-215. 13. Cuatico W, Parker Je.
Further
investigations on spinal
meningeal nerves and their role in pain production. Acta Neurochir 1989;101 : 1 26-128. human vertebral column. Am J Anat 1990;188:289-296. M,
Bjurholm
A,
32. Kramer J. J Intervertebral Disk Diseases: Causes, Diagllosis, Treatment and Prophylaxis. Thieme, Stuttgart, 1981 :38-39. 33. Krag MH, Seroussi RE, Wilder DG. Thoracic and lumbar inter
14. Groen GJ, Baljet B, Drukker J. Nerves and nerve plexuses of the 15. Ahmed
ties of contained and noncontained lumbar disc herniation. Spine 1997;22:2484-2488.
Kreicbergs
A,
nal disc displacement distribution from in vitro loading of human
Sch u l tzberg
M.
Neuropeptide Y, tyrosine hydroxylase and vasoactive intestinal polypeptide - immunoreactive nerve fibers in the vertebral b9dies, discs, dura mater and spinal ligaments of the rat lumbar spine. Spil1e 1993;18:268-273.
spinal motion segments: experimental resu l ts and
theoretical predictions. Spine 1987;12: 1 001-1007. 34. Kelsey J, White AA. Epidemiology and im pact of low back pain. Spine 1980;6:133-142. 35. Cochrane Report. Working Group
011
Back Pain. London, H MSO,
1979.
16. Kallakari S,Cavanaugh JM, Blagoev De. An immunohisto chemical study of innervation of lumbar spinal dura and longi tudinal ligaments. Spine 1998;23:403-4 1 1 .
36. Gowers W. Lumbago. BM! 1904;1 : 1 1 7. 37. Troup JD. Biomechanics of the lumbar spinal canal. Clin Biomech 1986;1 :31-43.
1 7 . Wyke B. The neurology of l o w back pain. In: Jayson M I V (ed)
38. Edgar MA, Park WM. Induced pain patterns on passive
TIle LU II/bar Spine and Back Pain, 2nd edn. Pitman Medical,
straight-leg raising in lower lumbar d isc protrusions. J Bone
Tu nbridge Wells, 1980.
Joint S u rg 1974;56B:658-667.
18. Roberts S, Eisenstein SM, Menage J, Evans EH, Ashton IK.
39. Mooney V. Differential d iagnosis of low back d i sorders.
Mechanoreceptors in intervertebral discs. Morphology, distri
Principles of classification. In: Frymoyer J (ed) The Adult Spine,
bution, and neuropeptides. Spine 1995;20:2645-2651 .
Raven Press, New York, 1 991 : 1 559. S.
40. Kostuik J P, Harrington 1, Alexander D, Rand W, Evans D. Cauda
Mechanosensitive afferent units i n the lumbar intervertebral
equina syndrome and lumbar disc herniations. J Bone foint S u rg
1 9 . Ya mashita
T,
Minaki
Y,
Oota
1 , Yokogushi
K,
Ishii
disc and adjacent muscle. Spine 1993;18:2252-2256. 20. Pal mgren
T,
Gronblad M, Virri J, Kaapa E, Karaharju E. An
immunohistochemical study of nerve structures i n the annulus fibrosus of human normal lumbar intervertebral discs. Spine 1 999;24:2075-2079. 21 . Wiltse LL, Fonseca AS, Amster J, Dimartino P, Ravessoud FA. Relationship of the dura, Hofmann's ligaments, Batson's plexus, and a fibrovascular membrane lying on the posterior surface of the vertebral bodies and attaching to the deep layer
1 986;68A:386-391 . 4 1 . Cyriax J H . Textbook of Orthopaedic Medicine, vol. 1 , Diagnosis of Soft Tissue Lesions, 8th edn. Bail l iere Tindall, London, 1982. 42. Dixon AStJ. Diagnosis of low back pair - sorting the complain ers. In: Jayson MIV (ed) The Lumbar Spine and Back Pain, 2nd end. Pitman Medical, Tunbridge Wells, 1980. 43. N achemson A. A dvances in low back pain.
Clin Orthop
1985;200:266. 44. Spitzer WOo Scientific approach to the assessment and manage
of the posterior longitudinal ligament. An anatomical, radio
ment of activity-related spinal disorders, a monograph for clini
logic, and clinjcal study. Spine 1993;18:1 030-1043.
cians, report of the Quebec Task Force on Spinal Disorders.
22. Scapinelli R. Anatomical and radiologic studies on the lumbo sacral meningo-vertebral ligaments of humans. J Spinal Disord 1990;3:6-15. 23. Plaisant 0, Sarrazin JL, Cosnard G, Schill H, Gillot e. The lumbar anterior epidural cavity: the posterior longitudinal
Spine 1987;12(7)(suppl). 45. Valkenburg HA, Haanen HCM. The epidemiology of low back pain. In: White AA III, Gordon SL (eds) American Academy of Orthopaedic S u rgeons Symposiu l1l on Idiopathic Low Back Pain. Mosby, St Louis, 1 982:9-22.
ligament, the anterior ligaments of the dura mater and the
46. MacNab 1. Backache. Williams & Wilkins, Baltimore, 1983:135.
anterior internal vertebral venous plexus. Acta Anal (Basel)
47. H irschberg G. Treating lumbar disc lesions. Tex St J Med
1996;155:274-281 .
1974;70:58.
24. Ohshima H , Hirano N , Osada R, Matsui H , Tsuji H . Morphologic
48. Nachemson AL, Elfstrom G. Intravital dynamic pressure mea
variation of lumbar posterior longitudinal ligament and the
su rements in lumbar discs: a study of common movements,
modality of disc herniation. Spine 1996;18:2408-2411. 25. Bashline SD, Bilott JR Ellis JP. Meningovertebral ligaments and their putative significance in low back pain. J Manipul Physiol TI,er 1996;19:592-596.
maneuvers and exercises. Scand ] Rehab Med 1970:(suppl 1):1-40. 49. Nachemson AL. Lumbar intrad iscal pressure. In: Jayson M (ed) The Lumbar Spine and Back Pain, Pitman Medical, London, 1987. 50. Waddell G. 1987 Volvo Award in clinical sciences: a new clinical
26. Gronblad M, Virri J, Tolonen J et al. A controlled immunohisto
model for the treatment of low back pain. Spine 1987;12:632-644.
chemical study of inflammatory cells in disc herniation tissue.
5 1 . Deyo RA, Tsui-Wu YJ. Descriptive epidemiology of low-back
Spille 1994;24:2744-275 1 . 27. Kang JD, Georgescu HI, McIntyre-Larkin L et al. Herniated lumbar intervertebral discs spontaneously produce matrix met
pain and its related medical care in the United States. Spine 1987;12:264-268. 52. Gilbert JR, Taylor DW, Hildebrand A. Clinical trial of common
alloproteinases, nitric oxide, interleukin-6, and prostaglandin
treatments
E2. Spille 1996;21 :271-277.
1985;291:791-794.
for
low
back
pain
in
fami l y
practice.
BMf
772 S E CTION T E N - T H E LUM BAR S P I N E
53. Lidstrom A , Zachrisson M . Physical therapy o n l o w back pain and sciatica: an attempt at evaluation. Scand ] Rehabil Med
8 1 . Farfan HF. Mechanical d isorders of the low back. Lea & Febiger, Philadelphia, 1973. 82. N achemson A . The lumbar spine - an orthopaedic challenge.
1970;2:37-42. 54. Deyo RA, Diehl AK, Rosenthal M. How many days of bed rest for acute low back pain? N Engi / Med 1 986;315:
Spine 1976;1:59. 83. Fagerlund MKJ, Thelander U, Friberg S. Size of lumbar disc hernias measured using computed tomography and related to
1 064-1 070. 55. Stankovic R, Johnell O. Conservative treatment of acute low
sciatic symptoms. Acta Radiologica 1990;31:555-558.
back pain; a prospective randomised trial: McKenzie method
84. McCullogh J A . Compu ted tomography before and after
of treatment versus patient education in 'mini back school'.
chemonucleolysis. In: Post MFD (ed) Compu ted TOll1ography of the Spine. Williams & Wil k i ns, B a lti more, 1983.
Spine 1 990;1 5 : 1 20-123. 56. Ombregt L. In: Cyriax JH (ed) lIIustra ted Manual of Orthopaedic
85. Boumphrey FRS, Bell GR, Modic M, Powers DF, Hardy WR. Computed tomography scanning after chymopapain injection
Medicine. Bu tterworths, London, 1983:212. 57. Frymoyer JW, Gordon SL. Research perspectives in low-back pain: report of a 1988 workshop. Spine 1989;14:1384-1388. 58. Kuslich SD, Ulstrom CL, Michael CJ. The tissue origin of low back pain and sciatica. Orthop Clin North A m 1991;22:181-187.
for herniated nucleus pulposus: a prospective study. Clin Orthop 1987;219:120-123. 86. Bertolini J, Miller J, Spencer D. The effect of intervertebral disc space narrowing on the contact force between the nerve root
59. Donelson R, Silva G, Murphy K. Centralization phenomenon;
and a simulated disc protrusion. Presented at the arUlual
i ts usefulness in evaluating and treating referred pain. Spine
meeting of the International Society for the Study of the Lumbar Spine, Toronto, Canada, 10 June 1982.
1990;15:211-213. Spille
87. Spencer DL, Irwin GS, Miller JAA. Anatomy and significance
6 1 . Urban l PG, McMullin JF. Swelling pressure of the lumbar
88. Marshall LL, Trethewie ER, Curtain Ce. Chemical radiculitis: a
intervertebral discs: infl uence of age, spinal level, composition
clinical, physiological and immunological study. Clin Ort/lOp
60. Nachemson
AL.
Disc
pressure
measurements.
of the l umbosacral nerve roots in sciatica. Spine 1983;8:672-679.
1981;6:93-97.
and degeneration. Spine 1988;1 3 : 1 79-187.
1977;129:61-67.
62. Adams MA, Dolan P, Hutton We. Diurnal variations in the stresses on the lumbar spine. Spine 1987;2:130-137. 63. Tyrrell AR, Reilly
T, Troup JDG. Circadian variations in stature
89. Gertzbein S. Degenerative disc d isease of the lumbar spine. Clin Orthop 1977;129:68-71 . 90. Marshall L, Trethewie E, Curtain e. Chemical irritation of nerve-root in d isc-prolapse. Lancet 1973;11:320.
and the effects of spinal loading. Spine 1985;10: 1 61-164. 64. Porter RW, Trailescu IF. Diurnal changes i n straight leg raising.
9 1 . Saal JS, Franson RC, Dobrow R, Saal ]A, White A, Goldwai the N. High levels of inflammatory phospholipase A2 activity in
Spine 1 990;1 5 : 1 03-106. 65. Andersson GBJ, Svensson H-O, Oden A . The intensity of work
lumbar disc herniations. Spine 1990;15:674-678. 92. Franson RC, Saal JS, Saal JA. Human disc phospholipase A2 is
recovery in low back pain. Spine 1983;8:880-884. 66. Bergquist-Ullman M, Larsson U. Acute low back pain in indu stry. Acta Orthop Scand 1 977;170(supp1 ):1-1 1 7
inflammatory. Spine 1992;17(suppl : 1 29-132. 93. Olmarker K, Rydevik B, Norborg e. Au tologus nucleus pu lpo
.
67. Troup JDG, Martin JW, Lloyd DCEF. Back pain in industry: a
sus induces neurophysiologic and
histologic changes in
porcine cauda equina nerve roots. Spille 1993;18:1425-1432.
prospective su rvey. Spine 1981 ;6:61-69. 68. Van Korff M, Saunders K. The course of back pain in primary
94. Rydevik B, Brown MD, Ehira T, Norborg C, Lundborg G. E ffects of graded compression and nucleus pulposus on nerve
care. Spine 1 996;24:2833-2839. 69. Mayer TG, Gatchel KJ, Kishino N et ai. Objective assessment of
tissue - an experimental study in rabbits. Proceed ings of the
spine function following industrial injury: a prospective study
Swedish Orthopaedic Association, Gotenborg, Sweden, 27
w i th
comparison
group
and
one-year
follow-up.
Spine
70. Troup JDG. Causes, prediction and prevention of back pain at 71 . Van Korff M. Studying the natural history of back pain. Spine 72. Klenerman L, Slade PD, Stanley 1M et al. The prediction of chronicity in patients with an acute attack of low back pain in 73. Otani K, Arai I, Mao G-P et al. Experimental disc herniation; evaluation of the natural course. Spine 1997;22:2894-2899. 75. Fisk B. Manipulation in general practice. NZ Med / 1971;74:172. 76. Armstrong J . L u mbar Disc Lesions. Williams & W i l ki ns, Traction techniques
for
low back pain. ]
Wright V. Sciatica and the intervertebral disc. An
98. MacNab I. The mechanism of spondylogenic pain. In: Hirsch C, Zotterman Y (eds) Cervical Pain. Pergamon Press, Oxford, 99. Rydevik B, Brown MD, Lundborg G. Pathoanatomy and pathophysiology of nerve root compression. Spine 1984;9:7-1 5.
78. Nachemson A . Review of mechanics of the lumbar disc. Rheu/1/at Rehabi/ 1975;14: 1 29. 79. Andersson GBJ, b rtengren R, Nachemson A. Intradiscal pres sure, intra-abdominal pressure and myo-electric back muscle to
posture
root ganglia and chronologically injured axons: a physiological basis for the radicular pain of nerve root compression. Pain
Musculoskel Med 1 986;April.
and
loading.
Clin
1977;3:25-4 1 . 1 0 1 . Garfin SR, Rydevik BL, Brown R A . Compressive neuropathy of spinal nerve roots. A mechanical or biological problem? Spine 1991 ;16:162-166.
Orthop
102. Mumenthaler M, Schliack H . Liisionen peripherer Nuven.
Spine
103. Hofmann M. Die Befestigung der Dura mater im Wirbel kanal.
Thieme, Stuttgart, 1973.
1977;129: 1 56. 1981 ;6:93-97.
MJ,
100. Howe IF, Loeser JD, Calvin WHo Mechanosensitivity of dorsal
Balti more, 1 965.
80. Nachemson
97. Smyth
1972.
74. Barbor R. Low backache. BM/ 1955;1:55.
related
/ Bone Joint S u rg 1988;70A:361-368. experimental study. ] Bone Joint S u rg 1958;40A:1401-1418.
a general practice setting. Spine 1 995;20:478-484.
acti v i ty
96. Takata K, Inoue S, Takahashi K, Ohtsuka Y. Swelling of the cauda equina in patients who have herniation of a lumbar disc.
1994;19:2041 5-2046S.
JE.
raising test versus radiologic size, shape, and positi0n of lumbar disc hernias. Spine 1992;17:395-399.
work. Scand J Work Environ Health 1984;10:419-428.
77. Lancourt
Aug 1982. Acta Orthop Scand 1983;54:670-671 . 95. Thelander U, Fagerlund M, Friberg S, Larsson S . Straight leg
1985;10:482-493.
AL.
Disc
pressure
measurements.
A rch Anat Physio (Anat Abt) 1899:403.
CHAPTER 52
104. Goddard MD, Reid JD. Movements induced by straight leg �aising in the lumbo-sacral roots, nerves and plexus and in the intrapelvic section of the sciatic nerve. J Neurol Neu ros urg
]13,
T H E D U RAL C O N C E PT 773
1 30. Nashold BS, Hrubec Z. L U lllbar Disc Disease. A TWe/l ty-year Clinical Follow-up Study. Mosby, St Louis, 1 97 1 . 1 3 1 . Weber H. Lumbar disc herniation. A controlled, prospective study with ten years of observation. Spine 1 983;8:1 31-140.
Psychiatry 1965;28 : 1 2-18. 105. Smith SA, Massie
-
Chesnut R, Garfin SR. Straight leg
raising. Anatomical effects on the spinal nerve root without and with fusion. Spine 1 993;18:992-999.
132. Alaranta H, Hurme M, Einola et at. A prospective study of patients with sciatica. Spine 1 990;15:1 345-1 349. 133. Saal JA, Saal JS. Nonoperative treatment of herniated lumbar
1 06. Estridge MN, Rouhe SA, Johnson NG. The femoral stretching test. J Nell rosurg 1982;57:813-8 1 7.
intervertebral disc with radiculopathy. An outcome study. Spine 1989;14:431-437.
107. Nachemson A. Intradiscal measurements of pH in patients with lumbar rhizopathies. Acta Orthop Scand 1 969;40:23-42. 108. Gertzbein SD, Tile M, Gross A, Falk R. Auto-immunity in degenerative disc disease of the lumbar spine. Orthop Ciin
134. Hurme M, Alaranta H . Factors pred icting the result of surgery for lumbar intervertebral d i sc hern i a tion. Spine 1 987; 1 2 : 933-938. 135. Frymoyer J, Hanley E, Howe J, Kuhlmann 0, Matteri R. Disc excision and spine fusion in the management of lumbar disc
North Am 1975;6:67-73. 109. Kliliuk PS, Pountain GD, Keegan AL, Jayson MIY. Serial measurements of fibrinolytic activity in acute low back pain and sciatica. Spine 1987;12:925-928.
disease. Spine 1 9 78;3 : 1 . 136. Young RH. Results of surgery in sciatica and low back pa in. Lancet 1952;i:245.
1 1 0. Rydevik B, Nordborg e. Changes in nerve function and nerve
137. Briceno e, Fazl M, Willinsky RA, Gertzbein S. Sequestered
fibre structure induced by acute, graded compression. J Neurol
intervertebral d i sc associated with vertebral erosion. Spille
Neurasurg Psychiatry 1980;43:1 070-1 082.
1989;14:898-899.
1 1 1 . )3rodal A. Neu rological Anatol1lY in Relation to Clinical Medicine, 2nd edn. Oxford University Press, New York, 1969.
1 38. Nofray JF, Gadom J, Becker Re, Resnick 0, Sartoris OJ. Extruded nucleus pulposus causing osseous erosion of the
112. Rasminsky M. Ectopic generation of impulses in pathological
lumbar vertebral body. Spine 1 988;13:941-944.
nerve fibres. In: Jewett DL, McCarroll HR Jr (eds) Nerve Repair
139. Vadala G, Dore R, Garbagna P. Unusual osseous changes in
alld Regeneration - its Clin ical and Experimental Basis. Mosby, St
lumbar herniated discs: CT features. J COlllp u t Assist TOlllogr
Louis, 1980: 1 78-185.
1985;9: 1 045-1049.
113. The Guarantors of Brain. Aids to the Examination of the Peripheral Nervous Systern. Bailliere Tindall, London, 1986.
140. Vincent JM, Baldwin JE, Sims C, Dixon AK. Vertebral 'corner' defect associated with lumbar disc herniation shown by
1 1 4. Leavitt 5, Garron DC, Whisler WW, Sheinkop MB. Affective and sensory dimensions of back pain. Pain 1978;4:273-281 . 1 1 5. Plum F. Personal communication. 1 99 1 .
magnetic resonance imaging. Spine 1 993;18:1 09-1 1 3 . 1 4 1 . S a a l J A , Saal JS, Herzog RI. The natural history of lumbar intervertebral disc extrusions treated nonoperatively. Spine
1 1 6 . Hall 5 , Bartleson JD, Onofrio BM et al. Lumbar spinal stenosis. Clinical features, diagnostic procedures and resu lts of surgical treatment in 68 patients. Ann Intern Med 1985;103(2) :271-275.
1990;15:683-686. 142. Teplick JG, Haskin ME, Spontaneous regreSSion of herniated nucleus pulposus. AJNR 1 985;6:331-335.
1 1 7. Falconer MA, McGeorge M, Begg Ae. Observations on the
143. Maigne JY, Rime B, Deligne B. Computed tomographic follow
cause and mechanism of symptom production in sciatica and
up study of forty-eight cases of nonoperatively treated lumbar
low back pain. J Neural Neurosu rg Psychiatry 1 948;11 : 1 3 .
intervertebral disc herniation. Spine 1992;17:1071-1 074.
1 1 8. O'Connell J E A . Protrusions of the lumbar intervertebral discs:
144. Bush K, Cowan N, Katz 0, Gishen P. The natural history of
a clinical review based on five hundred cases treated by exci
sciatica
sion of the production. J Bone Joint S u rg 1951;33B:8.
1 205-1222.
1 19. Spangfort E . Lasegues sign in patients with lumbar disc herni ation. Acta Orthopaed Scand 1971 ;42:459-460. operative diagnostic methods in lumbar disc surgery. Acta
discectomy: an objective approach. Spine 1979;4:129-134. prospective study of 100 new cases. Spine 1 981;6:1 75-179. 123. Spangfort EY. The lumbar disc herniation: a computer-aided operations.
Acta
Orthop
Scand
1 978;142(suppl):1 -95. cal studies of radicular symptoms. Spine 1 984;9:23-30. 125. Kadish LJ, Simmons E H . Anomalies of the lumbosacral nerve roots. J Bone Joillt Surg 1 984;66B:411-416.
1 45. Delauche-Cavalier Me, Budet e, Laredo JD et al. Lumbar disc vative
treatment
of
nerve
root
compression.
Spine
1 992;17:927-933. of the course of disc herniations in patients with proven 147. Matsubara Y, Kato F, Mimatsu K. Serial changes on MRI in lumbar disc herniations treated conservatively. Neuraradiolog1j 1 995;37:378-383. 148. Modic MT, Ross JS, Obuchowski NA et al. Contrast-enhanced the natural history. Radiology 1995;195:429-435. 149. Fraser RD, Sandhu A, Gogan WJ. Magnetic resonance imaging findings 1 0 years a fter treatment for lumbar disc herniation. Spine 1995;20:710-714.
1 26. Stary O. Pathogenesis of discogenic disease. Rev Czech Med
150. Dullerud R, Nakstad PH. CT changes after conservative treatment for
1956;2: 1 . 1 27. Ash CJ, Shealy CN, Young PA e t al. Thermography a n d the
radicul opathy.
l umbar
d isk
herniation.
Acta
Radiologica
1 994;35:415-419. 151. Komori H, Shinomiya MD, Nakai 0 et al. The natural history
sensory dermatome. Skel RadioI 1 986;15:40-46. 128. So YT, Aminoff MJ, Olney RK. The role of thermography in of lumbosacral
1 992;17:
MR imaging in acute lumbar radiculopathy: a pilot study of
124. Kikuchi 5, Hasue M, Nishiyama K, Ito T. Anatomic and clini
the evaluation
Spine
radiculopathy. A rch Phys Med Rehabi/ 1 993;74:3-8.
122. Blower PW. Neurologic patterns in unilateral sciatica: a
2504
disc pathol ogy.
146. Ellenberg MR, Ross ML, Honet JC et al. Prospective emulation
Ort/lOp Scand 1 972;43:234-238. 1 2 1 . Spengler OM, Freeman CWo Patient selection for lumbar
of
w i th
herniation; computed tomography scan changes after conser
120. Hakelius A, Hindmarsh J. The comparative reliability of pre
analysis
associated
Neu rology
1 989;39:1 154-1 158. 129. Hakelius A. Prognosis in sciatica. A clinical follow-up of surgical and nonsurgical treatment. Acta Orthop Scand 1970;129(suppI).
of herniated nucleus pulposus with radicu lopathy. Spine 1 996;21:225-229. 152. Hendry NGe. The hydration of the nucleus pulposus and its relation to intervertebral disc derangement. J Bone Joint Surg 1958;40 B : 1 32-144.
774 S E CTION TEN - T H E L U M BA R S P I N E
1 53. Naylor A. The biomechanical changes i n the human inter
165. Dvorak J, Gauchat M-H, Valach L . The outcome of surgery for
vertebral disc in degeneration and nuclear prolapse. Orthop
lumbar disc herniation I . A 4-17 years' follow-up with empha
Clin North Am 1971 ;2(2):343.
sis on somatic aspects. Spine 1988;13:1418-1422.
1 54. Ito Takui, Yamada M, Ikuta F et al. Histologic evidence of absorption
of
sequestration-type
herniated
disc.
Spine
166. Rish BL. A critique of the surgical management of lumbar disc disease in private neurosurgical practice. Spine 1984;9:500-504. 167. Berney J. Sciatiques chirurgicales et chirurgie des sciatiques.
1 996;21:230-234. 155. Ikeda T, Nakamura T, Kikuchi T et al. Pathomechanism of spon taneous regression of the herniated lumbar disc: histologic and immunohistochemical study. J Spinal Disord 1996;9:136-140.
Med Hyg 1980;38:2006-2013. 168. Walker N. Langzeitverlaufe nach lumbaler Discus-hernien Operation. Orthopade 1979;8:211-214.
156. Hirabayashi S, Kumano K, Tsu iki T, Eguchi M, Ikeda S. A dor
169. Martins AN, Ramirez A, Johnston J, Scl,wetzenau PR. Double
sally free fragment of lumbar disc herniation and its interest
blind evaluation of chemonucleolysis for herniated lumbar
ing histologic findings. A case report. Spine 1990;15: 1221-1223.
discs. A prospective study with random assignment. Clin
1 57. Parke WW, Watanabe R. The intrinsic vasculature of the 1 58. Suguro T, Oegema T, Bradford D. The effects of chymopapain on
prolapsed
human
i n tervertebral
d isc.
Clin
Orthop 1983;174:236-242. 170. Javid MJ et at. Safety and efficacy of chymopapain (chymodi
lumba-sacral spine nerve roots. Spine 1985;10:508-515. Orthop
1986;213:223-231. 159. Spencer DL, Miller JAA. The mechanism of sciatic pain relief by chemonucleolysis. Orthopedics 1983;6: 1 600-1603. 160. Ya tes DAH. Indications for spinal manipulation. Ann Phys Med 1964;10:146. 161. Sunderland S. Nerve and Nerve I njuries, 2nd edn. Churchill Livingstone, Edinburgh, 1978:1058. 162. WooLf AL, Till K. Pathology of the lower motor neurone in the light of new muscle biopsy techniques. Proc R Soc Med 1 955;48 : 1 89. 163. Ya tes DAH. Unilateral lumbosacral root compression. A n n Plrysiol Med 1 964;7(5):169-179. 1 64. Macnab I et al. Chemonucleolysis. Can J S u rg 1971;14:280.
actin) in herniated nucleus pulposus with sciatica - results of a randomized, double blind study. JAMA 1983;249:2489-2494. 1 7 1 . Feldman et al. Etude end double aveugle du traitement de la lombosciatique discale par chimionucleolyse. Rev Rhul11 Mal Os teoartic 1986;53 : 1 47-152. 172. Fraser RD. Chymopapain for the treatment of intervertebral disc herniation - the final report of a double blind study. Spine 1984;9:815-818. 173. Troisier O.
Sem ilogie et Traitemellt des Aigies Discales et
L igamen taires du Rachis. Masson, Paris, 1973:390. 174. Troisier O. Communication on the symposium on low back pain. Antwerp, 1982. BSSOM, De Haan, Belgium. 175. Ombregt L. Epidural local anaesthesia - results after two years of use in a general practice. SympOSium on low back pain. Antwerp, 1982. BSSOM, De Haan, Belgium.
CHAPTER CONTENTS
Introduction
The ligamentous concept
775
Mechanism of ligamentous pain Postural syndrome 776 Dysfunction syndrome 776
775
Postural syndrome 776 Posterior dysfunction syndrome 779 Facet joints 779 Iliolumbar ligaments 781 Supraspinous and interspinous ligaments
782
INTRODUCTION
Lesions of the posterior arch (posterior ligaments and facet joints) have long been considered an important source of low back pain. However, the classic work of Mixter and Barr in 1934, which focused attention on the disc;· overshadowed the importance of posterior liga mentous lesions. Disc lesions must be considered to be the main source of backache and sciatica but ligamen tous problems remain a possible basis for lumbar symp toms. In lesions of the lumbar spine, discs take the strain first but it is obvious that any change in height and mechanical properties of the disc will also influence the posterior ligamentous structures. There is anatom ical evidence for free nerve endings in the posterior liga ments and the capsule of the facet joint.l-3 In addition, a number of investigations have shown that low back pain can be produced by direct stimulation of facet joints and ligaments.4-6 Although ligamentous pain is diffucult to prove by technical investigations, it is possible to identify it on clinical grouds. 7-10 The ultimate proof of a posterior arch lesion is the improvement of pain and dysfunction after diagnostic infiltration with local anaesthesia. The structures discussed in this chapter are the supra and interspinous ligaments, the facet joints, and the intertransverse and the iliolumbar ligaments. The behaviour of the sacroiliac, sacrospinal and sacrotuber ous ligaments shows some similarity with that of the lumbar ligaments; however their disorders and treat ment are detailed in Chapter 63.
MECHANISM OF LIGAMENTOUS PAIN
Most of the stabilizing support for the lumbar spine in standing, sitting and flexion-extension is determined by the tension of the ligaments rather than the strength of the paravertebral muscles (Wyke:11 Ch. 11; Stokes and Frymoyer12). Postural strain therefore will affect the noci ceptors in the capsules of the facet joints and the ligaments of the posterior arch, which happens when prolonged or 775
776 SECTION TEN - THE LUMBAR SPINE
increased postural pressure falls on normal tissues, or when abnormal (traumatized, inflamed or deformed) lig aments are subjected to normal postural stress. The first prolonged or increased static loading of normal and healthy ligamentous tissues - is the 'postural' syndrome. The second - symptoms arising from abnormal (degener ated or inflamed) tissues subjected to normal mechanical stress - is the 'dysfunction' syndrome.
Box
53.2
Characteristics of dysfunction syndrome
• Intermittent pain, immediately produced during a particular position and abolished when the stress is released • Some lumbar movements are painful at the end of range
POSTURA L SYNDROME POSTURAL SYNDROME
Pathological changes in the structures responsible for the pain are not present. Only the maintenance of a stress on a normal tissue creates this type of pain - an example of what has been termed 'the bent finger' syndrome; if a finger is bent backwards, sooner or later pain will appear.9 If sufficient force is applied for long enough, mechanical deformation of the sensitive structures in the involved tissues induces pain. It is such lumbar aching that everyone experiences when a particular posture is maintained for a long period. Pain increases in intensity the longer the time spent in the position but the moment another position is adopted the pain will gradually dis appear (see Box 53.1).
DYSFUNCTION SYNDROME
It is not unlikely that, although in the postural syn drome the structures are normal and pain is initially produced by subjecting them to increased mechanical stresses, sooner or later damage to the tissues involved will follow. The ligaments can become elongated or inflamed, which results in pain of chemical origin and also in structural changes. In this new situation, pain will be provoked by stress on structures which have become pathological. It is this progression which.pro duces the dysfunction syndrome, defined as lumbar spine as the resul t of a normal mechanical stress on pathological ligaments (see Box 53.2).
Postural pain appears when normal ligaments are sub jected to abnormal mechanical stresses. This happens with inappropriate spinal loading - poor sitting or prolonged bent posi tions. Alternatively, abnormal mechanical stresses can originate when, as a result of decreasing intervertebral height, too great a load is applied posteriorly to the spine, a situation which can occur during a particular period in the ageing spine. The loss of turgor in the disc and the decrease in interverte bral space will first allow the posterior ligaments to become lax, causing some postural strain. Further diminution in disc height results in structural changes. At the posterior facets the joint surfaces override and simulate hyperextension (Fig. 53.1). In this position, considerably more weight falls on the facet joints and the posterior capsule becomes overstretched. Two types of fibre orientation have been described in the capsular fibres of the facet joint.14 Type I capsules have the fibres running diagonally from lateral-caudal to medial cranial; in type II, the direction is horizontal between the points of insertion on the lower and upper articular processes. Especially in type II, axial loading of the spine results in considerable stretching of the fibres as the upper articular process slides downwards over the lower. Pain may then result. A similar mechanism probably also accounts for liga mentous pain following disc excision and could also explain back pain after chemonucleolysis, which causes a sudden decrease in disc height.15
Postural pain in the ageing spine Box
53.1
Characteristics of postural syndrome 1-3
• Intermittent pain, induced by the maintenance of positions for a prolonged time and abolished by posture correction or movement • Time factor is important in differentiation from dysfunction pain: some time must pass before pain becomes apparent: the longer the posture is held, the more the pain • Spinal movements are thus full range and painless: the stress applied during lumbar tests is not maintained long enough to induce pain
Postural pain typically occurs in young patients (30 years of age or less). During this period, and because of the onset of the decrease in disc height, some instability and laxity of the posterior segment may occur. Then an unfavourable position imposes a high and continuous axial load on the spine, so stretching the ligaments and the capsules of the facet joints. In addition, continuing dehydration of the disc causes further narrowing of the intervertebral space, which in turn adds more tension in ' the ligaments. Continuing degeneration produces a stiff spine because of periarticular fibrosis and enlargement of the
CHAPTER 53
Figure 53.1
-
THE LIGAMENTOUS CONCEPT 777
Decrease in intervertebral space may result in stretching of the facet joint capsule. Normal (left), decreased intervertebral space (right).
facets. As a result, postural pain normally disappears as these changes advance after middle age (see Fig. 53.3).
History The localization of the pathological changes in the poste rior part of the lumbar spine means that dural symptoms are absent. The patient is usually young and female and has diffuse backache, with bilateral radiation over the iliac crests and the sacroiliac joints (Fig. 53.2); it is never
referred beyond the upper buttocks. When the postural pain originates from the sacroiliac ligaments, however, pain reference in the 51 and 52 dermatomes can be encountered (see eh. 63). The ache usually starts after being in one position for a considerable length of time - sitting or standing - and the intensity of the pain and the duration of the position are related. Barbor8 described the postural ligamentous pain as the 'theatre, cocktail party' syndrome, because these are characteristic examples of prolonged sitting or standing which produce low back pain. Lying down, for instance prone, often leads to increased pain, and walking can be painful, especially if the patient is merely slowly strolling. In contrast and surprisingly, to someone who is not familiar with the syndrome, the patient states that during activity and sports he or she is absolutely pain free. Postural pain (Fig. 53.3) is, as its name implies, a result of positions not movements.
Clinical examination The clinical examination is found to be quite normal: there is a full range of movement without the slightest pain. Dural and nerve root signs are absent.
Differential diagnosis
Figure 53.2
Pain localization in lumbar postural syndrome.
A patient seeking help for a lumbar problem who pres ents with a clear and detailed history but has no signs at all on clinical examination must be considered to have a genuine lesion and not a psychogenic disorder. The dif ferential diagnosis is then between a postural lumbar syndrome, a bruised dura mater, a self-reducing disc pro trusion or visceral pain referred to the back. In all these
778 SECTION TEN - THE LUMBAR SPINE
.j_.
Anterior wall'"
..J.
r\-� j....j
Concentric tears Radial tears Traction spurs Cysts Posterior displacements: Bulging Protrusion Prolapse
Hypermobility Compession and distraction Joint subluxation
Fissures and cavities Marked height decrease Circular and anterior displacements Gross osteophytosis Disc resorption
Spondylosis
Figure 53.3
Spondylarthrosis
The ligamentous concept in the ageing of the spine.
instances the clinical examination is not of help and dif ferentiation relies entirely on the history. In a bruised dura or referred visceral pain, the pain is independent of position. A bruised dura mater can be confirmed by epidural injection. If visceral disease is suspected, appro priate investigations should be made. A self-reducing disc is not always easy to differentiate from postural pain but, because the treatment is the same (sclerosing injec tions), the question is theoretical.
Treatment Classically, self-treatment and especially prophylaxis are recommended. The patient should be informed about the pain mechanism and taught how to avoid con stant static postures. If prolonged sitting is unavoidable, attention should be directed to a proper posture and good choice of furniture. Standing should involve regular movement of the body weight from one leg to the other. All such information and training can be given during a 'back school' programme (see p. 926). Contrary to general belief, it is unnecessary to give patients with postural back pain a programme of
strengthening exercises. Strong muscles will not prevent pain provoked by static mechanical stresses. Though these prophylactic measures should always be taken, it is our personal experience that the results are poor and that only a few patients improve. Most patients with postural backache maintain their complaints for years. Some learn to cope with the disability, until the pain gradually disappears as the result of progressive fibrosis and sclerosis of the posterior elements. Others become chronically disabled and frustrated. For these, one excellent treatment remains - induction of artificial sclerosis in the ligamentous structures. Chemical sclerosis was used to treat inguinal hernias between the wars and the resulting dense fibrosis of the tissues noted by Hackett. He adapted the method for the ligamentous periosteal junctions of the posterior lumbar arch as a treatment for chronic low back pain.4 Others fol lowed.16,17 The initial solution used was zinc sulphate and carbolic acid but a bewildering variety of other mate rials followed, indicating various soap derivatives and psyllium seed oil. Not surprisingly, considerable side effects were experienced: three instances of paralysis18,19 and two deaths after injection into the subarachnoidal space.20 Dextrose-phenol-glycerol solution, originally developed for treatment of varicose veins, had a good safety record21 and was introduced into spinal use by Ongley in the late 19S0S.1O The mixture provokes an effec tive inflammatory response, which leads to fibroblast proliferation and new collagen production (0. Troisier, cited by Cyriax:22 p. 339). At the periosteal junctions of the ligaments the fibrosis results in an increase in girth of the ligaments, with contraction and subsequent pain relief. As some of the phenol is injected at or around the medial and lateral branches of the posterior ramus, a direct effect on nerves may also occur23 and could explain the quick relief (sometimes from the day or days after the injections) in some patients. During 3 consecutive weeks, 3 ml of the solution mixed with 1 ml of lidocaine (lignocaine) 2% is infiltrated into the different lumbar ligaments at the ligamento periosteal junction, in the following sequence. In the first week the injection is made at the interspinous and supraspinous ligaments of L4-LS and LS-S1 and at the iliac insertions of the iliolumbar ligaments. In the second, the posterior aspects of the apophyseal joints of L4 and LS are infiltrated at both sides. In the third, injection is into the lateral aspects of the laminae of L4 and LS, where the ligamentum flavum blends with the medial aspects of the deeper layer of the lumbar fascia. In chronic poshlral backache, the results of these injections are fair. In our experience, about 70% of the patients become pain free after 6-8 weeks - the time required to induce sufficient sclerosis. The experience of others with facet denervation24-28 is similar, and Ongley,
CHAPTER 53 - THE LIGAMENTOUS CONCEPT 779
Box
�3.3
Summary of postural syndrome
•
Symptoms Vague lumbar pain produced by the maintenance of position Relationship between duration of posture and degree of pain Pain is abolished by change of position Pain is not referred below the upper buttocks Dural symptoms are absent
• • •
Signs None: full range of movement, no pain
Treatment Self-treatment and prophylaxis: back school Sclerosing injections
in a randomized study, has shown the effectiveness of the treatment in a group of patients suffering from low back pain for an average period of 10 years.1 ° Postural syndrome is summarized in Box 53.3.
•
Gross overriding of the articulating surfaces of the facet joints, occurring as the result of disc resorption in elderly people. Gross osteoarthritis of the facets, as seen in more than 50% of people above the age of 45.36-39 The angulation that occurs after a wedge fracture of the vertebral body. Posterior spondylolisthesis, when the inferior articular process shifts backwards on the superior articular process of the vertebra below. Adult spondylolisthesis, even with a totally disorganized joint.
In contrast, those who support the idea of facet syn dromes cite the considerable degree of pain relief after diagnostic injections of the joints with local anaes thetic,40-44 although others have had poor success rates.45 Evidence from studies of the spread of local anaesthetic and facet arthrography suggests that the use of more than 2 ml of anaesthetic may result in an unintentional epidural block, so explaining its early success.46
Potential causes of the 'facet joint syndrome' POSTERIOR DYSFUNCTION SYNDROME
As already outlined, posterior dysfunction syndrome is the appearance of pain when posterior structures affected by pathological change are subjected to mechanical stresses. The posterior structures involved are the facet joints, the supraspinous and interspinous ligaments and the iliolumbar ligaments. Disordered muscles are a great rarity, easily distinguished because they are contractile. Ligamentous lesions of the sacroiliac joint will be dis cussed in Chapter 63. FACET JOINTS
Arthropathy of the facet joints has for a considerable time been regarded as an important source of low back pain. In 1911, Goldthwait maintained that disease of the facet joint was the chief source of backache.29 By 1933, the term 'facet joint syndrome' had been introduced3o and in the 1960s and 1970s experiments showed that low back pain could be reproduced by injecting hypertonic saline into the facet jointS.31,32 However, the subject remains very controversial and there is much evidence against the idea. First, there is no sensory innervation in the synovial tissue of the articular capsule.33,34 Second, the frequency of grossly disordered joints in random radiographs of asymptomatic patients suggests that it is unlikely that minor disorders would cause pain.35 To this end, Cyriax22 listed lesions of the facet joints known to cause no problems:
The capsule of the facet joint is innervated by the dorsal ramus of the nerve corresponding to the adjacent verte bral body, which may also send branches to the joints above and below.2 However, free nerve endings have been found only in the capsule and not in the articular cartilage or the synovial tissue (WykeY p. 270; Gronblad et a[34). Inflammation could produce pain, as happens during a traumatic arthritis, and it has also been suggested that pain is caused by impingement of a synovial fold between the opposing facets.47,48 As neither the synovial membrane nor the fatty tissue is innervated, the latter seems unlikely. It is not known if advanced osteoarthro sis as such could be the source of a facet syndrome but it is probable that reduced spinal mobility can sometimes predispose to a sprain of the fibrous capsule.49 A sprain may also follow excessive strain directly on the posterior arch, which sometimes happens as the result of an unin tentional twist, usually in extension. Extension of the lumbar spine may be limited by impaction of the inferior articular process on the lamina below. If that happens on one side only, continued application of the extension movement will force the segment towards rotation around the impacted articular process which draws the inferior articular process of the contralateral facet joint further backwards. This may result in sprain of the capsule.50 A similar lesion may result from excessive rota tion: rotation is usually limited by the impaction of the facet joint opposite the direction of the movement (nor mally the axis of rotation is situated in the posterior third of the disc). If the torque continues, a new axis of rotation will be located in the impacted joint and the contralateral
780 SECTION TEN
-
THE LUMBAR SPINE
Figure 53.4 When extension is arrested at one facet only, the contralateral inferior articular process is further forced backwards into radiation, resulting in capsular sprain.
Figure 53.5
joint will be drawn backwards (Fig. 53.4).51 Although most posttraumatic inflammation subsides sponta neously in the course of a couple of days or weeks, it is conceivable that occasionally a chronic ligamentous sprain and lasting pain might result.
History The patient presents having hurt his back during a par ticular movement, frequently hyperextension but alterna tively hyperextension accompanied by side flexion. The pain is strictly unilateral and localized, sometimes with slight reference to the upper buttock or trochanteric area (Fig. 53.5).52 Because a facet joint is a lateral structure, it cannot give rise to a central pain. However, if there is a bilateral lesion, pain can be bilateral. There is absolutely no change in pain localization, whereas in disc lesions the movement of pain is an important diagnostic element: it can be at one side and move to the other, or it can pass from the paravertebral to the gluteal area, or root pain can follow backache. In facet joint lesions, however, the pain is always felt at the same spot. Dural symptoms, such as a painful cough or sneeze, are absent.53 Pain usually appears during extension, but standing and lying prone can also be painful.49,54 Sitting usually does not cause problems, because the spine is kept in mid-position, so putting little strain on the facet joints.
Clinical examination The patient stands straight. Usually there is a full range of movement, though extension may be slightly limited. Movements that cause pain at the end of range follow a typical, convergent pattern (Fig. 53.6): for instance, when
Reference of pain in facet joint lesions.
a left facet joint is at fault, left-sided flexion and extension are painfuI,55,56 Exceptionally, a divergent pattern can also indicate a facet joint lesion: for a left-side lesion, flexion and side flexion to the right then provoke the pain. Sometimes the pain can be provoked only by a com bination of extension with side flexion.42 A painful arc is always absent, as are dural signs (straight leg raising and neck flexion), typical for disco dural interaction and there are no root signs.57 Although some believe that pain on palpation over the facet joint is one of the diagnostic features of the lesion,58,59 palpation of the paravertebral region is non-specific because the tenderness so elicited often results from referral, typical of dural pain. Because facet joint lesions are rare, the diagnosis is never made without the confirmation of local anaesthetic injection. The technique is set out below but it is impor tant to remember that the results of the block are not always reliable. First, only small amounts of anaesthetic (no more than 1 ml at the dorsal aspect of the capsule) must be used to avoid unintentional epidural injection, which nullifies the test.45,46 Second, it has been shown that the infiltration is associated with a high false-posi tive rate of more than 50%.60
Treatment Once the diagnosis is made, treatment is infiltration of the posterior aspect of the joint capsule with 10 mg of triamcinolone. In long-standing cases, we prefer t� use phenol solution, since the triamcinolone often affords only temporary relief. Others have reported good results
CHAPTER 53 - THE LIGAMENTOUS CONCEPT 781
ILIOLUMBAR LIGAMENTS
Figure 53.6
Convergent and divergent patterns
after intra-articular injections of a mixture of lidocaine (lignocaine) and a corticosteroid suspension.39,61 and pain relief is equally good with intra-articular and periarticu lar injections, indicating that the pain may be of capsular origin, rather than synovial inflammation.62 Good out comes have also been described after injection with phenol aimed at denervating the joint23 and after radiofrequency 'denervation'.25,6 3 A summary of facet joint lesions is given in Box 53.4. Box
53.4
Summary of facet joint lesions
Presentation Localized and unilateral lumbar pain
Clinical examination Full range of movement with convergent or divergent pain Dural and radicular signs are absent
Treatment Infiltration of the posterior capsule with a corticosteroid suspension or phenol
The iliolumbar ligament arises from the tip and lower parts of the transverse process of the fifth lumbar verte bra. It splits into an anterior and a posterior band to insert at the anterior and posterior aspect of the top of the iliac crest64,65 (see p. 712). It plays an important role in the stabilization of the lumbosacral junction. Both anterior and posterior bands restrain flexion of L5 on the sacrum.66 Side flexion is controlled by the contra lateral band and extension by the anterior bands. The iliolumbar ligaments are also thought to be important in maintaining torsional stability of the lumbosacral junction.6 7 Because of the specific orientation of the facets of the lumbosacral junction, some rotation is per mitted between L5 and 51, in contrast to the lack of rota tion at the more superior lumbar joints and it seems reasonable to speculate that the iliolumbar ligaments fulfil the same function as the articular stabilization of the higher level.68,69 The stabilizing and anchoring func tion of the ligaments also modifies the outcome of acute disc displacements. At the L5-S1 level the strong liga ment prevents gross lateral deviations, as is usually seen in L3-L4 or L4-L5 protrusions. However, it is possible for the ligaments to become stretched during long standing disc displacements. The patient may then suffer from persistent and chronic pain after the primary lesion has been adequately treated by manipu lation, traction or surgery. Alternatively, iliolumbar strain can originate from sudden or repeated overstretching, as in forced rotation during flexion. Our personal experience includes instances in association football players, apparently as the result of repeated lumbosacral torsions; the differen tial diagnosis of groin pain in such circumstances includes strain of the iliolumbar ligaments.
History The patient suffers unilateral or bilateral localized pain at the lower lumbar area. The pain may spread along the iliac crest to the groin (Fig. 53.7).70,71 The symptoms may develop following injury, or persist after prior lumbago in which dural pain and gross disability have resolved but intermittent pain, appearing during particular movements or after main taining a particular posture for a certain length of time, remains. As in facet joint lesions, the pain always remains to one or both sides and is never central. There is no history of changing or moving pain, and dural symptoms are completely absent.
Clinical examination No deviation is visible in the standing position. There is a full range of movement. Side flexion away from the
782 SECTION TEN - THE LUMBAR SPINE
lesions but will also be positive if a hip lesion is present. Care should therefore be taken to perform this test only in those cases in which an iliolumbar lesion is already suspected and other sources of sacroiliac or groin pain are excluded.
Treatment Treatment consists of three weekly infiltrations with scle rosing solution at the insertion of the ligament at the upper aspect of the posterior superior iliac spine (see p. 920). Improvement usually starts some weeks after the infiltration and, if relief is gained, it is lasting. SUPRASPINOUS AND INTERSPINOUS LIGAMENTS
Figure 53.7
Pain reference in iliolumbar sprain.
painful side can cause pain at the upper sacroiliac region or in the groin (Fig. 53.8). Sometimes there is also pain at the end of flexion or extension. There are no dural or nerve root signs. Routine clinical examination is sometimes entirely negative and assessment of the sacroiliac joint and hip fails to reveal any abnormality. An additional provocative test can then be performed: the patient is positioned supine, and the hip is flexed to less than a right angle and adducted until the examiner reaches the ligamentous end-feel. Internal rotation together with simultaneous axial pressure on the femur will then exert a pull on the iliolumbar ligament. This test is not specific for iliolumbar
Figure 53.8
Patterns in iliolumbar lesions.
In vivo measurements taken from lateral radiographs of lumbar spines showed that the interspinous distance extends up to almost four times during full flexion,72 which could imply that the interspinous ligament is lax in the upright position and becomes taut only in the extremes of flexion. However, the orientation of the fibres in this ligament, which is obliquely from posterosuperior to anteroinferior, allows it to be active over a large range of motions during flexion.73,74 Over-stretching of the liga ments is therefore very rare, and it is doubtful whether this could be a cause of backache. Autopsy studies of a large number of subjects have shown that of subjects over 20 years, over 20% have rup tures of one or more of their supraspinous ligaments, occurring mostly at L4-L5 and L5-S1 segments,?5 These figures strongly suggest that ruptures of the supraspinous ligaments, defined by Newman as 'sprung , back /6 rarely are, of themselves, the cause of low back pain. It should be realized that, in disc degeneration, an intact supraspinous ligament probably plays an impor tant role in the prevention of posterior displacements. In such circumstances, the posterior fibres of the annulus fibrosus and the posterior longitudinal ligament no longer limit forward flexion because the instantaneous axis of rotation is not at the nucleus but more posteriorly, behind the posterior longitudinal ligamenf7 (Fig. 53.9). Flexion of the spine is then controlled by the supraspinous ligament (see p. 737). Although a 'sprung back' is certainly not the primary cause of pain, it can add to segmental instability and recurrent disc displacements. For this reason, sclerosis of the interspinous and supraspinous ligaments is part of the treatment of recur rent disc displacements (see p. 921). During full extension, the interspinous distances decrease to between 2 and 4 mm and the processes may meet as the bifid ligament buckles laterally on 90th sides,?8 The ligament is not trapped between the processes and, if pain originates in 'kissing spines', it is due to periostitis rather than to a damaged ligament.79
CHAPTER 53
(a)
'''''''��'r� ,
. �.
-
THE LIGAMENTOUS CONCEPT
783
(a)
.
�
(b)
Figure 53.9 Axes of rotation: (a) normal segment - posterior fibres of annulus and posterior longitudinal ligament limit forward fiexion; (b) degenerated disc fiexion of the spine is controlled by the supraspinous ligament. A, instantaneous axis of rotation.
History There is a localized and central pain (Fig. 53.l0a), which started after an unintentional hyperextension strain, for instance backwards bending during gymnas tics or diving. The pain does not spread over a large area. The patient states that standing upright and back wards bending cause discomfort. There are no dural symptoms.
Figure 53.10
Lesions of the supra- and interspinous ligaments: central pain (a), pain on backwards bending (b).
at the tips of two consecutive spinal processes, can be palpated. There are no dural or root signs.
Clinical examination
Treatment
Extension causes local pain (Fig. 53.l0b). Sometimes the end of flexion is also painful. Side flexions are usually free. The lesion is very localized and the patient often indicates the site with one finger. A tender spot, usually
Treatment consists of local infiltration of triamcinolone, which affords good results. No recurrences need be anticipated if the lesion has resulted from a single hyperextension episode.
REFERENCES CFJ, Gardner E. Anatomy of lumbosacral posterior rami and meningeal branches of spinal nerves. J Bone
1. Pedersen HE, Blunck
Joint Surg 1956;38A:377. 2. Bogduk N. The innervation of the lumbar spine. Spine 1983;8:286-293. 3. Stillwell D1. Nerve supply of vertebral colum. Anat Rec 1956;125:139.
4. Hackett GS. Joint Ligament Relaxatiol1 Treated by Fibro-osseous Proliferation, Thomas, Springfield, 1956. 5. Hirsch C. Studies on the mechanism of low-back pain Acta Orthop Scand 1951;20:261-274. 6. Kuslich SD, Ulstrom C1. The tissue origin of low back pain and sciatica. Orthop Clin North Am 1991;22:181-187. 7. Troisier O. Semiologie et Traitement des Aigies Discales et Ligamel1taires du Rachis. Masson, Paris, 1973.
784 SECTION TEN - THE LUMBAR SPINE
8. Barbor R. Treatment for chronic low back pain. Proc IVth Int Congr Phys Med. Paris, 1964. 9. MacKenzie RA. The LUlIlbar Spine. Spinal Publications, Waikane, New Zealand, 1981. 10. Ongley MJ, Klein RG, Thomas AD et al. A new approach to the treatment of duonic low back pain. Lancet 1987;JuI18:143-146. 11. Wyke B. The neurology of low back pain. In: Jayson MIV (ed) The Lurnbar Spille alld Back Paill, 2nd edn, Pitman Medical, Tunbridge Wells, 1980. 12. Stokes I, Frymoyer Jw. Segmental motion and instability. Spine 1987;12:688-691. 13. Van Wijmen PM. Lumbar pain syndrome. In: Grieve GP (ed) Modern Manual Therapy. Churchill Livingstone, Edinburgh, 1986:Chapter 41. 14. Hedtmann A, Steffen R, Methfessel J et al. Measurements of human lumbar spine ligaments during loaded and unloaded motion. Spine 1989;14:175-185. 15. McCulloch JA, McNab L Sciatica and Chymopapain. Williams & Wilkins, London, 1983:Chapter 11. 16. Peterson TH. Injection treatment for back pain. Am j Orthop 1963;26:320-325. 17. Myers A. Prolotherapy treatment of low back pain and sciatica. Bull Hasp joillt Dis 1961;2:48-55. 18. Hunt WE, Baird Wc. Complications following injections of sclerosing agent to precipitate £ibro-osseous proliferation. f Neurosurg 1961;18:461-465. 19. Keplinger JE, Bucy Pc. Paraplegia from treatment with scleros ing agents - a report of a case. JAMA 1960;73:1333-1336. 20. Schneider RC Williams JI, Liss L. Fatality after injection of scle rosiJ1g agent to precipitate £ibro-osseous proliferation. lAMA 1959;170:1768-1772. 21. Dodd H. Treatment of varicose veins with phenol solution. BMJ 1948;ii:838. 22. Cyriax JH. Textbook of Orthrapaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982:389. 23. Silvers HR. Lumbar percutaneous facet rhizotomy. Spine 1990;15:36-40. 24. Shealy CN. Facet denervation in the management of back and sciatic pain. Ciin Ortliop 1976;115:157-164. 25. Burton Cv. Percutaneous radiofrequency facet denervation. Appl Nellrap" ysiol 1976/77;39:80-86. 26. Florez J, Ucar S. Percutaneous rhizotomy of the articular nerve of Luschka for low back pain and sciatic pain. Acta Neurachir 1977;24:67-71. 27. Lora J, Long D. So-called facet denervation in the management of intractable back pain. Spine 1976;1:121-126. 28. McCulloch JA, Organ LW. Percutaneous radiofrequency lumbar rhizolysis. Can Med Ass j 1977;116:30. 29. Goldthwait JE. The lumbosacral articulation: an explanation of many cases of lumbago, sciatica and paraplegia. Boston Med Surg j 1911;164:365. 30. Ghormley RK. Low back pain with special reference to the articular facets with presentation of an operative procedure. JAMA 1933;101:17733-17777. 31. Hirsch C Inglemark B, Miller M. The anatomical basis for low back pain. Acta Ortliop Scand 1963;33:1. 32. Mooney V, Robertson J. The facet syndrome. Ciin Orthop 1976;115:149-156. 33. Wyke B. Articular neurology - a review. Physiotherapy 1972;58:94-99. 34. Gronblad M, Korkala 0, Konttinen Yet al. Silver impregnation and immunohistochemical study of nerves in lumbar facet joint plical tissue. Spine 1991;16:34-38. 35. Jackson RP. The facet joint syndrome: myth or reality? Ciin Orthop 1992;279:110-121.
36. Lewin T. Osteoarthrosis in lumbar synovial joints. Acta Orthop Scand 1966;73(suppl). 37. Park WM. The place of radiology in the investigation of low back pain. Ciin Rheum Dis 1980;6:93-132. 38. Wiesel SW, Bernini P, Rothman RH. Diagnostic studies in eval uating disease and aging in the lumbar spine. In: The Aging Lumbar Spine. Saunders, Philadelphia, 1982:Chapter 2. 39. Sanders HWA. Klinische betekenis van degeneratieve afwijkin gen van de lumbale wervelkolom en consequenties van het aan tonen ervan. Ned Tijdschr Geneeskd 1983;127:1374-1385. 40. Carrera GF. Lumbar facet jOint injection in low-back pain and sciatica. Neuraradiology 1980;137:665-667. 41. Destouet JM. Lumbar facet joint injection: indication, technique, clinical correlation and preliminary results. Radiology 1982;145:321-325. 42. Helbig T, Lee CK. The lumbar facet syndrome. Spille 1988;13:61-64. 43. Jackson RP, Jacobs RR, Montesano PX. Facet joint injection in low-back pain. A prospective statistical study. Spine 1988;13:966-971. 44. Schwarzer AC, Aprill CN, Derby R et al. Clinical features of patients with pain stemming from the zygapophyseal joints. Is the lumbar facet syndrome a clinical entity? Spine 1994;19:1132-1137. 45. MoraJ1e R, O'Connell D, Walsh MG. The diagnostic value of facet joint injections. Spine 1988;13:1407-1410. 46. Dory M. Arthrography of the lumbar facet joints. Radiology 1981;140:23-27. 47. Giles LGF. Lumbo-sacral and cervical zygapophyseal joint inclusions. Manual Med 1986;2:89. 48. Konttinen Y, Gronblad M, Korkala 0, Tolvanen E, Polak J. Immunohistochemical demonstration of subclasses of inflammatory cells and active, collagen-producing fibroblasts in the synovial plicae of lumbar facet joints. Spine 1990;15: 387-390. 49. Eisenstein SM, Parry CR. The lumbar facet arthrosis syndrome: clinical presentation and articular surface changes. j Bone Joint Surg 1987;69B:3-7. 50. Yang JH, King AJ. Mechanism of facet load transmission as a hypothesis for low back pain. Spine 1984;9:557-565. 51. Twomey LT, Taylor J, Furniss MM. Unsuspected damage to lwnbar facet joints after motor-vehicle accidents. Med j Allst 1989;151:210-217. 52. McCall IW, Park WM, O'Brien JP. Induced pain referral from posterior lumbar elements in normal subjects. Spine 1979;4:441-446. 53. Revel M, Poiraudeau S, Auleley GR et al. Capacity of the clini cal picture to characterize low back pain relieved by facet joint anesthesia. Spine 1998;23:1972-1977. 54. Lynch MC, Taylor JF. Facet joint injection for low back pain. J Bone joint Surg 1986;68B:138-141. 55. Lippitt AB. The facet joint and its role in spine pain: manage ment with facet jOint injections. Spine 1984;9:746-750. 56. Selby DK, Paris Sc. Anatomy of facet joints and its correlation with low back pain. Cantemp Orthop 1981;312:1097-1103. 57. Schroeder WF. The facet syndrome: diagnosis and treatment. Presented at the American Academy of Orthopedic Surgeons, Atlanta, Georgia, 1984. 58. Lewinnek GE, Warfield CA. Facet joint degeneration as a cause of low back pain. Ciin Orthop 1986;213:216-222. 59. W hite AH. Injection technique for the diagnosis and treatment of low back pain. Orthop Clill North Am 1983;14(3):353-367. 60. Schwarzer AC Aprill CN, Derby R et al. The false positive rate of uncontrolled diagnostic blocks of the lumbar zygapophyseal joints. Pain 1994;58:195-200.
CHAPTER 53
-
THE LIGAMENTOUS CONCEPT
785
61. Murtagh FR. Computed tomography and fluoroscopy guided
70. Collee G, Dijkmans AC, Vandenbroucke JP, Cats A. Iliac crest
al}aesthesia and steroid injection in facet syndrome. Spine
pain syndrome in low back pain: frequency and features. J RheulIlatoI1991;18:1064-1067.
1988;13:686-689. 62. Lilius G, Laasonen EM, Myllynen P. Lumbar facet joint syndrome;
71. Fairbans JCT, O'Brien JP. The iliac crest syndrome: a treatable
cause of low-back pain. Spine 1983;8:220-224.
a randornised clinical trial. J Bone Joint Surg 1989;71B:681-684. 63. Mehta M, Sluiiter ME. The treatment of chronjc backpain - a
72. Pearcy MJ, Tibrewal SB. Lumbar intervertebal disc and ligament
preliminary survey of radiofrequency denervation of the poste rior vertebral joints. Anaesthesia 1979;34:768-775. 64. Mitchell GAG. The lumbosacral junction. J Bone Joint Surg
73. Silver PHS. Direct observations of changes in tension in the
deformations measured in vivo. Ciill Orthop 1984;191:281-286.
1934;16:233-254. 65. Basadonna P-T, Gasparini D, Rucco V. IlIiolumbar ligament 66.
67.
68. 69.
insertions; in vivo anatomic study. Spine 1996;21:2313-2316. Leong JCY, Luk KDK, Chow DHK, Woo CWO The biomechanical functions of the iliolumbar ligament in maintaining stability of the lumbosacral junction. Spine 1987;12:669-674. Chow DHK, Luk KDK, Leong JCY, Woo CX. Torsional stability of the lumbosacral junction; significance of the iliolumbar liga ment. Spine 1989;14:611-615. Boebel R. Anatomische Untersuchungen am Ligamentum iliolumbale. Z Orti1op 1961:95-92. Yamamoto I, Panjabi MM, Oxlands TR, Crisco JJ. The role of the iliolumbar ligament in the lumbosacral junction. Spine 1990;15:1138-1141.
74. 75.
76. 77.
supraspinous and interspinous ligaments during flexion and extension of the vertebral column in man. J Anat 1954;88:550. Adams MA, Hutton WC, Stott JRR. The resistance to flexion of the lumbar intervertebral joint. Spine 1980;5:245. Rissanen PM. The surgical anatomy and pathology of the supraspinous ligaments of the lumbar spine, with special refer ences to ligament ruptures. Acta Orthop SCflnd 1966;46(suppl). Newman PH. The sprung back. J Bone Joint Surg 1952;34B:30. Hoag JM, Kosek M, Moser JR. Kinematic analysis and classification of vertebral motion. Part 1. J Am Osteopath Assoc 1960;59:899.
78. Heylings DJA. Supraspinous and interspinous ligaments of the
human lumbar spine. J Anat 1978;125:127. 79. Beks JWF. Kissing spines: fact or fancy? 1989;100:134-135.
Acta Neurochir
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS
The stenotic concept
Introduction
787 Definitions 787 Incidence 788 ,
Spinal stenosis
788
Pathological changes Symptoms 789 Signs 789 Radiography 790 Treatment 790
Lateral recess stenosis
788
791
Pathological changes 791 Lateral recess stenosis and natural history of the ageing spine 793 Symptoms 793 Signs 793 Radiography 794 Natural history 795 Treatment 795
INTRODUCTION
Compression of lumbosacral nerve roots by osteoarthritic changes in the lumbar spine has been recognized since 1900, when Sachs and Fraenke]1 published the case of a Russian tailor suffering from intermittent paresis of the legs, which improved markedly after removal of the thickened and enlarged laminae of Tll and T12. Further reports on the consequences of lumbar osteoarthrosis on the function of nerve roots followed.2,3 Patients suffering from root pain in whom the only operative finding was a marked thickening of the ligamentum flavum were also recognized,4-6 and excision of the ligaments produced considerable relief of symptoms. A hypertrophied liga mentum flavum as one possible cause for backache and sciatica was suggested both in 19377 and 1945.8 By 1945, congenital narrowing of the bony canal was recognized as responsible for pressure on the cauda equina8 and, in the same decade, for nerve entrapment at the foraminal leveI.9 Overhanging facets were also postulated to be a cause of nerve root irritation.1° The definitive account of developmental narrowing of the lumbar vertebral canal causing radicular symptoms was given in the 1950s.11,12 During recent decades there have been many publica tions on the different types of 'spinal stenosis' and a consensus has been reached on the classification and pathophysiology of the different types of this lesion.13-17 DEFINITIONS Definition of stenosis of the vertebral canal or the nerve root canal • The diameter(s) of the canal are narrowed to a degree that may cause compression of nerve roots in the cauda equina, lateral recess or one of the foramina
• Narrowing may be developmental or acquired and segmental or generalized
•
Idiopathi developmental stenosis of the bony lumbar vertebral canal is a genetic disturbance that reveals its pathological effect only when growth is complete.18 The narrowing is uniform over almost the whole length 787
788 SECTION TEN
-
THE LUMBAR SPINE
of the lumbar bony canal. A midsagittal diameter of 10 mm or less is an absolute stenosis the narrowing is capable of producing signs of compression of the neural content in the absence of other compressive agents. A relative stenosis has a diameter between 10 and 12 mm and can only lead to compression if other verte bral deformities, such as spondylitis posterior vertebral osteophytes, compound the narrowing. Acquired spinal stenosis is the consequence of arthrotic changes, disc herniations, postsurgical or post-trau matic lesions, or bone diseases, including tumours. Degenerative stenosis follows, as its name implies, degenerative changes in the spine. Such narrowing is segmental and most marked between disc and posterior articular processes. Between the stenotic regions the diameters of the vertebral canal are usually normal. Iatrogenic stenosis is the name sometimes given to stenosis resulting from surgical procedures that have caused considerable peridural fibrosis.19 Lateral recess stenosis indicates a narrowing of the ver tebral canal in its lateral portion (the lateral recess). The condition should be differentiated from a nar rowing of the entire vertebral canal (lumbar stenosis) caused either by a short sagittal or transverse diame ter or a combination of both. The two cause different clinical syndromes. Lumbar stenosis is related to both legs, often involving several dermatomes, the main symptom being neurogenic intermittent claudication. Lateral recess stenosis is characterized by root pain, confined to one dermatome only.
(a)
-
•
•
•
•
•
INCIDENCE
The frequency of lumbar spinal stenosis is low. A recent series of 443 lumbar spines yielded only six patients in a hundred with relative stenosis and none with absolute stenosis.20 Lateral recess stenosis is more common. In the same series, a trefoil vertebral canal was found in 15% of the examined vertebrae and the same incidence was found in an earlier study.21
SPINAL STENOSIS PATHOLOGICAL CHANGES
In developmental stenosis the laminae, pedicles and pos terior articular processes are increased in size (Fig. 54.1). Symptoms only arise in the third or fourth decade. The reason for this is that the bony stenosis is mostly relative, and degenerative changes are required to create narrow ing that effectively compresses the content of the canal.
(b)
Figure 54.1 (a) Normal spinal canal; (b) narrowed spinal canal in developmental stenosis.
Bulky bone overgrowth may well be tolerated as long as ' it lies in a normally developed spine. Degenerative stenosis results from gross anatomical changes alone (hypertrophy of the articular facets, osteo phytOSiS, thickening of the ligamenta £lava) or in combi nation with degenerative spondylolisthesis. The latter is a vertebral displacement with an intact neural arch. Although the exact mechanism is not fully understood, the combination of disc degeneration,22 general joint laxity,23 increased mechanical stress24 and structural abnormalities of laminae and facet25 may pre cipitate forward displacement of the whole vertebra. The common denominator in the development of degenerative vertebral slippage is the loss of the normal coronal orientation of the facet joints. Grobler et al demonstrated a significant increase in sagittal facet joint orientation in patients with degenerative spondylolisthe sis, compared with a normal population. 26,27 Association with narrowing of the intervertebral joint space and development of osteo arthrosis of the facets then leads to
CHAPTER 54 - THE STENOTIC CONCEPT 789
to one-third of the anteroposterior diameter of the supe rior border of the adjacent vertebral body.33 The displace ment does not progress continuously but is arrested by further degenerative changes of the intervertebral and facet jointS.34 The mechanisms that underlie the clinical symptoms in spinal stenosis are complex and poorly understood. There is pressure not only on the dural sac and nerve roots but also on the adjacent blood supply. Therefore, arterial obstruction, venous hypertension and pressure traction on nerve roots, qura and sinuvertebral nerves are all believed to be of importance.13,35--38 S YMPTOMS
Figure 54.2 (a) Normal position of upper and lower articular process; (b) position of lower articular prosesses in degenerative spondylolisthesis.
forward vertebral subluxation.28 Later on, buckling and hypertrophy of the ligamentum flavum may supervene. This results in stenosis between the lamina and the pos terior border of the underlying vertebra (Figs 54.2 and 54.3).29,30 The condition occurs mostly after the age of 50 years, is four to six times more common in women than in men and most frequently affects the L4-L5 levePl,32 The displacement is usually moderate, less than or equal -
The chief complaint is chronic and vague 'lumbo sciatica', which is poorly localized and usually associated with numbness and weakness of the legs. The most significant symptom of lumbar stenosis is neurogenic intermittent claudication, or 'pseudoclaudication'.39-4 1 As in true intermittent claudication, the pain is brought on by walking and relieved by rest. However, pseudoclaudi cation is believed to be secondary to mechanical com pression of the spinal content, whereas intermittent claudication is the result of vascular insufficiency42 (Table 54.1). The two conditions can be distinguished by their symptoms. In neurogenic claudication, leg pain is usually bilat eral, poorly localized and associated with paraesthesia and numbness. Although the pain is usually provoked during walking, it does not disappear on standing still, which can even aggravate the situation.43 The pain is relieved only by adopting a stooped posture or by sitting.44AS The main characteristic of neurogenic claudi cation is thus that it is generated by posture rather than by exercise. This postural mechanism explains whey a patient may have the same symptoms during recum bency in the prone position and does not usually experi ence symptoms while riding a bike.46-48 SIGNS
The physical findings are often minimal. The patient may have difficulty in standing erect and adopts a 'simian Table 54.1 Differences between neurogenic and vascular claudication
Figure 54.3 Stenosis between the lamina and the posterior border of the underlying vertebra in degenerative spondylolisthesis.
Localization Paraesthesia Walking Standing still Bending Cycling Lying prone
Neurogenic
Vascular
Vague, including the back Present Worse Worse Better No change Worse
Mostly in the calf Absent Worse Better No change Worse No change
790 SECTION TEN - THE LUMBAR SPINE
stance' with flattened lumbar lordosis and hips and knees slightly flexed. As a rule, flexion does not provoke symp toms in the legs, whereas maintained extension usually does.50,51 This can be explained by the fact that extension significantly decreases both midsagittal and subarticular sagittal diameter whereas flexion has the opposite effect.52 Straight leg raising is usually normal, as are reflexes. Because the lesion involves different levels and the compression of the roots is intermittent, there is often no demonstrable sensory deficit or muscle weakness. If there is some objective weakness, it is normally situated in the muscles supplied by the fifth lumbar and first sacral nerves.16 RADIOGRAPHY
Plain radiographs are sufficient to suggest the possibil ity of a narrow canal. Short pedicles and narrow inter vertebral foramina are clearly demonstrable on a suitable lateral projection (Fig. 54.4).53 Also hyper trophy of facets, disc resorption, retrolisthesis and degenerative spondylolisthesis can easily be seen on the same views.24,54 On the plain anteroposterior projections (Fig. 54.5), hypertrophy of the pedicles (A), hypertrophic articular processes (D), small interlaminar spaces (C) and some sagittalization of the articular facets may be seen (B).55,56 However, it is as well to remember that these radiographic findings are non-specific and can be seen in asymptomatic individuals. In those with clinical features there is no correlation between symptoms
(a)
(b)
and signs and the severity of the radiographic appear ances.58 They are helpful only in supporting the clinical diagnosis. In a symptomatic patient, the evaluation of spinal stenosis can best be made by CT, especially if this is done following intrathecal injections of contrast medium.59,6o This investigation gives an accurate morphological view, and allows exact measurements of the anteroposterior diameter of the canal and the interpedicle distance. TREATMENT
Non-operative, conservative treatment should be used first61-63 and includes relative rest and non-steroidal anti inflammatory drugs. Back school instructions in activities of daily living and pelvic tilting exercises to reduce the lumbar lordosis are given64,65 (see pp. 927-928). There seems to be evidence that calcitonin is beneficial for some patients with neurogenic claudication. About 40% find that with a short course of calcitonin, their walking distance improves.66 If the patient does not respond or if there is progres sive deterioration, surgery is required. Decompression of the stenotic area is the usual procedure.67,68 Some advocate spinal fusion after the decompression, in order to avoid postsurgical instability.69,7o The surgical outcome is good to excellent in 45-80% of operated patients,?I-76 Patients with a preoperative duration of symptoms of less than 4 years, with no preoperative back pain and without previous back surgery tend to have a better outcome.77-79
(c)
Figure 54.4 Interpretation of radiographic appearances of spinal stenosis (lateral projection): (a) normal intervertebral foramina; (b) developmental narrowing of the foramina; (c) degenerative narrowing of the intervertebral foramina.
CHAPTER 54
-
THE STENOTIC CONCEPT 791
n-�-----B
��fJtt¥.�:::::--:: c 1+1-1'-....,-- D - ,-+-
Figure 54.6
Figure 54.5 Interpretation of radiographic appearances of spinal stenosis (frontal projection) see text.
LATERAL RECESS STENOSIS
There are many terms used to describe stenosis at the lateral recess: lateral recess stenosis, subarticular stenosis, superior facet syndrome, intervertebral foramen stenosis, lateral gutter stenosis and radicular canal stenosis. The radicular canal is at the lateral aspect of the spinal canal. It begins at the point where the nerve root sheath emerges from the dural sac and ends at the intervertebral foramen. Its posterior border is formed by the ligamen tum flavum, superior articular process and lamina. The anterior border is the posterior aspect of vertebral body and disc, both covered by the posterior longitudinal ligament. The dural sac forms the medial wall and the internal aspect of the pedicle the lateral wall. The radic ular canal can be classified into three zones (Fig. 54.6): the entrance zone is medial and anterior to the superior articular process; the midzone is located under the pars interarticularis of the lamina and below the pedicle; the exit zone is the area surrounding the intervertebral foramen.Bo PATHOLOGICAL CHANGES
The radicular canal may be narrowed by different mechanisms but it usually is a combination of advanced intervertebral disc degeneration, associated with marked
The radicular canal: 1, entrance zone; 2, midzone; 3, exit zone.
narrowing of the intervertebral space and increasing arthrotic hypertrophy of the articular processes, which causes the entrapment of a nerve root. Compression of the nerve root can be the result of dif ferent mechanisms: subarticular entrapment, pedicular kinking, or foraminal impingement due to posterior joint subluxation (MacNab:B1 pp. 98-104). CyriaxB2 believed that the main reason for the compression lies in the fact that the posterior longitudinal ligament and the outer layers of the degenerated disc bulge in the upright posi tion, so impinging on the nearby nerve root. Recently, stenosis as a result of surgical procedures has become more frequent. Subarticular entrapment (Fig. 54.7)
This type of stenosis is related to the entrance zone. Emerging from the dural sac, the nerve root passes between the posterior aspect of disc and vertebral body and the anteromedial aspect of the superior articular facet of the same vertebra. Hypertrophic osteoarthrosis of the facet joint, especially involving the superior articular process, may considerably diminish the distance between both borders and thus compress the nerve root,B3 although there may be an additional compression by a thickened and folded posterior longitudinal ligamentB2,B4 (this is suggested by the observation that the pain is not constant but dependent on postureB5). The mechanism is as follows: increasing degeneration and anterior migration of discal tissue causes diminution of the intervertebral space and eventually leads to disc resorption and formation of gross anterior osteophytes. Consequently, the posterior longitudinal ligament which spanned a joint 1 cm high is now too long and will there fore bulge, especially in the standing or lordotic posi-
792 SECTION TEN - THE LUMBAR SPINE
Figure 54.8
The mushroom phenomenon: the buckling posterior longitudinal ligament causes pressure against the nerve root.
Pedicular kinking
This is a midzone stenosis. The mechanism is as follows: disc degeneration causes a considerable narrowing of the intervertebral space and the upper vertebral body descends. The pedicle may then press on the nerve root (Fig. 54.9), especially if the narrowing is asymmetrical, and cause inflammation and oedema, which will give rise to symptoms. An alternative source of the symptoms is that the nerve root is trapped in the gutter formed by the pedicle and the posterolateral aspect of the degenerated and bulging disc. Foraminal encroachment
This occurs at the exit zone in the intervertebral foramen. Narrowing of the intervertebral disc results in changes in Figure 54.7
Subarticular entrapment.
tion.86 The thickened and buckling ligament can then exert pressure against the nerve root, especially if the recess is narrowed by the hypertrophic superior facet. Pain in the upright posture which disappears on sitting and bending is better explained in this way than by pos tulating a static subarticular entrapment. Cyriax called this mechanism the mushroom phenomenon, because of the characteristic radiographic appearances of a long standing anterior shift of disc material, which results in a marked narrowing of the joint space and gross beak-like osteophytes (Fig. 54.8).
Figure 54.9
Pedicular kinking.
CHAPTER 54
Figure 54.10
Foraminal encroachment.
the position of the facet joints, which move telescopically in relation to each other - the inferior facet moving down wards. Because of the inclination of the joints, a down wards movement is accompanied by a backwards one and a small retrolisthesis is produced. In the foramen, the nerve root lies in close relationship to the tip of the supe rior articular process of the underlying vertebra, so that overriding may cause compression between the tip of the subluxated (and eventually enlarged) superior facet, and the pedicle or body of the vertebra above (Fig. 54. 10). Postsurgical fibrosis and stenosis
Surgical procedures on the spine can cause the formation of scar tissue around the dura and the nerve roots - a so called laminectomy membrane.87 After laminectomy the incidence is 9%; it is approximately the same after dorsal fusion. 19 Removal of a herniated disc, which decreases the intervertebral space, may also aggravate a pre-exist ing stenosis that has not been recognized at operation.88 Lateral compression of L5
Another, more exceptional cause of radicular entrapment is found at L5. A strong fibrous band - the corporotransverse ligament - runs from the undersurface of the fifth trans verse process to the side of the vertebral body (McNab:81 p. 53). The L5 nerve root can become trapped between this and the ala of the sacrum if there is a marked downwards and forwards drop of L5, for instance in degenerative spondylolisthesis at L5-S1.89 Compression can also occur in elderly patients with degenerative lumbar scoliosis, between the ala of the sacrum and the transverse process the 'far out' syndrome.9o It has also been suggested that enlarged lumbosacral ligaments can cause extraforaminal compression of the L5 roOt.91 In order to comprehend the mechanism that causes symptoms of radicular compression in a lateral recess stenosis, it is vital to understand that any impingement on the nerve root is intermittent and related to dynamic changes in the recess during changes in postures and movement. Most compression occurs when the canal is at its most narrow diameter; relief of the symptoms may be
- THE
STENOTIC CONCEPT 793
expected when the diameter increases. During an axial load on a degenerated spine, the lateral recess decreases in size: 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 pedicle tends to push downwards on the nerve root. Extension and, to a lesser degree, side flexion towards the painful side, will further narrow the space, and therefore add to more compression on the root.92,93 In contrast, compression is reduced during flexion, which stretches the posterior longitudinal liga ment and moves the superior articular process away from the foramen (Fig. 54. 11). Symptoms of root compression are caused not only by direct compression of the boundaries but also by inflammation and oedema in and around the nerve root.94,95 Swelling within an already confined space further increases the degree of compression.96 LATERAL RECESS STENOSIS AND NATURAL HIS TORY OF THE AGEING SPINE
Lateral root entrapment is characteristic of elderly patients with disc degeneration, marked intervertebral narrowing and spondylarthrosis of the posterior wall. SYMPTOMS
The patient is middle aged or elderly (the onset is seldom before the age of 50 years, and most patients are over 70). The complaint is of unilateral sciatica that comes on during standing and walking. Sometimes, but rather exceptionally, the root pain is bilateral. The pain does not usually start immediately on standing, only after some minutes or on walking. In the latter instance, claudication must be excluded: in vascular claudication the pain rapidly abates on standing still but in lateral recess steno sis it may persist until the patient sits. After some time, numbness and pins and needles in the foot may develop. Also bending forwards immediately relieves the pain, whereas extension movements increase it. There is some times nocturnal pain, caused by an increased lordosis in the prone position. Unlike radicular pain caused by a herniated disc, there is no change in symptoms over time: neither degree nor localization change, even over years, although the patient may progress in experiencing pain with less precipitating cause and incapacity increases. There are no dural symptoms. SIGNS
There is a striking contrast between the clear and severe symptoms and the almost complete absence of signs.
794 SECTION TEN - THE LUMBAR SPINE
Anterior wall ....
Loss of water content Loss of turgor Loss of height
I
Fibrotic degeneration of the nucleus Concentric tears Radial tears Traction spurs Cysts Posterior displacements: Bulging Protrusion Prolapse
•
Fissures and cavities Marked height decrease Circular and anterior displacements Gross osteophytosis Disc resorption
....1
Early degeneration
I�
�
Instability
1..-
I�
Lateral re�ess stenoSIS
1"-
I
Hypermobility Compession and distraction Joint subluxation
•
Subperiosteal osteophytes Enlargement of facets
Spondylarthrosis
Spondylosis
Figure 54.11
Capsular and ligamentous strain Changing axis of rotation
The stenotic concept in the ageing spine.
At presentation there is commonly restriction of the spinal extension, which is caused merely by the underly ing spondylarthrosis. That apart, spinal movements are quite normal and flexion particularly is of full range. Standing upright for inspection of the back sometimes brings on the familiar pain in the leg and bending for wards causes it to disappear almost immediately. Occasionally, increasing leg ache and paraesthesia are felt during extension or on side flexion towards the painful side. Straight leg raising is normal and painless and, as a rule, there is no weakness or sensory deficit. In long standing cases, there may be slight neurological deficit: a sluggish ankle jerk or a slight weakness of the toe extensors. However, in most cases of lateral recess stenosis, the clinical examination is completely normal, which means that - as is usual in this and alUed problems - the diagnosis is made entirely on the history: an elderly patient with root pain that comes on in the erect position
and immediately disappears on lying, sitting or bending forwards. RADIOGRAPHY
The diagnosis cannot be made from radiographs, because many patients with marked radiological signs of disc resorption and narrowing of the lateral recess do not have symptoms. However, once a clinical diagnosis has been made, radiography can determine the affected level and is therefore a good guide in planning treatment of the lesion. The characteristic changes on a lateral view are nar rowing of the intervertebral space, sometimes gross, beak-like anterior osteophytes (mushroom) and sub luxation of the facet joint, with anterior and superior movement of the superior articular process. 0,11 an anteroposterior view there is a narrowing of the inter laminar space, which is a characteristic feature of lateral recess stenosis; the interlaminar space is encroached if
CHAPTER 54 - THE STENOTIC CONCEPT 795
there is an overgrowth of posterior facets or an abnormal configuration of the laminae.55,97,98 Myelograms are difficult to interpret. Areas of sub articular narrowing can be very clearly demonstrated by CT. NATURAL HISTORY
Given the diagnosis, the condition is likely to become chronic. Symptoms get worse as the years go by and, without treatment, there is no improvement.99 TREATMENT
Occasionally, symptoms can be improved by reducing lumbar lordosis. The patient is thus instructed in the correct posture for activities of daily living (see p. 927). Failure of response to such a programme is an indica tion for nerve root infiltration with 20 mg triamcinolone (see p. 927). The chief difficulty is determining where the lesion is. When there is doubt, the injection can be given at the most likely level and, if improvement does not take place after 2 weeks, is repeated at the other level.
Locating the lesion is particularly difficult after laminec tomy and several attempts, at different locations, may be necessary. It may appear surprising that infiltration around the nerve root and the sinuvertebral nerve often causes per manent relief in lateral recess stenosis. Also, prolonged relief of radicular pain after injection of a local anaes thetic around the nerve root has been reported.lOO-102 These excellent results can be explained by the reduction of chronic irritation in ligaments and perineural tissues.94 Triamcinolone, injected at the appropriate point, sup presses inflammation and thus reduces the perineural swelling. As a result, relative narrowing of the canal is alleviated and the vicious cycle of anatomical stenosis and inflammation is broken. The good and permanent results sometimes seen after infiltration of a local anaes thetic alone are explained by a chemical effect on the C fibres of the dorsal root.102 When nerve root infiltration does not afford perma nent or semipermanent cure, surgery is indicated; it consists of decompression of the nerve root. Sometimes excision of an osteophyte by fenestration may be sufficient but more usually laminectomy with partial excision of the enlarged facets is necessary.103
REFERENCES 1. Sachs B, Fraenkel J. Progressive ankylotic rigidity of the spine. J Nerv Ment Dis 1900;27:1. 2. Goldthwaite JE. The lumbosacral articulation. An explanation of many cases of "lumbago", "sciatica" and paraplegia. Bast Med Surg J 1911;164:365. 3. Bailey P, Casamajor L. Osteoarthritis of the spine as a cause of compression of spinal cord and its roots. J Nerve Ment Dis 1911;38:588. 4. Towne EB, Reichert FL. Compression of the lumbosacral roots of the spinal cord by thickened ligamenta £lava. Ann Surg 1931;94:327. 5. Cramer F. A note concerning the syndrome of cauda eguina radiculitis. BI/ll Neurol lnst NY 1934;3:501. 6. Van Gelderen e. Ein orthotisches (lordotisches) Kauda syndrom. Acta Psychiatr Nellro/1948;23:57. 7. Spurling RG, Mayfield FH, Rogers JB. Hypertrophy of the lig amenta £lava as a cause of low back pain. JAMA 1937;109:928. 8. Sarpyener MA. Congenital stricture of the spinal canal. J Balle joint Surg 1945;27A:70. 9. Hirsch e. On lumbar facetectomies. Acta Orthop SWlld 1948;17:240-252. 10. Echoes DH, Rehfeldt Fe. Failure of disclose ruptured interver tebral disks in 32 operations for sciatica. J Neurosurg 1949;6: 376-382. 11. Verbiest H. Primaire stenose van het lumbale wervelkanaal bij volwassenen. Een nieuw ziektebeeld. Ned Tijdschr Geneeskd 1950;94:2415-2433. 12. Verbiest H. A radicular syndrome from developmental narrow ing of the lumbar vertebral canal. J Bone joint Surg 1954;36B:230. 13. Arnoldi CC, Brodsky AE, Cauchoix J et al. Lumbar spinal
14. Dorwart RH, Vogler IE III, Helms CA. Spinal stenosis. Radial Ciill North Am 1983;21:301-325. 15. Ehni G. Significance of the small lumbar spinal canal: Cauda eguina syndrome due to spondylosis. Part
I.
Introduction.
J Neurosurg 1969;31:490-494. 16. Kirkaldy-Willis W H, Paine KW, Cauchoix J et al. Lumbar spinal stenosis. Ciin Orthop Rei Res 1974;99:30-50. 17. Paine KWE. Clinical features of lumbar spinal stenosis. Ciill Ort/lOp 1976;115:77-82. 18. Verbiest H. Stenosis of the lumbar vertebral canal and sciatica. Neurosurg Rev 1980;3:75-89. 19. Brodsky A. Post-laminectomy and post-fusion stenosis of the lumbar spine. Ciin Orthop 1976;115:130-139. 20. Eisenstein E. The morphometry and pathological anatomy of the lumbar spine in South African negroes and Caucasoids with specific reference to spinal stenosis. } Bone Joint Surg
1977;59B:173-180. 21. Epstein JA, Epstein BS, Levine L. Nerve root compression, associated with narrowing of the lumbar spinal canal. J Neural Neurosurg Psychiatry 1962;25:165-176. 22. Tail1ard WF. Etiology of spondylolisthesis. Ciill Orthop 1976;117:30-39. 23. Porter RW, Hibbert e. Vertebral displacement in spondylolis thesis. Ciill Biomech 1989;4:58-63. 24. Fitzgerald JAW, Newman PH. Degenerative spondylolisthesis. J Bone Joint Surg 1976;58B(2):184-192. 25. Grobler LJ, Robertson PA, Novotny JE, Pope MH. Etiology of spondylolisthesis. Assessment of the role played by lumbar facet joint morphology. Spine 1993;18:80-91.
26. Grobler L, Robertson P, Novotny J, Pope M. Etiology of
stenosis and nerve root entrapment syndrome. Definition and
spondylolisthesis. Assessment of the role played by lumbar
classification. Ciill Orthop Rei Res 1976;115:4-5.
facet joint morphology. Spille 1993;18:80-92.
796 SECTION TEN - THE LUMBAR SPINE
27. Ryan MD. L4-L5 degenerative spondylolisthesis in mono zygous twins. Spine 1994;19:985-986. 28. Herkowitz HN. Spine update: degenerative lumbar spondylo listhesis. Spille 1995;20:1084-1090. 29. Junghans H. Spondylolisthesis ohne Spalt im Zwischen gelenkstuck (Pseudospondylolisthesen). Arch Orthop Trallma
SlIrg 1930;29:118.
30. MacNab 1. Spondylolisthesis with an intact neural arch: the so-called pseudospondylolisthesis. ] Bone Joint Surg 1950;32B:325. 31. Newman PH. Stenosis of the lumbar spine in spondylolisthe sis. Clin Orthop 1976;115:116-12l.
32. Cauchoix J, Benoist M, Chassaing V. Degenerative spondylo listhesis. Ciill Orthop 1976;115:122-129. 33. Feffer HL, Weisel SW, Chuckler JW et at. Degenerative spondyl osis. To fuse or not to fuse. Spine 1985;10:287-289. 34. Matzunaga S, Sakou T, Morizondo Y et al. Natural history of degenerative spondylolisthesis. Pathogenesis and clinical course of the slippage. Spille 1990;15:1204-1210. 35. Kirkaldy-Willis WH, Wedge JH, Yong-Hing K et at. Pathology
51. Katz IN, Dalgas M, Stucki G et at. Degenerative lumbar spinal stenosis; diagnostic value of the history and physical examina tion. Arthritis Rheum 1995;38:1236-1241. 52. Inufusa A, An HS, Lim T et al. Anatomic changes of the spinal canal and intervertebral foramen associated with flexion extension movement. Spine 1996;21:2412-2420. 53. Babin
E.
Radiology
of
the
narrow
lumbar
canal.
Tn:
Wackenheim A, Babin E (eds) The Narrow Lumbar Canal, Springer, Berlin, 1980. 54. Venner RM, Crock HY. Clinical studies on isolated disc resorp tion in the lumbar spine.] Bone Joint SlIrg 1981;63B:491-494. 55. Babin E, Capesius
P,
Maitrot D. Signes radiologiques osseux
des varietes morphologiques de canaux lombaires etroits. Alln
Radial 1977;20:491-499. 56. Jones RAC, Thomas JLG. The narrow lumbar canal. A clinical and radiological review. ] Bone ]oillt Surg 1968;50B:595-605. 57. Amundsen T, Weber H, Lilleas F et at. Lumbar spinal stenosis; clinical and radiological features. Spille 1995;20:1178-1186. 58. Jonsson B, Almertz M, Sjoberg C, Stromqvist B. A prospective and consecutive study of surgically treated lumbar spinal
and pathogenesis of lumbar spondylosis and stenosis. Spille
stenosis - Part 1: clinical features related to radiographic
1978;3:319-328.
findings. Spine 1997;22:2932-2937.
36. Ooi Y, Mita F, Satah Y. Myeloscopic study on lumbar spinal
59. Schnebel B, Kingston S, Watkins R, Dillin W. Comparison of
canal stenosis, with special reference to intermittent claudica
MRI to contrast CT in the diagnosis of spinal stenosis. Spine
tion. Spille 1990;15:544-549.
1989;14:332-337.
37. Parke WE. The significance of venous return impairment in
60. Bolender N-F, Schonstrom N, Spengler D. Role of computed
ischemic radiculopathy and myelopathy. Ort/wp Ciin North Alii
tomography and myelography in the diagnosis of central
1991;22:213-221. 38. Kauppila LI, Eustace S, Kiel DP, Felson DT, Wright AM.
spinal stenosis.] Bone Joint Surg ] 985;67 A:240-246.
61. Amundsen T, Weber H, Nordal HJ et al. Lumbar spinal steno
Degenerative displacement of lumbar vertebrae; a 25-year
sis: conservative or surgical management? A prospective 10-
follow-up study in Framingham. Spine 1998;23:1868-1874.
year study. Spine 2000;25:1424-1436.
39. Auquier L, Hirsch JF, Paolaggi JB et al. Stenose du canal rachi
62. Simotas
AC,
Dorey
FJ,
Hansraj
KK,
Cammisa
F
Jf.
dien lombaire et claudication sciatique. Rev Rheum 1972;39:
Nonoperative treatment for lumbar spinal stenosis. Clinical
429-437.
and outcome results and a 3-year survivorship analysis. Spille
40. Wilson CB. Significance of the small lumbar spine canal: cauda equina compression syndromes due to spondylosis. Part 3: intermittent claudication. ] Neurosurg 1969;31:499-506. 41. Ganz Je. Lumbar signal stenosis: postoperative results in terms of preoperative posture-related pain. ] Neurosurg 1990;72:71-74. 42. Keenan GF, Ashcroft GP, Roditi GH et al. Measurement of lower limb blood flow in patients with neurogenic claudica
2000;25(2):197-203. 63. Atlas Sf, Keller RB, Robson D, Deyo RA, Singer DE. Surgical and nonsurgical management of lumbar spinal stenosis: four year outcomes from the Maine Lumbar Spine Study. Spine 2000;25(5):556-562. 64. Ritchie JH, Fahnri WH. Age changes in lumbar intervertebral discs. Can } Surg 1970;13:65. 65. Onel
D,Sarl
H,
Dinmez
e.
Lumbar
spinal
stenosis:
tion using positron emission tomography. Spine 1995;20:
clinical / rad iologic therapeutic evaluation in 145 patients.
408-411.
Conservative treatment or surgical intervention? Spille 1993;18:
43. Nicola GC, Nizzoli V. Claudication intermittente des membres inferieurs par stenose total du canal lombaire. Neurochirurgia 1974;17:48-57. 44. Simkin PA. Simian stance: a sign of spinal stenosis. Lancet 1982;ii:652-653. 45. Hall S, Bartleson JD, Onofrio BM, Baker HL et at. Lumbar spinal stenosis. Clinical features, diagnostic procedures and
291-298. 66. Porter RW, Miller CG. Neurogenic claudication and root claudication treated by calcitonin: a double blind trial. Spine 1989;13:1061-1064. 67. Grabis S. The treatment of spinal stenosis.
68. Fast A, Robin GC, Floman Y. Surgical treatment of lumbar
results of surgical treatment in 68 patients. Ann Intern Med
spinal
1985;103:271-275.
1985;66:149-151.
46. Penning L, Wilmink JT. Posture-dependent bilateral compres sion of L4 or L5 nerve roots in facet hypertrophy, a dynamic CT-myelographic study. Spine 1987;12:488-500. 47. Kapila A, Chakeres DW. Flexed sitting manoeuvre for com plete lumbar myelography in patients with severe spinal stenosis and apparent block. Radiology 1986;160:265-267. 48. Bartels RH, Frenken Cw. Lumbale spinale stenose. Ned Tijdschr
Geneeskd 1993;137:529-532. 49. Porter RW. Spinal stenosis and neurogenic claudication. Spine 1996;21:2046-2052. 50. Gaskill MF, Lukin R, Wiot JG. Lumbar disc disease and stenosis. Radial Ciin North Am 1991;29:753-764.
j Bone joillt Surg
1980;62A:308-313. stenosis
in
the
elderly. Arch
Plrys Med Rehabil
69. Frymoyer JW, Selby OK. Segmental instability: rationale for treatment. Spine 1985;10:280-286.
70. Postachini F. Management of lumbar spial stenosis.] Bone Joint
Surg 1996;78B:154-164. 71. Hall S, Bartleson JD, Onofrio BM et al. Lumbar spinal stenosis, clinical features, diagnostic procedures and results of surgical treatment in 68 patients. Ann Intern Med 1985;103:271-275. 72. Verbiest H. Results of surgical treatment of idiopathic devel opmental stenosis of the lumbar vertebral canal. j Borre Joint
Surg 1977;59B:181-188. 73. Paine KWE. Results of decompression for lumbar spinal steno sis. Ciin Orthop 1976;115:72-76.
CHAPTER 54
-
THE STENOTIC CONCEPT 797
74. Jonsson B, Annertz M, Sjoberg C, Stromqvist B. A prospective
90. Wiltse LL, Guyer RD, Spencer CW, Glenn WV, Porter IS. Alar
qnd consecutive study of surgically treated lumbar spinal
transverse process impingement of the L5 spinal nerve: the far
stenosis - Part II: five-year follow-up by an independent
out syndrome. Spine 1984;9:31-41. 91. Olsewski JM, Simmons E, Kallen FC, Mendel FC. Evidence
observer. Spine 1997;22:2938-2944.
75. Turner J, Ersek M, Herron L, Deyo R. Surgery for lumbar
from cadavers suggestive of entrapment of fifth lumbar
spinal stenosis. Attempted meta-analysis of the literature.
spinal nerves by lumbosacral ligaments. Spine 1991;16:
Spine 1992;17:1-8.
336-347.
76. Ishac R, Alhayek G, Fournier 0, Mercier P, Guy G. Results of surgery for lumbar spinal stenosis in patients aged 80 years or more. A retrospective study of thirty-four cases. Rev Rhul11 Engl 1996;63(3):196-200. 77. Herno A, Airaksinen 0, Saari T, Miettinen H. The predictive
93. Willen J, Danielson B, Gaulitz A et al. Dynamic effects on the
value of preoperative myelography in lumbar spinal stenosis.
lumbar spinal canal: axially loaded CT-myelography and MRI
Spine 1994;19:133-1338.
92. Zander DR, Lander PH. Positionally dependent spinal steno sis: correlation of upright flexion-extension myelography and computed tomographic myelography. Can
Assoc Radio I
1998;49(4):256-261.
in patients with sciatica and / or neurogenic claudication. Spine
78. Katz IN, Stucki G, Lipson SJ et al. Predictors of surgical outcome in degenerative lumbar spinal stenosis. Spine 1999; 24(21):2229-2233. 79. Herno A, Airaksinen 0, Saari T, Sihvonen T. Surgical results of
94. Mumenthaler M, Schliack H. Liisionen peripherer Nerven Thieme, Stuttgart, 1973. 95. Garfin SR, Rydevik BL, Brown RA. Compressive neuropathy
lumbar spinal stenosis. A comparison of patients with and
of spinal nerve roots. A mechanical or biological problem?
without previous back surgery. Spine 1995;20:964-969.
1997;22:2968-2976.
80. Lee CK, Rauschning W, GleIm W. Lateral lumbar spinal canal
Spine 1991;16:162-165. 96. Rydevik B, Brown MD, Ehira T, Norborg C, Lundborg G.
stenosis: classification, pathologic anatomy and surgical
Effects of graded compression and nucleus pulposus on nerve
decompression. Spine 1988;13:313-320.
tissue - an experimental study in rabbits. Proceedings of the
81 MacNab 1. Backache. Williams & Wilkins, Baltimore, 1983. 82. Cyriax JH. Textbook of Orthopaedic Medicine, vol I. Diagnosis of Soft Tissue Lesiolls, 8th edn, Bailliere Tindall, London, 1982:281-282. 83. Epstein JA, Epstein BS, Rosenthal A, Carras R, Lavine L.
Swedish Orthopaedic Association, Gbteborg, Sweden, 27 August 1982. Acta Orthop Scand 1983;54:670-671.
97. Vouge M. Interapophysolaminar spaces of the lumbar spine and their utility in the diagnosis of narrow lumbar canal. In:
Sciatica caused by nerve root entrapment in the lateral recess:
Wackenheim A, Babin E (eds) The Narrow Lumbar Canal.
the superior facet syndrome. I Neurosurg 1972;36:584-589. 84. Cyriax JH. Treatment of lumbar disc lesions. BMJ 1950;ii:1434. 85. Penning L. Functionele radio-anatomie van lumbale stenose. Ned Tijdschr Mall Ther 1990;9:36-48. 86. Beatty RA, Sugar 0, Fox TA. Protrusion of the posterior longi
Springer, Berlin, 1980. 98. Wilmink JT, Korte JH, Penning L. Dimensions of the spinal
tudinal ligament simulating herniated lumbar intervertebral disc. J Neurol Neurosurg Psychiatry 1968;31:61-66. 87. LaRocca H, MacNab 1. The laminectomy membrane. J Bone loint Surg 1974;56B(3):825-830. 88. Verbiest H. Fallacies of the present definition, nomenclature, and classification of the stenoses of the lumbar vertebral canal.
Spine 1976;1:217-225. 89. Transfeldt EE, Robertson 0, Bradford OS. Ligaments of the lumbosacral spine and their role in possible extra-foraminal spinal nerve entrapment and tethering. J Spinal Discord
1993;6:507-512.
canal in individuals symptomatic and non-symptomatic for sciatica: a CT-study. Neuroradiology 1988;30:547-550.
99. Porter RW, Hibbert C, Evans C. The natural history of root entrapment syndrome. Spine 1983;8:345-349. 100. Tajima T, Furakawa K, Kuramochi E. Selective lumbosacral radiculography and block. Spine 1980;5:68-77. 101. Haueisen DC, Smith BS, Myers SR, Pryce ML. The diagnostic accuracy of spinal nerve injection studies. Clill Orthop 1985;198:179-183. 102. Dooley JF, McBroom RJ, Taguchi T, MacNab r. Nerve root infiltration in the diagnosis of radicular pain. Spine 1988;13: 79-83. 103. Kirkaldy-Willis WH, Wedge JH. Young-Hing K et al. Lumbar spinal nerve lateral entrapment. Clin Orthop 1982;169:171.
THIS PAGE INTENTIONALLY LEFT BLANK
Clinical examination of the lumbar spine
CHAPTER CONTENTS ,
History
799
Introduction 799 Localization of the symptoms 800 Pathogenesis 800 Problem solving 801 Age and daily activities 801 Routine of history taking 802 Pain 802 Paraesthesia 806 Danger to S4 nerve roots 807 What is the patient's reaction to the symptoms? Inspection 808 The shape of the normal trunk
The pathological trunk Functional examination
831
Epidural local anaesthesia Technical investigations
INTRODUCTION
812
830
Accessory tests
HISTORY
808
808
Examination standing 812 Examination supine 819 Examination in the prone-lying position Palpation
808
832 833
Plain lumbar radiography 833 Other imaging studies 833 Electrodiagnosis 834
827
Evaluating the symptoms and signs of backache and I or sciatica is never easy. Despite the increasing accessibility of very sophisticated technical aids for the assessment of a patient with a lumbar problem, diagnosis should still be made clinically, on the basis of history and physical examination. The history offers unique opportunities that the other diagnostic techniques do not possess. Examination tech niques only give a cross-section' snapshot' . History indi cates: the evolution of the disease; the record of past and present suffering; and the basis for future treatment, pre vention of relapse and prognosis. History also gives the examiner an idea of the degree of disablement the problem has produced. For these reasons a careful history, detailed and in chronological sequence, is the first and most important aid. History taking can not be done in a hurry. The exam iner must have a lot of time and patience, especially with patients who are unable to give precise responses to questions. Most patients have difficulties in organizing their story or in remembering every detail. For a satis factory diagnosis, however, it is essential to obtain a description of the past and present pain in meticulous detail. Therefore the examiner should develop a specific technique of questioning which is chronological and precise. The answers (both positive and negative) form a pattern that is related to knowledge of applied anatomy, biomechanics and pathogenesis. Taking a history thus translates the patients' complaints into an anatomical and biomechanical context and finds a correlation with one of the well-known syndromes. The nature of the symptoms and the way that symp toms produce disability is very informative. Also, the evolution of the symptoms, so important in the diagno sis of low back disorders, can be obtained only from the history and not from the clinical examination. The following case report makes this clear: a patient presents with backache, which started suddenly, followed a few days later by unilateral sciatica and numbness of the 799
800 SECTI O N TEN - T H E L U M BAR SPI N E
outer two toes; the backache ceased the moment the sci atica appeared. This is the story of SI root compression, with neurological deficit, almost certainly caused by a large annular irreducible d isc protrusion at the level of L5. From these few items in the history, not only can the diagnosis be established but also therapeutic implica tions can be made: manipulative treatment will be of no help in this case, and the patient should either be treated by epidural local anaesthesia or await spontaneous recovery. In practice, the patient's symptoms are not always as obvious as in this idealized case but it does give an idea of the value of a good history. After the history has been taken the examiner should have a fair idea of the diag nosis or at least be able to distinguish genuine backache from that referred from elsewhere in the body or of psy chogenic origin. The history can also differentiate mechanical from inflammatory disorders. In the large group of mechanical syndromes, discodural, ligamento us and stenotic disorders all have their own typical behaviour: onset, localization, appearance and evolution. The clinical examination tends only to confirm the infor mation derived from the history. LOCA LIZATION OF T H E SYMPTO M S
Symptoms are grouped under the headings lumbago, backache and sciatica. These terms are used as follows: •
• •
Lumbago: a sudden attack of severe low back pain, causing some degree of fixation and twinges on attempted movement. Backache: discomfort in the lower back. Sciatica: pain that strictly radiates from the buttock to the posterior thigh and calf. It is restricted to a specific dermatome (L4, L5, SI or S2) and may be accompanied by paraesthesia and motor and / or sensory deficit. In practice, however, the term is inaccurately used if pain and paraesthesia are felt in the anterior part of the thigh and / or lower leg (L2-L3).
PATH O G E N E S I S
In lumbar spine problems, the mechanism of causation is usually reflected in the behaviour of the pain. Localization of the symptoms, their evolution and rela tion to activity and posture differs according to the tissue involved. Pain in the lumbar and pelvic-gluteal area is usually of local origin but it may also be referred from intra-abdominal or pelvic lesions. Sometimes lumbar pain is devoid of any organic basis and is then labelled as non-organic or 'functional'. Local organic disorders may or may not be related to activity. The former are called activity-related spinal disorders, the latter non-activity related spinal disorders (Box 55. 1 ).
Box 55.1 Origin of low back pain Organic disorders Activity-related spinal disorders D i scodural and discoradicular disorders Capsul oligamentous di sorders Stenotic di sorders Non-activity-re/ated spinal disorders Inflammati ons (septic and rheumatic) Osseous disorders Acquired defects Tumours Metabolic di sorders Pain referred to the back Vi sceral disorders Non-organic disorders
Activity-related spinal disorders (eh. 57)
These are caused by a mechanical dysfunction of parts of the lumbar spine. Of these, discodural interactions are paramount, but capsular or ligamentous lesions and spinal stenosis are other possible causes. Discodural interactions may cause all three major syn dromes: lumbago, backache and sciatica. Both articular and dural symptoms are present. These lesions have a characteristic evolution: because the discal displacement seldom remains stable, the localization and intensity of the symptoms vary with the localization and intensity of the dural impingement. Lesions of the facet joints are characterized by localized pain. There is absolutely no change in localization. Dural and root symptoms are also absent. Ligamentous pain typically occurs in relatively young people. It is created by prolonged or increased postural stress and abolished by correction of posture. In long standing cases, movements also become painful at full range. In disorders of the lumbar ligaments, pain is always intermittent and vague and never referred below the upper buttocks. Lesions of the iliolumbar or sacro iliac ligaments, however, may give rise to slight refer ence of pain in the groin and the back of the upper thigh, respectively. Again, neither dural nor root symptoms are present. In central spinal stenosis chronic and vague lumbo-sciat ica is brought on by walking or standing and relieved by stooping or sitting. Pain is often associated with feelings of numbness and weakness in both legs. These patients are never under 30 years old and more often are over 60. In stenosis of the lateral spinal recess, a middle-aged or elderly patient complains of unilateral sciatica coming on during standing and walking. Sitting or bending forward alleviates the pain immediately. As in ce11tral spinal stenosis, dural symptoms and signs are absent, as are root signs.
CHAPTER 55
Non-activity-related spinal disorders (Ch. 58)
•
TheS'e include:
•
• • • •
Inflammatory diseases, both septic and rheumatological. Osseous disorders, such as osteoporosis, fractures or tumours. Acquired defects of the vertebral arch. Intraspinal lesions, such as neuroma, metastases and cysts.
In ankylosing spondylitis, pain may vary in an unex pected way. One day the patient awakes without any dis comfort and able to do any kind of heavy work. Next week early awakening may be with a painful back and disablement persists for the rest of the day. This d iffers markedly from the patient with discodural backaches, in whom the pain starts at the moment of rising or when an attempt is made to put o n socks o r pantihose. The back thus aches during certain movements or positions, whereas others ease the pain. In rheumatoid conditions, the pain is typically experi enced most severely in the morning and improves throughout the day. In malignant di sease, pain is unremitting and worse at night. Lumbar pain increases steadily even after root pain has set in; its distribution is not confined to a single dermatome. Pain referred to the back
Pain in the back that is completely unrelated to move ment or posture and has little temporal pattern suggests a referred source from intra-abdominal or pelvic lesions, such as those of the aorta, and the genitourinary and gas trointestinal tract. In the initial stages of these diseases, the history may signal the disease by the existence of warning signs. Some of these are briefly discussed here. Warning • Pain in the upper l umbar region suggests the possibil ity of aortic aneurysm, neoplasm, caries, ankylosing spondyl i tis or may result from vi sceral disease. • Steadily increasing lumbar pain, especially in elderly patients also occurs i n malignant di sease • Graduall y expanding and increasing pain is associated with a l esion increasing in size, for example neoplasm or neuroma; a good example of this i s a patient with backache, fol l owed by sciatica i n which the pain i n the back worsens instead of dimi nishes. • Continuous pain, not altered by movement and posture is ominous; it should be remembered, however, that 'endless' pain may also be present in psychogenic disorders.
PROBLEM SOLV I NG
While taking a history the examiner endeavours to find an answer to the following questions?
• • • •
-
CLI N I CA L EXAMI NATI O N 801
Is this an organic or non-organic lesion? Do the symptoms point to activity-related disorders? If yes, is it a disc lesion? What sort of disc lesion is present? What other type of lesion is more in accordance with the symptoms? What type of person is the patient? Is it obvious that the degree of pain and effect on daily activities tally with appearance and behaviour and interfere with the disablement that is outlined?
Because low back pain is most often caused by a soft tissue lesion and so frequently attributed to d isc di sor ders, the history serves in the first place to veri fy if this is the case. 'All discs are alike, all other lesions are dif ferent' is Cyriax's statement, which has proved itself in orthopaedic practice. Therefore, in d isc displacements of all types, a confirmation of the facts detailed i n Chapter 5 3 is expected. The history also provides an opportunity to interpret the credibi lity of the patient's story, again by looking for 'unlikelihoods' - facts that do not correlate with one of the well-known syndromes. If during the history the slightest doubt arises, the clinicians should be on the alert. More 'unlikelihoods' should then be sought in the patient's story or during the following clinical examina tion. In contrast, when the patient states exactly what is expected and normal for a comparable case, there is certainly no reason to doubt the reliability nor will a search for possible psychoneurotic components be nec essary. Patients devoid of a physical cause will rarely escape detection if the history is properly taken. In these patients, none of the well-known physical patterns emerges - the rules and facts of referred pain do not fit. They do not so much describe their symptoms as the degree of suffering. They fail to supply relevant answers and, if the examiner insists, questions are often resented. During the history the interviewer should obtain specific data on the following: • •
•
Age and daily activities Symptoms: pain paraestheSia influence of posture, movements or coughing / sneezing bowel or bladder problems / S4 root Patient's reaction to these symptoms.
AG E AND DAI LY ACTI V ITIES
Disc lesions causing backache and sciatica are most common between the ages of 20 and 50 years. Over 60, the frequency decreases. Under the age of 20, disco dural interactions are rare, although not impossible.
802 SECT I O N TEN - T H E LU M BAR SPI N E
Table 55.1 Age-dependent disorders Age (years)
Disorder
15 1 5-35 20-40 20-50 Elderly
Spondylolisthesis Ankylosing spondylitis Reiter's syndrome Disc lesions Spinal and lateral recess stenosis
Sciatica caused by a posterolateral disc protrusion can be expected from adolescence to old age. In elderly patients, lateral recess stenosis is more fre quently expected to be the cause of root pain (Table 55.1). Also, degenerative spinal stenosis is a disease that occurs predominantly in the elderly. Spondylolisthesis can provoke posterior ligamentous pain in the young. Postural ligamentous pain is also more frequent in young patients who stand at work. This syndrome nor mally persists until degeneration of the spine restricts mobility and stabilizes the 'motion segment', the mobile connection of two neighbouring vertebrae including the intervertebral disc and zygapophyseal joints. Ankylosing spondylitis typically provoke alternating sciatica between 15 and 35 years of age. It is four to nine times more frequent in men.] Back pain as the presenting symptom of Reiter's syn drome is also most common between the ages of 20 and 40 years, with males predominantly affected? The activities undertaken in the patient's profession, hobbies and sports will give additional information that is extremely important in judging the actual functional incapacity and in designing the treatment strategy. Most patients do not suffer from pain, rather from the disabil ity the pain provokes. It is obvious that disco dural back ache will produce more disability in a truck driver who has to sit the whole day than in a patient who has light and varying work. For some, normal activities are unre stricted but their favourite sport is impossible, and this is a major concern. Profession and activities are also important in relation to treatment, recurrences and prophylaxis. If a bricklayer gets lumbago every second year, his back can be judged to be reasonably stable and manipulation will help him sufficiently each time there is a new attack. If by contrast, a clerk gets attacks of lumbago five times or more a year, these repeated events indicate that the back is very unsta ble. Al though manipulation may solve the problem for a short time, it is obvious that stronger prophylactic measures will be necessary; successful manipulation should be followed by sclerosing injections, back school and / or a good lumbar support.
ROUTINE OF HISTORY TAKING.
In disorders of the low back, symptoms can diversify. The clinician must try to obtain a clear impression not only of present discomfort but also of fonner events (see Box 55.4, p. 806). Pain is the most frequent and important symptom and usually the one that forces the patient to seek medical help. Other symptoms are not always mentioned sponta neously but should be asked about: the presence of paraesthesia, numbness, a cold foot or incontinence. Symptoms are usually presented by the patient in a very disorganized way. The interviewer then tries to create 'order in the dis-order'. The best approach is chronological, the patient being asked about the events leading up to the onset of the symptoms and then to recount chronologically what has happened since. PAI N
All different aspects o f pain should b e investigated: local ization, onset, evolution and duration of the perceived 'actual' pain; any influence of movement and posture; and the presence of dural symptoms. It is also very useful to obtain information on the same factors in previous attacks (Box 55.2). In disorders of the low back, the pain may be experi enced as backache, as gluteal pain with or without refer ence to one or both legs, or as typical root pain. Actual pain Side and level. The patient is first asked if he feels the pain now and to point to its location. The method chosen
Box 55.2 Pain: important reminders Actual pain Localization Side: unil ateral , bil ateral or central? Level: upper l umbar, l ower lumbar, gluteal , l eg? Onset When did the pain start?: days, weeks, months or years ago How did the pain start?: suddenl y, gradually Evol ution Relationship between back pain and leg pain? Rel ationship between pain and activity What posture or movement makes the pain worse? Is a cough painful? What eases the pain? Is there nocturnal pain?
Previous pain episodes Earliest manifestation? Localization? Frequency of attacks? Pain-free interval s? Previous treatment?
CHAPTER 55 - CLINICAL EXAMINATION 803
may indicate emotional stability or instability. In the former, the patient generally places the palm of his hand at the site of maximal pain and moves it across his body to demonstrate the route of radiation. A psychologically unstable patient never touches the painful area but only points it out vaguely with the thumb.2 Back pain may be localized centrally, unilaterally or bilaterally. Central pain can never be referred from a unilateral structure, for example a facet joint or a sacroiliac joint. Bilateral pain also hardly ever has a central origin. Unilateral pain in one buttock is typical of a discodural problem. Sometimes the sacroiliac joint is responsible but a strained muscle is a rarity. Apart from dural pain reference, bilateral leg pain can sometimes be caused by two simultaneous protrusions, one compressing the fourth, the other the fifth nerve root on the opposite side. However, bilateral root pain is more often the result of spondylolisthesis, spinal stenosis, lateral recess stenosis or metastases. Bilateral osteoarthris of the hip joints, intermittent claudication due to thrombosis in the iliac arteries and tabes may also create pain in both legs. The level of the pain is also important. In backache with dural reference, pain is situated in the lower lumbar region, perhaps radiating upwards to the lower parts of the thorax or downwards to the sacral area or the buttocks. If the patient points to the upper lumbar area, the investigator should immediately be on the alert. Malignant diseases in the lower back have a great preference for this area (see p. 852). In sacral, coccygeal or perineal pain, compression of the 54 root is a real possibility and constitutes an absolute contraindication to manipulation. Further information on bladder and rectal function and sexual potency should be obtained. In sciatica, unilateral pain in the relevant dermatome results from pressure on the dural sleeve of one of the lower lumbar nerve roots (L4, L5, 51 or 52). It is impor tant, although not always easy, to distinguish radicular pain from pain caused by pressure on the dura mater. The latter is referred extra segmentally and therefore experienced over a larger area, not restricted to one der matome. Such dural pain is diffuse, vague and spreads upwards to the chest or down both thighs, sometimes reaching the ankles. When the patient presents with a clearly outlined and severe ache in the leg, it is easy to recognize the segmental pain of root compression. However when, as happens occasionally, referred dural pain in the leg is present, the difference between seg mental and dural pain can be more difficult to establish, especially if the pain is felt more strongly in the leg. The difference between radicular and dural pain is extremely important both in diagnosis and treatment.
Every effort should therefore be made to obtain a precise description of the localization and characteris tics of the pain. To a patient, a leg is a leg, and most are not precise about whether the pain is in the front or back of the thigh, whether it spreads beyond the knee and whether it is localized or generalized. Pain in one lower buttock only is rarely dural; more commonly it is a segmental reference from 52. Onset of pain Low back disorders may be acute, chronic or recurrent. The patient should identify the first time when the symptoms occurred, 'When did your back problem start?' is thus an important question. A long history of, say, 20 years of 'suffering' from backache requires further questioning on whether the problem is continuous or intermittent. It may be that there was but one attack of acute lumbago 20 years ago with a second attack 2 days ago; or a constant and daily ache may have been present over the whole period of 20 years; or the problem may be recurrent incapacitating backache six times a year. It is obvious that although in all three instances the history extends over a period of 20 years, the diagnostic and therapeutic approach will differ, as will the prophylactic measures to be taken. Information about the duration of symptoms is also extremely important in cases of sciatica. There is no limit to the duration of radicul ar pain resulting from lateral recess stenosis. In discoradicular interactions a course terminating in spontaneous recovery is the rule. Once the protrusion has shifted to one side, symptoms tend to abate; the protrusion has settled itself outside the inter vertebral joint and there it lacks nutrition and shrivels away. As a rule, the patient recovers within 12 months of the onset of the radicular pain. However, this only applies in patients under 60 years of age. The next question concerns the speed of onset: 'How did it start: was the onset sudden or gradual?' Very often the patient cannot remember. Especially in long-standing cases, it is difficult to recall whether the symptoms appeared suddenly or gradually. Backache brought on over some hours, or even the morning after doing some heavy work involving much stooping and lifting, suggests a soft disc lesion slowly increasing in size, i.e. a soft nuclear displacement. Cyriax used to say: 'Pulp oozes, cartilage subluxates in an instant'. In this type of discal displacement, traction is usually the treatment of choice, except in very acute cases where it is strongly contraindicated. An epidural injec tion is then the alternative. Acute lumbago starting suddenly, at the moment the patient bent forward or lifted a weight is typical of a hard, annular disc displacement. In a case that is not too acute, manipulation is almost always successful in one or two sessions.
804 SECTION TEN - THE LUMBAR SPINE
In most discoradicular interactions, pain typically starts in the back and sooner or later shifts into one leg. 'Shifting pain' of this nature strongly indi cates a disc lesion. If backache gradually increases and after some time extends into one leg and finally involves the back and both legs, a progressive lesion such as a tumour is very l ikely and the examiner should be on the alert. Pain starting in the leg, slowly getting worse over a period of months and finally spreading upwards to the posterior aspect of the thigh is very suggestive of a primary posterolateral protrusion compressing the Sl root. The lesion occurs in young adults and is always nuclear. Chronic sciatic pain in the elderly, extending over months to years, is typical of radicular pain from a nar rowed lateral recess. 'Alternating pain' in the legs suggests bilateral sacro iliac arthritis, which is usually a manifestation of early ankylosing spondylitis. Less often it indicates a disc lesion in a very unstable lumbar intervertebral joint. Cou rse of the pain.
Sequence of
backa che
and
root p a i n:
which
pain
Usually, backache is followed by root pain and ceases when the root pain begins. From that point, the mechanism of gradual spon taneous recovery starts. However, there are exceptions and there is no point in awaiting spontaneous recovery in patients over 60. Root pain without previous backache, which is caused by a primary posterolateral protrusion, has been shown to be irreducible by manipulation. All displacements of this nature appear to be nuclear, moving posterolaterally from the onset.
came fi rst. backache or root pain?
In activity-related spinal disorders it is obvious that there is a relationship between the symptoms and posture or exertion. What factors influence the symptoms?
In a discodural interaction the ache is increased by stooping, lifting, sitting or coming upright after sitting and is relieved during walking and in recum bency. However, there are some characteristic histories slightly different from the usual findings for disc lesions. For example, a patient between 20 and 40 years of age may awake wi thout any pain and remain asymptomatic over the next few hours, even on exertion. During the day backache comes on, slowly getting worse. On going to bed, the pain ceases after an hour or so. This is the typical history of a 'self-reducing' disc lesion. A patient may complain of pain in the lower back which comes on with prolonged standing. The ache gets worse and is finally followed by bilateral root pain, even tually with paraesthesia in both feet. Sitting or lying down results in cessation within a minute. In young
patients this pattern suggests a spondylolisthesis. If the patient is elderly, stenosis of the spinal canal should be suspected . In 'ligamentous postural' syndromes, pain is particu larly increased by maintenance of a particular posture, whereas altering the position relieves the pain gradually. Moreover, the longer the position is maintained the more intense the pain becomes. Barbor3 described the discom fort of ligamentous pain as 'the theatre, cocktail party syndrome': it is impossible to sit at the theatre or stand at the cocktail party without low backache occurring. In contrast, the symptoms are relieved by activity. This syndrome is typically found in the young. Coughing and sneezing. Another factor that may influence symptoms is raised intra-abdominal pressure during coughing and sneezing (see Box 55.3). Pain in these circumstances may be a dural sign produced by a sudden increased intradural pressure, which in turn causes sudden expansion of the dura pressed against the protrusion. Although it is very often related to a disc pro trusion, it is clear that any space-occupying lesion in the lumbar spinal canal compressing the dura mater (e.g. a neuroma) may evoke the same response. Often the patient will not mention it spontaneously, so the investi gator must inquire about coughing and sneezing. In disc lesions, coughing and sneezing normally increase the lumbar or gluteal pain. However, when they also increase the pain in the leg, manipulative reduction will almost certainly fail. Epidural injections should then be tried. A neuroma may evoke the same sign but the pain is usually felt more in the leg than in the back. In active sacroiliitis, pain on coughing is felt in the buttock and sometimes radiates into the thigh. It results from the painful distraction of the joint caused by' the momentarilty increased intra-abdominal pressure.
Posture and exertion.
Box 55.3 Low back pain disorders in which coughing produces symptoms Intraspinal lesions Intradural Neuroma Extradural Disc protrusion Disc infections Metastasis Epidural abscess Haematoma
Extraspinal lesions Sacroiliac joint Arthritis Strain
CHAPTER 55
- CLINICAL
EXAMINATION 805
'Ea rly morning' pain. This wakes the patient and eases on getting up, after which it is possible to do quite heavy work; the pattern is suggestive of ankylosing spondylitis. The pain is felt centrally in the whole lumbar region and varies from day to day. Sometimes early morning pain is caused by a disco dural interaction. The increased hydration of the disc during recumbency possibly exacerbates an existing small posterior bulge, which then slowly compresses the dura mater, so waking the patient before dawn. This type of disc lesion is best treated by epidural local anaesthesia. It should be emphasized that these histories are quite different from the usual story for a patient with a small disc lesion who has a painful stiff back on getting up in the morning. Turning in bed is also mentioned as causing a twinge and is quite different from increasing pain in a recumbent position.
recovery becomes more and more likely to succeed. Later recurrences at the same level are no longer likely. In major or long-standing sciatica, epidural local anaesthesia may relieve the pain during the period of spontaneous recovery. If this fails and pain remains unbearable, chemonucleolysis or surgery are indicated. Root pain that does not get better within a year or even gets worse after, say, 8 months is suggestive of conditions other than d isc lesions, such as neuroma or lateral recess stenosis.
This results from a large protrusion with a high degree of inflamma tion. For this reason, manipulation and traction will be of no help and the patient is best treated by an epidural injection. If lumbar movements or posture do not influence the pain, there is certainly not a mechanical lesion and the condi tion may be the result of some other pathological dis order such as intra-abdominal or spinal malignancy or infection, a bruised dura or bruised nerve root sleeve.
Age. If a patient states that backache or attacks of lumbago have occurred since childhood, spondylolis thesis with a secondary disc lesion should be suspected.
Root pain worsening during the night.
The d u ration of pain. Lumbago usually recovers spon taneously within a week because of the strong counter pressure exerted by the posterior longitudinal ligament, which gradually reduces the large posterocentral displacement. In backache, there is no predictable time limit: the pro trusion is small and remains more or less in contact with the rest of the intervertebral content of disc, end-plates and ligaments, thus receiving sufficient nutrient supply to maintain it. Because of a decrease in intervertebral height, the counterpressure exerted by the posterior longitudinal ligament becomes less effective. As a result, the discal tissue may remain displaced for years, with or without remission. Spontaneous recovery probably never occurs, whereas reposition by manipulation or traction is simple and is indicated regardless of how long the patient has had the problem. In sciatica, the protrusion has slipped posterolaterally and becomes extra-articular. Consequently the bulge is cut off from its nutrient supply. Slow but continuous shrinking sets in from the moment the backache has ceased and results in spontaneous remission of the sciatic pain within 8-12 months. Therefore treatments such as manipulation and traction are worth trying but only during the first 6 months. Once this time limit has passed, they are not relevant because the process of spontaneous
Previous attacks
Previous attacks should be related to age, localization, origin, evolution, influence of movement and posture. Also important are the frequency of attacks, the type of treatment and its result.
Localization of symptoms. In disc lesions, the localization of symptoms is determined by the site of the pressure on the dura mater or nerve root. In a new episode, the pain may have similar localization. However, in that a disc may easily shift and compress sensitive structures at other places, repeated attacks of backache caused by the same disc may provoke pain on different sides. Reports of former attacks, not located on the same side, point to a disc protrusion as the cause of the problem. A shifting pain means a shifting lesion, and only the disc is free to move from one side to another. Pain changing from one buttock into the other is also seen in early ankylosing spondylitis with involvement of the sacroiliac joints. In capsular and ligamentous disorders or in spinal stenosis, localization is fixed, and remains unchanged over a long period. Cause. A disc is damaged by prolonged wear and tear but symptoms only become manifest at the moment of inter nal derangement. An annular crack can also be caused by one single injury but if there is a time gap between the injury and the onset of pain it will usually be very difficult to prove the aetiological significance of the latter. Evolution. Episodic backache for years does not suggest progressive, serious disease. More suspicion arises if an elderly patient, for the first time in his life, gets backache which is progressive. When pain is continuous, it is there fore vital to know if it is getting better or worse, is unchanging or is variable. Frequency of attacks. The frequency of previous attacks gives information about the stability of the disc; it should
806 SECTION TEN - THE LUMBAR SPINE
always be considered in relation to the profession of the patient. If the frequency is less than once a year in a person doing heavy work every day, the implication is that the disc is relatively stable. Treatment other than reduction and back school instruction is not required. I n contrast, in a patient undertaking a fairly light job, attacks of lumbago three or four times a year indicate an unstable disc. Reduction is then only part of the solution. The back needs to be stabilized by a corset, sclerosing injections into the surrounding inert structures or even by operative intervention. Pain-free intervals . The degree of pain and d isability in between the attacks must be assessed. Have the symp toms disappeared completely and can the patient do everything this is wished between the bouts of pain, or has the pain never completely receded? In the former, reduction has been complete and a manipul ative attempt will probably succeed again; in the latter, either the d isc has not been reduced completely or there remains a second (ligamentous) lesion. In either event, continuing pain is a bad prognostic sign for manipula tion or traction alone.
be on guard. Although manipulation can safely be tried, it will not always be tolerated. Traction, however, should definitely be abandoned, because traction makes matters worse, usually at the moment it is released. The safest and most effective treatment is epidural local anaesthe sia. It almost always affords immediate relief although the large displacement remains present, continuing the marked deviation and limiting the joint movements. Manipulation, carried out from the next day, is much better tolerated and usually gives good results. Num bness or even weakness. The patient states that the foot flops during walking or that rising on tiptoe cannot be done: this suggests a large posterolateral protrusion not reducible by manipulation or traction. Box 55.4 summarizes the routine of taking a pain history. Table 55.2 outlines some typical histories.
PARA E STH ESIA
When the patient states that there are 'pins and needles', this is pathognomonic of pressure on or inflammation of the peripheral nervous system. In practice, the cause is
Previous treatment It is also necessary to determine whether the symptoms disappeared spontaneously or as the result of some specific treatment.
Discodural interactions
Box 55.4 Summary of pain history -
Location
The history may also serve to obtain an idea of the degree of discodural interactions.
Central, unilateral, bilateral
Ma rked a rticular symptoms (twinges) and postural devi
Onset
These are characteristic of intense discodural contact. The deformity is noticed by the patient or by others. The typical case is acute lumbago in which the patient is painfully locked i n flexion by a large central protrusion at the posterior aspect of a lumbar interverte bral joint. Any attempt to extend the lumbar spine squeezes the protrusion further backwards and increases the already painful pressure on the dura mater. The adop tion of the flexed position decreases the pressure of the subluxated part of cartilage on the dura mater. A large posterolateral protrusion is accompanied by some deviation of the lumbar spine in lateral flexion, so projecting one hip sideways. The patient is not able to move in the opposite direction. Such lateral deviation suggests a lesion at the fourth or perhaps the third lumbar level. When the lumbar spine is fixed in flexion or in lateral flexion because of root pain, all conservative treatment is likely to fail and surgical management or chemonucleo lysis is indicated. If a patient with acute lumbago states that twinges are felt on even the slightest movements, the therapist should ation.
Level ('forbidden area', S4 dermatome) Low back/leg Sudden/gradual
Evolution Shifting pain Expanding pain Alternating pain Sequence of backache-root pain Usual evolution - primary posterolateral protrusion
Factors influencing pain Relation between symptoms and posture/activities Typical histories: Self-reducing disc lesion, spondylolisthesis Spinal stenosis Ligamentous postural syndrome Pain on coughing, in back/leg Twinges Early morning pain/nocturnal pain No influence on movement or posture
Duration of pain No time limit for backache Spontaneous recovery in unilateral sciatica
Previous attacks Frequency Pain-free periods
CHAPTER 55 - CLINICAL EXAMINATION
807
Table 55.2 Some typical histories Diagnosis
Age
Pain localization
Discodural backache
15-70
Lumbar gluteal
Postural syndrome
30 or younger
Lumbar
Provokes
Eases
Lateral recess stenosis
Elderly
Leg, unilateral segmental
Standing and walking provoke Sitting, lying or bending forward eases
No influence
Sciatica
usually 20-50
Leg, unilateral segmental
Sitting often provokes Supine lying often eases
Provokes
Ankylosing spondylitis, 'active stage'
15-35
Lumbar; less often unilateral gluteal
Often worst on waking
May aggravate pain already present
Spondylolisthesis
15-35
Lumbar, bilateral sciatica
Prolonged standing provokes
Largely unconnected with exertion
Spinal malignant disease
No particular age Increasing central backache in an elderly patient
(Upper) lumbar, legs; multisegmental distribution
No particular postures, worse at night
Muscle spasm markedly limits movements
pressure. These symptoms are extremely important but are often not mentioned by the patient, so the examiner must enquire about them. Two different syndromes causing paraesthesia must be considered: nerve root compression and pressure on the spinal cord. Pressure on a nerve root results in a typical set of symptoms: pain and paraesthesia, strictly related to the segment involved. Pressure on the dural sleeve of a nerve root causes severe segmental pain. Pins and needles indicate that the nerve fibres are irritated and they are always felt in the distal extremity of the der matome. For this reason, it is vital to determine their exact areas; an accurate dermatomal distribution of paraesthesia is always a better pointer to the affected nerve root than is the pain itself. In external compression of the nerve root, the sheath is compressed before the fibres and pain will therefore appear before paraesthesia. In discoradicular interac tions, the sequence of segmental pain first, followed later by pins and needles and perhaps numbness is therefore an 'inherent likelihood' . If the paraesthesia appear before the pain begins, other lesions such as a neuroma or tumour should be suspected. In lateral recess stenosis, pain and paraesthesia usually appear simultaneously. Also the symptoms do not tend to change over months or years. If the paraesthesiae are painless, disc protrusion is an unlikely cause. Spondylolisthesis, disseminated sclero sis, diabetes or pernicious anaemia are more l ikely. In
Dural symptoms +
+
+
Posture
Exertion
Sitting provokes Walking eases
Bending provokes
these circumstances, pins and needles are also more diffuse. Painless paraesthesia in both feet or in all four limbs suggests compression of the spinal cord. The symptoms extend beyond the borders of innervation of any root or peripheral nerve. Neck flexion may also bring on the pins and needles. DAN G E R TO S4 N E RV E ROOTS
These roots are situated in the midline of the spinal canal, well protected by the posterior longitudinal ligament. In a large posterocentral protrusion, this ligament is placed under increased pressure. Finally the l igament may rupture, so threatening the S4 roots. Because mobility tests for the fourth sacral roots do not exist, it is almost impossible to evaluate their function. The diagnosis should be made entirely on history: pain and/or pins and needles in the perineum, anus or genitals. In a progressing situation, loss of bladder or bowel control and ' saddle' anaesthesia complete the picture, and laminectomy is mandatory. It should be re-emphasized that manipulation is absolutely contra-indicated; even traction is not at all safe if the slightest suspicion of compression of the fourth sacral roots arises. Some patients are timid and do not mention these symptoms. So it is important to ask about them in the next three types of cases in which a large posterocentral protrusion is to be suspected: acute lumbago, acute perineal pain and bilateral sciatica.
808 SECTION TEN - THE LUMBAR SPINE
WHAT I S THE PATIE NT'S REACTION TO THE SYMPTOM S?
History taking should also determine how much the patient is disabled by the symptoms. Some patients are stoical, others react in a hypersensitive way. Before active therapy such as manipulation is instituted, the presence of pronounced psychological factors must be established. For this reason, the patient should be encouraged to relate how far his daily activities are disturbed. La ter, after the clinical examination, how bad the handicap really is can be established. For example, if it is obvious that di sablement is severe for a minimal lesion, it is likely that mental depression is more responsible for the symptoms and should be treated first. It is also unwise to treat actively a patient who seems to have undeniably psychoneurotic behaviour or is involved in a compensation claim. During the history and clinical examination, the exam iner should feel that therapist and patient are on the same side and the patient is strongly motivated towards improvement. If this is not the case, active methods of treatment are to be avoided.
tissue structures on both sides should be symmetrical (Fig. 55.1a). The thoracic and lumbar vertebrae should be vertically aligned. The angles of the scapulae should be level with the seventh thoracic spinous process; the iliac crest should line up with the fourth lumbar verte bra. The lower extremities should more or less share the body load and be in good alignment: the hip joints not adducted or abducted, knees not bowed or knock kneed, feet parallel or toeing out slightly and the cal caneal bones neither pronated nor supinated. From the side (Fig. 55.1b), the curves of the thoracic and lumbar vertebrae should be slightly convex posteri orly and anteriorly, respectively. The pelvis should be in the neutral position, i.e. the anterior superior iliac spines lie in the same vertical plane as the symphysis pubis. Hip, knee and ankle joints should be neither flexed nor hyperextended. T H E PATHOLOG ICA L TRUNK Posterior view
Many lumbar spinal disorders present with asymmetrical posture. Therefore it should be checked whether both iliac crests, the anterior and posterior superior spines and the
INSPECTION
One important feature of this part of the examination is gaining an idea of the degree of disability. The clinician should observe the patient from the moment he or she enters the consulting room. In particular the following are noted : •
• •
•
How does the patient enter the room? A posture deformity in flexion or a deformity with a lateral pelvic tilt, possibly a slight limp, may be seen. How does the patient sit down and how comfortably/uncomfortably does he or she sit? How does the patient get up from the chair? A patient with low back pain may splint the spine in order to avoid painful movements. What is the facial expressions? Is it in accordance with the pain the patient seems to suffer?
Then the patient undresses so that posture can be observed, especially the lower back, pelvis and lower extremities. This is best done in good and uniform light; light falling from a unilateral source will give unilateral shadows, which may give a false idea of shape and posture. THE SHAPE OF T H E NORMAL TR U NK
From the posterior aspect, the shoulders and pelvis should appear level and the bony as well as the soft
(a) Figure 55.1
(b) The shape of the normal trunk.
CHAPTER 5 5 - CLINICAL EXAMINATION 809
greater trochanters are level in relation to each other. I f they ,are not, there may be some 'pelvic torsion'. In this situation, the two liliac bones have rotated slightly in opposite directions. One posterior iliac spine is situated higher than the other, whereas from the anterior side the position of the superior iliac spines are just opposite. A more common reason is some lateral pelvic til t in the frontal plane because of anatomical changes above or below the greater trochanter, such as changes of the femoral head and neck or anatomical leg length discrep ancy from growth disturbance. A deformity of the bones and joints of the leg may also be responsible. (Fig. 55.2a). When a leg length difference is the source of the scoliosis, it is also called static. To diagnose the latter, boards of various thickness are placed under the foot of the shorter limb, until the pelvis becomes horizontal. There is no clear evidence as to the significance of dif ferences in leg length in the generation of spinal symp toms. If a platform under the shorter limb eases or even abolishes the pain while standing or on lumbar flexion or extension, a raised heel is advised. Some physicians rec ommend correction of any kind of leg length inequality. However, in a study in people of working age, Soukka et a/4 could not establish mild leg length inequality (5 mrn or less) as a factor contributing to low back pain. They further concluded that the risk of low back pain did not substantially increase with an inequality of 10-20 mm. Correction is therefore only of importance in recurrent attacks of lumbago and in the presence of a difference of more than 20 mm. It is possible that correction of such a difference may decrease the shearing strain on the affected intervertebral joints.
L5-S1 seldom result in marked lateral deviation, because of the stabilizing action of the iliolumbar ligaments on the joint, although some pelvic tilt remains possible. In lumbar disc displacements, six possible types of deviation (sciatic scoliosis) exist: •
•
•
Static scoliosis
(Fig. 55.2b). In a primary, so-called sciatic scoliosis, caused by painful disorders in the lower lumbar spine, correction in this way will not alter the deviation, showing that it is intrinsically lumbar. Sciatic scoliosis
(Fig. 55.2c). The curve of an idio pathic scoliosis, present since childhood, differs from the tilt of the spine associated with recent disc problems in that it is accompanied by a lower thoracic or lumbar rotation deformity. If this is not evident in the erect posture, it will become obvious during flexion. A so called razor back eminence of the thoracic cage is then easily seen.
Idiopathic scol iosis
(Fig. 55.2d). In a psychogenic scolio sis, the wrong level is held fixed: although the pain is alleged to be lumbar, the patient holds neck, shoulders and thoracic spine in deviation whereas the lumbar spine remains vertical In disc lesions, gross lateral deviation usually results from displacements at the L4 or L3 levels. Disc lesions at
Psychogenic scoliosis
• • •
Towards the painful side. This shows that the displacement is situated medially, i .e. at the axilla of the nerve root. Away from the painful side. In this case the protrusion lies lateral to the nerve root, which is drawn away by the deviation of the trunk. Alternating deviation. This demonstrates that the dura mater slips from one side to the other of a small midline protrusion. It is also diagnostic of a protrusion at the fourth lumbar level. Deviation standing, which disappears during flexion. No deviation when standing erect but marked deviation on attempted trunk flexion. This is often seen in root pain. A momentary deviation when the trunk is flexed halfway. The patient is seen to deviate suddenly at a particular moment during flexion, returning to a symmetrical posture as this point is passed. Usually pain is felt at the moment of deviation but occasionally it is not. This sign indicates that a fragment of disc alters its position at the back of the intervertebral joint and temporarily touches the dura mater.
Lateral view
Together with anterior pelvic tilt, this is often the result of weak abdominal muscles but it also compensates for a flexion deformity of the hip joint in cases of gross osteoarthrosis.
Increased l u m b a r lordosis.
This is typical in acute lumbago. A large posterior projection accounts for a block at the back of the joint; any attempt to straighten the back results in a painful squeezing of the dura mater by the subluxated fragment. The patient stands in flexion deformity, with or without a lateral pelvic tilt. Kyphotic posture.
In young patients, this is characteristic of ankylosing spondylitis or adolescent osteochondrosis. In the elderly, it may indicate osteitis deformans or senile osteoporosis. Exaggerated thoracic kyphosis.
This is caused either by gross thinning of two adjacent discs or by a wedge-shaped fracture of a vertebral body, which may result from osteoporosis, tuberculous caries, neoplasm or osteitis deformans. The sign thus calls for a radiograph.
Ang u l a r kyphosis.
Flattened back. Patients with lumbar spinal stenosis or lateral recess stenosis usually present with a flattened back. They stay in a slightly stooped position, eliminating the normal lumbar lordosis.
8 1 0 SECTION TEN - THE LU MBAR SPINE
Figure 55.2 Types of scoliosis: (a) static; (b) sciatic; (c) idiopathic; (d) psychogenic.
(a)
(b)
(c)
(d)
If this is not compensated by an equally excessive thoracic kyphosis, it is suggestive of spondylolisthesis. The whole spine lies in a plane ante rior to the sacrum. This is characterized by a mid- or low lumbar shelf at the spinous processes which, if not visible, can be palpated: when the hand slides gently downwards along the spinous processes, it engages the Excessive
lordosis.
step at the fourth or fifth level (Fig. 55.3b). In concealed spondylolisthesis the shelf disappears during recum bency and radiography in this position may not reveal the displacement. Reduction of the space between the i l iac crest ar'ld the
This indicates disc-space narrowing at consecutive levels or marked osteoporosis.
thoracic cage.
C H APTER 55 - CLI N ICAL EXA M I N AT I O N 8 1 1
(a)
(c)
Muscles Wasting . Wasting of the paraspinal muscles is rare but may indicate chronic inflammatory disease, such as ankylosing spondylitis or tuberculosis, or point to poliomyelitis or a myopathy. It may also be seen after a previous spinal operation because of denervation. Marked wasting of the calves, hamstrings or the buttock occurs in fifth lumbar and first sacral root palsy. In severe arthritis of the hip, the buttock, hamstrings and quadriceps will show visible wasting.
Asymmetric spasm of the paraspinal or gluteal muscles, making them stand out compared to the normal side, is an ordinary finding in discodural or discoradicu lar problems and is then accompanied by an adaptive Spasm .
(b)
Figure 55.3
Palpation of the iliac crests (a), shelf (b) and muscle spasm (c).
posture in flexion or in side flexion. In slight cases, the difference in tension can be palpated (Fig. 55.3c). However, spasm of the sacrospinalis muscles, holding the lumbar spine in lordosis, is suggestive of serious disease such as metastasis. Muscle spasm, accompanied by visible flexion and / or lateral deformity is also a very bad prognostic sign in sciatica. The protrusion nearly always proves irreducible and laminectomy is the only successful measure. Skin and hair
A midline dimple or tufts of hair may suggest a variety of congenital, osseous or neurological disorders. In over 80% of all cases of occult spinal dysraphism, excess hair is present in the midline.
8 1 2 SECTION TEN - T H E LU M BAR S P I N E
The colour of the skin may be an indication of vascular disorders. If the foot turns a dusky red on standing but blanches on elevation, advanced arterial obstruction is present. If this is associated with a painful limb, intermittent claudi cation is a real possibility. In Sudeck's atrophy, the dependent ankle and foot are almost black. :fUNCTIONAL EXAMINATION
i v,," M 1.
•
I
_ ,-
l
'
. "r
��• • '
Y
.
Table 55.3 Summary of lumbar movements performed standing Movement
Pain and/or limitation
Disorder
Extension
Painful limitation
Large protrusion Small protrusion + spondylosis Spinal stenosis + spondylosis Serious disease
Painless limitation
Spondylosis Long-standing ankylosing spondylitis Vertebral hyperostosis
Pain at full range
Small protrusion Ligamentous lesion Capsular lesion Sacroiliac joint lesion Hip joint lesion
Deviation
Strong suggestion of disc protrusion
Painful limitation of both side flexion movements
Serious disease Ankylosing spondylitis
Painless limitation of both side flexion movements
Spondylosis Advanced osteoporOSis Osteitis deformans
Painful limitation of one side flexion move men
Large disc protrusion, L4 Serious extra-articular lesion
Pain at full range
Small disc protrusion Minor fracture Sprained ligament Capsular lesion Muscular lesion
Painful arc
Disc lesion
Painful limitation
Large disc protru�ion Serious disease (+ limitation of both side bending movements) Major lesion at the buttock
Painless limitation
Spondylosis
Pain at full range
Small disc protrusion Sprained ligament Capsular lesion Injured muscle Sacroiliac joint lesion Minor lesion at the buttock Hip jOint lesion
: ,
I.
Before the examination of lumbar movements is begun, the patient should be asked if there is pain at this moment and, if that is so, to point out its site. If pain free, the usual location is indicated. If this is in the upper lumbar or lower thoracic area, i.e. the 'forbidden' area, one should be on the alert (Fig. 55.4). Serious conditions such as neo plasm or caries are often situated there. It is also an area in which pain may occur in aortic aneurysm or visceral disease. Disc lesions at this area are extremely rare. In order to avoid missing important findings, an orderly scheme of examination must be followed in which different tests are successively performed stand ing, supine and lying prone.
Side flexion
EXA M I N ATION STA N D I N G Procedure
Four active movements are examined while the examiner watches the patient from behind: backward bending, side bending to each side and forward bending (Fig. 55.5 and Table 55.3) completed at full range by neck flexion.
Flexion
I
�:� (\' : /"1 I
..
--�
•
•
Figure 55.4 The 'forbidden' area.
Painful arc
Disc protrusion
Deviation
Large disc protrusion Large intraspinal lesion
Extension is recorded by noting the accentuation of the lumbar curve, as well as how far the patient, can lean back before the pelvis tilts . Lateral flexion is measured by determining how far the patient can run his or her hand down the side of the
CHAPT E R 55
C LI N I CAL EXAM I N AT I O N 8 1 3
(c)
(a)
(e)
(d) Figure 55.5
•
-
Examination standing: (a) backward bending; (b, c) forward bending; (d, e) side bending.
leg. At full range the lumbar spine should be curved uniformly in both directions. The patient is not allowed to bend forward or backward while performing the movement. The range of forward flexion is assessed by noting the distance of the fingertips from the floor. When
complete body flexion has been attained, the lumbar spine is flattened or in young people even slightly convex. As forward being puts an increased load on a patho logical disc, causing a persistent ache that obscures the responses to other movements, it is preferable to examine
8 1 4 SECT I O N TEN - T H E L U M BA R S P I N E
this movement last. However, i n ligamentous disorders and in stenosis of the spinal canal, bending forward may be pain free or may cause only minor discomfort. The patient is also asked to flex his or her neck when ever forward bending becomes painful or at the full range of flexion. This movement stretches the dura by traction exerted from a distance and pulls it painfully against any anterior projection lying in front of it. Pain provoked on neck flexion is a normal finding in cases of a large posterior bulging, for example, a disc protrusion in acute lumbago. Movements shoul d be performed smoothly and gradually. Any deviation and I or restriction is noted and painfulness ascertained. The range of lumbar movements is maximal between 2 and 13 years of age (Fig. 55.6) As a movement is performed, the patient should tell the examiner when he or she feels the pain and where. A painful arc should then be sought by asking for an increase in the range to the point at which the pain may disappear. Such a painful arc is pathognomonic for a disc lesion.
whereas the others are not, or are less painful (Fig. 55.7). If there is l imitation of range, its degree is unequal and corresponds with the degree of pain. The severity of the signs depends on the size of the displacement. The most striking example of the partial articular pattern is an attack of acute lumbago from a gross discodural interaction. Although all movements commonly hurt, pain and limitation on one movement will be more serious than in the opposite direction. A distinctive asymmetry is present. Pain may be felt centrally or unilaterally, depending on the position of the protrusion. If the attack of lumbago is caused by a posterocentral displacement, flexion and extension are very painful and grossly restricted, whereas side flexion is only painful at the end of the range. In a gross unilateral protrusion one side flexion may be com-
Findings
After testing the four lumbar movements, one of the following patterns may emerge: • • • • •
A partial articular pattern (PAP), with or without deviation. A painful arc of movement. End of range painful. Full articular pattern. Full range, no pain.
Partial a rticular pattern. This i s very suggestive of inter nal derangement and strongly suggests a disc protrusion. So one or more of the lumbar movements are painful,
Figure 55.6
Lumbar lateral flexion diminishes with age.
Figure 55.7
-
Examples of partial articular patterns.
_._---
CHAPT E R 5 5 - C L I N ICAL EXAM I N ATION 8 1 5
pletely blocked and painiul, together with flexion and extension, whereas side flexion to the opposite side is not limited and causes only slight discomfort. In backache caused by internal derangement some movements are slightly limited or only painiul at their extremes, and others are normal. Restriction of move ment is not as striking as in acute lumbago. Rarely lesions of the posterior arch, i.e. posterior liga ments and capsules of the facet joints, cause a partial articular pattern but neither restriction nor a painful arc is to be expected here. Spinal deviation is also absent. Painful a rc. A painful arc may occur during or on the way back from forward bending or side bending. It always means that a fragment of disc shifts, jarring the dura mater momentarily via the posterior longitudinal liga ment. Sometimes a painiul arc exists when the trunk passes the vertical on swinging from one side to the other. The sign is usually associated with a partial articular pattern but it can also be an isolated finding. Sometimes there is only a painless momentary devia tion, which implies an arc unnoticed by the patient; a fragment of disc alters its position at the back of the inter vertebral joint, without touching the dura mater. A painless click is a sign of abnormal articular displacement that is insufficient to irritate sensitive structures. It is not defined as an arc and its clinical significance is unclear. The finding of a partial articular pattern together with a painful arc leads to three important conclusions: • •
•
Convergent
It is never psychogenic. It is pathognomonic of a disc protrusion - the dura comes into contact with the protrusion and slips over it. It indicates that the protrusion is small and reducible.
This is a common symptom in a small disc protrusion. However, it can also be the result of stretching an injured muscle or a sprained ligament or capsule. The discovery that resisted move ment in the opposite direction is painless excludes the muscles. In a sprained ligament there is never a painful arc, and dural signs or root signs are absent. The move ment that is supposed to stretch a ligament is also pre dictable: in sprain of the supraspinous and interspinous ligaments, full flexion is painful. If the iliolumbar liga ments are sprained on one side only, side flexion away from that side is painful, although there may also be pain on full flexion or on full extension. In a capsular lesion of one of the apophyseal joints, movements also cause pain at the end of the range but now a convergent or divergent pattern is to be expected. This means that in a left-side joint, extension and side flexion to the left or flexion and side flexion to the right are painiul (Fig. 55.8). Pain at the end
of movement.
Divergent Figure 55.8
Pain (coloured side) at the end of movement.
However, it should be remembered that posterior dysfunction syndromes of the facet joints are rare. This diagnosis should therefore never be made without confirmation by diagnostic local anaesthesia. F u l l a rticu l a r pattern (Fig. 55.9). If all movements are painiul and / or restricted in a uniform pattern, arthritis, arthrosis, fracture or malignant disease is suspect. In this respect, age and habitus are very important. Therefore gross limitation in every direction is quite normal in an elderly person but in adolescence it is usually a sign of serious disease. The typical example is a patient with ankylosing spondylitis who has a flat lumbar spine combined with bilateral limitation of side flexion and gross rigidity on forward flexion. The same limitations are present in
8 1 6 SECT I O N TEN - T H E L U M BA R S P I N E
•
•
Figure 55.9
Full articular pattern.
patients may complain of bilateral sciatica as well. Inspection often shows a mid or low lumbar shelf. 'Bruised'dura mater or dural sleeve. These patients have started with an ordinary attack of lumbago and / or sciatica. There is a constant ache in the back or the limb, unaltered by movement or posture and most often worse at night. Epidural local anaesthesia abolishes the symptoms for a time, which indicates a dural origin. The injection may also be a very effective therapeutic measure . Spinal stenosis. Pain comes on only during standing and walking. Lumbar movements, except perhaps extension, do not provoke the pain. But if the patient is asked to stand for a while, vague symptoms of lumbosciatica arise, which cease when the back is flexed. There is some clinical similarity with spondylo listhesis causing symptoms itself; however the patient is much younger.
Interpretation
tuberculosis of the disc or vertebra, malignant or benign neoplasms, Paget's disease and chronic osteomyelitis. The finding of a full articular pattern is therefore often a warning sign and an indication for technical in vestiga tions. F u l l range. without pain. Sometimes none of the four lumbar movements causes any discomfort. This may occur in the following circumstances. •
•
•
•
History of a lumbar disc lesion but without displacement at the time of examination is a well-known event in patients presenting with a self-reducing type of disc lesion. Every morning the patient awakes comfortable and able to bend the back in every direction without any pain. After some hours the back begins to ache. Seen early in the morning, all clinical tests are nega tive for such a patient. Another example is the patient who is seen some days after an attack of acute lumbago. Because of spontaneous recovery all symp toms may have been lost and no disc protrusion is present at the time of examination. Pain referred to the back in cases of visceral disease. If pain is not aggravated by activity or relieved by rest, which is usually the case in activity-related disorders, this is an important feature. A careful history usually elicits other symptoms. Ligamentous postural syndrome. The pain is only pro voked after standing or walking for a long time. Spinal movements are painless for the simple reason that the stress applied during the tests is not sufficient to induce the pain. Spondylolisthesis without a disc lesion. This disorder resembles the ligamentous postural syndrome but
Extension. The movement is initiated by contraction of the paravertebral muscles, whereas the iliopsoas and abdomi nal muscles relax smoothly to allow the movement to its extreme. During extension the respective surfaces of the inter vertebral joint tilt. This reduces the vertebral interspaces posteriorly and drives the nucleus anteriorly which is checked by the anterior fibres of the annulus and the anterior longitudinal ligament.
In acute lumbago, extension is usually completely blocked because of a large posterocentral protrusion. This limita tion is part of a gross partial articular pattern. In sciatica, if trunk extension is considerably limited by severe pain shooting down the back of the limb, the prognosis is very poor and laminectomy is almost always indicated. Painful /imitation as part of a partial articular pattern.
Painful limitation as part of a full a rticular pattern.
Elderly patients normally show painless limitation of extension as the result of spondylosis. However, if a disc lesion is superimposed, extension may also become painful. The presence of a full articular pattern with bilat eral painless limitation of side bending and, to a lesser degree, forward bending, makes it obvious that two dis orders are present: osteophytosis together with a small disc protrusion. Serious disease is thus excluded and this is confirmed if a radiograph of the spine is obtained. A similar picture may be seen in spinal stenosis. There are symptoms of vague lumbosciatica, sometimes together with paraesthesiae and numbness, increased on exten sion but often relieved by flexion. These patien ts are usually elderly and extension is therefore also limited as the result of degeneration.
CHAPTE R 5 5
In lateral recess stenosis, extension may provoke pain and / or paraesthesia in one leg only. Painful limitation of extension may also indicate ankylosing spondylitis. In this disorder, both side flexions will also be very restricted. Painless limitation. In middle-aged or elderly people, painle�s limitation of extension results from osteophyte formatJon and / or diminished intervertebral joint space. In long-standing ankylosing spondylitis, pain ceases hel ,: : b?n� ankylosis is complete. Then not only exten SIOn IS hmlted but also both side flexions. The anatomical abnormalities in vertebral hyperostosis (Forestier disease) also create increasing stiffness in the spine of the elderly. These patients, however, rarely have significant disability or pain.
In unilateral backache because of a disc protrusion, a common pattern is for extension to be of full range and painful centrally, whereas flexion causes ��ilate�al pain, at the region of the posterior superior Ihac spme or in the buttock. In third lumbar root pain, the root is stretched on extension and relaxed on flexion. Therefore extension is usually painful and flexion often produces relief. In sciatica, extension sometimes causes pain in the lower limb instead of the back. If the patient is under the age of 60, manipulation will almost certainly fail. Central and localized pain on full extension sometimes result from local periostitis at a spinal process. This is easily proved by local anaesthesia at the painful spot. Unilateral pain at the upper sacroiliac region or in the groin on full extension may result from a lesion of the iliolumbar ligaments. It then is usually found together with pain on side flexion away from the painful side and possibly with pain on flexion. In backache caused by a lesion of the capsule of a facet joint, a convergent pattern may be expected: as well as extension, side flexion towards the pain will also produce pain at the end of range. It is sometimes difficult to find the source of the problem if trunk extension creates pain felt in the buttock or the lower limb. It is obviously non-muscular in almost every instance, because at the end of range the sacrospinalis and buttock muscles are relaxed. So when the pain is felt in one buttock only, its origin may be in the lumbar spine, the sacroiliac joint or the hip joint. When it is combined with segmental pain over the front of the thigh, the lesion must originate in the third lumbar �e.gment: a third lumbar disc lesion or arthritis at the hip J � mt. They can be differentiated by performing an exten SIOn movement of the lumbar spine after flexing the hip to 90° a position that avoids extension strain falling on t�e hip joint. If the pain is felt at the back of the thigh, the fifth lumbar and the sacroiliac joint are likely to be Pain on full range.
-
-
CLI N I CAL EXAMI NATI O N 8 1 7
strained. Further investigation will then differentiate between these two locations. Deviation. Sometimes the lumbar spine is seen to deviate slightly during extension so as to avoid pain. This invol untary manoeuvre strongly suggests a disc protrusion. Side flexion. This movement is initiated by the para vertebral muscles, the psoas major and the external and internal oblique abdominal muscles on the same side. Contralateral muscles relax smoothly, controlling the movement. At the end of the range the thorax and iliac crest approximate laterally. The vertebrae tilt towards the si�e of flexion. At the same time the nucleus pulposus is dnven to the opposite side, checked by the lateral part of the annulus fibrosus. Painful limitation of both side flexion movements. Cyriax stated that: 'Al l serious diseases of the lumbar spine result in limitation of the range of both side flexion movements'. The finding of this sign should be treated as a warning sign in young and midd le-aged patients. Malignant and benign neoplasm, tuberculosis, chronic osteomyelitis, ankylosing spondylitis and fractures are strongly suspected. Painless limitation of both side flexion movements. This is a normal finding in the elderly and associated with spondylosis, advanced osteoporosis or osteitis defor mans; extension and flexion will also be restricted. Painful limitation of one side flexion movement. This usually results from a large unilateral protruSion. The joint is blocked at one side only. At the fourth or third lumbar level, these protrusions usually are associated with a lateral deviation of the lumbar spine on standing and lying. If side flexion away from the symptomatic side is painful and limited, manipulative reduction is likely to gIve a good result, although it may take special tech niques and several sessions to produce a lasting cure. In contrast, if side flexion towards the painful side hurts in a patient under the age of 60, manipulation often fails and traction is more likely to succeed. If this move ment also causes pain in the lower limb instead of in the lumbar region or the upper buttock, reduction is almost certain to fail. If ross limitation of side flexion away from the painful . ? SIde IS the only positive finding, a serious extra-articular lesion must again be suspected. Abdominal neoplasm or a neuroma at the lumbar or lower thoracic level com monly shows this warning sign. Pain a t full range. Together with a partial articular pattern, this indicates internal derangement at an inter vertebral joint, and the earlier remarks in relation to manipulative treatment remain the same. However, the
8 1 8 SECTION TEN - T H E L U M B A R S P I N E
absence o f any limitation means that the protrusion is small and also ind icates that manipulation should succeed more quickly. Pain at the end of side flexion exceptionally arises from a fracture, a muscular lesion or a sprained ligament. •
• •
In a lesion of the sacrospinalis or quadratus lumborum (rare), pain results from stretching the injured muscle. Resisted side flexion in the opposite direction is also painful, whereas passive side flexion in this direction can be expected to be painless. A minor fracture of a transverse process or a lower rib has the same clinical pattern as a muscle lesion. In unilateral posterior ligamentous dysfunction syndrome, side bending away from the painful side suggests a lesion of either the contralateral iliolumbar ligament or the capsule of a facet joint. In the former anteflexion and extension may also be painful, whereas a facet joint is apt to show a divergent pattern of painful movements: apart from side flexion, forward flexion is painful at the end of range.
Painful arc. A painful arc on side flexion indicates a disc lesion, usually at the fourth lumbar level. An arc may present as a slight momentary pain when the patient moves his trunk from one side to the other. Alternatively the arc may be quite extensive, preventing the patient from moving, unless he is encouraged. Flexion. This is a complex movement that influences not only the lumbar spine and its neural contents but also the sacroiliac and hip joints. The movement is initiated by contraction of the iliopsoas and abdominal muscles. It then proceeds due to the force of gravity, the paraverte bral muscles, gluteal muscles and hamstrings relaxing smoothly to allow the movement to be carried out to its extreme. At the end of the range, the vertebral column is stabilized only by the passive action of vertebral liga ments fixed to the bony pelvis. Bending forward causes pelvic rotation together with flexion of the lumbar spine. Normally a smoothly graded ratio exists between the degree of pelvic rotation and that of lumbar flattening. This constitutes the 'lumbar-pelvic rhythm', which is difficult to quantify. However, at any phase of body flexion, the extent of lumbar curve flatten ing must be accompanied by a proportional degree of pelvic rotation around the transverse axis of the two hip joints. During these movements, a posterior shift of the hips in a horizontal plane takes place simultaneously, in order to maintain balance, an integral part of the pelvic portion of the lumbar-pelvic rhythm. The rhythm is dis turbed if any of the component parts lacks function.s
In an acute and severe discodural interaction, pain grossly limits trunk flexion because the weight of the body on forward bending further increases Painful limitation.
the size of the protrusion. In addition, this movement also stretches the dura and draws it strongly forward against the protrusion. Flexion of the neck performed at the moment of maximum lumbar flexion further stretches the dura from above and therefore increases the pain. Flexion may also be limited by root pain. If this is the only sign, it usually indicates a primary posterolateral protrusion such as that found in young adults. The sign is then regarded as a root sign rather than an articular sign. In secondary posterolateral protrusions, trunk flexion may also be painful and limited because of pain felt posteriorly in one leg. Commonly, howevel� this sign is associated with pain felt in the lower back or upper buttock on one or two other lumbar movements. Again, neck flexion may provoke or increase the pain in the limb, as it draws the nerve root structures more against a projection into the spinal canal. Fixation in lordosis. During flexion the lumbar spine may stay fixed in lordosis because of spasm of the sacrospinalis muscles. If both side bending movements are also markedly limited, serious disease is to be expected, such as neoplasm, tuberculosis, osteomyelitis or ankylosing spondylitis.
Central or unilateral pain in the low back on full flexion is a common articular sign found in most cases of backache and results from a small midline protrusion contacting the dura mater. It is usually accompanied by pain on some of the other spinal movements as part of a partial articular pattern. Rarely, localized central pain is caused by a sprained supra- or interspinous ligament. The only clinical findings are then pain at the end of flexion and extension. If pain on full flexion is felt on one side and at the level of the sacroiliac joint or the buttock, a small disc protrusion compressing the dura unilaterally is likely. However, this must be differentiated from a lesion of the sacroiliac joint, hip joint or gluteal structures, all of which are also stretched at the end of flexion. A strained iliolumbar ligament may be a possible source of unilat eral pain. Side flexion away from the painful side is then also painful. An inflamed capsule of the facet joints may give rise to local unilateral pain, perhaps with slight ref erence to the upper buttock. Side bending away from the painful side is painful - the divergent pattern. A painful reaction on extension and side flexion to the painful side is more common - the convergent pattern. It should be noted that, if the accessory movement of neck flexion, performed at the moment of full flexion, provokes or increases the pain in the back or buttock, all l igamentous, facet joint, sacroiliac or hip lesions �an be excluded. This sign points to a space-occupying lesion in the spinal canal contacting the dura mater. Pain at the end o f ra nge.
C H APTE R 55
-
CLIN ICAL EXAMI NATI ON 8 1 9
In elderly people limitation of flexion, in combination with limitation of extension and both side movements is normal and results from spondylosis. However, if a small lesion (disc or ligament) is superim posed on this condition, flexion is also painful. In L3 root compression, flexion is usually full and painless, because this movement relaxes the nerve.
Painless limitation.
A painful arc on flexion always means that a fragment of disc shifts, jarring the dura mater halfway through the movement. The pain disappears when the patient continues forward bending. Painful arc.
Lateral deviation of the spine together with lateral pelvic tilt also points to a disc lesion and sug gests a large protrusion. It is caused by the way the spine accommodates such a protrusion, preventing it from pressing on the dura mater or the dural investment of the " nerve root. In unilateral pain, although standing upright symmetrically, the spine sometimes deviates on flexion. Patients may also present with a deviation while stand ing upright. On bending forwards, the tilt to one side either increases or disappears. In other patients the devi ation alternates, one way on bending forward, the other way on straightening up, the implication being that the dura mater has to be held to one or other side of the small projection.
Lateral deviations.
The last test in the standing position is rising on tiptoe, which examines the strength of the calf muscles and thus the integrity of the S1 / S2 segment. The patient is invited to perform the test, first on the good then on the bad leg. The examiner steadies the patient with both hands, without taking any weight. Inclining the body forward and flexing the knee is evidence of weakness (Fig. 55.10). This test is best repeated several times in order to discover those cases with only slight weakness. Rising on ti ptoe.
Warning Standing
• Impossible to stand for a moment because of severe pain • Full articular pattern • Limitation of the range of both side flexion movements in young and middle-aged patients • G ross limitation of side flexion away from the painful side as the only positive finding • Fixation in lordosis during flexion together with marked limitation of both side flexion movements.
EXAMINATION S U PI N E
The patient i s asked to lie supine. The way he o r she moves to get on the couch should correspond to his or her previous performance and to the information
Figure 55. 1 0
Rising o n tiptoe.
gained from the history. In suspected exaggeration or 'malingering', careful observation of the patient's atti tude can be informative. For example, turning from a sitting to a supine position places particular strain on the low back, and especially in acute lumbago it can be expected that the patient will use the support of their arms. The move on and off the couch also means that the psoas muscles must be in good condition. If the patient, before lying down, is able to sit on the couch with their legs stretched out, straight leg raising must be of ful l range. Other discrepancies will be d iscussed in Section 16. Sacroiliac joints
Pain in the buttock frequently results from disorders of the lumbar spine. However, in disorders of the hip or sacroiliac joint, the pain may be experienced in the same area. To resolve this puzzling phenomenon and to exclude sacroiliac disorders, a specific test should be done to exert tension on the capsule and ligaments of the sacroiliac joint without affecting the lumbar spine or the hip joint. Distraction of the iliacs is the best basic test that fulfills this condition. The sacrioiliac joints are tested as follows.
820 S E CTI O N TEN - T H E LU M BAR S PI N E
The examiner places the hands o n the anterior superior spines of the ilium with the arms crossed (Fig. 55.11). Pressure is exerted in a downward and outward direction and should be evenly distributed to prevent moving the lumbar region. In a positive test, a deep-seated unilateral ache is evoked at the gluteal and / or posterior crural area. In acute lumbar pain syndromes, it may be necessary to perform this test with the patient's forearm supporting the low lumbar area. In this way, the lumbar segments are better prevented from moving into flexion. This measure also prevents a tender part of the sacrum or of one of the posterior superior iliac spines from being pressed painfully against the couch. Confirmation of unilateral pain strongly indicates sacroiliitis or strain of the anterior sacroiliac ligaments. In contrast, if the patient states that the pain is felt centrally, it is clear that this is irrelevant, because it is impossible for a unilateral structure to refer pain centrally. Probably it has more to do with the appear ance of referred tenderness at the dorsal part of the sacrum, which is pressed against the couch. Discomfort at the anterior superior iliac spines can also be ignored. The distraction test at the sacroiliac joint is very sensi tive. If a patient has symptoms referable to these joints, this manoeuvre will always elicit them. The test is extremely important clinically. Usually there is almost nothing in the nature and extent of sacroiliac pain that distinguishes it from a disc protru sion compressing either the dura mater or the dural extent of the Sl and S2 nerve roots. The fact that the pain probably comes and goes i rrespective of posture and exertion, or often changes sides, draws attention to the possibility of sacroiliac arthritis. To make the matter more confusing, a cough also hurts because the increase in abdominal pressure painfully distracts the ilium from the sacrum. Also, routine clinical examination does not usually differentiate sacroi liac arthritis from a disc lesion: the lumbar movements may increase the pain a
little at ful l range; flexion can be very painful and even limited; and straight leg raising may also prove to be painful. It should therefore not be surprising that the diagnosis is easily missed and that patients are often treated on the assumption that a disc lesion is present, which may even lead to unnecessary laminectomy. Moreover, a normal radiographic appearance of the sacroiliac joints does not always exclude an arthritis, for symptoms may precede the radiological evidence by months or even years. It is therefore vital never to forget the sacroiliac d istraction test during routine lumbar examination. Even in the slight cases of arthritis or after subjective recovery, the test remains positive. A positive test indicates that more investigations should be done, by performing other clinical tests dealt with in Section 1 1 . Radiography, CT and the erythrocyte sedimentation rate are useful technical investigations. Hip joints
After testing the sacroiliac joints, three basic tests are per formed to examine the hip joints. These are necessary to d ifferentiate between the lumbar spine and the hip joints as causes of obscure pain in one buttock and / or the anterior thigh. First, the uninvolved side is tested over its range, for end-feel and possible pain on flexion, lateral and medial rotation. The thigh is moved into flexion until it touches the abdomen (Fig. 55.12a). The movements of rotation are tested while the hip joint is held in 90° of flexion. One hand stabilizes the femur at the knee, the other is placed at the distal end of the lower leg and performs the rotation movement (Fig. 55.12b, c). In minor lumbar lesions, none of these movements usually hurts at the back. In a patient with severe lumbar pain, some of these tests may also provoke pain in a minor way. Indeed, at the full range of hip flexion, both the lumbar spine is flexed and traction exerted slightly on the sciatic nerve roots. Breig and Troup7 stated that full medial rotation at the hip stretches the sciatic nerve trunk and may cause ache in the buttock in the presence of sciatica. The same applies to the sacroiliac joints. Moving the hip joint beyond full range involves the next link of the moving chain - the sacroiliac joint ':" and may evoke sacroiliac pain. Full lateral rotation at the hip stretches the anterior sacroiliac ligaments and full medial rotation has the same effect on the posterior liga ments (see Ch. 63). Straight leg raising test
Figure 55. 1 1
Testing the
sacroiliac joints.
The straight leg raising (SLR) test is performed to esti mate the mobility of the dura mater as well as the dural investments of the nerve roots at the fourth lumbar to second sacral segments.
CHAPTER 55 - CLINICAL EXAMINATION 821
careful study 1 5 of those between 35 and 55 years of age showed a downward movement of 1 .5 mm for the fourth lumbar root, 3 mm for the fifth and 4 mm for the first sacral root. This work also confirmed that the third lumbar root, just as the third and fourth sacral roots, do not shift during the manoeuvre. In a study of 50 consecutive surgical patients with clin ical and radiographic evidence of lumbar disc herniation, it was shown that straight leg raising was the most sensi tive preoperative physical diagnostic sign (96% ) for correllating intraoperative pathology of lumbar disc heniation. The sign has also been helpful in diagnosing discodural backache. 1 6
(a)
of the test. However, the significance of neither the presence nor the absence of the signs should be overestimatedY SLR as an isolated phenom enon has n o diagnostic significance and must always be interpreted in association with other clinical fin dings. As can be seen in Box 55.5, limitation of the mobility of nerve roots and dural tube is not pathognomonic for a d isc lesion. Conversely, a completely painless SLR does not exclude a disc lesion. Circumstances that produce a negative test i n discoradicular problems are:
Significance
•
(b) • • •
Cases where the nerve root emerges a little higher up in the foramen and does not come into contact with the protrusion. Protrusions at the second or third lumbar level. The third and fourth sacral nerve roots are not influenced by the manoeuvre. Minor protrusions interfere only slightly with the dura mater and therefore do not influence its mobility.
lesions. During SLR any space-occupying lesion situated at the anterior wall of the vertebral canal at the fourth and fifth lumbar and the first and second sacral segments may interfere with the dura mater and / or the nerve root structures and thus
Intraspinal space-occupying
(c)
Box 55.5 Stra ight leg raising (SLR) --
Figure 55.12
rotation.
Testing the hip joints: (a) flexion; (b) medial rotation; (c) lateral
This test was first presented by JJ Frost in 1 881 with reference to his teacher, Ernest Charles Lasegue. Frost proposed the test to aid in distinguishing hip from sciatic pain.s Later, a number of workers7,9-11 demonstrated that this movement exerts tension on nerve roots and dural tube. The mobility of the nerve roots at the intervertebral foramen has also been investi gated and shows a range of 2-8 mm on SLR1 2-1 4. A H istorical note.
The SLR test may be positive in:
Intraspinal lesions Discogenic Protrusion Non-discogenic Tumour Neuroma
Extraspinal lesions Sacroiliac joint lesions Major lesions at the buttock Major lesions at the hip j oint Lesions of the hamstring muscle belly Non-organic disorders
822 SECTI O N TEN - T H E LU M BAR S PI N E
painfully limit the movement. This often results from disc protrusion but is also seen in tumours and neuromas. However, the sign is absent in lateral recess stenosis and hypertrophic apophyseal joints, where pressure is exerted from behind, which may affect the dural invest ment of the nerve roots but does not influence their mobili ty. Indeed, duri ng SLR nerve roots are dragged not only downwards but also forwards, and for this reason escape the pressure that comes from behind. The examiner should be on guard against apparent cases of acute lumbago without any dural signs. A pathological fracture, osteomyelitis or Calve's disease should be suspected. These non-mechan ical disorders do not influence the dura, which in turn results in a negative SLR.
Apparent acute lumbago.
In these, SLR is also always of full range, because the movement cannot pull directly on these rootS. 1 2 However, the root pain in a lesion at these levels may be aggravated on full SLR. Traction on the root is then caused via a pull on the dura from the roots below. Disc lesions at the second or third lumbar level.
It is also possible for tightness of the hamstrings to limit the manoeuvre. Limitation of motion, sometimes up to 50°, together with posterior thigh pain, may be experienced. By raising the leg on the other side, a similar degree of tightness differentiates from true muscle spasm, when the muscles contract defensively because of involvement of the dura and I or nerve roots. Hamstring tightness.
Straight leg raising may also be painful, though not limited, in these
Painful disorders of the sacroiliac joint.
Figure 55.13
Straight leg raising.
d isorders. At full range the sacrotuberous and sacrospinous ligaments, as well as the superior and infe rior bands of the anterior sacroiliac ligament are tight ened. I S From this point, the sacrum and the iliac bone move together, which also puts a rotational strain on the joint at the contralateral side. Major lesions at the buttock. These also influence the manoeuvre of SLR, for example, osteomyelitis or neo plasm at the ilium or the upper femur, fractured sacrum or chronic septic sacroiliac arthritis. In these conditions, SLR is painful and slightly limited, whereas passive hip flexion with the knee flexed is more limi ted and much more painful. This striking pattern of physical findings is known as the 'buttock sign' (see p. 1007). Perform ing the test. Before testing, it should be assumed that there is at least 90° of flexion at the hip joint, other wise conclusions cannot be drawn. Then the leg is lifted from the anatomical position upward by supporting the foot at the calcaneus. To prevent the knee from bending, the other hand is placed on its anterior aspect (Fig. 55.13). From 15 to 30°, tension is exerted on the sciatic nerve. This in turn pulls on roots L4, L5, SI and S2 and the dural tube, which is stretched from below. The patient should not be allowed to rotate the pelvis forwards or to abduct and externally rotate the leg at the hip, in order to escape painful stretching. The range, end-feel and degree of discomfort are first estimated on the painJess side, then on the painful side. At the end of range, movement is restricted by tension of the hamstring muscles, which exemplifies the constant length phenomenon. At this point, the angle between the
CHAPTER 5 5
leg and the couch varies from 60 to 1 20°. In impaired mobiJity of the dura mater and / or one of the two lower lumbar and upper sacral nerve roots, involuntary spasm of the hamstring muscles abruptly prevents further movement. At this point, the patient may state that pain in the back or leg is reproduced, a sign that the dura or the dural investments of the nerve roots are compressed. The range of movement varies inversely with the size of the space-occupying lesion. However, SLR often causes only slight pain in the back or the leg starting at 60° and the movement may be con tinued up to 90°, which implies that mobility of the dural structures is not really impaired and there is only slight contact. Therefore, the examiner must not fail to force SLR gently, as long as this causes only slight pain and the hamstring muscles do not abruptly terminate the move ment. Otherwise a painful arc may be missed or those unCOmmon cases in which pain begins at, say, 45° but the leg can be moved to 90° without increased discomfort (see Box 55.6 for an outline of the six stages in the straight leg raising test). Pa inful arc. The finding of a painful arc is very important because it proves that a disc lesion is the source of pain and disability. The patient feels a transient pain on the way up or perhaps on the way down. A painful arc may be an isolated finding during SLR but is usually associ ated with pain at the extreme of movement. This sign indicates that the protrusion momentarily catches the nerve root which then slips over it. Such a protrusion is small in size, and therefore manipulation can be expected to succeed quickly. It also implies that the symptoms are not caused by a muscular or ligamentous strain, and that a psychogenic disorder can be excluded.
-
CLINICAL EXAMINATION 823
Cross-leg straight leg raISIng test. This test is positive when moving the uninvolved leg reproduces the com plaints of back or sciatic pain. This results from a move ment of the dura and the contralateral nerve, which is dragged downwards and medially. It strongly suggests an axial localization of the protrusion and points to the fourth lumbar level1 9 but some20,2 1 have failed to correlate the position of the disc protrusion in relation to the root at laminectomy. However, a very high incidence of sequestration or extrusion is seen at operation in patients with cross-leg painP Although the sensitivity of this test is low (about 0.25), it has been established to be a very specific sign (0.90-0.97) in lumbar disc herniation.22
At full range the manoeuvre may also strain the contralateral sacroiliac joint. After taking up all the slack in the ligaments on the uninvolved side, the movement puts a rotational strain at the contralateral joint. Straining the contralateral sacroiliac joint.
At the moment SLR becomes painful, the patient is asked to flex his or her neck, while keeping the trunk still. This often increases the pain by pulling on the dura mater from above, adding tension to the impaired dural structures. This clear 'd ural sign' excludes the possibility of a sacroiliac major buttock or hamstring lesion (Fig. 55.14).
Straight leg raising with neck flexion.
Bragard's test. The presence of nerve irritability can also be confirmed with the manoeuvre known as Bragard's test. The raised leg should be lowered until the pain is relieved. At that position the foot is dorsi-flexed, which causes a recurrence of pain as a result of stretching the sciatic nerve via the tibial nerve.23
Box 55.6 Stages in the straight leg raising test: six stages can be disting u ished and each used as a criterion to ascertain the size of the protrusion Full and painless
This does not exclude disc protrusions. In the supine position these may be too small to make contact with the dura or the dural sleeve and thus these structures can move freely
Pain on full range
A small protrusion is likely
Painful arc
Suggestive of a small protrusion. The dura or nerve root slips over the projection
Painful and limited without neurological deficit
The protrusion is larger, limiting the mobility of the dura or the dural sleeve of one of
Painful and limited with neurological deficit
A large posterolateral protrusion is compressing a nerve root, impairing mobility and conduction. The severity of the palsy takes over from SLR as the criterion of the degree
the lower lumbar or upper sacral nerve roots
of interference Full and painless with neurological deficit
A large posterolateral protrusion has become maximal, compressing the nerve root so intensively that it has become ischaemic and atrophies
824 SECT I O N TEN - T H E L U M BAR S P I N E
Figure 55.14
Modified straight leg raising: with neck flexion.
The 'bo wstring' sign. This is also suggested to be a very reliable test of root tension.9 In this, SLR is carried out until pain is reproduced. At this level, the knee is slightly flexed until the pain abates. The examiner rests the limbs on the shoulder and places the thumbs in the popliteal fossa, over the sciatic nerve. If sudden firm pressure on the nerve gives rise to pain in the back or down the leg, the patient is almost certainly suffering from significant root tension. lumbago and stra i g ht leg raising . The degree of limita tion corresponds to the degree of discodural contact. In large posterocentral protrusions, SLR is limited bilater ally. Unilateral lumbago often restricts the manoeuvre on the affected side only or to a greater degree on that side than on the other. Any change in discodural contact alters the range of SLR instantly. Hence, the sign is very useful in assessing the effect of treatment. So, during a manipulation session, before starting traction, or during a period of bed rest, SLR is a good test for estimating progress without stress ing the lesion. From the moment SLR becomes negative, active movement of the lumbar spine while standing becomes the new criterion for testing. In this position, the intradiscal pressure is raised, which may cause renewed discodural contact. Sciatica and stra i g ht leg raising . The test is also very useful in sciatica but here is used to ascertain the degree of discoradicular compression. If the root is not yet atrophic, the degree of restriction of SLR is proportional to the pressure exerted �:)ll the nerve root. However, from the point at which conduction becomes impaired, which is coupled with neurological signs, the degree of interfer ence affords the new criterion of the size of the protru sion. Indeed, although the protrusion has got larger, restriction of SLR may not have altered or may even have returned to full range. In the latter case, the patient has developed an ischaemic root palsy. The protrusion has
become maximal in size but, as a result of the ischaemia, the nerve root has lost its function, including that of pain conduction. Dural sleeve pain thus ceases and SLR returns to full range. The patient is subjectively better pain free - but the lesion is anatomically worse. The large protrusion will undoubtedly be seen on CT although the SLR test has become negative. Non-organic disorders and stra ight leg raising. The range of SLR must always be compared with the range of trunk flexion on standing. Because intradiscal pressure is higher on standing and bending forward, restriction is expected to be greatest on this test or at least equal to SLR, in which the body weight is off the joint. The con verse does not hold; many perfectly genuine disc lesions restrict trunk flexion but not SLR. Unless this difference is appreciated, patients with medicolegal claims may suffer injustices. However, the inconsistencies likely in psychogenic disorders should be recognized, in order to avoid treat ment of a spinal lesion that does not exist. If there is any doubt, additional tests should be performed to establish such inconsistency. For example, if the patient sits on the couch with the legs outstretched in front, discrepancy between the degree of alleged limitation of SLR and the degree of hip flexion necessary to sit on the couch confirms the suspicion.
Testing the integrity of spinal segmental innervation
'
This is carried out next, by testing motor and sensory conduction of the nerve roots together with tendon reflex activity. This includes examination of muscle strength, sensation and reflexes of the entire lower extremity to detect and locate neurological disorders with relative accuracy. Comparison should always be made with the ' contralateral side. When signs of interference with nerve conduction are found, the degree of involvement should also be esti-
CHAPTE R 5 5
mated. Motor conduction may be found to be reduced but in discoradicular interactions there is seldom com plete paralysis. Detection of such signs is important, both for diagno sis and treatment. Specific motor weakness is the most reliable localizing physical sign of nerve root involve ment. Sensory changes are subjective and are easily affected by the emotional state of the patient. Reflex changes may result from a previous episode of nerve root compression. Disturbance of spinal segmental innervation indi cates that the protrusion is too large and located too far laterally for attempts at reduction by manipulation or traction to succeed. A disc protrusion usually affects one root only. However, because of the obliquity of the lumbar nerve roots, a large protrusion may lie at the interval between two roots, catching the motor part of the upper and the sensory part of the lower root. This clinical observation is seen in L4 protrusions affecting the fourth and fifth roots, as well as in L5 protrusions with palsy of the fifth lumbar and first sacral roots. Impaired conduction of more than two roots is so rare that neoplasm should first be suspected. The same applies to bilateral root palsies. Diffuse weakness of all muscle groups, particularly the psoas muscle, is highly suggestive of a psychological disorder.2, 1 9 (See p. 853.) All tests of conduction should be repeated before each session of manipulation or attempted traction, especially if the patient does not respond in the expected way. It is possible that during the interval between sessions a root palsy develops, which makes further attempts at reduc tion futile.
Figure 55. 1 5
Resisted flexion of the hip.
-
C L I N I CAL EXAM I N ATION 825
Tests for motor conduction.
There are four tests in the
supine position. Resisted flexion o f the hip. This tests the L2 and L3 nerve roots. It is performed with the hip joint flexed to 90° so as to eliminate activity of the rectus femoris as much as pos sible. Both hands are placed at the distal end of the thigh and the patient attempts to resist the strong force applied by the examiner (Fig. 55.15). At the same time, it is neces sary to stabilize the ilium with one knee placed against the ischial tuberosity. If the attempted movement is weak and painful, neo plasm should be suspected. A second lumbar root palsy is hardly ever caused by a disc protrusion (1 in 1000 lumbar protrusions) and serious disease is more likely, for example a neuroma or metastasis. The latter may be located vertebrally or at the upper femur. In a third lumbar root palsy, resisted flexion of the hip is only slightly impaired but there is striking loss of power of the quadriceps.
This tests the L4 nerve root. The patient lies supine with the hips and knees extended. The patient holds the ankle in full dorsi-flexion and should resist the full weight of the examiner's body (Fig. 55.16). Resisted dorsiflexion of the foot.
Resisted dorsiflexion o f the big toe. This tests the L4 and L5 nerve roots. The examiner places the thumb on the nail bed of the great toe and the fingers on the ball of the foot. The patient is asked to resist the examiner's attempt to plantiflex the great toe (Fig. 55.1 7). Resisted eversion of t h e foo t. This tests the L5 and SI nerve roots. One hand stabilizes the ankle at the medial side, the other hand is placed at the outer side of the
826 SECT I O N TEN - T H E L U M BAR S P I N E
Figure 55. 1 6
Resisted dorsiflexion of the foot.
Figure 55. 1 8
• • •
Resisted eversion of the foot.
Big toe and two adjacent toes: L5. Outer border of the foot, together with the two outer toes: S1 . Sole of the heel: S2
Disturbed sensory conduction in both legs is atypical in disc lesions but does occur in spondylolisthesis or neoplasm.
Figure 55.17
Resisted dorsiflexion of the big toe.
forefoot. The patient is asked to resist the examiner's attempt to move the foot into dorsiflexion and inversion (Fig. 55.18). When weakness is present, it is necessary to be aware of efforts to substitute the eversion movement by rotating the leg outward at the hip. It should be emphasized that, in performing these tests, the patient with normal motor nerve conduction will be able to resist the strongest power exerted by the examiner, except in dorsiflexion of the great toe, where the examiner will be stronger. These are performed next. The various areas are compared bilaterally at the same time (Fig. 55.19).
Tests for sensory conduction.
• • •
Front of the thigh: L2. Front and inner side of the lower leg to just above the foot: L3. Big toe alone: L4.
Figure 55. 1 9
Testing for sensory conduction.
CHAPTER 55
-
CLI N I CA L EXAMI NATION 827
Knee reflex text. This may be diminished in lesions of the third- lumbar root. Each knee is raised in turn with one hand and the ligamentum patellae struck with the reflex hammer (Fig. 55.20).
Testing the integrity of the spinal cord
The integrity of the spinal cord should be tested in all patients suspected of an upper motor neurone lesion. Clinical syndromes that suggest this are: • • • • •
Root palsy affecting more than one root, especially if this is bilateral. Backache in the upper lumbar area. Complaint of weakness in both legs. Paraesthesia in both feet. Backache with a spastic gait.
The reverse end of the reflex hammer is run with a firm stroke over the plantar surface of the foot from the calca neus along the lateral border to the forefoot, ending at the ball of the great toe (Fig. 55.21 ). In a positive reaction the great toe extends, while the other toes plantar flex and splay (positive Babinski's sign). In a negative reaction the toes either do not move at all or flex uniformly (negative Babinski's sign). Warning Supine • A positive sacroiliac distraction test • Acute lumbago without any dural signs • B uttock sign • Discrepancy between trunk flexion and straight leg raise • Signs of interference with conduction of more than one root. • L2 root palsy • Bilateral nerve root palsy • Complete paralysis • A significantly warmer foot on the affected side.
Figure 55.21
Testing for Babinski's sign.
Examination of the circulation
This is optional and depends on the history and the findings at inspection. If intermittent claudication is suspected, the pulses of the femoral, posterior tibial and dorsalis pedis arteries should be felt (Fig. 55.22). If the pulse is diminished or absent at the femoral artery the d iagnosis is almost a certainty. Absence of a pulse at the ankle often exists without any vascular disorder. In cases of claudication of the buttock, the internal iliac artery may be blocked on its own and the pulse of the femoral artery is normal (see Section 12). Oedema in one foot is suggestive of venous thrombosis. Local heat is found in patients with inflamed varices and in osteitis deformans of the tibia. Neoplasm at the upper two lumbar levels may interfere with the sympa thetic nerves; if so, the foot on the affected side is significantly warmer than the other. EXA M I NATION IN THE PRO N E- LYING POSITION
This starts with the ankle reflex test. Ankle reflex test
Figure 55.20
Knee reflex test.
The foot is raised by one hand. Then all the slack of the p lantiflexors is taken up by the little finger pushing the foot into dorsiflexion, before striking the Achilles tendon (Fig. 55.23). This reflex is diminished or absent unilaterally in fifth lumbar and first or second sacral root palsy. It is well known that once lost, this reflex does not return in about half the cases. Hence in a new attack of lumbago, the absence of the ankle jerk does not confirm recently impaired root conduction.
828 S E CTI O N TEN - T H E L U M BAR S PI N E
(a) Figure 55.23
Ankle reflex test.
Absence of the reflex on both sides may have no significance but is one of the findings in tabes, malignant disease and spondylolisthesis, when the emerging nerve roots are involved bilaterally. Passive knee flexion
(b)
Next, passive knee flexion is performed to test the mobility of the third lumbar root (Fig. 55.24). In posterolateral disc protrusions at this level, flexion of the knee is painful at its extreme and occasionally limited in range. Pain is felt in the back and / or the ante rior part of the upper leg, depending on whether the test provokes a disco dural or a discoradicular interaction. Wasserman described the manouevre in 1918. It was performed in soldiers with anterior thigh and leg pain where the straight leg raising test was negative. 24 A false-positive femoral stretching test has also been reported in osteoarthritic hip joints, diabetic neuropathy, anticoagulant medication, retroperitoneal haemorrhage and ruptured aortic aneurysm.25,26
(c) Figure 55.22 Feeling the pulses of (a) femoral, (b) posterior tibial and (c) dorsalis pedis arteries.
Figure 55.24
Passive knee flexion.
CHAPTER 5 5 - C L I N ICAL EXAM I N AT I O N 829
Tightness of the rectus femoris may also influence this movement. The patient experiences anterior thigh pain, which must be differentiated from the painful reaction in an L3 nerve root entrapment. By flexing the non-painful side, the degree of pain and limitation can be compared and in this way distinguished from the defensive reflex muscle spasm in an L3 root involvement. During this test, the pull of the rectus femoris on the anterior inferior spine of the ilium forces the lumbar spine into extension, which may also provoke lower lumbar pain. This test is considered positive when flexion of the knee on the asymptomatic side reproduces the symptoms on the affected side. It is hypothesized to be a valid manoeuvre to help in the diagnosis of symptomatic disc herniation.27 However, it i s a far less constant sign, a n d in most third lumbar root lesions stretching is painfu l but not limited. Crossed femoral stretching test.
This tests the 51 and 52 nerve roots. The examiner resists attempted flexion at the same time stabilizing the pelvis (Fig. 55.26). Normally, the examiner is just stronger than the patient. Weakness indicates a lesion of the first or second sacral root. Painful weakness indicates a partial rupture of one of the hamstrings.
Resisted flexion of the knee.
The 51 and 52 nerve roots are tested by asking the patient to contract the buttocks strongly (Fig. 55.27). Weakness is demonstrated by a decreased prominence on the affected side and loss of tone on palpation. Testing the buttock muscles.
.-... �--I Testing motor conduction
There are three tests in the prone-lying position. This tests the L3 nerve root. The examiner tries to resist attempted extension with his flexed elbow, at the same time fixing the upper leg strongly just above the knee (Fig. 55.25). The normal patient is stronger than the examiner. Gross weakness goes together with weakness of the psoas, which is partly supplied by the same nerve root. If weakness is bilateral, spinal neoplasm or myopathy should be suspected. Painful weakness indicates a partial rupture of the quadriceps and, in more obvious instances, a fractured patella. Resisted extension of the knee.
Figure 55.25
Resisted extension of the knee.
Figure 55.26
Resisted flexion of the knee.
Figure 55.27
Testing the buttock muscles.
830 SECT I O N TEN - T H E LU M BAR SPI N E
PA LPATION To detect irreg u l a rities of the l u mbar spinous p rocesses .
The index and middle fingers run quickly down the spine feeling for any abnormal projections (Fig. 55.28). If one is found, it may indicate wedging of a vertebral body or complete loss of two adjacent disc spaces. It should also prompt suspicion of bone erosion of a vertebral body (osteoporosis, tuberculous caries, secondary deposit or an old fracture), which requires radiography. The finding of a shelf, most often at the interspace of L4-L5, or loss of a shelf palpable on examination in the standing position, indicates spondylolisthesis. Pressu re towards exte nsion . Next a series of pressures towards extension are exerted to detect the level of the lesion. Starting at the sacrum each lumbar segment is 'sprung' in turn, and it should be noted at which level pain and muscle guarding are most provoked (Fig. 55.29).
Figure 55.28
Palpation for irregularities of the spinous processes.
Figure 55.29
Pressures towards extension.
In mechanical disorders the expectation is that the painful level is in the lower lumbar area. If the upper lumbar area is the site of pain, the clinician must be on the alert. Serious disease is to be expected and technical investigations are indicated. The test also serves to check the end-feel. In the young, the end-feel should be elastic, whereas in elderly persons it is hard because of spondylosis. A hard end-feel in patients under 40 years old suggests ankylosing spondylitis. Functional examination and palpation are summa rized in Table 55.4. Warning Prone-lying • An abnormal proj ection of one of the spinous processes • Pain and muscle guarding provoked by pressure towards extension in the upper lumbar area • A hard endfeel in patients under forty.
CHAPTER 55 - C L I N I CAL EXAMI NATION 8 3 1
Table 55.4 Summary o f functional examination and palpation ,
Standing
Inspection
Test
Testing
Deviation
In the sagittal plane In the frontal plane (6 types) Level Side Bone Skin Muscle
Pain Irregularities
Lumbar movements
Supine
Range, pain, painful are, deviation Range, pain, painful are, deviation
Flexion (+ neck flexion)
Range, pain, painful are, deviation Range, pain, painful are, deviation
Motor conduction
Rising on tiptoe
S1 and S2
Sacroiliac joint
Distraction
Inflammation of sacroiliac joint
Hip joint
Flexion External rotation Internal rotation
Lesions of the hip joint and buttock Lesions of the hip joint and buttock Lesions of the hip joint and buttock
Mobility of dura mater and nerve roots L4-S2
Straight leg raising
Range Pain Painful arc Crossed straight leg raising Neck flexion 'Buttock sign'
Motor conduction
Resisted flexion of hip joint Resisted dorsiflexion of foot Resisted extension of big toe Resisted eversion of foot
L2 and L3 L4 L4 and L5 L5 and S1
Sensory conduction
Front of thigh Front of thigh, inner side of lower leg Big toe Big toe and adjacent toes Outer border of foot and two outer toes Sole of heel
L2 and L3 L3 L4 L5 S1 S2
..
Prone
Extension Side flexion
Knee reflex
Patellar tendon
L3
Plantar reflex
Plantar surface of foot
Spinal cord
Ankle reflex
Achilles tendon
L5, S1 and S2
Mobility of L3 nerve root
Passive flexion of knee
Range Pain
Motor conduction
Resisted extension of knee Resisted flexion of knee Contraction of buttock muscles
L3 S1 and S2 S1 and S2
Palpation
Lumbar spinous processes
Irregularities
Extension pressure
Sacrum and lumbar vertebrae
Pain End-feel
ACCESSORY TESTS
Finally, the history will sometimes lead to the perform ance of resisted movements. These are particularly desir able when: •
A fracture of the last rib or a transverse process is sus pected after a unilateral injury to the lumbar spine,
•
resulting in a local pain only. Such minor fractures show themselves clinically as muscle lesions and strong contraction of the sacrospinalis muscle pro vokes the pain at the site of the fracture. Radiography confirms the diagnosis. The patient firmly believes a muscle sprain has occurred. However, at the lumbar region this scarcely ever occurs. It is only the combination of painful resisted
832 S E CTI O N TEN - T H E LU M BAR S PI N E
•
extension with painless passive extension that di rects attention to the muscle. However, in some (acute) d isc lesions resisted movements may also provoke pain because of increased compression of the joint. The patient is suspected of psychogenic symptoms. Pain that is provoked by resisted movements is particularly likely in such circumstances. These patients are prone to equate effort with pain. There are three resisted movements (Fig. 55.30).
• • •
Prone lying, resisted trunk extension. Standing, resisted side flexion. Side lying, resisted side flexion.
Trunk extension in the prone position is resisted by placing one hand on the upper thorax posteriorly, the other on the back of the knees. On resisted side flexion with the patient standing, the examiner opposes the movement by applying his hip to the patient's, grasping the latter's far shoulder. Then the patient is asked to bend away from the examiner. In the side-lying position, with the body weight now off the joint, the patient crosses the arms in front of the
.
..... .:. �
..
?"-.� -::.".
(b)
(a) Figure 55.30
(c) Accessory tests: resisted trunk extension and resisted side flexion.
chest; the examiner steadies the patient's thighs during this movement. Then the patient is asked to j ust lift the thorax off the couch.
.
EPIDURAL LOCAL ANAESTHESIA ,
.
..
Cases are sometimes met in which neither the history nor the physical signs clearly indicate one particular lesion. Although examination will show that the symptoms arise from a mechanical disorder, it may be uncertain whether a disc lesion, a disorder of the posterior structures or a sacroiliac lesion is present. The use of local anaesthesia may then be helpful. A weak solution of procaine can be introduced epidu rally via the sacral route. The solution desensitizes the dura mater and the dural investments of the nerve roots. In a discodural or discoradicular interaction, the pain will cease for the duration of the anaesthesia. In addition, epidural local anaesthesia induced for diagnostic pur poses may also yield permanent improvement. Alternatively, if a disorder of the posterior lumbar elements (facet or ligaments) is probable, local anaes-
CHAPTER 55
thesia of the suspected structure should be performed. Five minutes after infiltration the patient is asked to undertake the movements that previously were painful. If these no longer cause distress, the correct area has clearly been chosen and the diagnosis is confirmed. The infiltration must be precise, however, as false inferences may be drawn, a fact that is especially true for the infiltration of facet joints. It has recently been shown that, when relatively large volumes are injected into the facet joint, some extravasation occurs through the thin anterior capsule into the epidural space.28 Facet arthrog raphy confirms that epidural extravasation of dye takes place when more than 2 ml are injected in the facet joint.29 More than this amount of local anaesthetic injected into a facet joint may thus result in an uninten tional epidural block.
TECHNICAL INVESTIGATIONS PLAIN LU M BAR RADIOGRAPHY
Most observations made on plain radiographs are of little or no value.30,3] In particular congenital anomalies, such as transitional vertebra, occult spina bifida and asymmet ric facet orientation are not clinically significant.32 It has also been repeatedly shown that there is no relationship between clinical symptoms and radiological changes associated with degeneration.33-40 The poor diagnostic value of radiographs in patients with low back pain can also be appreciated from the observation that radiographs of the individual with symptoms remain unchanged over time, despite the fact that the symptoms come and go. Because radiographs do not show the posi tion of cartilage, they also are of no value in diagnosing actual disc lesions. Radiographs therefore remain a very poor method of indicating causes of past, present or future low back pain.4] It is common to order routine radiographs to reduce the risk of missing serious disorders. The possibility is in fact slight, and one series of 68 000 spinal radiographs found only 1 in 2500 with serious disorders not suspected clinically.42 In contrast, it should be remembered that serious disease does not always show up immediately on a radiograph - about 30% of the osseous mass of a bone must be destroyed before a lesion is radiologically evident43 - so that too much reliance on the radiographic appearances can give a false feeling of security. In the short term, it is wiser and safer to rely on the history and the clinical examination: if symptoms and signs warrant (i.e. warning signs are found), the patient should be assumed to have a serious disease and, rather than manipulative treatment being undertaken, specific tests should be performed.
-
CLINICAL EXAMINATION 833
A further deterrent in radiographic evaluation of the lumbar spine is that it should be remembered that it is the single largest source of gonadal irradiation.44 The total gonadal dose from a five-view lumbar spine examination is 75 millirads in men and 382 millirads in women45 - unnecessary46 oblique views are responsible for 65% of the irradiation dose.47 Ha1l48 estimated that the gonadal dose in women, when only a three-view examinati on is made, is equal to those of plain radiographs of the chest performed daily over a period of 6 years. Radiographic 'labels' may confuse or bias patients and should never be transmitted to them as statements of disease because there is no evident correla tion between the radiographic appearances and the actual complaints. To the patient, a statement such as 'your back shows a marked degree of arthrosis' means that he is incurable.49 It implies a back that is crumbling like rotten cheese: the situation is definite, incurable and hopeless. The diagnosis of 'osteoarthrosis' condemns the sufferer and many patients become really depressed when they hear that the back is 'worn out'. An anxious or overconcerned patient will then suffer more from the idea that the back is beyond redemption and that no proper treatment for 'osteoarthrosis' exists, than he or she might from the back pain that is experienced. Technical investigation has become a problem rather than an aid. The radiograph does not help the patient, rather it may increase his disability.5o
Conclusion: plain radiographs of the lumbar spine have a very limited value. They have a low specificity, require a high degree of gonadal irra diation in females, are relati vely cost-ineffectives1 and have substantial risk of negative psy chological repercussions in suggestive patients. A clinician should always be very ca reful and restrictive in using radi ography. The results should be interpreted in the context of the normal a geing spine. A negative radiogra phic examina tion does not always exclude serious disease.
OTH E R I MAG I N G STU D I E S
Ever since 1921, attempts have been made t o increase the contrast in imaging between the various structures in the spine. Initially gas was introduced into the subarachnoid space.52 Next, positive contrast myelography with iodized oil solutions was begun in 1922.53 Gross toxic effects from this, including severe arachnoiditis and late meningeal disorders led to the development of safer, water-soluble contrast agents.54 From the early 1940s, lumbar discs have been injected with contrast material in order to detect disc degenera tions and disc ruptures.55 However, discography has
834 SECTION TEN - T H E LUMBAR SPI N E
always been controversial. In the past decade, several authorities have seriously questioned its use: it is painful, expensive and without diagnostic value;56 the sensitivity, specificity and predictive value are less good than myel ography, CT and MRI,57 and the risk of postdiscography disci tis is high.58,59 Discographic studies are therefore considered obsolete.60,61 Recently, high-resolution CT and MRI have in many ways revolutionized the diagnosis of spinal disorders. These techniques not only visualize the bony anatomy and pathological features of the spine but can also confirm disc displacements or bony stenosis. They have therefore become the foundation of diagnostic imaging of the spine. Unfortunately, for a variety of reasons, the ability to visualize spinal disorders has not solved the diagnostic problems and the therapeutic dilemmas. First, CT and MRI are highly sensitive but relatively unselective. In other words, these techniques have a very high prevalence of abnormal findings in images of asymptomatic individuals; postmortem studies show the existence of large, symptomless disc protrusions in almost 40% of cadavers;62 myelograms in asymptomatic patients show defects in 37%;63 CT scans in subjects over 40 years of age show abnormality in more than 50% .64 Also MRI studies demonstrate the high incidence of disc degeneration in asymptomatic patients.65-69 'To get a MRI scan to see if there is anything wrong with the spine' is therefore usually the beginning of a very dangerous process'?o Second, the accuracy of CT and MRI i n anatomical diagnosis i s between 8 3 and 87% . 71,72 Although additional imaging techniques are strongly indicated for the evaluation of patients presenting with warning symptoms and signs suggestive of neoplastic or infectious disorders, they have only limited value in the diagnosis of mechanical disorders of the lumbar spine. 73 It can not be stressed enough that the excessive reliance on diagnostic studies without precise clinical correlation can lead to erroneous (and disastrous) treat ment. The diagnosis of most spinal disorders depends on a detailed history and physical examination. So does the treatment. The increased tendency that has devel oped over recent years to recommend operation in the presence of a positive CT scan is a major error. Given the high number of asymptomatic disc protrusions, many patients will go forward to an unnecessary operation. The presence of a disc protrusion and its size are unim portant; it is the impact of the protrusion on the sur rou nding pain-sensitive structures that determines management. Imaging can usually not d istinguish symptomatic from asymptomatic disc herniation in that
it is usually unable to detect the degree of inflammation, the degree of pain or the functional impact on a nerve. Clinical examination can do so provided it is intelli gently interpreted.
E LECTRO DIAG NOSIS
The use of electromyography (EMG) was introduced 50 years ago,?4 Refinement of the technique, together with additional testing procedures (electrodiagnosis), now make it possible to analyse and document nerve root dys function (level, degree and chronicity),?5 Though it is the only laboratory study that directly assesses the physio logical integrity of the roots, the test will not be helpful in patients with so-called non-compressive radiculopathy?6 the protrusion compresses only the dural nerve root sleeve and not the fibres. Also, EMG examination is very time dependent. Studies may be falsely negative if they are performed too early or too late in the course of sciatica. When it is done before sufficient fibrillation potentials have developed throughout the muscle, the result will be normal. This will also be the case in chronic radiculopathies, when muscles have been completely reinnervated. In addition, the cause of the process leading to the denervation cannot be determined. Fu rthermore, in severe compressive neuropathies, the (serious) func tional loss is detected easily during a proper clinical examination. These factors cause electrodiagnosis to have very low specificity and sensitivity,?7 This diagnostic tech nique is therefore not important in lumbar disorders, except when an objective documentation of the physiological integrity of the lumbar roots is required, which is sometimes the case when there are medicolegal implications.
Conclusion: • Additional imaging modalities are highly sensitive and relatively unselective • There is a high prevalence of abnormal findings on images of asymptomatic individuals • (T and M R I techniques are extremely important in the evaluation of patients with symptoms and signs of non mechanical (neoplastic or infectious) disorders • In mechanical lesions, excessive reliance on diagnostic studies without precise clinical correlation can lead to erroneous (surgical) treatment
CHAPTER 55 - CLI N I CAL EXA M I NAT I O N 835
REFERENCES <
1 . Korst v d JK. Gewrichtsziekten. Boh.n, Scheltema & Holkema, 2. MacNab 1 . Backache. Williams & Wilkins, Baltimore, 1979. 3. Barbor R. Treatment for chronic low back pain. Proceedings of the rvth International Congress on Physical Medicine, Paris, 1964. 4. Soukka A, Alaranta H, Tallroth K, Hellovaara M. Leg-length inequality in people of working age. Spine 1991;16(4):429-43l . 5 . Cailliet R . Low Back Pain Syndromes, 2nd edn. FA Davis, Philadelphia, 1975.
1 048-1055. 3 1 . Sanders HWA et al. Klinische betekenis van degeneratieve afwijkingen van de lumbale wervelkolom en consequenties van het aantonen ervan. Tijdschr Geneeskd 1 983;127:1 374-1385. 32. Park WM. The place of the radiology in the investigation of low back pain. Clin Rheum Dis 1 980;6:93-132. 33. Splithoff CA. Lumbosacral junction: rontgenographic compari
6. Laslett M. The reliability of selected pain provocation tests for
son
of
patients
with
and
without
backache.
JAMA
1 953;152: 1 6 1 0-1613.
sacroiliac joint pathology. Spine 1994;19(11 ) : 1 243-1249. 7. Breig A, Trou p JDG. Straight-leg raising. Spine 1979;4:242. 8. Dijck P. Lumbar nerve root. The enigmatic Eponyms. Spine
34. Fullenlove TM, Williams AJ. Comparative rontgen findings in symptomatic and asymptomatic backs. JAMA 1 957;168: 572-574.
1984;9(1) :3-6. 9. De Buermann W. Note sur un signe peu corum de la sciatique. Reserches experimentales. A rch Physiol Norm PathoI 1884;16:375. 10. Fajersztajn J. Ober das gekreuzte Ischias Phanomen. Wien Klin
35. La Rocca H, MacNab 1. Value of pre-employment radiographic assessment
of
the
lumbar
spine.
Can
Med
Assoc
J 1969;101:383-388. 36. Wiltse LL. The effect of the common anomalies of the lumbar
Wehnschr 1901;14:4 l . 1 1 . Smith MJ, Wright V. Sciatica and the intervertebral disc. J Bone
spine upon disc degeneration and low back pain. Orthop Clin
North Am 1971;2:569-582.
Joint surg 1958;40A:1401. 12. Inman VT, Sounders JB. Clinico-anatomical aspects of lumbo
37. Magora A, Schwartz A. Relation between the low back pain syndrome and X-ray findings. scand J Rehabil Med 1976;8:
sacral region. Radiology 1942;38:669. 13. Falconer MA, McGeorge M, Begg CA. Observations on the cause and mechanism of symptom production in sciatica and low back pain. J Neurol Neurosu rg Psychiatry 1948;11: 1 3-26. 14. Charnley J. Orthopaedic signs in the diagnosis of disc protru
1 1 5-125. 38. Torgeson WD, Dotler WE. Comparative rontgenographic study of the asymptomatic and symptomatic lumbar spine. J Bone
Joint surg 1976;58A:850-853. 39. Wiesel SW, Bernini P, Rothman RH. The aging lumbar spine. In:
sion. Lallcet 1 95 1 ; i : 186-192. 15. Goddard MD, Reid JD. Movements induced by straight-leg raising in the lumbo-sacral roots. J Neural Neurosu rg Psychiatry
Diagnostic Studies in Evaluating Disease and Aging in the Lurnbar Spine. Saunders, Philadelphia, 1982. 40. Dabbs VM, Dabbs LG. Correlation between disc height narrow
1 965;28:12. 16. Supic MD, Broom MJ. Sciatic tension signs and lumbar disc herniation. Spine 1994;19:1 066-1 069. 1 7. Kosteljanetz
30. Frymoyer JW, Newberg A, Pope MH et al. Spine radiographs in patients with low back pain. J Bone Joint surg 1 984;66A:
Utrecht, 1980.
M,
Bang
F,
Schmidt-Olsen
ing and low-back pain. Spine 1990;15:1 366-1369. 41. Van Tulder MW, Assendelft
S.
The
clinical
significance of straight-leg raising (Lasegue's sign) in the diag nosis of prolapsed lumbar disc. Spine 1 988;13(4):393-395. 18. Kapandji IA. The Physiology of the Joints. Volume 3; The Trunk and
radiographic
findings
and
WJJ,
Koes B, Bouter LM. Spinal
nonspecific
low
back
pain;
a
systematic review of observational studies. Spine 1 997;22: 427-434. 42. Brolin I. Product control of lumbar radiographs. Uikartidnil1gen 1975;72:1 793-1795.
Vertebral Column. Churchill Livingstone, 1974. 19. Cyriax J. Textbook of Orthopaedic Medicine, vol I, Diagnosis of Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982.
43. Edelstyn GA, Gillespie PG, Grebbel FS. The radiological
20. Edgar MA, Park WM. Induced pain patterns on passive
44. Liang H M , Katz I N , Frymoyer JW. Plain radiographs i n evalu
straight-leg raising in lower lumbar disc protru sion. J Bone Joint
ating the spine. In: Frymoyer JW (ed) The Adult Spine. Raven
21. Rothman RH, Simeone FA. The Spine, 2nd edn. Saunders, Philadelphia, 1988:602. 22. Oosterhuis HJGH. Fysische diagnostiek - lumbosacrale radicu laire prikkelingsverschijnselen. Ned Tijd Geneeskd 1990;143(12): 612-620.
45. Shaigetoshi A, Russell W. Dose to active bone marrow, gonads and skin from rontgenography and fluoroscopy. Radiology 1971;101 : 669-678. 46. Rhea JT, DeLuca SA, Llewellyn HJ, Boyd RJ. The oblique view: an u nnecessary component of the initial adult lumbar spine
23. Reilly BM. Practical Strategies in Outpatient Medicine. Saunders, Philadelphia, 1 984. 24. Estridge MN, Rouhe SA, Johnson NG et al. The femoral stretch ing test. A valuable sign in diagnosing upper lumbar disc herniation. J Neurosurg 1982;57:813-8 1 7. 25. Calverly JR, Mulder DW. Femoral neuropathy. Neu rology
examination. Radiology 1 980;134:45-47. 47. Scavone JG, Latshaw RF, Weidner WA. Anteroposterior and lateral radiographs: an adequate lumbar spine examination.
AJR 1981;136:715-717. 48. H a l l
FM.
Overutilization
of
radiological
examinations.
Radiology 1976;120:443-448. 49. Rockey PH, Tompkins RK, Wood RW, Wolcott BW. The useful
1960;10:963-967. 26. Cianci PE, Piscatelli RL. Femoral neuropathy secondary to retroperitoneal hemorrhage. JAMA 1969;210:1100-11 0 1 .
P,
Young-Hing K e t a l . Crossed femoral stretch
ing test. A case report. Spine 1996;21:1 584. 28. Morane R, O'Connell D, Walsh MG. The diagnostic value of facet joint injections. Spine 1988;13:1407-1410. 29. Dory M. Arthrography of the lumbar facet joints. Radiology 1981;140:23-27.
tions. Clin RadioI 1967;18: 1 58.
Press, New York, 1991 :302.
surg 1974;56B:658.
27. Kreitz BG, Cote
demonstration of skeletal metastases: experimental observa
ness of X-ray examinations in the evaluation of patients with back pain. J Fam Pract 1978;7:455-465. 50. Verjaal A. De Rugpijnpatient bij de neuroloog. In: Kingma MJ, Verjaal A, Weijel JA (eds). R ugpijn. De Erven Bohn, Amsterdam, 1973:46-62. 5 1 . Liang M, Komaroff AL. Rontgenograms in primary care patients with acute low back pain: a cost-effectiveness analysis.
A rch Intern Med 1982;142 : 1 1 08-1112.
836 S E CT I O N T E N - T H E LU M BAR SPI N E
52. Jacobaeus He. O n insufflation o f air into the spinal canal for
diagnostic purposes in cases of tumors in the spinal canal. Acta
Prevalence of lumbosacral intervertebral disc abnormalities
Med Scand 55:555-564. 53. Siccard JA, Forrestier IE. Methode general d'exploration radio
logique par I'huile iodee (Lipiodol). Bull Mem Soc Med Hop Paris 1 922;46:463-469. 54. Grainger RG, Gumpert J, Sharpe OM, Carson J. Water soluble
lumbar radiculography: a clinical trial of Dimer-X, a new con trast medium. c/in Radial 1971 ;22:57-62.
on MR images in pregnant and asymptomatic non-pregnant women. Radiology 1989;170 : 1 25-128. 67. Boden SO, 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. 68. Buirski G, Silberstein M. The symptomatic lumbar disc in
55. Lindblom K. Protrusions of the discs and nerve root compres
sion in the lumbar region. Acta Radial Scand 1 944;25:1 95-21 2 . 5 6 . H o l t Jr, EP. The question of lumbar discography.
j Bone joint
patients with low-back pain. Magnetic resonance imaging appearances in both a symptomatic and control population.
Spine 1993;1 8 : 1 808-1 81 1 . 69. Jensen Me. Brant-Zawadzki MN, Obuchowski N , Modic MT.
Surg 1 968;50A:720-726. 57. Gibson
symptomless women. Lancet 1 986;Dec 13:1 366-1367. 66. Weinreb JC, Wolbarsht LB, Cohen JM, Brown CE, Maravilla KR.
MJ, Buckley J, Mawhinney R. Magnetic resonance
imaging and discography in the diagnosis of disc degeneration: a
Magnetic resonance imaging of the lumbar spine in people without back pain. N Engl j Med 1994;331:69-73.
comparative study of 50 discs. j Bone joint Surg 1 968;68B:369-373.
70. Boden SO. The use of radiographic imaging studies in the
58. Fraser RD, Osti OL, Vernon Roberts B. Discitis after discogra
evaluation of patients who have degenerative disorders of the
phy. j Bone joil7t Surg 1 987;69B:31-35. 59. Sachs BL, Vanharanta
H, Spivery MA.
lumbar spine. j Bone joint Surg 1 996;78 A : 1 1 4-124. Dallas di scogram
description: a new classification of CT / discography in low back d isorders. Spine 1987;12:287-294.
60. Shapiro R.
tomography. Spine 1984;9:552-556. 72. Zsernavicky J, Juppe M. A comparison of myelography and
Lumbar discography: an outdated procedure.
j Neurosurg 1 986;64:686-691 .
computer tomography in lumbar disc herniation. Intel'll Orthop 1 989;13:51-55.
6 1 . Nachemson A . Lumbar discography - where are we today?
73. Frymoyer JF, Gordon S.
New Perspectives in Low Back Pain.
Am Acad Orthop Surg, Park Ridge, 1988:45-47.
Spine 1 989;14:555-557. 62. MacRae DL. Asymptomatic intervertebral disc protrusion.
Acta
74. Shea
PA, Wood s WW, Werden DH.
Electromyography in
diagnosis of nerve root compression syndrome. Arch Neural
Radial 1 956;46:9. 63. Hi tselberger WE, Whitten
71. Bell GR, Rothman RH, Booth RE. Study of computer assisted
RM. Abnormal myelograms in
asymptomatic patients. J Neurosurg 1 968;28:204. 64. Wiesel SW, Tsourmas N, FeHer HL, Citrin CM, Patronas N. A
study of computer-assisted tomography: 1 . The incidence of
Psychiatry 1 950;64:93-104. 75. Glantz RH, Haldemann S. Electrodiagnosis. In: Frymoyer JW
(ed) The Adult Spil7e, Raven Press, New York, 1991 :541-548. 76. Wilbourn AJ, Aminoff MJ. AAEE Minimonograph 32: the elec
positive CAT scans in all asymptomatic group of patients. Spine
trophysiologic examination in patients with radiculopathies.
1984;9:549-551 .
Muscle Nerve 1988;11 : 1 099-1 1 1 4 .
65. Powell Me. Wilson M, Szypryt P, Symonds EM. Prevalence of
lumbar disc degeneration observed by magnetic resonance in
7 7 . Hudgins WR. Computer-aided diagnosis of lumbar disc herni
ation. Spine 1983;8:604-6 1 5 .
CHAPTER CONTENTS ,
Definitions
Lumbar instability
837
838 Inert structures 838 Contractile structures 838 Neuromuscular control 838
Anatomy
Classification of lumbar instability
839
Instability and the clinical concept of mechanical lesions of the lumbar spine 840
Segmental instability and discodural interactions 840 Segmental instability and ligamentous lesions 840 Segmental instability and the stenotic concept 840 841 Clinical observations 841 Radiological observations 841 Bracing 842
Diagnosis of lumbar instability
Tr�atment of lumbar instability
Sclerosant treatment Surgery 844
843
842
Although lumbar instability is considered to be responsi ble for the majority of chronic or recurrent backaches, the word 'instability' is still poorly defined. There exist a number of different definitions but as yet there are no clear and validated clinical features by which instability might be diagnosed. It is also not clear how instability as such might set up pain and disability. It is generally accepted that instability does not cause any trouble but predisposes to other conditions such as (recurrent) disc displacements, strain of the posterior ligaments and the zygapophyseal joints and nerve root entrapment.
DEFINITIONS At the most simple level, instability is a lack of stability, a condition in which application ot' a small load causes an inordinately large, perhaps catastrophic displacement.1 This is also the description given by the American Academy of Orthopaedic Surgeons who state: 'Segmental instability is an abnormal response to applied loads, characterized by motion in motion segments beyond normal constraints'.2 A biomechanically more accurate definition of segmental instability, using a 'neutral zone' concept has been pro posed by Panjabi. The neutral zone concept is based on the observation that the total range of motion (ROM) of a spinal motion segment may be divided into two zones: a neutral zone and an elastic zone (Fig. 56.1).3 The neutral zone is the initial portion of the ROM during
Stress
Figure 56.1 In segmental instability, the stabilizing system is unable to maintain the spinal neutral zone (NZ) within the physiological limits ROM, range of motion. .
837
838 SECTION TEN - THE LUMBAR SPINE
which spinal motion is produced against minimal inter nal resistance. The elastic portion of the ROM is the portion nearer to the end-range of movement that is pro duced against substantial internal resistance. Segmental instability is thus defined as a decrease in the capacity of the stabilizing system of the spine to maintain the spinal neutral zones within the physiological limits in order to prevent neurological deficit, major deformity and/ or incapacitating pain.4 This definition describes joints that early in range and under minor loads may exhibit excessive displacement. The clinical definition of instability is: 'a condition in which the clinical status of a patient with low back problems evolves, with the least provocation, from the mildly symptomatic to the severe episode'.s Others consider instability to exist only when sudden aberrant motions such as a visible slip or catch are observed during active movements of the lumbar spine or when a change in the relative position of adjacent vertebrae is detected by palpation performed with the patient in a standing position versus palpation performed with the patient in a prone position.6
ANATOMY In order to be clinically useful, the structures that are responsible for instability must be specified. The stabiliz ing system of the spine can be conceptualized as consist ing of passive (inert) and active (contractile) parts and a neural control system. INERT STRUCTURES
The passive subsystem consists primarily of the vertebral bodies, discs, zygapophyseal joints and joint capsules and spinal ligaments. The passive subsystem plays its most important stabilizing role in the elastic zone of spinal ROM (i.e. near end-range)? and numerous studies have been conducted that demonstrate the relative con tributions of passive structures to segmental stability. The posterior ligaments of the spine (interspinous and supraspinous ligaments), along with the zygapophyseal joints and joint capsules and the intervertebral discs are the most important stabilizing structures when the spine moves into flexion.8-11 End-range extension is stabilized primarily by the anterior longitudinal ligament, the ante rior aspect of the annulus fibrosus and the zygapo physeal joints.12,13 Rotational movements of the lumbar spine are stabilized mostly by the intervertebral discs, the zygapophyseal joints and, for the L4-LS and LS-Sl segments, also the iliolumbar ligaments.14 Injury to the inert stabilizing system may have impor tant implications for spinal stability. Intervertebral disc
degeneration, weakening of the posterior longitudinal ligaments and early degeneration of the facet joints may increase the size of the neutral zone, increasing the demands on the contractile subsystem to avoid the development of segmental instability.3 CONTRACTILE STRUCTURES
The active subsystem of the spinal stabilizing system includes the spinal muscles and tendons and the thoracolumbar fascia that contribute to stability in two ways. The first and lesser mechanism is to pull directly against the threatened displacement (which is of course not possible if the latter is a fragment of disc). The second, and more important, contribution is indirect: whenever the muscles contract, they exert compressive loads on the spine, which in turn achieves a stabilizing effect. In other words by compressing joints in a neutral position, muscles may make it less easy for joints and discs to move. During the last decades, a variety of studies have doc umented the stabilizing effect of muscles on the lumbar spine.IS-I8 The lumbar erector spinae muscle group pro vides most of the extensor force required for many lifting tasks.1 9 Rotation is produced primarily by the oblique abdominal muscles. The multifidus muscle seems to be able to exert some segmental control and is therefore pro posed to function as a stabilizer during lifting and rota tional movements of the lumbar spine.2o The role of the oblique abdominal and transversus abdominis muscles in spinal stability has been the subject of much debate. The abdominals have been thought to play a stabilizing role, either by increasing intra-abdominal pressure or by creating tension in the lumbodorsal fascia.21 NEUROMUSCULAR CONTROL
The neural control system may also play an important role in stabilization of the spine. Panjabi describes the stability system as being composed of an inert spinal column, the spinal muscles and a control unit.22 In this model, changes in spinal balance resulting from position and load are monitored by transducers embedded in the ligaments that relay the information to the control unit. When the conditions that challenge spine stability are detected, the control unit activates the appropriate muscles to protect, restore or avoid instability. Evidence for this hypothesiS is found in studies showing that patients with low back pain (LBP) often have persistent deficits in neuromuscular controp3,24 This hypotheSis was further supported by a recent electromyographic study demonstrating that a primary reflex arc exists from mechanoreceptors in the supraspinous ligament to the multifidus muscles. Such a reflex arc could be triggered
CHAPTER 56
-
LUMBAR INSTABILITY 839
by application of loads to the isolated supraspinous liga ment; which in turn initiates activity of the multifidus muscles at the level of ligament deformation as well as one level above or below.25 Anterior
Posterior
CLASSIFICATION OF LUMBAR INSTABILITY The major categories of segmental instability are shown in Box 56.1.26 Tumours, infections and trauma are beyond controversy. They produce mechanical weaken ing of the anterior columns and can be diagnosed by medical imaging and by biopsy. Spondylolisthesis is a more controversial category. The condition is rarely pro gressive in teenagers or adults and can therefore be con sidered as stable in these age groupS.27 However, it has been: suggested that concurrent occurrence of severe disc degeneration at the level of listhesis may lead to progression of slip and turn an asymptomatic and stable lesion into a symptomatic one.28 More difficulties arise with respect to so-called ' degen erative instability'. The ageing of the lumbar spine has been discussed thoroughly (see Ch. 51). Grossly, it occurs in three sequential phases: dysfunction, instability and restabilization.29 During the early phase of degeneration (dysfunction), small annular tears and early nuclear degeneration appear in the disc and ligamentous strains develop in the posterior ligaments and in the capsules of the zygapophy seal joints. The unstable phase includes reduction of the disc height, gross morphological changes in the disc and laxity of the spinal ligaments and facet joints. These changes lead to increased and abnormal range of move ment and to increased liability to disc displacements. During the restabilization phase, further physiological changes in the disc, such as increased collagen and decreased water content, together with the development of spinal osteophytes and gross osteoarthrosis of the zygapophyseal joints result in an increased stiffness of the spine and consequent stabilization (Fig. 56.2). Biomechanical studies, both in vivo and in vitro have confirmed this hypotheSiS: loss of stiffness, accompanied by annular tears or even nuclear disruption have been produced in the laboratory by repetitive loading cycles Box 56.1 Lumbar segmental instabilities: classification
1. 2. 3. 4. 5. 6.
Fractures and fracture dislocations Infections involving anterior columns Primary and metastatic neoplasms Spondylolisthesis in children Degenerative instabilities (Progressive scoliosis in children)
Dysfunction phase
loss of turgor
Ligamentous strain
Early degeneration
II
Unstable phase
disc
Instability
degeneration
III Restabilization phase
Ligamentous elongation
osteophytes/
Osteophytes/
disc resorption
facet enlargement
Stabilization
Figure 56.2 The three sequential phases in the degenerative process of the lumbar spine.
which simulate normal human exposures.3D In other experiments, load applications to degenerative segments have revealed loss of stiffness, sometimes with quite dra matic results.31 However, difficulty remains in translating these anatomical and functional changes into clinical descriptions that could serve as a basis for diagnosis and treatment. A further classification system for degenerative lumbar instability (see Box 56.2), based on a combination of history and radiographic findings, has been proposed.32
primary instability is one where there has been no prior intervention or treatment which might account for the development of the process. A secondary instability involves surgical destruction of one or more of the restraining elements of the spine. Secondary instabilities may develop after discec tomies.33 decompressive laminectomies, spinal fusions and chemonucleolysis.34
• A
•
Box 56.2 Degenerative lumbar instabilities Primary instabilities Axial rotational Translational Retrolisthetic (Scoliotic) Secondary instabilities Post-disc excision Post-laminectomy Post-fusion Post-chemonucleolysis
840 SECTION TEN - THE LUMBAR SPINE
Rotational instability is still a hypothetical entity and so far normal radiological limits have not been identified.35 Translational instability is the most classical and best known of primary degenerative instabilities. It is char acterized by excessive anterior translation of a vertebra during flexion of the lumbar spine. In an early stage it presents with disc space narrowing and traction spurs: in a later stage it represents degenerative spondylo listhesis. However, an terior translation is a normal component of flexion and the difficulty that arises once again is to set a limit of normal translation: many asymptomatic individuals exhibit anterior slips of more than 3 mm;36 4 mm of translation occurs in 20% of asymptomatic patients.37 Retrolisthesis develops when degeneration of the disc and the consequent decrease in disc height force the zygapophyseal joints into extension (see eh. 51, p. 734). Again it has been shown that similar appearances occur in asymptomatic individuals.38 Therefore, the simple detection of retrolisthesis on a radiograph is not an operational criterion for instability.
INSTABILITY AND THE CLINICAL CONCEPT OF MECHANICAL LESIONS OF THE LUMBAR SPINE Segmental instability by itself is not painful and a subject with clear radiological signs of instability may be com pletely unaware of the condition. However, an unstable segment makes the spine more vulnerable to trauma; a forced and unguarded movement may be concentrated on the hypermobile segment and produce a posterior disc displacement. Repeated injuries may also produce chronic irritation of posterior structures such as liga ments and zygapophyseal joints. An anterior or posterior shift of a vertebra may narrow the lateral recess to such a degree that the respective nerve roots become com pressed. Spinal instability is not a painful condition but may predispose to secondary lesions: • • •
Ligamentous sprain Recurrent discodural interactions Nerve root compression in a narrowed lateral recess.
SEGMENTAL INSTABILITY AND DISCODURAL INTERACTIONS
It can be postulated that a hypermobile segment may pre dispose to recurrent disc displacements leading to recur rent or chronic discodural interactions. Pain arises not from instability of the segment itself but from the insta bility of a fragment of disc lying within it.
The typical history is usually that of recurrent back pain, which begins either suddenly or gradually depend ing on the consistency of the shifted fragment ('nuclear' or 'annular') (see p. 791, Dural concept). There are bouts of backache a few times a year and between the attacks the patient is fit and the back is painless. However, the slightest sudden movement or unaccustomed posture leads to a new discal shift resulting in a renewed disco dural interaction and pain. It is obvious that in this case treatment should not solely be addressed to the reduction of the displaced frag ment of disc but that also treatment of the instability should be undertaken. SEGMENTAL INSTABILITY AND LIGAMENTOUS LESIONS
Postural ligamentous pain appears when normal liga ments are subjected to abnormal mechanical stresses (see p. 773, Ligamentous concept). This may occur during the dysfunction stage: some loss of turgor in the disc and the decrease in intervertebral joint space causes some laxity of the segment and an increase of the neutral zone. The facet joints override with the upper articular processes sliding downwards over the lower. The joints adopt the extension position and the posterior capsules become overstretched. As instability proceeds, more tension is imposed on the ligaments and the facet joint capsules, leading to more postural ligamentous pain. The patient is usually a young adult, complaining of diffuse backache, with bilateral radiation over the lower back and the sacroiliac joints. The pain typically starts after maintaining a particular position for a long time and the intensity of the pain depends on the duration of the position. By contrast, there is absolutely no pain during activity or sports and all lumbar movements are free. SEGMENTAL INSTABILITY AND THE STENOTIC CONCEPT
Instability and the subsequent retrolisthesis may narrow the radicular canal and subsequently compress the nerve root (see p. 785, Stenotic concept). Usually the process results from a combined anterior pressure exerted by a buckled posterior longitudinal ligament and a posterior compression of the superior articular process. The mech anism is as follows: considerable narrowing of the inter vertebral disc space causes the posterior longitudinal ligament, which contains some fragments of remaining disc tissue, to bulge dorsally. This is especially the ca§e in the standing or lordotic position. Because of the inclina tion of the facet joints, narrowing of the disc and increased laxity of the segment also result in retrolisthesis
CHAPTER 56
of the upper vertebra which brings the nerve root in close contact with the tip of the anterior articular process of the vertebra below (Fig. 56.3). The history is of a middle-aged or elderly patient with unilateral or bilateral sciatica. The pain comes on during standing or walking and disappears on sitting or bending forwards. DIAGNOSIS OF LUMBAR INSTABILITY The term 'segmental instability' is often abused and it has become fashionable to label any lumbar pain that is aggravated by movement as lumbar instability. The statement: 'you suffer from lumbar instability' should be made with great reserve in that it is very hard to satisfy the criteria that justify the use of this term. A diagnostic 'gold standard' for instability has not yet been identified. Diagnosis is usually based on history, clinical exami nation, functional tests and imaging. Some elements can be found in the patient's history. It is believed that fre quent recurrences of LBP precipitated by minimal pertur bations, lateral shifts in prior episodes of LBP, short-term relief from manipulation and an improvement of symp toms with the use of a brace in previous episodes of LBP are confirmatory data for instability.39 CLINICAL OBSERVATIONS
Some authors state that the palpation of increased mobil ity with passive intervertebral motion testing is indica tive of instability.4o The validity of these techniques, however, has never been demonstrated.41 Others have proposed that aberrant motions such as the instability catch occurring during active ROM testing indicate insta-
Figure 56.3
Retrolisthesis narrows the nerve root canal.
-
LUMBAR INSTABILITY 841
bility.6,42,43 The instability catch has been described as a sudden acceleration or deceleration of movement, or a movement occurring outside of the primary plane of motion (e.g. side bending or rotation occurring during flexion) and is proposed as an indication of segmental instability. However, this definition of an 'instability catch' is far too broad, because in the present description it also includes the common painful arc sign which indi cates a momentary discodural interaction during move ment (see p. 753, Dural concept). In our opinion Macnab's reversal of the normal spinal rhythm is much more characteristic of segmental insta bility.44 In a normal lumbar-pelvic rhythm, there is a smoothly graded ratio between the degree of pelvic rotation and that of lumbar flattening. This rhythm may be disturbed in regaining the erect posture after forward flexion. In order to avoid putting an extension strain on the lumbar spine, the patient first slightly flexes the hips and knees in order to tuck the pelvis under the spine and then regains the erect position by straightening the legs (Fig. 56.4). RADIOLOGICAL OBSERVATIONS
Radiological measurements have been the most consis tently reported method to establish instability, although again there is much controversy. Disc space narrowing is a sign of questionable signifi cance because this is a common age-related finding. A second observation is the presence of traction spurs (Fig. 56.5) as described by MacNab.45 The spur is consid ered to result from tensile stresses being applied to the outer annular fibres which attach to the vertebral body46 (see p. 736). The third observation is the presence of spinal malalignment. This radiological assessment is based on the early observations of Knutsson who defined
Figure 56.4
Reversal of the normal spinal rhythm.
842 SECTION TEN - THE LUMBAR SPINE
Box 56.3 Diagnosis of lumbar segmental instability -
History Chronic postural back pain and/or recurrent discodural interactions
Traction spurs
<
Clinical examination Full range of movement No dural signs Reversal rhythm when regaining the erect posture from a flexed position Radiography Traction spurs Anterior translation of more than 4 mm during functional radiographs
Figure 56.5
Traction spurs.
instability as 3 mm or more of anterior translation measured between flexion and extension. However, as discussed earlier there exists much debate about the upper limit of normal translations. Boden and Wiesel emphasized that any slip should be greater than 4 mm before instability could be considered.36 Others con cluded that a minimum of 4 mm of forward displacement was necessary at the L3-L4 and L4-L5 levels to define instabili ty,47 while at the L5-51 level displacements of greater than 5 mm were necessary for accurate meas urements (Fig. 56.6).48,49 Furthermore, it has also been suggested that many instabilities do not occur at the extremes of flexion and extension, which is the usual technique utilized in routine radiographic studies. BRACING
Lastly, it has been proposed that a trial of bracing should produce pain relief in a patient with instability. a
Figure 56.6 Radiographic methods to evaluate anterior (AO) and posterior (PO) translation during flexion and extension (after Dupuis et a/50).
In general, the results have not been diagnostic, possibly because spinal braces usually produce little or no spinal immobilization. The diagnosis of segmental instability should be made with great reserve. The features outlined in Box 56.3 may point to an instability.
TREATMENT OF LUMBAR INSTABILITY
Patient education may be an important component in the treatment of patients with segmental instability. Education should first of all focus on avoiding loaded flexion movements as they may create a posterior shift of the disc.51 Patients should also be made aware of the importance of avoiding end-range positions of the lumbar spine because these overload the posterior passive stabilizing structures (see p. 921; Prevention of lumbar spine disorders). Physical therapy for segmental instability focuses on exercises designed to (what is generally believed) improve stability of the spine. During the last decades all sorts of strengthening programmes have been designed in order to actively stabilize the unstable segment: the type of advocated treatment ranges from simple and intensive dynamic back extensor exercises to specific training of dynamic stability and segmental control of the spine. As the lumbar erector spinae muscles are the primary source of extension torque for lifting tasks, strengthening this muscle group has been advocated.52 Intensive dynamic exercises of the extensors proved to be significantly superior to a regime of standard treatment of thermotherapy, massage and mild exercises in patients with recurrent low back pain.53-55 The abdominal muscles, particularly the transversus abdominis and oblique abdominals, have also been proposed to ph�y an important role in stabilizing the spine by co-contracting in anticipation of an applied load. However, exercises
CHAPTER 56 - LUMBAR INSTABILITY 843
proposed to address the abdominal muscles in an isolated manner usually involve some type of sit-up manoeuvre that imposes dangerously high compressive and shear forces on the lumbar spine56 and may provoke a posterior shift of the (unstable) disc (Fig. 56.7). Alternative techniques should therefore be applied when training these muscles. Some authors strongly suggest the transversus abdo minis57 and the multifidus muscles to provide a specific contribution to the stability of the lower spine58,59 and an exercise programme that proposes to retrain the co contraction pattern of the transversus abdominis and multifidus muscles has been described.6o The exercise programme is based on training the patient to draw in the abdominal wall while isometrically contracting the multifidus muscle and consists of three different levels: •
•
•
First, specific localized stabilization training is given. Lying prone, sitting and standing upright the patient performs the isometric abdominal drawing-in manoeuvre with co-contraction of the lumbar multifidus muscles. During the phase of general trunk stabilization the co-contraction of the same muscles is carried out on all fours, and then elevating one arm forwards and/ or the contralateral leg backwards, or on standing upright and elevating one arm forwards and/ or bringing the contralateral leg backwards. Third, there is the stabilization training. Once accurate activation of the co-contraction pattern is achieved, functional movements such as standing up Intradiscal pressure in % of that of the standing positi on
Figure 56.7
Sit-up manoeuvres may dangerously increase intradiscal pressure.
from a sitting or lying position, bending forwards and backwards and turning are trained. All daily activities are then integrated. A significant result of a randomized trial has recently been reported comparing this exercise programme with one of general exercise (swimming, walking, gym exer cises) in a group of patients with chronic LBp'61 Despite the positive results with muscular training programmes, it remains difficult to understand how training of the lumbar and abdominal muscles can improve segmental stability. Not only have the muscles (except for the multifidus) multisegmental attachments to the lumbar vertebrae but they are also not very well oriented to resist the displacements. Because they mainly run longitudinally, they can only resist sagittal rotation and are not able to resist anterior or posterior shears. However, whenever the muscles contract, and especially when they do this simultaneously, they exert a compres sive load on the whole lumbar spine, as well as on the unstable segment. By compressing the joints, the muscles make it harder for the joints and for the intradiscal content to move.62 The most important contribution of trained muscles to spinal stability may therefore be the creation of a rigid cylinder around the spine and an increased stiffness. It is important, however, that exercises should only be prescribed as a matter of prevention after the actual problem - usually a discodural interaction - has been solved by manipulation, mobilization, traction or passive postural exercises.
SCLEROSANT TREATMENT
Sclerosing injections, given to the posterior ligaments are the conservative treatment of choice in segmental instability of the spine. The therapy involves the injection of an irritant phenol 2%, dextrose 25%, glycerol 15% - into the inter and supraspinous ligaments, the posterior capsule of the facet joints and the deep part of the fascia lumborum at the affected level(s). The infiltration produces a local inflammatory reac tion which is followed by an increased proliferation of fibroblasts and the production of new collagen fibres. The final outcome is tightening, reinforcement and loss of normal elasticity of the connective tissue which decreases the mobility and increases the stability of the injected segments.63-65 The beneficial effect of the treatment method was recently shown in a double-blind controlled study that demonstrated a statistically significant difference between the active therapy group and those who received only injections with a saline solution.66
844 SECTION TEN - THE LUMBAR SPINE
· Technique A series of infiltrations is made in all the dorsal liga ments at two consecutive motion segments (usually Sl-L5-L4) and at the iliac insertions of the iliolumbar ligaments. Over 4 consecutive weeks 3 ml of the solu tiOll, mixed with 1 ml of lidocaine (lignocaine) 2% is injected. The techniques are shown on page 918 but it is well to remember that in order to stay clear of any vital structures, including the structures in the spinal canal, the injection should be made only when the tip of the needle touches bone. • • •
•
is at least 40% higher in the US than in any other country and is five times higher than in the UK.69 Although there have been no randomized trials evaluat ing the effectiveness of lumbar fusion for spinal insta bility, the feeling remains that the operation should be reserved for patients with severe symptoms and radio graphic evidence of excessive motion (greater than 5 mm translation or 10° of rotation) who fail to respond to a trial of non-surgical treatment.70 The latter should consist of a combination of patient education, physical training and sclerosing injections.
The first injection is at the interspinous and supraspinous ligaments. The second injection is given at the posterior capsules of the zygapophyseal joints. The third injection is given at the lateral aspects of the laminae where the ligamentum flavum and the medial aspects of the deeper layer of the fascia lumborum merge. The fourth injection aims at the insertion of the iliolumbar ligaments and the insertion of the thoracolumbar fascia on the posterior superior iliac spine (Fig. 56.8).
SURGERY
The indications for spinal fusion in the treatment of degenerative instability are controversial. The basic problem lies, as discussed earlier, in the definition and the diagnosis of the disorder. However, despite the fact that indications for the procedure are uncertain, costs and complication rates are higher than for other surgical procedures performed on the spine, and long-term out comes are uncertain, the rate of lumbar spinal fusion is increasing rapidly in the United States.67,68 The rate of back surgery and especially of spinal fusion operations
Figure 56.8 Sclerosing injections in the treatment of segmental instability: 1, interspinous and supraspinous ligaments; 2, facet joint capsules; 3, deep layer of the fascia lumborum; 4, iliolumbar ligaments.
REFERENCES 1. Pope MH,
Panjabi M. Biomechanical definitions of spinal
instability. Spine 1985;10:255-256.
lumbar spinal ligaments: an in vitro biomechanical study. Spine
2. American Academy of Orthopaedic Surgeons. A glossary on
spinal
terminology.
American
7. Panjabi MM, Goel VK, Takata K. Physiologic strains in the
Academy
of
Orthopaedic
Surgeons, Chicago, 1985:34.
JRR. The resistance to flexion of
the lumbar intervertebral joint. Spine 1980;5:245-253.
3. Panjabi MM. The stabilizing system of the spine, part
II:
neutral zone and instability hypothesis. J Spinal Disord 1992;5:390-396.
9. McGill
SM.
Estimation
of
force
and
extensor
moment
contributions of the disc and ligaments at L 4- L 5 . Spine 1988;13:1395-1402.
4. Panjabi MM, Oxland TR, Yamamoto I, Crisco
JJ. Mechanical
behavior of the human lumbar and lumbosacral spine as shown by three-dimensional load-displacement curves. J Balle Joint
10. Solomonow M, Zhou B, Harris M, Lu Y, Baratta
5. Kirkaldy-Willis W, Farfan H. Instability of the lumbar spine.
Ciin Orthop 1982;165:110-123.
RY. The
ligamento-muscular stabilizing system of the spine. Spine 1998;23:2552-2562. 11. Kong WZ, Goel VK, Gilbertson LG, Weinstein
Surg 1994;76A:413-424.
6. Paris SY. PhYSical signs of instability.
1982;7:192-203. 8. Adams MA, Hutton MC, Stott
IN.
Effects of
muscle dysfunction on lumbar spine mechanics. A finite element study based on a two motion segments model. Spine
Spine 1985;10:277-279.
1996;21:2197-2206.
CHAPTER 56 - LUMBAR INSTABILITY 845
Haher TR, O'Brien M, Dryer JW et al. The role of the lumbar facet joints in spinal stability: identification of alternative paths of loading. Spine 1994;19:2667-2670. 13. Sharma M, Langrana NA, Rodriguez J. Role of ligaments and facets in lumbar spinal stability. Spine 1995;20:887-900. 14. Basadonna P-T, Gasparini D, Rucco V. Iliolumbar ligament insertions; ill vivo anatomic study. Spine 1996;21:2313-23. 15. Bogduk N, Macintosh JE, Pearcy MJ. A universal model of the lumbar back muscles in the upright position. Spine 12.
1992;17:897-913. 16.
Hodges PW, Richardson A. Inefficient muscular stabilization of the lumbar spine associated with low back pain. Spine 1996;21:2640-2650.
17. 18.
19.
20. 21.
22.
Gudavalli MR, Tirano JJ. An analytical model of lumbar motion segment in flexion. I Mallip Physiol Ther 1999;22:201-208. Gardner-Morse M, Stokes lA, Laible JP. Role of muscles in lumbar spine stability in maximum extension efforts. I Orthop Res 1995;13:802-808. Macintosh JE, Pearcy MJ, Bogduk N. The axial torque of the lumbar back muscles: torsion strength of the back muscles. Aust N.Z I SlIrg 1993;63:205-212. Macintosh JE, Bogduk N. The biomechanics of the lumbar multifidus. Clill Biolllecli 1986;1:205-213. V leeming A, Pool-Goudzwaard AL, Stoeckaert R, van Wingerden JP, Snijders e. The posterior layer of the thoraco lumbar fascia: its function in load transfer from spine to legs. Spille 1995;20:753-758. Panjabi M. The stabilizing system of the spine 1. Function, dysfunction, adaptation and enhancement. J Spinal Oisord 1992;5:383-389.
Hodges PW, Richardson A. Evaluation of the relationship between the findings of a laboratory and a clinical test of trans versus abdominis function. Physiother Res Internat 1996;1:30-40. 24. Luoto S, Taimela S, Hurri H et al. Psychomotor speed and pos tural control in chronic low back pain patients: a controlled follow-up study. Spine 1996;21:2621-2627. 25. Solomonow M, Zhou B, Harris M, Lu Y, Baratta RV. The ligamento-muscular stabilizing system of the spine. Spine
Hayes MA, Howard TC, Gruel CR, Kopta JA. Rontgenologic evaluation of lumbar spine flexion-extension in asymptomatic individuals. Spine 1989;14:327-331. 38. Lehman T, Brand R. Instability of the lower lumbar spine. Orthop Trans 1983;7:97. 39. Delitto A, Erhard RE, Bowling RW. A treatment-based classification approach to low back syndrome: identifying and staging patients for conservative treatinent. Plrys Ther 37.
1995;75:470-485.
Maitland GD. Vertebral Manipulation, 5th edn. Butterworth Heinemalm, Oxford, 1986:74-76. 41. Maher CG, Adams R. Reliability of pain and stiffness assess ments in clinical manual lumbar spine examination. Phys TireI' 40.
1994;74:801-809. 42. 43.
44. 45. 46.
47.
48.
23.
1998;23:2552-2662.
Frymoyer Jw. Segmental instability. In: Frymoyer JW (ed) The Adult Spine. Raven Press, New York, 1991:1873-1891. 27. Axelsson P, Johansson R, Stromqvist B. Is there increased inter vertebral mobility in isthmic adult spondyllisthesis? A matched comparative study using steroephotogrammetry. Spine
49.
50.
26.
51. 52.
2000;25:1701-1703. 28. 29. 30. 31.
32.
Floman Y. Progression of lumbosacral isthmic spondylolisthesis in adults. Spine 2000;25:342-347. Kirkaldy-Willis W. Mallaging Low Back Paill. Churchill Livingstone, New York, 1988:55. Adams MA, Hutton We. Prolapsed intervertebral disc: a hyperflexion injury. Spine 1982;7:184-191. Wilder DG, Pope MH, Frymoyer JW. The biomechanics of lumbar disc herniation and the effect of overload and instabil ity. I Spinnl Oisord 1988;1:16-33. Frymoyer JW, Pope MH. Segmental instability. Semin Spine Surg 1991;3:109-118.
Wietfeld K. Diagnostik und konservative Therapie lumbaler Instabilitiiten nadl Nucleotomien. Orthop Praxis 1995;12:977-980. 34. Sepulveda R, Kant AP. Chemonucleolysis failures treated by PUP. Clin Orthop 1985;193:68-74. 35. Farfan HF, Gracovetsky S. The nature of instability. Spine
53.
54.
55.
56.
33.
1984;9:714-719. 36.
Boden SO, Wiesel SW. Lumbosacral segmental motion in normal individuals. Have we been measuring instability properly? Spine 1990;15:571-576.
Nachemson A. Lumbar spine instability: a critical update and symposium summary. Spine 1985;10:290-291. Ogon M, Bender BR, Hooper OM et al. A dynamic approadl to spinal instability, part II: hesitation and giving-away during interspinal motion. Spille 1997;22:2859-2866. MacNab 1. Backache. Williams & Wilkins, Baltimore, 1983:119. MacNab 1. The traction spur: an indicator of segmental instabil ity. J Bone Joint Surg 1971;53A:663-670. Nathan H. Osteophytes of the vertebral column. An anatomical study of their development according to age, race, and sex with considerations as to their etiology and significance. I Bone loillt Surg 1962;44A:243-268. Hayes MA, Howard TC, Gruel CR, Kopra JA. Roentgenographic evaluation of lumbar spine flexion extension in asymptomatic individuals. Spine 1989;14:327-331. Woody J, Lehmann T, Weinstein J et al. Excessive translation on flexion-extension radiographs in asymptomatic populations. Presented at the meeting of the International Society for the Study of the Lumbar Spine, Miami, Florida, 1988. Shaffer WO, Spratt KF, Weinstein J, LehmannN TR, Goel V. Volvo award in clinical sciences. The consistency and accuracy of roentgenograms for measuring sagittal translation in the lumbar vertebral motion segment. An experimental model. Spine 1990;15:741-750. Dupuis PR, Young-Hing K, Cassidy JD, Kirkaldy-Willis WHo Radiologic diagnosis of degenerative lumbar spinal instability. Spine 1985;10:262-276. McGill SM. Estimation of force and extensor moment contribu tions of the disc and ligaments at L4-L5. Spille 1988;13:1395-1402. Callaghan JP, Gunning JL, McGill SM. The relationship between lumbar spine load and muscle activity during extensor exer cises. Phys Ther 1998;78:8-18. Malmiche C, Hesselsoe G, Bentzen L, Christensen I, Lundberg E. Clinical trial of intensive muscle training for chronic low back pain. Lancet 1988;24-31;2(8626-8627):1473-1476. Manniche C, Lundberg E, Christensen I, Bentzen L, Hesselsoe G. Intensive dynamic back exercises for chronic low back pain: a clinical trial. Pain 1991;57:53-63. Hansen FR, Bendix T, Skov P et al. Intensive dynamic back muscle exercises, conventional physiotherapy, or placebo control treatment of low back pain. Spine 1993;18:98-107. McGill SM. Distribution of tissue loads in the low back during a variety of daily and rehabilitation tasks. I Rehabil Res Oev 1997;34:448-458.
Hodges PW. Is there a role for transversus abdominis in lumbo pelvic stability? Manual Therapy 1999;4(20):74-86. 58. Hides J, Stokes MJ, Saide ML et al. Evidence of lumbar multi fidus muscle wasting ipsilateral to symptoms in patients with acute/subacute low back pain. Spine 1994;19:165-172. 59. Wilke H, Wof S, Claes LE et al. Stability increase of the lumbar spine with different muscle groups. Spine 1995;20:192-198. 57.
846 SECTION TEN - THE LUMBAR SPINE
Richardson CA, Jull GA. Muscle control-pain control: what exercises would you prescribe? Manual Therapy 1995;1:2-10. 61. O'Sullivan PB, Twomey LT, Allison GT. Evaluation of specific stabilizing exercise in the treatment of chronic low back pain with radiologic diagnosis of spondylolysis or spondylolisthesis. Spine 1997;22:2959-2967. 62. Wilke HJ, Wolf S, Claes LE, Arand M, Wiesend A. Stability increase of the lumbar spine with different muscle groups: a biomechanical in vitro study. Spille 1995;20:192-198. 63. Liu Y, Tipton C Matthes R et al. An in situ study of the influence of a sclerosing solution in rabbit medial collateral ligaments and its junction strength. Connect Tissue Res 60.
64.
65.
66.
67.
68.
1983;11:95-102.
69.
Maynard J, Pedrini V, Pedrini-Mille A, Romanus B, Ohlerking F. Morphological and biochemical effects of sodium morrhuate on tendons. J Ortilop Res 1985;3:236-248.
70.
Klein R, Dorman T, Johnson C. Proliferant injections for low back pain: histologic changes of injected ligaments and objec tive measurements of lumbar spinal mobility before and after treatment. J Neurol Orthop Med Surg 1989;10:123-126. Klein R, Eek B, DeLong B, Mooney V. A randomized double blind trial of dextrose-glycerine-phenol injections for cllronic, low back pain. J Spinal Disord 1993;6:23-33. Deyo RA, Ciol MA, Cherkin DC et al. Lumbar spinal fusion: a cohort study of complications, reoperations, and resource used in the Medicare population. Spine 1993;18:1463-1470. Davis H. Increasing rates of cervical and lumbar spine surgery in the United States, 1979-1990. Spille 1994;19:1117-1124. Cherkin DC, Deyo RA, Loeser JD, Bush T, Waddell G. An international comparison of back surgery rates. Spille 1994;19: 1201-1206.
Sonntag V KH, Marciano FF. Is fusion indicated for lumbar spinal disorders? Spine 1995;20(suppl):138S-142S.
Mechanical disorders of the lumbar spine: differential diagnosis
Activity-related lumbar disorders have a multifactorial origin. Diagnostic precision is difficult, and imaging techniques usually have a relatively low specificity. Nevertheless, the clinician is asked to make an accurate diagnosis,
to
choose
an
appropriate
management
strategy and to determine prognosis. Therefore there is a need for a classification of spinal disorders based on simple clinical criteria. With the infor mation gained from history and examination, clinical syndromes can be defined and used as a basis for a classification which also embraces the concepts that have been described . •
Syndromes - Lumbago (see Box 57.1) - Backache (see Box 57.2) - Sciatica (see Box 57.3)
•
Concepts (see Fig. 57.1) - Dural - Ligamentous - Stenotic Both syndromes and concepts have to be considered in
the context of the normal changes in the ageing lumbar spine.
847
848 SECTION TEN - THE LUMBAR SPINE
Box 57.1 Lumbago Definition
A sudden attack of severe and incapacitating backache
Mechanism
Always caused by disc displacement, and thus comes entirely under the dural concept. A large posterior shift of disc material compresses the dura mater: mechanism is dual; there is a discodural interaction
Symptoms
Slow onset if the displacement is nuclear: nuclear lumbago Sudden onset if the shift is annular: annular lumbago Articular: twinges; severe pain during particular positions and movements, especially pain on sitting and on bending Dural: Extrasegmental pain; pain on coughing and sneezing
Signs
Articular: deviation; gross partial articular pattern Dural: Painful neck flexion; limited SLR
Natural history
Spontaneous cure within 2 weeks in most cases
Treatment
Hyperacute lumbago: epidural Annular lumbago: manipulation Nuclear lumbago: bed rest in psoas position; mobilizations-McKenzie techniques; no traction in the presence of 'twinges' or of deviation
Fibrotic degeneration of the nucleus Concentric tears Radial tears Traction spurs Cysts Posterior displacements: Bulging Protrusion
Hypermobility Compession and distraction Joint subluxation
Prolapse
Fissures and cavities Marked height decrease Circular and anterior displacements Gross osteophytosis Disc resorption
Spondylosis
Figure 57.1
Spondylarthrosis
The three ciinicallumbar concepts in relation to the natural ageing
of anterior and posterior walls of the vertebral column.
CHAPTER 57
-
MECHANICAL DISORDERS: DIFFERENTIAL DIAGNOSIS 849
Box 57.2 Backache
Definition
Pain in the lumbar area, with or without radiation in a dural diffuse manner In most cases pain does not radiate beyond the gluteal folds Pain can be acute or chronic, intermittent or constant
Mechanism
Acute and recurrent backache: almost always caused by a discodural interaction, thus symptoms and signs are very similar to acute lumbago, although milder. Dural symptoms and signs are sometimes subtle or even absent. A clear non-capsular pattern or a painful arc during flexion is pathognomonic for a small central disc protrusion Chronic backache: caused by either a discodural interaction or a lesion of a posterior structure (facet or ligament) Differential diagnosis depends on the clinical picture
Symptoms Discodural bachache
Ligamentous postural syndrome
Ligamentous dysfunction syndrome
Moment of onset is known
Pain comes on gradually
A hypertension trauma is often present
Acute: annular lesion
Moment of onset is known
Gradual: nuclear lesion Pain intensity is not constant but can
Pain appears during some postures;
fluctuate
intensity depends on duration
provokes pain
Pain is often unilateral but bilateral
Bilateral and vague pain, seldom
Localized and strictly unilateral pain,
radiation is possible
radiating beyond the glutei
Pain is constant during the posture that
except in bilateral facet joint lesion; Central pain in lesion of the supra- and interspinous ligaments
Localization changes: shifting pain
No change in localization
No change in localization
Sometimes dural symptoms
No dural symptoms
No dural symptoms
Twinges?
Never twinges
No twinges
Pain is caused by movements
Pain is caused by posture, increases
Pain is caused by posture and increases
with maintenance of posture and
with maintenance of posture, sometimes
disappears during movement
with particular movements
Sitting and bending are particularly
Standing and strolling are particularly
Movements and postures that increase
painful
painful
the lumbar lordosis are painful
DiscoduraI backache
Ligamentous postural syndrome
Ligamentous dysfunction syndrome
Partial articular pattern
Full range
Signs Full range, sometimes pain at the end of range Facet lesions: convergent or divergent patterns Sometimes painful arc
No painful arc
No painful arc
Sometimes positive dural signs; pain
No dural signs
No dural signs
Improvement after manipulation/
No improvement after manipulation/
No improvement after manipulation/
traction
traction
traction
or limitation of SLR; neck flexion increases the pain
Natural history
Unpredictable: backache may recover spontaneously, but often does not. Chronic backache in particular shows no tendency to spontaneous cure
Treatment
Acute backache
-
Annular: manipulation and prevention (back school); Nuclear: traction (epidurals)
Recurrent backache
-
Annular: manipulation and sclerosing injections (or back school) Nuclear: traction and sclerosing injections (or back school)
Chronic backache
-
Discodural: manipulation and traction Bruised dura mater: epidurals Self-reducing disc: back school and prevention; sclerosing injections Postural ligamentous: sclerosing injections Dysfunction of posterior structures: triamicinolone/sclerosing injections
850 SECTION TEN - THE LUMBAR SPINE
Box 57.3 Sciatica Definition
Radicular pain resulting from compression of the dural investment of a nerve root Pain is limited to the dermatome of the root involved. If there is parenchymatous involvement, the pain is accompanied by paraesthesia, motor and/or sensory deficit
Mechanism
Radicular compression can result either from a posterolateral disc herniation or from a narrowed lateral recess Discoradicular conflicts have a typical age of onset and typical natural history Entrapment of the nerve root in the lateral recess occurs in elderly patients; there is virtually no spontaneous evolution
Symptoms Discoradicular interactions
Lateral recess stenosis
• Young to middle-aged patients • Evolution in the pain localization
• Middle-aged to elderly patients • No evolution of the symptoms
Secondary posterolateral protrusions:
No moving pain
first backache then leg ache Primary posterolateral protrusions: pain starts in the calf and moves upwards
• Dural symptoms • Spontaneous recovery within 1 year in most cases • As a rule sitting and bending is worst, although continuous pain is possible
• No dural symptoms • No tendency to spontaneous recovery • Pain on standing and walking, disappears during sitting and forward bending Sometimes pain in prone-lying position
Signs Discoradicular interactions
Lateral recess stenosis
• Partial articular pattern
• Full range or slight capsular pattern due to the
• Limited flexion, sometimes with deviation
• Sometimes limited extension • Pain provocation after standing for a while • Normal mobility of the nerve roots; sometimes slight pain
osteoarthrosis
• Impaired nerve root mobility: positive SLR
at end of SLR
or L3 stretch
• Often signs of parenchymatous involvement/loss
• Seldom signs of parenchymatous involvement
of motor and/or sensory functions, sluggish reflexes
• Diagnostic response after epidural local anaesthesia
• No diagnostic response after epidural local anaestr,esia
Treatment Discoradicular interactions: see pp. 905-915 and Chapter 59
Lateral recess stenosis: Back school Nerve root blocks Surgery
CHAPTER CONTENTS Intr�duction
851
Warning signs in backache and sciatia Disorders 855 Spondylolisthesis 855 Osseous disorders 857 Rheumatological disorders 861 Infections 863 Intraspinal lesions 864 Pain referred to the back 867
851
Non-mechanical disorders of the lumbar spine �••tr.!Ilf'��" JO- �,�-';::�W(" !!!">"INTRODUCTION tl�· _,..l,�,,_.;t
.
�
,
_
The majority of lumbar spine syndromes encountered in clinical practice result from mechanical - activity related - disorders. They can be classified into dural, ligamentous and stenotic syndromes. Lumbar syndromes, however, can also stem from non-mechanical - non-activity-related - disorders affecting the spine. These are: inflammatory diseases, both septic and rheumatological; tumours and infiltrative lesions; metabolic disorders; and acquired defects in the neural arch. Finally, pain in the lower back, groin and pelvic area can be referred from visceral organs (see p. 655 and 867). Pain in buttocks, groin and limb, as the result of reference from the sacroiliac and hip joints, although 'activity-related', does not have a spinal origin and is discussed thoroughly in the chapters on the hip joint and sacroiliac joint. Although the occurrence of non-mechanical (non activity related) disorders is rare, it is important to dif ferentiate them as quickly as possible from mechanical activity-related lesions. This is never easy, because these disorders frequently mimic the other, more specific lumbar lesions. Sometimes the diagnosis is made radio logically but very often this is of no help, especially in the early stages of an inflammatory or neoplastic disease. A thorough history and clinical examination are what will first draw attention to the possibility of a non activity related disorder: the history may show an unusual localization or an atypical evolution of the pain; particular clinical signs may arouse suspicion. Most of all, however, it is the comparison between history and clinical examination, resulting in the existence of 'unlikelihoods' that focuses attention on the probability of a non-mechanical disorder. ... ,
,
-
,
WARNING SIGNS IN BACKACHE AND SCIATICA -
.
Symptoms and signs that almost invariably point to non-mechanical disorders are termed 'warning signs' here. The finding of such signs indicates that the exis tence of a non-specific disorders in the lumbar spine is 851
852 SECTION TEN - THE LUMBAR SPINE
very likely. A patient presenting with a warning sign should never be considered to be suffering from a common mechanical disorder until the contrary has been proved. It is important, therefore, always to have confirmatory investigations done (radiography, bone scan, CT and blood examination) to settle the diagnosis. It is also the duty of a physiotherapist who is asked to give active treatment (manipulation or traction) to a patient presenting with warning signs, to report this to the doctor, and to send the patient back with a request for further thorough examination. SYMPTO M S
Warning Warning signs that may be detected during the history are: • Pain in the 'forbidden area' • Increasing, slowly aggravating pain • Expanding, instead of moving pain • Continuous pain, unaltered by position or movement • Sciatica with too long an evolution • Bilateral sciatica • Increasing postoperative backache
However, if the history is that of continuing backache, gradually expanding and worsening despite the appear ance of root pain, a non-mechanical disorder should be suspected. In addition, a history of pain which first spreads to one dermatome but after some time also involves the neighbouring dermatomes should be con sidered to be the history of an increasing lesion, which is almost never of a disc. When pressure against the dura mater increases when pressure on the nerve root (or roots) sets in, the lesion responsible for the pain will not be a moving disc protrusion but a rapidly (neoplasm) or slowly (neuroma) increasing lesion. Continuous pain
Typical of mechanical disorders is that postures and activities have a certain influence on the pain: backache because of disc lesions is usually increased by sitting and bending and relieved by recumbency, ligamentous pain has a typical postural nature and the radicular pain caused by a narrow lateral recess increases in the upright position and eases on sitting. When a patient's pain is more or less continuous and no posture can be found for its relief, a serious spinal or extraspinal lesion should be suspected. Sometimes however, an emotionally dis traught patient or a patient with hyperacute lumbago will claim that the pain is continuous. Further history
Pain in the 'forbidden areal
In the upper lumbar region pain is very seldom the result of a mechanical lesion. Disc lesions almost never occur at the first and second levels1 and even third lumbar lesions constitute only 5% of lumbar disorders.2 Also ligamen tous lesions and recess stenosis do not seem to occur at these upper lumbar levels. Hence, if a patient has pain at the upper lumbar level - the 'forbidden area' (Fig. 58.1) the suspicion is aroused that a non-mechanical lesion is present. Ankylosing spondylitis, neoplasm, tuberculosis, aortic thrombosis or reference from a viscus may then be the possibilities (Cyriax:3 p. 26).
I
•
\\:,1\
Increasing pain
Lumbar pain steadily worsening over a number of weeks suggests malignant disease. This is especially true in elderly patients who have had increasing central back ache over a short time. Expanding pain
A familiar symptom in disc lesions is that of a moving pain: the pain is central at first and becomes unilateral; or the backache changes sides; or there has been backache initially which after a time has turned into leg ache. Thus, in disc displacements, back pain may move to different localizations, or the backache eases when the unilateral root pain comes on.
Figure 58.1
The 'forbidden area'.
CHAPTER 58
taking will disclose that although there is continuous dis ability, there may be some positions in which the pain eases somewhat, while servere twinges make other movements absolutely impossible. It is obvious that in these cases the pain is of mechanical origin . Sciatica lasting too long
It is unusual for sciatica from a posterolateral disc pro trusion to last longer than a year. The normal develop ment is a root pain which becomes rapidly worse and reaches a peak within 1-4 weeks. Severe symptoms then persist for a few weeks or months, thereafter improving. At the end of a year, nearly all patients have recovered. However, it should be remembered that patients over 60 years of age, especially those who still have some back ache after the root pain has appeared, do not always show this tendency to improve. Additionally, in cases of root compression caused by a narrowed lateral recess, the pain can remain present for months or years, without showing any tendency to worsen or improve. If root pain continues to worsen after 9 months, the cause is almost certainly not a disc lesion, and a non mechanical disorder, such as a neuroma or epidural cyst, is more likely. Rarely, sciatic pain that lasts longer than usual is caused by an adherent nerve root.
•
•
Spondylolisthesis can cause bilateral radicular pain which presumably results from the forward movement of the listhetic vertebra, pulling the nerve roots painfully against the shelf formed by the stable vertebra below. A disc lesion resulting in bilateral sciatica is rare and should always be taken seriously, because it means probably a massive protrusion, which presents a danger to the 54 root. Bladder incontinence and numbness in the saddle area may then accompany the bilateral root pain. Rarely a disc develops two protrusions, one at each side of the posterior
NON-MECHANICAL DISORDERS 853
longitudinal ligament; alternatively two protrusions, one at the fourth and one at the fifth level are present. BiLateraL LateraL recess stenosis, or a narrowed spinal canaL can also be causes of bilateral sciatica. In the former, the typical history of increasing pain in the upright position is informative. In the latter, the patient mentions neurogenic claudication. Malignant disease: rapidly increasing bilateral sciatica, often spreading into the limbs in a distribution which corresponds to too many dermatomes indicates malignant disease.
•
•
Increasing backache a fter lumbar surgery
Intervertebral disc space infections most often follow sur gical enucleation of a herniated disc. After initial relief of the preoperative pain, severe and steadily increasing lumbar pain appears. SIGNS
Warning Clinical signs that constitute warning are: • Discrepancy between the marked articular signs and the absence of dural signs
• Gross limitations of both side flexions • Gross limitation of side flexion away from the painful
Bilateral sciatica
For the purposes of differential diagnosis, it is important not to confuse bilateral extrasegmental dural reference of pain with bilateral radicular pain. To an experienced examiner it is not difficult to distinguish between the two. Dural pain is dull, deep, diffuse, ill-defined and spreads to different dermatomes. Although dural pain often reaches the ankles, it never extends to the feet. Radicular pain is sharp, well-localized and within the borders of the dermatomes. The pain can reach the feet, except in the more exceptional cases of L1-L3 radicular pain and can also be accompanied by distally localized paraestheSia and numbness. If the patient presents with real bilateral sciatica, a number of conditions must be taken into consideration:
-
side as the only positive finding
• • • • • • •
Flexion with a rigid lumbar segment Radicular pain and muscle spasm Discrepancy between pain and neurological deficit I nvolvement of multiple nerve roots Deficit of L 1 and L2 nerve roots Buttock sign A warm foot on the affected side
Discrepancy between articular and dural signs
In that acute lumbago is basically a compression of the anterior part of the dural tube, dural signs should always be present. If a history of acute lumbago is described and marked articular signs are present but the patient has no dural signs at all, a disc lesion is unlikely and other more serious lesions should be considered, for instance: •
•
•
A pathological fracture of a vertebra, resulting from a malignant disease or from senile osteoporosis, shows gross limitation of spinal movements but straight leg raising may remain normal and painless. AnkyLosing spondylitis: an acute sprain of the stiffened lumbar joints will result in an acute lumbago but dural signs are completely absent. In chronic afebrile osteomyelitis of a lumbar vertebral body there is a gross contrast between the marked articular signs and the complete absence of dural signs.
854 SECTION TEN - THE LUMBAR SPINE
Gross and bilateral limitation of side flexions
The range of side flexion diminishes with a patient's age. Some symmetrical limitation is therefore a normal finding in the elderly. However, bilateral limitation of these movements in younger or middle-aged patients is not normal and, if this sign is present, non-mechanical, and usually serious, diseases of the lumbar spine are strongly suggested. A lumbar localization of ankylosing spondylitis often presents with this sign, but so also can malignant or benign neoplasms, Paget's disease, chronic osteomyelitis and old fractures.
itations of side flexion and must always be taken seri ously. It is sometimes seen in an acute lumbago caused by an ordinary disc lesion but most often it indicates a spinal localization of ankylosing spondylitis or a more serious non-mechanical disorder of the spine. Care should be taken not to confuse this sign with a normal flexion range in a patient with marked kypholordosis. In such a case, the spine may stay horizontal at the end of the flexion, although the lumbar segment has undergone a consider able flexion movement. Radicular pain and muscle spasm
Gross limitation of side flexion a way from the painful side
Gross limitation of side flexion away from the painful side (Fig. 58.2) is a common finding in acute disc lesions, in which it always appears in combination with other limited and painful movements, together forming the non-capsular pattern. However, when limitation of side flexion away from the painful side is the only positive lumbar feature, a disc lesion is never present and a serious extra-articular lesion must be suspected. This pattern sug gests an abdominal neoplasm, usually a carcinoma of colon or kidney, although a neuroma at the lumbar or lower thoracic level should also be considered. Flexion with a rigid lumbar segment
Patients with serious disease of the lumbar spine flex from their hips; the lumbar spine is held in lordosis by spasm of the sacrospinalis muscle. The patient bends like an old-fashioned butler. This characteristic type of flexion - the lumbar spine held rigid and the body flexing as a whole at the hips - sometimes accompanies bilateral lim-
In sciatica from a disc lesion, trunk flexion is limited because of pain felt in the limb, the patient being unable to stretch the sciatic nerve beyond a certain point. Usually this limitation is associated with some spasm of the sacrospinalis muscle. However, when side flexion or extension provokes radicular pain and also induces muscle spasm, more serious spinal diseases must be suspected, rather than a disc lesion. Discrepancy between pain and neurological deficit
In disc lesions, some muscle weakness will be present only after a history of severe radicular pain. This does not mean that the patient must still have sciatic pain at the moment that paresis is detected. For instance, in root atrophy, the radicular pain disappears the moment weakness becomes obvious. Although there is not very much pain at this stage, the history is that of a recent and severe sciatica. If, by contrast, a patient presents with severe weak ness without a record of severe pain in the limb, spinal metastases are likely. In disc lesions, it is very unusual to find complete paresis of a muscle except when two con secutive roots are involved, as sometimes happei1s in combined L4-L5 lesions at the fourth lumbar level and which leads to a drop foot. Involvement of multiple nerve roots
Although one lumbar disc protrusion often compresses two adjacent nerve roots, triple palsies or bilateral palsies almost always result from metastases or from neuralgic amyotrophy. Deficit of L 1 and L2 roots
Figure 58.2 Gross limitation of side flexion away from the painful side is a warning sign for serious disease.
Dis lesions at the first and second lumbar levels are extremely rare; the estimated frequency is between 0.3 and 0.5%.4-6 Also, lateral recess stenosis leading to muscular weakness does not occur at the upper lumbar levels. Therefore, if weakness of the psoas mus,cle is encountered, the initial diagnosis should never be a disc lesion but rather a serious non-mechanical disorder. In a neoplasm at the second lumbar level, a bilateral paresis is
CHAPTER 58
likely to appear. If unilateral weakness is accompanied by pain 1n the iliac fossa, brought on when the muscle con tracts, a neoplasm at the il iac crest or in the pelvis is pos sible. If the weakness is accompanied by pain in the thigh, a metastatic invasion of the upper femur is proba ble (see Ch. 69).
•
Presence of the 'sign of the buttock'
When the sign of the buttock is encountered, a serious lesion in the lumbopelvic area is always present (see Ch. 68). This can be a malignant deposit in the sacrum, iliac bone or femur, a septic arthritis of the sacroiliac joint or a rectal abscess. •
A warm foot on the a ffected side
In radicular pain caused by disc lesions, patients often complain that the foot and the leg on the affected side feel cold, which is often confirmed by palpation. If, by con trast; the affected side is warmer, neoplasm at the upper lumbar level should be suspected (Cyriax:3 p. 292). The explanation is probably interference by the tumour with the sympathetic nerves at L1 and L2.
•
- NON-MECHANICAL DISORDERS
855
elongation without lysis or an acute fracture (subtypes a, b and c). If a defect in the pars interarticularis can be identified, but no slip has occurred, the condition is called a 'spondylolysis'. In degenerative spondylolisthesis an advanced degeneration of the facet joints and a progressive change in the direction of the articular processes allow the vertebra to slip forwards. The condition occurs four times as frequently in females than in males and nearly always at the fourth lumbar level (Cyriax:3 p. 288; Rosenberg10). The slip is never severe. This condition has been discussed in the chapter on the stenotic concept. Traumatic spondylolisthesis results from a fracture of a posterior element other than the pars interarticularis. Pathological spondylolisthesis develops as the result of weakness caused by a local or generalized bone disease.
In this chapter we discuss only the spondylolytic spondylolistheses. AETIO LOGY
DISORDERS SPONDYLOLISTHESIS
In 1 782, the Belgian gynaecologist Herbiniaux described a severe case of lumbosacral luxation, which he consid ered as a potential obstetrical problem? A precise definition of spondylolisthesis was first given by Kilian in 1 8548 - a spinal condition in which all or a part of a vertebra (spondylo) has slipped (olisthy) on another. Wiltse et al.9 described five major types: •
•
Dysplastic spondylolisthesis is secondary to a congenital defect of the first sacral-fifth lumbar facet joints, with gradual slipping of the fifth lumbar vertebra. Isthmic or spondylolisthetic spondylolisthesis is the most common type of spondylolisthesis. The basic lesion is in the pars interarticularis. The vertebra above can slip as the result of a lytic process, an
Box 58.1 Non-activity-related disorders of the lumbar spine
Isthmic spondylolisthesis has been defined as 'a condi tion in which fibrous defects are present in the pars inter articularis, which permit forward displacement of the upper vertebrae and separation of the anterior aspects of the vertebra from its neural arch' (Fig. 58.3).11 The aetiol ogy of this bony defect has been discussed for decades
1--- Superior articular facet
Transverse process
+----Inferior articular facet
-
Acquired defects in the neural arch (isthmic spondylolisthesis) Osseous disorders Rheumatological disorders Infections Intraspinal lesions Pain referred to the back Pseudoradicular pain
Figure 58.3 Spondylolisthetic spondylolisthesis: fibrous defects in the pars interarticularis permit forward displacement of the upper vertebra and separation of the anterior part of the vertebra from its neural arch.
856 SECTION TEN - THE LUMBAR SPINE
but it is now widely accepted to be the result of a con genital weakness. The defect itself is not present at birth, however, but develops in childhood, probably as the result of repeated stress and trauma.12-I4 Stress fractures form in the weakened pars interarticularis; fibrous tissue fills the gap, and further tension enlarges the defect.Is Forward slipping of the vertebral body therefore occurs most frequently between the ages of 1 0 and 15 years, and progression is unlikely after adolescence.16,17 The reported incidence of spondylolisthesis is between 4 and 7%,18, 1 9 although a higher incidence has been reported among Eskimos (18_56%).20,21
G RAD I N G
Spondylolysis is visualized b y a n oblique view of the lumbar spine which shows the well-known 'collar on the Scottie dog's neck'. Forward slipping is best visual ized on a lateral radiograph and the amount of listhesis is graded by the Meyerding's system (Fig. 58.4):22 the upper sacrum is divided into four parallel quarters and the degree of slipping is calculated from the distance that the posterior edge of the fifth lumbar vertebra has shifted on the posterior edge of the sacrum in relation to the total width of the upper sacrum. Grade I is a shift of less than 25%, grade II between 25 and 50%, grade III between 50 and 75% and grade IV more than 75%. Some authors emphasize that there is a significant difference in measurements when the radiographs are taken with the patient in a recumbent rather than erect posi tion. 23
II
Figure 58.4
Grades of spondylolisthesis (from Meyerding)22
CLIN ICAL F I N D I N G S
I t should b e emphasized that most cases of spondylo listhesis are asymptomatic. Even severe displacements may be present in very active patients, without the slightest discomfort. In a radiological study of 996 adult patients with low back pain, MacNab found spondylo listhesis in only 7.6%, which is not significantly higher than in the population as a whole (4_6%).24 Therefore caution must be taken before ascribing back pain or sci atica to spondylolisthesis and the radiological demon stration of a defect in a patient with back pain does not always indicate that the source of the symptoms has been discovered.25 Spondylolisthesis can produce backache or sciatica in two ways: spondylolisthesis as the basis of a secondary disc lesion and the spondylolisthesis itself causing symptoms. Spondylolisthesis with secondary disc lesion
As early as 1945, Key stated that symptoms in spondylo listhesis were far more often caused by a disc lesion than by slippage of the vertebra.26 The clinical features are exactly the same as in patients without spondylolis thesis, and nothing in the history or clinical examjnation arouses suspicion, except some irregularity of the spinous processes on examination. Radiographs carried out in the erect posture disclose the slip. It is obvious that the management of disc lesions occurring in spondylolis thetic spines is exactly the same as in those without bony defects. The only difference is probably the liability to recurrence of acute or chronic disco dural conflicts. As in
III
IV
CHAPTER 58
other forms of lumbar instability, sclerosing injections can have' a good preventive outcome after reduction has taken place. Spondylolisthesis of itself causing symptoms
Spondylolisthesis can cause both backache and sciatica. The former has postural ligamentous characteristics: the ache is central, sometimes with vague and bilateral radi ation over the lower back. The discomfort is associated more with maintaining a particular position than with exertion. Dural symptoms are absent. There are no artic ular signs or symptoms; lumbar mobility is full and painless. Root signs are also absent. The only clinical finding is a bony irregularity palpated over the spinous processes. Treatment is that of ligamentous backache and consists of sclerosing injections (see pp. 918-923). Spondylolitic sciatica very much resembles a bilateral lateral recess stenosis but the patient is much younger. Increasing pain and paraesthesia appear in the standing position and may force the patient to sit or lie down, which caJ.ses the symptoms to disappear. Dural symp toms are absent. Clinical examination reveals little: there is a normal range of movement without pain. Root signs, such as positive straight leg raising, weakness or sensory loss are not found (J Cyriax, personal communication, 1 983; Calliauw and Van Velthoven27). The cause of sciatic pain in spondylolisthesis is unknown. The different hypotheses are: •
•
•
•
The forward movement of the listhetic vertebra drags on the nerve roots, which engage painfully against the shelf formed by the stable vertebra below (Cyriax:3 pp. 287-290). A fibrocartilaginous mass, with or without small ossicles, may form at the defect in the pars interarticularis. Adhesions around the nerve root and compression result.28 With the forwards and downwards drop of the vertebral body, the pedicles descend on the nerve roots and kink them as they emerge through the foramen.24 A forwards slipping of the vertebral body moves the transverse processes in a forwards and downwards direction, allowing the L5 roots to be pinched between the sacrum and transverse process (the 'far-out' syndrome29).
TREATM ENT
Patients with an accidentally detected spondylolisthesis do not need treatment. If the pain is caused by a second ary disc lesion, the patient is treated by the normal pro cedures used in discodural or discoradicular problems: manipulat�on, traction or epidural anaesthesia. The lia bility to recurrences after successful treatment, however, is much increased and in patients with both spondylolis-
-
NON-MECHANICAL DISORDERS 857
thesis and a d isc lesion the displacement will reappear. In these instances, sclerosing injections are used as a prophylactic measure. Spondylolisthesis which of itself causes lumbar pain should always be treated non-surgically. Sclerosing injec tions to the ligaments often give good results. If leg pain is a significant problem, nerve root infiltra tions can often abolish it. The patient can also be advised to wear a corset during occasional strenuous activity. If root pain cannot be abolished by these conservative measures, surgery should be considered. Surgical interven tion can also be considered if the listhesis is progressive or the patient presents with a Meyerding grade III or IV. In situ posterior arthrodesis, from the sacrum to the fourth lumbar vertebra, with or without removal of the loose posterior element of the fifth lumbar vertebra has been the accepted standard for surgical treatment. There have, however, been repeated reports of pseudoarthrosis in up to 60% of subjectsy,3o The range of further progres sion of the listhesis despite solid arthrodesis is also high, up to 25%.31-33 Recently, reduction of the listhesis and stabilization, whether by bilateral lateral fusion or interbody fusion has been recomrnended.34 It should be remembered, however, that even in grade III and IV listhesis, good results have been described after non-surgical treatment. Harris compared the outcome in 1 1 patients treated non-surgically with that in 21 patients treated by posterior interlaminar fusion. Although the results were slightly better in the surgical group, all but one non-surgical patients remained active and required only minor adjustments to their lifestyle to cope with the mild symptoms. None developed disabling pain, or neurological symptoms, or incontinence of the bowel or bladder.35 Apel et aP6 reported on the long-term results (40 years) after surgical and non-surgical treatment of grade I and grade II spondylolisthesis. Of the conserva tively managed patients, all functioned well. Among those undergoing surgery, poor results were confined to those patients in whom the fusion failed, and a pseudarthrosis developed (40%). Frennered et af37 stated that operative treatment for low-grade spondylolisthesis does not seem to give better results than conservative treatment. A recent prospective study, however, con cluded that surgical management of adult isthmic spondylolisthesis improves function and relieves pain more efficiently than an exercise programme.38
OSSEOUS DISORDERS
OSTEOPOROSIS
Osteoporosis is a metabolic disease, related to several d ifferent disorders. It is characterized by a reduction of
858 SECTION TEN - THE LUMBAR SPINE
bone mass which occurs predominantly in the axial skeleton, the femoral neck and the pelvis. By radio graphic criteria, 18% of men and 29% of women between the ages of 45 and 79 years of age have evi dence of osteoporosis and more sensitive methods for determining vertebral bone mineral density show that 50% of women past the age of 65 have asymptomatic osteoporosis.39 The radiographic appearances are changes in bone porosity, trabecular pattern and verte bral body shape (the so-called biconcave fishmouth ver tebrae).4o It is a common mistake to believe that these changes account for patients' backache. It should be remembered that uncomplicated osteoporosis does not cause any symptom except some loss of height of the spine. Thus the major explanation for long-standing back pain in the elderly does not appear to be related to spinal osteoporosis and, if a radiograph shows uncom plicated osteoporosis in a symptomatic patient, other sources for the pain should be sought.41 Osteoporosis may however lead to a pathological fracture. If this takes place, a sudden pain in a girdle distribution will result. PAG ET'S DI S EASE
Osteitis deformans or Paget's disease of bone42 is a local ized disorder characterized by a remarkable hyperactiv ity of osteoclasts and subsequent increase of osteoblastic bone deposition. As a result, the normal bone architecture is completely disturbed.43 In a vertebral body this can result in softening, broadening and collapse of the bone. The disease is reported to occur in approximately 4% of individuals over the age of 40.44 In the majority, the disease is restricted to a few bones. It must be emphasized that most patients with Paget's disease are asymptomatic.45 The main problem for the cli nician therefore is not the discovery of the Paget's disease but the association of the back symptoms with the Pagetoid lesion. Back pain and the associated angular kyphosiS arise as the result of collapse of the vertebral body. Sometimes new bone growth in the vertebral arch may compress nerve roots, resulting in a spinal stenosis or a lateral recess stenosis.46,47 FRACTURES Crush fracture of the vertebral body
This causes a wedge deformity. It usually occurs at the upper lumbar or at the thoracolumbar level and usually results from axial trauma or from flexion injuries. Wedging of a vertebral body may also result from a pathological fracture which is the consequence of senile osteoporosis, tumour, Paget's disease or tuberculous caries.
Immediate posttraumatic pain is referred bilaterally in the appropriate dermatome. The diagnosis is not missed if backache follows a gross trauma. In a pathological frac ture, however, the patient probably does not recall an injury that can be related to the onset of the symptoms. Nothing in the history then warns the examiner of the possibility of a crushed vertebra. However, if the history is taken carefully, and compared with the clinical findings, some unlikelihoods will immediately become obvious. They are: •
• • • •
The pain is usually located in the upper lumbar area: pathological fractures occur more often in the 'forbidden area'. Dural signs are absent: although the patient describes an intense backache, coughing does not hurt. Inspection reveals an angular kyphOSiS. Examination shows a capsular pattern, with symmetric limitation of lateral flexion. There are no dural signs: straight leg raising is normal, which is always suspicious in a case of acute lumbago.
The girdle pain lasts a week or two, whereafter a local ized bone pain remains. After 3 months the fracture will have united and symptoms have ceased. Although a wedged vertebra results in lasting malalignment of the related posterior joints, usually little ligametous pain results. Any continuous pain after the fracture has healed is from a coincident disc lesion. Indeed, any force sufficient to break bone will also threaten disc tissue and it is not hard to imagine that, after a crush fracture of a vertebral body, the disc above or below the lesion may also be damaged. The possibility of a coincident disc dis placement should therefore be considered in a case with persistent pain. Because of the permanent kyphosis and the possible elongation of supra- and interspinousliga ments, the protrusion may be very unstable and difficult to treat. Although manipulation usually affords excellent results, the improvement is not lasting unless sclerosing injections are given to stabilize the joint. Spondylolysis
Symptoms of back pain are often attributed to the existence of a spondylolysis (fatigue fracture in the pars interarticularis) in one of the lower lumbar vertebrae (L4 or L5). However, only a small proportion of subjects with spondylolysis presents with disabling low back pain.12 The relation between unilateral or bilateral back pain and a fatigue fracture of the pars interarticularis therefore remains unclear.48 Recent histological studies, however, could iden�ify a well-developed ligamentous structure covering the defect ('the spondylolysis ligament') and containing thin unmyelinated nerves.49,50
CHAPTER 58 - NON-MECHANICAL DISORDERS 859
Infiltration of bupivacaine hydrochloride (Marcain) into .,the pars defect can produce temporary symptom relief. Direct repair of the pars defect by internal fixation and bone grafting was effective in 90% of the cases.51 Fractures of the transverse processes
These may occur after direct trauma to the back. Alternatively they result from gross muscular effort, fre quently a resisted rotation strain; lumbar manipulation is a rare cause of fracture. The patient complains of posttraumatic and localized unilateral pain. Clinical examination reveals a partial articular pattern, with pain during side flexion away from the affected side. However, there is also pain during resisted movements: resisted side flexion to the painful side and resisted extension in the prone-lying position are both positive. The lesion may appear insignificant on radiograph. Pain usually ceases after a fortnight. If pain persists, a coincident disc lesion should be suspected. Alternatively, an emotionally unstable patient may capitalize on radio logical evidence of a 'fractured spine'. Stress fractures of the lumbar pedicle
Stress fractures of the contralateral pedicle in patients with unilateral spondylolysis has recently been reported.52,53 and termed 'pediculolysis'.54 The develop ment of a unilateral spondylolysis probably leads to a redistribution of forces, resulting in a stress fracture of the contralateral pedicle. Alternatively, not a fracture but a compensatory sclerosis and hypertrophy of the contra lateral pedicle develop.55,56 To date, it is not clear if the lesions are responsible for particular clinical syndromes.57
TUMOURS
Classically, neoplastic lesions in the lumbar spine are classified as benign or malignant lesions. The latter are subdivided into primary malignancies and metastases. Benign and primary malignant neoplasms are rare in the lumbar spine, whereas secondary deposits are common. Although the diagnosis of tumours of the lumbar spine is largely dependent on radiological examinations, it must be remembered that 30% of the osseous mass of bone must be destroyed before a lesion is radiologically evident.58 Therefore radiographs do not reveal early disease and too much reliance on radiographic appear ances can give both the patient and the physician a false feeling of security. Therefore, in the diagnosis of neoplas tic lesions, the history and clinical examination remain vital. Special attention must be paid to warning signs. When routine radiographs fail to support the clinical impression, a radioisotope scan must be obtained, in
order to demonstrate the presence of a malignant lesion and the extent of the spinal involvement. Benign tumours
Benign tumours of the vertebrae predominantly affect patients under the age of 30 years and are mostly local ized in the posterior wall. Chronic localized backache that is not dependent on posture and movement and does not ease with recumbency is the main characteristic of a benign tumour. Clinical examination may show a limited range of flexion due to a muscle spasm. If the lesion compresses nerve roots, slowly progressing sciat ica will supervene. Early detection of the lesion on the radiograph is not always easy. Osteoid osteoma. This constitutes about 12% of all benign hlmours (Dahlin and Unni:59 pp. 88-101) and appears mostly in children and adults below the age of 30 years. The pain is frequently exacerbated at night and is often relieved by small doses of aspirin.6o Treatment consists of local excision of the tumour. Osteoblastoma. This is a rare benign neoplasma of bone but has a predilection for the spine: approximately 40% of all osteoblastomas are found in the posterior elements of the spine and sacrum.61 The tumour is seen most fre quently in males under the age of 30 years.62 The back pain is localized, insidious in onset, with a duration of months or years and not as severe as in osteoid osteoma. Clinical examination may reveal muscle spasm and localized tenderness. Because of the expansive nature of the tumour, slowly progressive compression of nerve root(s), with radicular pain and evidence of neurological deficit, may occur. Haemangiomas. These account for less than 1% of symptomatic primary bone tumours (Mirra:63 pp. 492-497), although postmortem studies have demon strated that asymptomatic lesions exist in 1 2% of all ver tebral columns. This implies that most of these lesions remain asymptomatic throughout life. The thoracic spine is the location for 65%, the cervical spine 25% and the lumbar for only 1 0% . Patients with symptomatic haemangiomas are usually between 40 and 50 years of age.64 The main complaints is localized pain. Clinical examination may show limitation of movement from muscle spasm and localized tenderness. Increased weakening may results in a pathological fracture, which in turn may cause neurological symptoms.65 Since vertebral haemangiomas are usually asymptomatic and have a benign course, treatment is expectant. Radiation seems to afford a good outcome in patients with con stant, disabling pain.66 Eosinophylic granuloma. This is a rare bone lesion char acterized by the infiltration of bone with histiocytes,
860 SECTION TEN - THE LUMBAR SPINE
mononuclear phagocytic cells and eosinophils. It was first described by Jaffe and Lichtenstein in 1944.67 It occurs most commonly in children and adolescents68 and only 10% of the lesions are localized in the spine. Local and constant back pain is the first symptom. Clinical examination shows muscle spasm and local ten derness. If the lesion affects a vertebral body, a flatten ing - vertebra plana - will result. This spontaneous collapse of the vertebral body in children was first described by Calve in 192569 and was thought to be a manifestation of osteochondritis juvenilis.69 It seems that the collapse of the vertebra induces spontaneous healing of the granuloma, in that symptoms usually cease after the body has collapsed?O,71 This is a benign, cystic vascular lesion of bone. The majority of aneurysmal bone cysts occur in the long bones of the extremities of young adults.72 The lumbar spine is affected in only 10% of cases?3 The clinical presentation is lumbar pain that usually has an acute onset and increases in severity over a short period of time. Depending on the location and size of the lesion, the other clinical manifestations vary. If the lesion is at the spinous or transverse processes, the pain remains locaF4 If the vertebral body is affected, the lesion may expand, which can result in weakening of the bone, pathological fractures and serious neurological deficits. Although aneurysmal bone cysts are benign lesions, they may cause severe damage because of their expansive characteristics. The lesion therefore must be diagnosed early and treatment instituted without delay in order to keep disability to a minimum. Treatment is by surgery, radiotherapy or cryotherapy. Aneurysmal bone cyst.
Ma lignant tumours
Malignant tumours of the spine predominantly affect patients over the age of 50 and are mostly localized in the anterior spine elements. Metastatic lesions of the axial skeleton are much more common than primary malig nant lesions (chordoma, myeloma and chondrosarcoma), the overall ratio being 25:1 (Francis and Hutter;75 Mirra:63 pp. 448-454). Chordoma. This is a slowly developing malignant tumour that originates from the remnants of notochordal tissue and therefore occurs exclusively in the midline of the axial skeleton. It has a predilection for either end of the spinal column: 50% of cases occur in the sacrum and 38% in the skull base?6 The lesion is rarely reported below the age of 30 years and most tumours become evident between the ages of 40 and 70?7 Chordomas are slow-growing tumours with a locally invasive and destructive character. The common sacral tumours may be difficult to detect. The patient initially presents with localized pain in the
sacral area or with coccygodynia. The pain is dull, con stant and not relieved by recumbency. Often it is of long duration and only moderate, so that it does not force the patient to see the doctor.78 Chordomas of the sacrum extend anteriorly into the pelvis. Because the dural sleeve is not involved, presacral invasion of the nerve roots does not provoke radicular pain. Straight leg raising is also not limited. However, gross muscular weakness of one or both legs, together with considerable sensory deficit is detected. Sometimes the patient presents with urinary or bowel incontinence as wel1.79 Such a gross paresis in the absence of root pain always suggests a tumour. A radi ograph of the lumbar spine and sacrum discloses lytic bone destructions with calcified foci and a pre-sacral soft tissue mass.80,81 Patients with chordomas of the lumbar spine may present with localized central lumbar pain sometimes radiating bilaterally. Involvement of nerve roots may induce bilateral sciatica. Clinical examination then shows muscle spasm and bilateral weakness.82 Treatment consists of total resection of the tumour, which usually presents a major problem. Often partial resection, followed by radiation therapy, is the only option.83 Chemotherapy is ineffective.84 Chondrosarcoma. A malignant tumour that forms in car tilaginous tissue. The tumour is frequently located in the pelvis and lumbar spine and grows extremely slowly. The usual age of onset is between 40 and 60 years (Dahlin and Unni:59 pp. 227-259). The tumour may be symptomless over many years. Local pain is very suggestive of actively growing tumour. When neural elements are compressed by the tumour, abnormalities are found on neurological examination. The treatment of choice is total resection of the tumour. Myeloma. This is a malignant tumour of plasma cells and is the most common primary tumour of bone; the spine is almost always involved. The disseminated form is multi ple myeloma and accounts for 45% of all malignant bone tumours (Dahlin and Unni:59 pp. 193-207). The patients are usually in an older age group, in that the disease is rare below the age of 50 years. Plasmacytoma is the solitary form and affects the spine in about 50% . of the patients.85 The most common complaint is of back pain, which does not vary with exertion although initially may be relieved somewhat by bed rest. Malignant disease is suggested by steady worsening of the backache which eventually becomes continuous, irrespective of posture or movement. As the backache becomes more severe sciatica, which is often bilateral, appears.86 The facts that the backache does not cease after the root 'pain comes on and that the root pain is bilateral, immediately draws attention to the possibility of an expanding
CHAPTE R 58 - NON-M ECHAN ICAL D I SORD E RS 861
lesion. Alternatively, the backache is sudden as the resul-t of a pathological fracture. Findings on clinical examination depend on the extent of the disease. In the early stage, there is usually only lumbar muscle spasm and localized tenderness. In later stages, angular kyphosis and signs of nerve root com pression at different levels can be seen. Finally, signs of generalized illness, such as fever, weight loss and pallor, become prominent. Radiographically, multiple myeloma is characterized by the presence of round lytic defects in the bone without any surrounding reactive sclerosis. Occasionally, lytic defects may not be obvious, and the radiograph shows nothing more than a diffuse osteopenia.87 In such circum stances the differential diagnosis must be made by laboratory examinations,88 which consistently reveal an elevated erythrocyte sedimentation rate - seldom les than 100 mm / h. Characteristically, abnormal Bence-Jones pro teins can be demonstrated in the urine.89 The most impor tant test is serum protein electrophoresis, which identifies a monoclonal spike in more than 75% of the patients and hypogammaglobulinaemia in 9%.90 The usual course of multiple myeloma is one of gradual progression . Systemic therapy with melphalan and cortisone may improve clinical symptoms, but the average survival seldom exceeds 5 years.91 Metastatic tumours. The most common malignant tumour in the spine is metastatic cancer. The prevalence of metastases increases with increasing age, and patients who are aged 50 years or older are the population at greatest risk. Neoplasms frequently associated with spinal metastases are of prostate, 92 breast, lung, thyroid and colon.93 Up to 70% of patients with a primary neo plasm will sooner or later develop metastases in the tho racolumbar spine.94 The predilection of metastases for the lumbar spine may be explained by the functioning of Batson's plexus. This is a venous network, located in the epidural space between the bony spinal column and the dura mater. Because this plexus has no valves to control blood flow, metastatic cells may easily enter it and lodge in the connected sinusoidal systems of the red bone marrow of the vertebral bodies.95 Some suspicion may arise when, for the first time, a patient over the age of 50 presents with an attack of low back pain. Especially if the pain has a gradual onset and increases in intensity over time, the patient should be suspected of suffering from a malignant disease. The concern should be even greater if there is a prior history of malignancy. In the beginning the pain is localized but very soon it spreads down the leg in a distribution not corresponding to a single root. Sometimes there is bilat eral sciatica and the lumbar pain does not ease but even becomes worse when the sciatica appears. Because the
tumour often extends into the epidural space, dural symptoms may be present. However, not all skeletal metastases cause pain: symptoms may occur only when the lesion is complicated by a pathological fracture.96 Results of the clinical examination depend on the stage; at first, there will be muscle spasm, markedly limiting movements, especially side flexions. Localized tenderness, particularly at the 'forbidden' upper lumbar area causes more suspicion. Later, distinctive neurologi cal signs will immediately draw attention to the possible existence of a spinal neoplasm: • • • • •
Bilateral weakness Weakness of the psoas muscle Signs of involvement of two or three consecutive roots, or non-adjacent roots Discrepancy between pain and weakness A warm foot on the affected side.
It is important to stress that radiographs may be normal and are not reliable early in the course of a metastatic lesion. Clinical symptoms and even signs of gross muscular weakness may appear before the radio graph shows erosion or collapse of bone.97 If the clinical features of metastasis are present but the radiographic examination remains negative a bone scan may be neces sary to establish the diagnosis.98 MRI examination is a quite sensitive complementary technique and appears to be more specific for metastasis in certain locations of the spine.99 Cure is seldom possible and treatment of metastatic deposits in the spine is palliative: it includes radiation therapy, corticosteroids and decompressive laminectomy.
RHEUMATOLOGICAL DISORDERS
AN KYLO S I N G SPON DYLITIS
This disease usually affects the sacroiliac joints initially, and then appears in the thoracolumbar area. Thereafter, the lower lumbar, the thoracic and the cervical spine also become affected100 (see Ch. 63). Although the lesion invariably starts at the sacroiliac joints, it is possible that this does not cause any symptoms and the first complaint is then of backache. Backache in ankylosing spondylitis is typicall y inter mittent; it comes and goes irrespective of exertion or rest. However, the pain and the stiffness are greatest in the morning and usually improve with movement. Several segments at the upper lumbar and thoracolumbar level become involved at about the same time. 1 01 Because the pain is usually limited to the central part of the spine and does not refer laterally, the patient complains of vertical distribution (Fig. 58.5a). This contrasts with the more or
862 SECT I O N TEN - T H E L U M BA R S P I N E
(a)
(b)
lumbar and thoracolumbar spines. First there are signs of osteitis of the anterior corners of the vertebral bodies. This results in the typical 'squaring' of the vertebrae. Healing of the inflammation leads to a reactive sclerosis in the anterior portions of the vertebral bodies. Later on, thin, vertically orientated calcifications of the annulus fibrosus and anterior and posterior longitudinal liga ments appear. These growing 'syndesmophytes' can enclose the whole axial skeleton, which is then called a 'bamboo spine'.102 R H E U MATOI D ARTH R ITIS
Figure 58.5 Localization of pain affecting the upper lumbar level in ankylosing spondylitis (a), dural reference of low back pain in a lumbar disc disorder (b).
less horizontal, gluteal and asymmetrical reference of dural pain in a lumbar disc disorder (Fig. 58.5b). Inspection usually shows a flat lumbar spine, together with the beginning of an upper thoracic kyphoSiS. The motion of the spine is impaired in a symmetrical way, which is best demonstrated by a gross limitation of side flexion in both directions. There is also upper lumbar tenderness and the end-feel during a downwards thrust on the prone spine is hard. Sometimes an acute increase in pain caused by a sprain of the stiffened lumbar joints can simulate an attack of lumbago. The patient then states that lifting something heaving caused immediate and agonizing pain at the upper lumbar level. Although the history probably sug gests a disc protrusion, there is a complete absence of dural signs, which is rather unusual in such an acute case. Furthermore, there is a symmetrical limitation of side flexion and the pain on the palpation is upper lumbar, in the ' forbidden area'. Diagnosis is confirmed by radiography of the sacro iliac joints. Because lumbar manifestations occur some years after sacroiliac manifestations, plain radiographs of the latter will almost certainly reveal the typical nar rowed joint spaces and surrounding sclerosis. In later stages, radiographic abnormalities also appear in the
Rhematoid arthritis, a systemic chronic inflammatory disease which involves synovial joints, may affect the facet joints of the lumbar spine, although it is found more frequently in the cervical articulations. The disease does not affect the sacroiliac joints.103 Those who develop low back pain secondary to rheumatoid arthritis usually have a long-standing history of disease in the joints usually affected by the illness.104 Pain stems from the facet joints and therefore its refer ence does not spread beyond the hips. l OS The symptoms are inflammatory in nature, with pain and stiffness increasing with rest, greater in severity in the morning and improving during activity. Clinical examination reveals limitation of movement in a capsular way and localized tenderness. The diagnosis is based upon the typical history, the clinical appearances of the peripheral joints and the characteristic laboratory findings. REITER'S SYN DRO M E
This is a triad of urethritis, arthritis and conjunctivitis.106 It is the most common cause of arthritis in young men and primarily affects the joints of the lower extremity. The disease results from the interaction of a specific infec tion and a genetically predisposed host. Although back pain is a frequent symptom of patients with Reiter's syn drome, pain usually stems from the sacroiliac joint and lesions of the lumbar spine are rare lO7 (see Ch. 63). AN KYLO S I N G HYPE ROSTOSIS
This disease is also known as the vertebral hyperostosis of Forestier.108 More recently 'diffuse idiopathic skeletal hyperostosis' (DISH) has been suggested, in recognition of the frequent combination of both spinal and extraspinal foci. l o9 According to autopsy findings, it seems to be a common entity in the eldery.l l0 Despite the impressive anatomical abnormalities, most patients rarely have significant disability from the illiless, the principal complaint being increasing stiffness. Some patients develop a vague and local ache in the entire
CHAPT E R 58 - NON-M ECHAN ICAL DISORD ERS 863
trunk. III Clinical examination shows marked limitation of movement at every spinal joint. Dural and radicular signs are of course absent. Laboratory parameters are normal and the diagnosis of DISH is a radiographic one. The criteria are a flowing calcification along the anterolateral aspect of four con tiguous vertebral bodies, preservation of the normal intervertebral disc height and absence of apophyseal arthrosis or sclerosis. 112 Treatment is seldom necessary, in that the complaints are rather minor.
INFECTIONS
Infections of the spine are rare. However, it is important to remember them as a potential source of backache. An early diagnosis is vital, because the prognosis of infections of the vertebral column is excellent if the disease is recognized early. Infections involving the lumbar spine include vertebral osteomyelitis, inter vertebral discitis and herpes zoster, and viral infection of the dorsal root ganglia.
VERTE BRAL OSTEOMYE LITIS Pyogenic vertebral osteomyelitis
This occurs as the result of haematogenous spread through the blood stream. Pelvic lesions, such as urinary tract or rectosigmoid infections, preferentially spread to the vertebral column through the venous plexus of Batson. l 13 During recent decades the clinical features of vertebral osteomyelitis have changed. ll 4 Before the antibiotic era, it used to be a disease of chil dren and adolescents, with a rapid evolution and in most cases caused by Staphylococcus aureus. Now, the mean age of patients reported with osteomyelitis is 50 years, the onset is insidious and the development is Slow.ll5 The diagnosis of vertebral osteomyelitis is frequently missed because the patient's symptoms are ascribed to mechanical problems. Onset of back pain is insidious and it becomes more and more severe. The central ache is usually constant, although it is sometimes increased by exertion. If the lesion becomes more invasive, the patient will find it difficult to stand or sit upright. In a later stage, the infec tion may extend beyond the bone and can produce a psoas abscess: the patient may then present with an abdominal syndrome or with hip pain.n6 Should the infection drain into the spinal canal, an epidural abscess or meningitis will result.II7 In the early stage, the signs may be insignificant, with only slight limitation of movement. As a rule, side
flexions are symmetrically limited. Local tenderness at the affected level can be detected during passive forcing of extension in the prone-lying position. Because the first and second lumbar vertebrae are the levels in the axial skeleton most commonly affected, lIB the discovery of pain at the 'forbidden area' during selective examination will alert the examiner. As the pain worsens, side flexions become more and more limited and muscle spasm limits flexion. Because of severe pain, the patient finds it more and more difficult to remain upright. This could suggest an attack of lumbago but when it comes to further clinical exami nation, straight leg raising is found to be of full range and completely painless. Patients with psoas muscle irritation also present with decreased hip motion and a painful weakness of hip flexion. It is important to notice that, in most cases, fever and signs of general illness only appear if an abscess forms.119 Radiographic evidence of the disease follows the symptomatic onset by 1-2 months. Bone scintigraphy usually demonstrates abnormalities at an earlier stage of disease although it should be remembered that false positives and negatives do occur. Computed tomography may also show bony changes before their appearance on routine radiographsYo Treatment includes antibiotics and bed rest. The choice of antibiotic is dependent on the identification of the organism causing the infection. Tuberculous vertebral osteomyelitis
This has a clinical course that can be distinguished from pyogenic infections. Before the antibiotic era, it was a disease of children but nowadays patients with spinal tuberculosis have an average age between 40 and 50 years.121 Alcoholics and drug addicts are at greatest risk of developing the disease.122 Tuberculous spondylitis occurs as the result of haematogenous spread from foci in either the lungs or the genitourinary tract. The lesion begins under the bony endplate and, although initially only the vertebral body is affected, in a later stage the infection can spread to disc, soft tissues and spinal cord. Abscess formation is present in about 50% of the cases.123 The disease is very insidious, and the time elapsing before a diagnosis is made may be as long as 3 years.I24 Initially there is a vague and localized backache. Later the pain can spread to the buttock. A careful history also reveals the existence of constitutional problems such as anorexia, weight loss, intermittent fever and night sweats. Limitation of movement in a capsular way and muscle spasm, together with localized tenderness over the involved vertebra, are the main clinical findings in the
864 SECTI O N TEN - T H E L U M BAR S P I N E
early stage. Later there is localized bony deformity, resulting from vertebral collapse or neurological abnor malities. Because of the insidious nature of the disease and the insignificant and local symptoms, the onset of paraplegia is sometimes the first manifestation of tuber culous spondylitis.125 Because the disease has a slow development, patients with tuberculous spondylitis usually present with identifiable destruction of vertebral bodies. Investigation by CT seems to be the best way of searching for abscess forma tion.126 Treatment consists of antituberculous drugs and immobilization. Surgery must be considered if, despite antituberculous therapy, abscesses progress.
I NTERVERTE BRAL DISC S PACE I N F ECTI O N S
Infections o f the intervertebral disc can develop second ary to haematogenous invasion via the blood stream. The primary lesion is usually an infectious endocarditis or a urinary tract infection.126 The most common cause for spondylodiscitis, however, is a direct complication of disc surgery. 1 27-1 29 The clinical picture is that of an acute lumbago which appears 1 week to 2 months after the discectomy. The pain radiates in a dural manner to the gluteal region, groin and limbs, is exacerbated by movement and is relieved by absolute rest. Dural symptoms are present. There are dural and articular signs. Fever is rarely present but the erythrocyte sedimentation level is usually elevated.130 Since the condition closely resembles a disco dural conflict, nothing except the previous disc surgery will draw attention to the possibility of an infection. It is therefore wise to consider every case of 'acute lumbago' occurring in the first months after discectomy as a discitis until the reverse is demonstrated. Radiographs do not show abnormality during the first few weeks. The earliest change is a decrease in the height of the affected intervertebral disc space. Later, relative sclerosis and irregularity at the vertebral end plates will be noted. If a disc infection is suspected, a bone scintillation scan is indicated and identifies an area of increased bone activity in the adjacent verte brae. 131 During the last decade MRI has become the radiological method of choice for establishing the diag nosis of spondylodiscitis, in particular with regard to differentiating between cases with and without abscess formation.132,133 Treatment includes antibiotics and immobilization. The childhood form of discitis develops in children between 2 and 6 years old. The patient presents with antalgic posture, muscular defence, unexplained fever and increased erythrocyte sedimentation rate.134,1 35
H E RPES ZOSTER
This is a sequela of previous infection with chicken pox. After the termination of the illness, the virus remains dormant in the posterior spinal sensory ganglia. During a period of low host resistance, the virus multiplies, which results in pain and skin lesions.136 Herpes (shingles) occurs more frequently in the elderly and in patients with impaired immune function. The patient complains of segmental pain which is burning or shooting in character. Since the pain antedates the appearance of the vesicles by 4-7 days, the early diag nosis can be missed and the patient may be mistakenly regarded as suffering from sciatic pain, although exami nation of the lumbar spine and the neurological examina tion of the limbs are norma1.138 Sometimes, however, dysaesthesia in the area of skin supplied by the affected nerve root can be detected. Once the skin lesions develop in a segmental distribution, the diagnosis will be obvious. Sometimes patients with herpes zoster may also demon strate a mild and temporary paresis in the motor nerve that corresponds to the affected level. Treatment is directed at controlling the pain.
INTRASPINAL LESIONS
Pathological processes may affect tissues inside the spinal column (Fig. 58.6). In the lumbar area they can be extradural or intradural. EXTRAD U RAL LESIONS Extradural neoplasms
These are metastatic lesions that have invaded the intraspinal space from contiguous structures. They
Figure 58.6 Intraspinal lesions: 1 , extraspinal, osseous lesions; 2, intraspinal, extradural lesions; 3, intraspinal, intradural lesions.
CHAPT E R 58 - N O N -M ECHAN ICAL D I SO R D E RS 865
usually remain extradu ral because the dura is resistant to invasion by the neoplasm. Epidural abscesses and epidural haematomas
These present as acute backache with severe dural signs and symptoms. There is a rapid progression to bilateral sciatica and neu rological weakness.139-141 Intraspinal synovial cysts
Cysts arising from the synovium-lined facet joints can exert pressure on the nerve root sleeve and cause unilat eral sciatica. 1 42 Cauda equina compression has also been reported.143 Diagnosis is made by CT or MRI and the treatment is surgicaP44 I NTRADURAL LESIONS Arachnoiditis and arachnoid cysts
Inflammatory changes to the arachnoid space (arach noiditis) develop after myelography with iophendylate, in spinal injuries and as a complication of haemorrhages or meningitis. 14s The patient complains of diffuse and constant back pain, sometimes radiating to both legs. Paraesthesia and dysaesthesia may be present. The prognosis is poor and there is no effective treatment. Neurofibromas and meningomas
Meningomas and neurofibromas are slowly growing benign tumours, arising from meninges and spinal nerves. They are rarer at the lumbar spine than at the cervical level. As intradural spinal tumours can compress the dura mater, the nerve roots and the nerve root sleeves, dural and radicular symptoms and signs will be present and the clinical picture usually mimics a herni ated disc - between 0.8 and 1 .0% of patients presenting with symptoms consistent with disc herniation have intraspinal tumours.146,147 If the tumour involves the nerve roots of the first or second level, diagnosis is not very difficult because first and second lumbar disc lesions are extremely rare. At the lower lumbar levels, however, neuromas are very difficult to detect, which explains the considerable delay in diagnosis.148, 149 The patient presents with back pain and / or root pain. Sometimes the pain increases at night or in the supine position. Dural symptoms, such as pain during coughing and sneezing, are always present - a neuroma is unlikely if a cough does not hurt. Unlike a disc lesion, coughing usually hurts in the limb rather than in the back. Clinical examination shows limitation of spinal move ments and straight leg raising. Motor and sensory deficit together with reflex disturbances can be present. Differential diagnosis of neuromas and lumbar disc lesions is almost impossible if only the actual symptoms and signs are considered. However, when the duration
and evolution of the symptoms are analysed, certain fea tures should arouse suspicion. The evolution of radicular pain in neuroma is that of a slowly progressive lesion. This is completely different from the evolution in disco radicular interactions, in which the sciatica becomes rapidly worse and reaches a peak within 1-2 months; severe symptoms may then persist for a certain length of time, which seldom exceeds 2 months. Although primary posterolateral protrusion in young patients can have a slower and more gradual onset, the evolution usually does not take more than 6 months. Hence any case of root pain that is getting worse at the end of 18 months is suspect (Cyriax:3 p. 293). Also, increasing backache after root pain has set in must alert the exam iner. The range of straight leg raising is not much help in the differential diagnosis: if the lesion lies upwards in the canal, straight leg raising may be normal, but if the neuroma lies near the intervertebral foramen it will be markedly and often bilaterally restricted.1so Palsies affecting two non-adjacent roots may suggest a neuroma, and bilateral sciatica should also alert the cli nician to the possibility of a cauda equina tumour (see Fig. 58.7).152 Late manifestations are marked motor deficit, with drop foot or widespread weakness and muscle atrophy. Bladder dysfunction also tends to be a late manifestation, although u rinary and rectal inconti nence sometimes appear early in the evolution. l s3 If the clinical picture suggests neuroma, an epidural injection with 50 ml of 0.5% procaine should be given. Because the fluid is forced between spinal wall and the dural sac, it cannot touch the neuroma or the nerve root. Although the introduction of the fluid creates consider able and sometimes unbearable root pain, it has no immediate effect on the symptoms or on the range of straight leg raising if this is tested some minutes later. Had the root pain been caused by a discodu ral conflict, the injection would have created some anaesthesia immediately afterwards. No improvement of straight leg raising after the epidural injection therefore strongly suggests the possibility of a neuroma and the patient should be referred for a myelogram. Computed tomog raphy is not the technique of choice because a lesion higher up in the spinal canal will always be missed. In addition, as disc protrusions are often asymptomatic,1s4 the clinical picture may be wrongly ascribed to such a cause, surgical opinion sought and an exploration of the disc undertaken. Craig et a[lS5 summarized this in 1952 when they stated: ' It is not unusual at this clinic to remove a spinal cord tumor from a patient who has had a previous operation for protruding disc without relief of symptoms'. Treatmeht consists of laminectomy and total excision of the tumour, which gives excellent results provided there is not too much neurological dysfunction.
866 SECTION TEN - T H E L U M BAR SPI N E
Discoradicular Interaction
Symptoms
Neuroma
Backache ceases when root pain comes on Root stabilizes after 2-4 months
Backache increases Root pain continues to worsen after 8 months Persisting or increasing root pain after 1 year
Recovery of root pain after 1 year
A cough always hurts, mostly in the limb
A cough sometimes hurts in the back
c
'ro c..
o Signs
3
6
Months
- Backache
- Backache
- Root pain
- Root pain
9
12
Root signs evolve in the course of 1-4 weeks They continue unchanged for 6-8 months
Recovery may be expected within 1 year after onset Palsy is uniradicular or involves two adjacent roots
(L4-L5 or L5-S 1 )
o
3
6
Months
9
12
Root signs appear insidious
Progression is very slow, month by month No spontaneous recovery, but steadily
increasing weakness
Triple palsies, a palsy affecting two non-adjacent roots or a bilateral palsy are all possible
Straight leg raising may be positive or negative in both cases and is therefore no help in differential diagnosis
Figure 58.7
Differential diagnosis of discoradicular conflict and neuroma in the lower lumbar area.151
Differential diagnosis.
The following conditions may
resemble a neuroma. There are rare cases of root adher ence to the posterior aspect of the intervertebral joint, which occur after the herniation has shrivelled away as the result of the natural course of the disc lesion. The patient's sciatica gets slowly less and after 2 years the pain may have gone. However, the patient continues to find that they cannot bend forwards, and examination shows about 45° limitation of straight leg raising on the affected side. Attempted trunk flexion causes pain in the back and the leg. Apart from that, there are no other com plaints and the sciatic pain is slight. The pain also does not increase; there is no appreciable neurological deficit and certainly not an increasing one. The condition thus
Adherent nerve root.
presents as sciatica, usually in a young man in whom the symptoms have abated but the signs continue. As in neuroma epidural local anaesthesia does not alter the range of straight leg raising. Increasing protrusion on an a trophied root. The patient had severe sciatica some years ago. Sudden loss of pain, together with considerable weakness of one or two roots, indicates that a root atrophy took place. There has been no recovery from the palsy and one day, without pain, the patient notices increased weakness and more numbness. This can be explained by a further protru sion of disc substance at the original level. Because it impinges against the atrophied nerve root there is no pain, but there is further loss of sensory and motor conduction.
C H APTER 58
The patient is suffering from sciatica, which is improving (as expected) after some months. After a while, a new disc lesion develops at an adjacent level, impinging against an adjacent or a con tralateral root. Of course, weakness extending to another level after some months' sciatica is suspect, but the dif ferential diagnosis will easily be made on a myelogram. A second disc protrusion.
Neuralgic amyotrophy (Cyriax:3 p . 300). This uncommon parenchymatous disorder of the peripheral nerves usually afffects three to four consecutive roots at the same side. The origin is unknown but the disease has a sponta neous and complete recovery within a year. The patient, usually a man between 50 and 70, experi ences a sudden and severe ache in one leg. The pain is considerable and not altered by position or motion. There is no pain on coughing or sneezing. After about 3 months the .symptoms slowly ease, and 6 months after the onset they have disappeared. Examination shows a full range of movement and full and painless straight leg raising. Considerable muscle weakness is detected where the muscles are innervated by two to three different roots. An important differential diagnostic finding is that the palsy is maximal from the first and does not increase or spread to the other limb. There is no sensory loss. There is no treatment for this condition. As the pain ceases, so the muscles gradually recover. The disorder completely resolves 1 year after its onset.
PAIN REFERRED TO THE BACK
It should be remembered that back pain occurs not only due to lesions of bones, discs and ligaments but also can be referred from intra-abdominal or pelvic lesions. The prominent feature will then be the complete absence of articular, dural and radicular signs during routine clinical examination. Lesions of the aorta and genitourinary or gastrointestinal diseases should be suspected in such circumstances. LESIONS OF THE AORTA
An arterial aneurysm is a localized or diffuse enlarge ment of an artery. In the abdominal aorta it occurs most commonly in men over the age of 50 years.I56 The major ity of patients with a stable abdominal aneurysm are asymptomatic, and pain is only associated with enlarge ment or rupture. Most frequently the pain is abdominal, dull and steady. Sometimes the main symptom is severe and increasing backache, accompanied by L3 pain in the left leg. IS? Increasing back pain and L3 pain in an elderly patient with a negative functional examination should
-
N O N -M ECHAN ICAL D I SORDERS 861
therefore always arouse suspicion. The patient should be referred immediately for ultrasonography and CT of the abdomen. These methods are non-invasive and very reliable in identifying the location of the lesion.l58 Acute occlusion of the abdominal aorta presents as acute and severe low back pain and abdominal pain together with acute claudication of the lower extremities.159 G E N ITO U R I NARY D I S EASES
The colic and excruciating pain caused by a kidney or ureteral stone is well known. The pain is sudden, sharp and has a spasmodic character. It is upper lumbar and radiates to the lateral flank and along the course of the ureter into the ipsilateral flank and along the course of the ureter into the ispilateral testicle (men) or labium (women). Renal infarction causes a sudden and sharp pain in the costovertebral angle. Renal cancers may present as increasing upper lumbar and flank pain, which is con stant and dulP60 Clinical examination reveals a limita tion of the side flexion away from the painful side as the only finding. This warning sign should always prompt the physician to refer the patient for further internal examination. Diseases of the bladder and the prostate rarely cause lumbosacral pain. Lesions of the testis, however, often cause backache and back pain may be a presenting symptom in 1 0-21% of patients with testicular carci noma.161 Patients may even present with back pain in the absence of any testicular symptom. 1 62 In testicular carci noma, the pain is dull and persistent, localized over the lumbosacral and paravertebral region. Functional lumbar examination is completely negative, but exami nation of the testicles reveals a testicular mass together with diffuse induration. In women, referred pain from the genital organs (uterus, fallopian tubes or ovaries) is possible, although backache from gynaecological causes should not be overestimated. For instance, malposition of the uterus, in times past regarded as a main source of backache in women, certainly does not cause any back trouble.163 In contrast, endometriosis, a disease associated with the presence of endometrial tissue outside the uterine cavity, is often associated with intermittent back pain. The pain is lower lumbar and often irradiates to the buttocks or thighs. The symptoms characteristically increase at the time of menstruation and persist throughout the entire period of bleeding. Other symptoms associated with the disease are dyspareunia, infertility and menorrhagia.I64 It is a well-known fact that women complain more often of low back pain during pregnancy. The incidence reported varies between 24 and 49%.] 65-1 68 The increase in backache during pregnancy is not very well understood.
868 SECT I O N TEN - T H E LU M BAR S P I N E
Hormonally induced laxity probably allows increased biomechanical stress on the pelvis and spine, which results in more postural ligamentous pain164,] 69 But there are several studies indicating that pregnancy is also a risk factor for lumbar disc herniations.165,1 66 Pelvic inflammatory disease, an acute or chronic infec tion of the fallopian tubes, is also associated with pain at the lower back, radiating into the buttocks. The chief clin ical symptoms, however, will be lower abdominal and pelvic pain, with a feeling of pelvic pressure.J67 GASTRO I NTESTINAL DISEASES
Diseases of the pancreas, stomach, duodenum and colon may be associated with low back pain. The gallbladder has a TS-T9 origin and pain is therefore felt in the thoracic region. Cyriax described cases of gastric ulcer adherent to the lumbar spine. The back symptoms are connected both with eating and with posture. The pain is upper lumbar, with radiation into one or other iliac fossa. It is not brought on by exertion but appears during eating. The only finding during clinical examination is central discomfort during extension. The combination of pain
influenced by posture and abdominal visceral function brings the diagnosis to mind, and the diagnosis is confirmed by gastroscopy. A peptic ulceration of the posterior duodenal wall can also cause low back pain. Again the pain is localized to the L2-L3 lumbar level, but appears 1-3 hours after the meal, and is relieved by further intake of food. The pain has no relation to physical activity.17O Sometimes there is tenderness at the upper lumbar ('forbidden') area. Pain from chronic pancreatitis or carcinoma of the pan creas is felt in the epigastrium and is referred to the upper lumbar area.l 71 Disease processes that affect the head of the pancreas cause pain to the right of the spine, while lesions of the tail are felt at the left side. Lesions of the colon - both diverticulitis and carci noma - can be associated with low back and flank pain.172 Patients with a rectal carcinoma often complain of sacral pain. Invasion of the nerve roots at the front of the sacrum gives rise to gross weakness of the muscles in both legs. As the dural sleeve is not affected here, the lesion does not provoke pain and the weakness often remains silent. Similar back pain may be the fi rst sign of recurrence after apparently successful excision of a rectal cancer.
REFERENCES 1 . D e Palma A , Rothman R H . The Intervertebral Disc. Saunders, Philadelphia, 1970. 2. Albert TJ, Balderston RA, Heller JG et al. Upper lumbar disc herniations. J Spinal Disord 1993;6:351-359. 3. Cyriax J H . Textbook of Orthopaedic Medicine, vol 1, Diagnosis of Soft Tissue Lesions. 8th edn. Bailliere Tindall, London, 1982:263. 4. Gurdjian ES, Thomas LM. Neckache alld Backache. Thomas, Springfield, 1 970.
5. Armstrong J. L U lllbar Disc Lesions. Wi l l iams & Wilkins, Baltimore, 1 965. 6. Kramer J . I ntervertebral Disk Diseases. Thieme, Stu ttgart, 1981 :148. 7. Herbiniaux G . Traite sur Divers Accouchements Laborieux, et sur les Polypes de la Matrice. Be Boubers, Bruxelles, 1 782. 8. Kilian HF. Schilderungen neuer Beckenformen und ihres Verhalten irn Leben. Basserman und Mathy, Mannheim, 1854. 9. Wil tse L, Newman P, MacNab 1. Classification of spondylolysis and spondylolisthesis. Clin Orthop 1976;117:23-29. 1 0 . Rosenberg N. Degenerative spondylolisthesis predisposing factors. j Bone Join t Surg 1 975;57A:467. 1 1 . American Academy of Orthopaedic Surgeons, Committee on the Spine. A Glossary on Spinal Terminology. American Academy of Orthopaedic Surgeons, Chicago, 1987. 12. Wil tse LL, Widell EH, Jackson ow. Fatigue fracture: the basic lesion in isthmic spondylolisthesis. I Bone Joint S u rg 1975;57A : 1 7. 13. Lonstein J E . Spondylolisthesis in children. Cause, natural history, and management. Spine 1999;24(24):2640-2648. 14. Hutchinson MR. Low back pain in elite rhythmic gymnasts. Med Sci Sports Exer 1999;31(11):1 686-1688.
15. Sairyo K, Goel VK, Grobler LJ, Ikata T, Katoh S. The pathome chanism of isthmic lumbar spondylolisthesis. A biomechanical study in immature calf spines. Spine 1 998;23(13):1442-1446.
16. Fredrickson BE, Baker 0, McHollick W et al. The nahHal history of spondylolysis and spondylolisthesis. j Balle joillt Surg 1984;66A:699-707. 1 7. Turner RH, Bianco AJ Jr. Spondylolysis and spondylolisthesis in children and teenagers. j Bone Joint Surg 1971;53A:1298-1306. 18. Moreton RD. Spondylolysis. I Am Med Assoc 1966;195:671-674. 19. Neugebauer FL. The classic: a new contribution to the history and etiology of spondyloli sthesis. Ciin Orthop 1976;117:4-22. 20. Stewart TO. Incidence of separate neural arch in the lumbar vertebrae of Eskimos. A lii ] Phys AntiJropo/ 1931 ;16:51-62. 2 1 . Kettelkamp DB, Wright DG. Spondylolysis in the Alaskan Eskimo. J Bone loint Surg 1971;53A:563-566. 22. Meyerding HW. Low backache and sciatic pain associated with spondylolisthesis and protruded intervertebral disc. J Bone joillt Surg 1 941 ;23:46 1 . 23. Lowe RW, Hayes TO , Kaye J , Bagg JR, Leukens C A Jr. Standing roentgenograms in spondylolisthesis. Clin Ortliop 1976;117:80-84. 24. MacNab 1. Backache. Williams & Wilkins, Baltimore/ London, 1977:50. 25. Virta L, Roonemaa T. The association of mild-moderate isthmic lumbar spondylolisthesis and low back pain in middle-aged patients
is
weak
and
it
only
occurs
in
women.
Spine
1993;18: 1496-1503. 26. Key JA. Intervertebral disc lesions are the commonest callse of low back pain, with or without sciatica. Ann Surg 1945;121:534. 27. CalJiauw L, Van Velthoven V. Ervaringen bij de behandeling van spondylolisthesis. Ned Tijdschr Geneeskd 1987;43(13):849-858.
CH APTER 58 - N O N-M ECHAN ICAL D I SORDERS 869
28. Gill GC, Manning Je, White HL. Surgical treatment of spondylo listhesis without spine fusion. Excision of the loose laminar with decompression of the nerve roots. j Bone joint Surg
53. Garber JE, Wright AM. Unilateral spondylolysis and contra lateral pedicle fracture. Spine 1986;11:63-66. 54. Gunsburg R, Fraser R. Stress fractures of the lumbar pedicle: case reports of ' Pediculolysis' and review of the literature. Spine
1955;37 A:493-520. 29. Wiltse LL, Guyer RD, Spencer CW, Glenn WV, Porter IS. Alar transverse process impingement of the L5 spinal nerve: the
1991;16: 1 85-189. 55. Maldague BE, Malghem JJ. Unilateral arch hypertrophy with spinous process tilt: a sign of arch defici ency. Radiology
far-out syndrome. Spine 1984;9:31-41. 30. Wiltse LL, J ackson Ow. Treatment of spondylolisthesis and
1976;121:567-574. 56. Wilkinson RH, Hall JE. The sclerotic pedicle: tumour or pseudo
spondylolysis in children. Clin Orthop 1976;117:92-100. 31 . Laurent LE, Osterman K. Operative treatment of spondylo
tumour? RadiologJj 1974;111 :683-688. 57. Sherman FC, Wilkinson RH, Hall JE. Reactive sclerosis of a
listhesis in young patients. Clin Orthop 1976;117:85-91 . 32. Johnson JR, Kirwan EO. The long-term resu lts o f fusion ' in situ' for severe spondylolisthesis. J Bone Joint Surg 1983;65 B ( 1 ) :
pedicle and spondylolysis in the lumbar spine. J Bone joint SlIrg 1977;59A:49-54. 58. Edelstyn GA, Gillespie PG, Grebbel
43-46. 33. Seitsalo S, Osterman K, Schlenzka 0, Poussa M . Severe spondylolisthesis in children and adolescents. J Bone joint
FS. The radiological
demonstration of skeletal metastases: experimental observa tions. Clin Radial 1967;18:158. 59. Dahlin DC, Unni K . Bone Tumors. General Aspect and Data all 8542
Surg 1990;77B:259-265. 34. Steffee AD, Sitkowski OJ. Reduction and stabilization of grade
Cases, 4th edn. Thomas Springfield, 1986. 60. Saville DP. A medical option for the treatment of osteoid
IV spondylolisthesis. Clin Orthop 1988;227:82-89. 35. Harris IE, Weinstein SL. Long-term follow-up of patients with grade III and IV spondylolisthesis. Treatment with and without
osteoma. Arthritis Rheulll 1981 ;23:1409. 61. Marsh BW, Bonfiglio M, Brady LP, Enneking WF. Benign osteoblastoma : range of manifestations. j Balle loillt Surg
posterior fusion. J Bone joint SlIrg 1 987;69A:960-969. 36. Apel OM, Lorenz MA, Zindrick MR. Symptomatic spondylo listhesis in adults: four decades later. Spine 1989;14:345-348. 37. Frennered AK, Danielson BI, N achemson AL, Nordwall AB. Midterm follow-up of young patients fused in situ for spondylo
1975;57A: 1 . 62. Nemoto 0, Moser R,Van Dam B . Osteoblastoma o f the spine. A review of 75 cases. Spine 1 990;15 : 1 272-1 280. 63. Mirra J. Bone Tumors: Diagnosis and Treatment.
Lippi ncott,
Philadelphia, 1980.
listhesis. Spine 1991;16:409-416. 38. Moller H, Hedlund R. Surgery versus conservative manage ment in adult isthmic spondylolisthesis: a prospective random ized study: Part 1. Spine 2000;25(13) : 1 711-1715.
64. Schmorl G, Junghanns H . The Human Spine in Health and Disease, 2nd edn. Grune & Stratton, New York, 1971 :325. 65. Mohan V, Gupta SK, Tu li SM, Sanyal B. Symptomatic vertebral
39. Riggs BL, Wahner HW, Dunn WL, Mazes RB, Offord K P, Melton LJ III. Di fferential changes in bone mineral density of appendic ular and axial skeleton with aging. j Clin Invest 1981;67:328. 40. Parfitt AM, Duncan H . Metabolic bone disease affecting the spine. In: Rothman RH, Simeone FA (eds) The Spine, 2nd edn.
hemangiomas. Clin Radial 1980;31:575. 66. Manning JH. Symptomatic hemangioma of the spine. Radiology 1 951;56:58. 67. Jaffe HL, Lichtenstein L. Eosinophilic granuloma of bone. Arch
PathoI 1944;37:99. 68. Cheyne e. Histiocytosis X. j Bone Joint Surg 1971;53B :366.
Saunders, Philadelphia, 1982:775-905. 41 . Zetterberg C, Mannius S, Mellstrom D. Osteoporosis and back
69. Calve JA. Localized a ffection of spine suggesting osteochondri
pain in the elderly: a controlled epidemiologic and radiographic
tis of vertebral body, with clinical aspects of Pott's disease.
study. Spine 1990;15 :783-788.
J Bone joint Surg 1925;7:41.
42. Paget J. On a form of chronic inflammation of bone (osteitis 43. Barry He. Paget's Disease of Bone. E & S Livingstone, Edinburgh,
71 . Ippolito E, Farsetti P, Tudisoc e . Vertebra plana. I Bone joillt Surg 1984;66A:1 364.
1969. 44. Altman RD. Musculoskeletal manifestations of Paget's disease
72. Biesecker JL, Marcove RC, Huvos AG, Mike V. Aneurysmal bone cyst: a clinicopathologic study of 66 cases. Cancer
of bone. Arthritis Rheum 1 980;23 : 1 1 2 1 . 45. Altman RD, Brown M, Gargano GA. Low back pain in Paget's
1970;26:615. 73. Hay MC, Patterson D, Taylor TKF. Aneurysmal bone cysts of
disease of bone. Clin Orthop 1987;217:152. 46. Hartman JT, Dohn OF. Paget's disease of the spine with cord and nerve root compression. j Bone Joint Surg 1966;48A: 1079-1084. 47. Weisz GMM. Lumbar canal stenosis in Paget's diseases: the staging of the clinical syndrome, its d iagnosis and treatment.
the spine. J Bone Joint Surg 1978;60B:406. 74. Dabska M, Buraczewski J. Aneurysmal bone cyst: pathology, clinical course and radiologic appearance. Cancer 1969;23:371 . 75. Francis KC, Hutter RVP. Neoplasms of the spine in the aged.
Clin Orthop 1963;26:54.
Clin Orthop 1986;206:233. 48. Buck JE. Further thoughts on the direct repair of the defect in
76. Huvos AG, Bone Tumors: Diagnosis, Treatment and Prognosis, Saunders, Philadelphia, 1979:373-391 .
spondylolysis. j Bone joint Surg 1979;61 B : 1 23. 49. Schneidermatm GA, McLain RF, Hambly MF, Nielsen SL. The pars defect as a pain source - a histologic study.
70. Weston WJ, Goodson GM. Vertebra plana. J Bone joillt Surg 1959;41B:477.
deformans). Trans R ChiI' Soc Land 1877;60:37.
Spine
1995;20:1761-1 764. 50. Eisenstein SM, Ashton lK, Roberts S, Darby AJ. Innervation of the spondylolysis ' ligaments'. Spine 1994;19:912-916. 5 1 . Wu SS, Lee CH, Chen PQ. Operative repair of symptomatic spondylolysis following a positive response to diagnostic pars injection. j Spinal Disord 1999;12( 1 ) : 1 0-16.
77. Mindell ER. Chordoma. J Bone joint Surg 1981;63A:50] . 78. Hudson TM, Galceran M. Radiology of sacrococcygeal chor doma: difficulties in detecting soft tissue extension. Clin Orthop 1983;175:237. 79. Congdon Ce. Benign and malignant chordomas: a clinico anatomical study of twenty-two cases. Am j PathoI 1 952;28:793. 80. Sundaresan N, Galicich JH, Chu FCH,
Huvas AG. Spinal
chordomas. J Neurosurg 1979;50:312.
52. Aland C, Rineberg BA, Malberg M, Fried SH. Fracture of the
81. Cheng EY, Ozerdemoglu RA,Transfeldt EE, Thompson RC Jr.
pedicle of the fourth lumbar vertebra associated with contra
Lumbosacral chordoma. Prognostic factors and treatment. Spine
lateral spondylolysis. J Bone joint Surg 1986;68A:1454-1455.
1 999;24(16):1 639-1645.
870 SECTI O N TEN - T H E LU M BAR SPI N E
82. Bjornsson J . Wold LE, Ebersold MJ, Laws ER. Chordoma of the mobile spine. A clinicopathologic analysis of 40 patients. Callcer 1993;71(3):735-740. 83. Boriani S, ChevalJey F, Weinstain IN et al. Chordoma of the spine above the sacrum. Spine 1996;21:1569-1577. 84. Kamrin RP, Potatos IN, Pool JL. An evaluation of the diagnosis and treatment of chordoma. ] Neural Neurosurg Psychiatry 1 964; 27:157. 85. Valderrama JAF, Bullough PG. Solitary myeloma of the spine. I Bone Joint Surg 1 968;50B:82. 86. Paredes JM, Mitchell BS. Multiple myeloma: current concepts in diagnosis and management. Med Clill North Am 1980;64:729. 87. Wooltenden JM, Pitt MJ, Durie MGM, Moon TE. Comparison of bone scintigraphy and radiography in multiple myeloma. Radiology 1980;134:723. 88. Gompels BM, Votaw ML, Martel W. Correlation of radiological manifestations of multiple myeloma with immunoglobulin abnormalities and prognosis. RadiologJJ 1972;104:509. 89. Bence-Jones H. On a new substance occuring in the urine of a patient with mollities ossium. Phil Trans R Soc Land (BioI) 1984;1:55. 90. Kyle RA. Multiple myeloma: review of 869 cases. Mayo Clil1 Proc 1 975;50:29. 91 . Costa G, Engle RL Jr, Schilling A et al. Melphalan and pred nisone - an effective combination for the treatment of multiple myeloma. A,n I Med 1973;54:589. 92. Johnson TL Jr. Diagnosis of low back pain, secondary to prostate metastasis to the lumbar spine, by digital rectal exam ination and serum prostate-specific antigen. I Manip Physiol Ther 1994;17(2): 107-11 2. 93. Galasko CSB. Skeletal Metastases. Butterworths, Boston, 1986. 94. Fornasier VL, Horne JG. Metastases to the vertebral column. Cancer 1 975;36:590. 95. Batson Ov. The function of the vertebral veins and their role in the spread of metastasis. Ann Surg 1940;112:138. 96. Constans JP, De Divitis E, Donzelli R et al. Spinal metastases with neurological manifestations: review of 600 cases. ] Neurosu rg 1 983;59 : 11 1 . 97. EmselJem H A . Metastatic disease of the spine: diagnosis and management. South Med ] 1986;76:1405. 98. Shaberg J, Gainor BJ. A profile of metastatic carcinoma of the spine. Spine 1 985;10:19. 99. Gosfield E 3rd, Alavi A, Kneeland B . Comparison of radio nuclide bone scans and magnetic resonance imaging in detect ing spinal metastases. I Nucl Med 1993;34(12):2191-2198. 100. Hard FD, MacLagen NF. Ankylosing spondylitis: a review of 184 cases. Ann Rheum Dis 1 975;34:87. 101 . Kinsel la TD, MacDonald FR, Johnson LG. Ankylosing spondylitis: a late re-evaluation of 92 cases. Can Med Assoc I 1 966;95: 1 . 102. Dale K. Radiographic changes of the spine in Bechterew's synd rome and allied d isorders. Scand J Rheumatol 1979; 32(suppl): 103. 103. Graudal H, de Carvalho A, Lassen L . The course of sacroiliac involvement in rheumatoid arthritis. Scand J Rheumatol 1979;32(suppl):34. 1 04. Resnick D. Thoracolumbar spine abnormalities in rheumatoid arthritis. Ann Rheum Dis 1978;37:389. 105. Sims-Williams H, Jayson MIV, Baddeley H. Rheumatoid involvement of the lumbar spine. Ann Rheum Dis 1 977;36:524. 106. Bauer W, Engleman EP. A syndrome of unknown etiology characterized by urethritis, conjunctivitis, and arthritis (so called Reiter's disease). Trans Assoc Am Phys 1942;57:307. 107. Russell AS, Davis P, Percy JS, Lentle Gc. The sacroiliitis of acute Reiter's syndrome. J Rheumato/ 1 977;4:293.
108. Forestier J, Rotes-Querol J. Senile ankylosing hyperostosis of the spine. Ann Rheum Dis 1 950;9:321 . 109. Resnick D, Shaul SR, Robins JM. Diffuse idiopathic skeletal hyperostosis (DISH): Forestier's disease with extraspinal manifestations. RadiologJJ 1975;115:513. 110. Boachie-Adjei 0, Bullough PG. Incidence of ankylosing hyper ostosis of the spine (Forestier's disease) at autopsy. Spille 1987;12:739-741 . 1 1 1 . Forestier J , Lagier R. Ankylosing hyperostosis o f the spine. Ciill Ortilop 1971 ;74:65. 112. Harris J, Carter AR, Glick EN, Storey GO. Ankylosing hyper ostosis. 1. Clinical and radiological features. Ann Rheum Dis 1974;33:210. 113. Wiley AM, Trueta J. The vascular anatomy of the spine and its relationship to pyogenic vertebral osteomyelitis. ] Bone Joillt Surg 1959;41B:796. 114. L i feso R. Pyogenic spinal sepsis in adults. Spille 1990;15:1265-127 1 . 1 1 5 . Sapico FL, Montgomerie J Z . Pyogenic vertebral osteomyelitis: report of nine cases and review of the literature. Rev Infect Dis 1979;1:754. 116. Ross PM, Fleming JL. Vertebral body osteomyelitis: spectrum and natural history: a retrospective analysis of 37 cases. Ciill Orthop 1976;118:190. 1 1 7. Baker AS, Ojemann RG, Swartz MN, Richardson EP Jr. Spinal epidural abscess. N Engl ] Med 1975;293:463. 118. Garcia A Jr, Grantham SA. Hematogenous pyogenic vertebral osteomyelitis. J Balle Joillt Surg 1960;42A:429. 119. Digby JM, Kersley JB. Pyogenic non-tuberculous spinal infec tion: an analysis of thirty cases. J Bone ]oil1t Surg ] 979;61B:47. 120. Kattapuram SV, Philips We,. Boyd R. CT in pyogenic osteomyelitis of the spine. A]R 1983;140:1199. 121. Lifeso RM, Weaver P, Harder O. Tuberculous spondylitis in adults. J Bone Joint Surg 1985;67A:1405-1413. 122. Forlenza SW, Axelrod JL, Grieco MH. Pott's disease in heroin addicts. JAMA 1979;241:379. 123. Janssens JP, De Haller R. Spinal tuberculosis in a developed country. A review of 26 cases with special emphasis on abscesses and neurological complications. Ciill OrtllOp 1990;257:67-75. 124. Gorse GJ, Pais MJ, Kusske JA, Cesario TC. Tubercu lous spondylitis: a report of six cases and a review of the literature. Medicine 1983;62:1 78. 125. Eismont FJ, Montero C. Infections of the spine; In: Davidoff RA (ed) Handbook of the Spinal Cord. Marcel Dekker, New York, 1987: 411-449. 126. Rivero MG, Salvatore AJ, de Wouters L. Spontaneous infec tious spondylodiscitis in adults. Analysis of 30 cases. Medicina (Buenos Aires) 1999;59(2): 1 43-150. 127. Pilgaard S. Discitis (closed space infection) following removal of lumbar intervertebral disc. J Bone ]oillt Surg 1969;51A:713. 128. Kylanpaa-Back ML, Suominen RA, Salo SA et al. Postoperative disci tis: outcome and late magnetic resonance image evalua tion of ten patients. Ann Chir Gynaeco/ 1 999;88(1):61-64. 129. Hansen SE, Gutschik E, Karle A, Rieneck K, Vinicoff PG. Spontaneous and postoperative spondylodiscitis. A material concerning 23 patients. Ugeskr Laeger 1998;160(41):5935-5938. 130. Onofrio BM. Intervertebral disci tis: incidence, diagnosis and management. Clin Neurosurg 1980;27:481 . 1 3 1 . Norris S, Ehrlich MG, Keirn DE, Guiterman H , McKusick KA. Early diagnosis of d isc-space infection using gallium-67. , Nucl ' Med 1978;19:384. 1 32. Maiuri F, Iaconetta G, Gallicchio B, Manto A, Briganti F. Spondylodiscitis - clinical and magnetic resonance diagnosis. Spine 1997;22:1 741-1746.
CHAPTER 58 - N O N- M ECHAN I CAL D I SO R D E RS 871
133. Wirtz DC, Genius I, Wildberger JE et al. Diagnostic and thera peutic management of lumbar and thoracic spondylodiscitis an evaluation of 59 cases. A rch Orthop Trau ma S u rg 2000;120(5-6):245-251 . 134. Crawford AH, Kucharzyk OW, Ruda R et al. Discitis in chil dren. Ciin Orthop 1991;266:70-79. 135. Engelbert RH, Van der Net J, Schoenmakers MA. Twee kinderen met discitis. Casuistische mededelingen. Ned Tijdschr Geneeskd 1993;137:1 614-1616. 136. Straus SE. Varicella-zoster virus infections: biology, natural history, treatment and prevention. Ann Intern Med 1988;108:221. 137. Burke BL, Steele RW, Beard OW et al. Immune response to varicella-zoster in the aged. Arch Intern Med 1 982;142:291 . 138. Helfgott SM, Picard DA, Cook JS. Herpes zoster radiculopathy. Spine 1993;18:2523-2524. 139. Thomas JE, Howard FM Jr. Segmental zoster paresis - a disease profile. Neurology 1972;22:459. 140. Markham JW, Lynge HN, Stahlman GEB. The syndrome of spontaneous spinal epidural hematoma. Report of three cases. J Nellrosurg 1967;26:334. 141 . Hancock DO. A study of 49 patients with acute spinal extradural abscess. Paraplegia 1973;10:285-288. 142. Abdullah AF, Chambers RW, Daut DP. Lumbar nerve root compression by synovial cysts of the ligamentum f1avum. 1 NeUlosurg 1984;60:617-620. 143. Baum JA, Hanley EN. Intraspinal synovial cyst simulating spinal stenosis. Spine 1 986;11:487-489. 144. Lemish W, Apsimon T, Chakera T. Lumbar intraspinal synovial cysts. Recognition and CT diagnosis. Spine 1989;14:1378-1383. 145. Shaw MOM, Russel JA, Grossart KW. The changing pattern of spinal arachnoiditis. ! Nellrol Neurosurg Psychiatry 1978;41:97. 146. Epstein JA. Common errors in the diagnosis of herniation of the intervertebral disk. Industrial Medicine 1970;39:488. 147. Waddell G. An approach to backache. Br ! Hosp Med 1 982;28:1 87-19 1 . 148. Norstrom CW, Kernohan JW, Love J G . One hundred primary caudal tumors. !AMA 1969;178:1071-1077. 149. Ker NB, Jones CB. Tu mors of the cauda equina: the problem of differential diagnosis. 1 Bone Joint Surg 1985;67B:358-362. 150. Guyer RD, Collier RR, Ohnmeiss DO et al. Extraosseous spinal lesions mimicking disc disease. Spine 1988;13:228-231 . 151. Ombregt L . Tumoren van d e cauda equina: het belang van vroege diagnostiek. Ned Tijdschr Geneeskd 1986;130(8):371-372. 152. Fearnside MR, Adams CBT. Tumours of the cauda equina. J Nellrolog Nellrosurg Psychiatry 1978;41:24-31 . 153. Garfield J, Lytle SN. Urinary presentation o f cauda equina lesions without neurological symptoms. Br J Urol 42:551-554.
154. Wiesel SW, Tsourmas N, FeHer 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 1 984;9:549-551 . 155. Craig WM, Svien HJ, Dodge H W JR, Camp WM. Intraspinal lesions masquerading as protruded lumbar intervertebral discs. lAMA 1952;149:250-253. 156. Gore I, Hirst AE Jr. Arteriosclerotic aneurysm of the abdominal aorta: a review. Prog Cardiovasc Dis 1973;16:1 13. 157. Barratt-Boyes BG. Symptomatology and prognosis of abdomi nal aortic aneurysm. Lancet 1957;ii:716. 158. Amparo EG, Hoddick WK, Hricak H, Sollitto R, Justich E, Filly RA, Higgins CB. Comparison of magnetic resonance imaging and ultrasonography in the evaluation of abdominal aortic aneurysm. RadiologJJ 1 985;154:45 1 . 159. Filtzer DL, Bahnson HT. Low back pain d u e t o arterial obstruc tion. ! Bone Joint Surg1959;41 B:244. 160. Gibbons RP, Montie JE, Correa RJ Jr, Mason JT. Manifestations of renal cell carcinoma. UrologJJ 1 976;8:201 . 1 6 1 . Paulson OF, Einhorn L, Peckham M, William Sc. Cancer of the testis. In: De Vita VT, Hellman S, Rosenberg SA (eds) Cancer: Principles and Practice of Oncology. Lippincott, Philadelphia, 1982:786-822. 162. Cantwell BMJ, Mann KA, Harris AL. Back pain - a presentation of metastic testicular germ cell tumours. Lancet 19876;i:262. 163. Jeffcoate TNA. Pelvic pain. BM] 1 969;ii:431 . 164. O'Connor DT. Endometriosis. Churchill Livingstone, New York, 1987. 165. Mantle MJ, Greenwood RM, Currey HLF. Backache in preg nancy. Rheum Rehabi/ 1977;16:95-10 1 . 166. Svensson H-O, Andersson GB, Hagstad A , Jansson P-O. The relationship of low-back pain to pregnancy and gynecologic factors. Spine 1990;15:371-375. 167. Ostgaard HC, Andersson GBJ, Karlsson K. Prevalence of back pain in pregnancy. Spine 1991;16:549-552. 1 68. Kristiansson P, Sviirdudd K, von Schoultz B. Back pai n during pregnancy. A prospective study. Spine 1996;21:702-709. 1 69. Mens JMA, Vleeming A, Stoeckaert R, Stam HJ, Snijders CJ. Understanding peripartum pelvic pain. Implications of a patient survey. Spine 1996;21: 1363-1370. 170. Ross JR, Reave LE III. Syndrome of posterior penetrating peptic ulcer. Med Ciin North Arn 1 966;50:461 . 1 7 1 . Bank S . Chronic pancreatitis: clinical features and medical management. Am ] GastroenteroI 1986;81 : 1 53. 1 72. Falterman KW, Hill CB, Markey JC, Fox JW, Cohn T Jr. Cancer of the colon, rectum and anus: a review of 2313 cases. Cancer 1974;34:951 .
THIS PAGE INTENTIONALLY LEFT BLANK
CHAPTER CONTENTS Introduction Manipulation Traction
Treatment of the lumbar spine
873 87S
893
Alternative procedures for reducing nuclear protrusions 901 Injections
903
Epidural local anaesthesia 903 Nerve root blocks 914 Injection of ligaments 918 Prevention of lumbar spine disorders Spinal surgery
INTRODUCTION
921
928
Surgery for discodural or discoradicular interactions Surgery for spinal stenosis and lateral recess stenosis 930 Lumbar arthrodesis 931
928
Treatment of mechanical disorders of the lumbar spine should be selected by the nature of the underlying problem. If this is neglected, an inadequate or inappro priate type of treatment may be given, disappointing the patient, the physician and the therapist. A wide variety of non-smgical treatments are advocated in the management of low back pain. Back school instruc tions, bed rest, cryotherapy, medication, exercises, manip ulation, traction, mobilization, local blocks, epid ural infiltrations and spinal orthosis all claim to have their suc cesses but until now controlled studies of large, unselected populations have not demonstrated the superiority of any one of these measmes,1-7 which thus supports the view that there seems to be no definite evidence that any treat ment for low back pain is much better than the placebo effect.8,9 Some authors even suggest that the main effects of the therapies are produced not through the reversal of physical weaknesses targeted by the corresponding exercise method but rather through some ' central' effect, perhaps involving an adjustment of perception in relation to pain and disability.lO Obviously these studies have reinforced therapeutic nihilism. In that conservative measures are not proven to be effective, the patient is told to learn to live with the disability until it disappears spontaneously.ll However, in analysing the results, one striking factor emerges - the lack of a proper diagnosis. In current clin ical trials on the effectiveness of treatment for lumbar disorders, only the course of a symptom (pain) is evalu ated in randomized groups of patients. This is com pletely wrong. Controversies over treatment are usually the result of stu dies performed on widely differing lesions. A group of patients complaining of 'backache' is very heterogeneous. Even if, in most cases, the d isc is responsible for the pain, the mechanism will differ con siderably from patient to patient. Before any kind of randomization is done, the individual disorders in any group of patients should be clearly identified; treatment could then be given not to a symptom but to a well defined condition.12 We therefore believe that before treatment of any kind is instituted, a clear diagnosis 873
874 SECTION TEN - THE LUMBAR SPINE
must be made and the physician must have a distinct idea of the underlying cause. Treatment can then be pre scribed selectively, according to the type and the sever ity of the lesion. For example, a recent systematic review of randomized clinical trials on spinal manipulation could find no evidence of effectiveness, except in some subgroups of patients, with clearly delineated clinical inclusion criteria. 1 3 The history and clinical examination almost always indicate the best method of treatment for an individual patient. It is our personal experience that, if conservative treatment techniques are employed intelligently, there is definite evidence that in each case one treatment is better than another or than the p lacebo effect. Also, only a few patients will remain wholly unrelieved, in which cases surgery may be required. Even when surgery is indi cated, then the decision must be made on clinical grounds alone. An abnormality seen on imaging and not confirmed by the clinical examination is not an indication for surgery.14 Before any form of treatment, conservative or surgical, is instituted, answers to the following questions must be obtained.
Is the pain caused by a spinal disorder? It is important to exclude psychogenic pain and pain of visceral origin referred to the back.
Is the condition an 'activity-related' (mechanical) spinal disorder? It is obvious that specific, non-mechanical disorders causing backache or sciatica, for example rheumatic diseases, tumours and infections, need other types of treatment.
If the spinal disorder is activity-related (mechanical), to which 'concept' does it belong? Is the disorder a d i scod u ra l or d i scoradicular i nterac tion? In a clear combination of both articular and dural signs and symptoms, the answer will be obvious. In a moderate discodural backache, however, where the patien t p resents with articular signs only, it may be more difficult to make the d iagnosis of internal derange ment with certainty. However, a p artial a rticu l a r pattern, except in a few cases of ligamentous pain, always indicates a d isc lesion. A deviation, whether in the upright position or on flexion defines a protrusion. Also, the presence of a painful arc, whether during side flexion or forward flexion, is the signature of a small posterior or posterolateral bulge. If there is proof of a disc lesion, and the patient is motivated to take active treatment, conservative therapy consists of one or more of the fol lowing measures:
• • •
•
Reduction of the displacement: achieved by manipulation or traction. Maintenance of reduction: obtained by sclerosing injections and I or back school instructions. Desensitization of the dura mater: acute or gross inflammation requires desensitization of the dura mater before manipulation or traction is attempted. Alternatively, if the dura mater remains inflamed after the discodural contact as ceased, the treatment is epidural local anaesthesia. Desensitization of the dural nerve root sleeve: in intense discoradicular contact leading to some degree of parenchymatous involvement, attempts at reduction fail. De-inflammation and desensitization of the dural sleeve, while spontaneous recovery is awaited, is then a good and defensible therapeutiC approach. Epidural local anaesthesia via the sacral canal is the technique of choice. Should this fail, a sinuvertebral and nerve root block can be substituted. Desensitization of the dural sleeve is also recommended when the discoradicular contact has lasted for some time or when the nerve root remains inflamed after the conflict has ceased (Fig. 59.1).
Is the disorder a ligamentous problem? Ligamentous dis orders are characterized by postural pain, absence of dural symptoms and a full range of movement. Symptoms and signs make it possible to differentiate between a postural and a local dysfunctional syndrome. In the former, treatment consists of the induction of artificial sclerosis in the posterior ligamentous structures. The latter usually responds to local infiltration with tri amcinolone or sclerosants. Is the disorder a stenotic problem? Spinal stenosis, sug gested by the p resence of 'neurogenic intermittent clau dication', is very difficult to treat conservatively. L,ateral recess stenosis, however, characterized by long-standing sciatic pain in an elderly patient, which appears during walking or standing and disappears during sitting or bending, responds extremely well to nerve root infiltra tions with triamcinolone. What sort of person is the patient? What attitude does the patient have towards the problem? Is there a desire to get better? Is there any compensation claim? Is there evidence of psychoneurosis? Will active and sometimes unpleasant forms of treatment be tolerated? These ques tions must be addressed when devising a treatment plan. If treatment is employed along these lines, only a few patients will remain without any relief. This approach has also proved to be safe and, at the same time is a meaning ful, realistic and practical response to the enormousliabil ity of lumbar disorders in terms of cost and needless human suffering. In 1986, the annual cost of back pain in
CHAPTER 59 - TREATMENT OF THE LUMBAR SPINE 875
Lumbosciatic pain ,
I 1
1
1
1
1
1
Sacroiliac disorders
Hip disorders
Spinal disorders
Visceral disease
Psychogenic pain
1 Discogenic
I
I 1
Discodural
Discoradicular
Reduction: • Manipulation • Traction
Reduction: • Manipulation • Traction
Maintenance of reduction: • Back school
Maintenance of reduction: • Back school
•
Sclerosants
Desensitization of dura mater: •
Epidurals
•
I
1 Mechanical
I
Ligamentous
-.l
1
1 •
J I
I
Postural syndrome •
I
Postural advice Sclerosants
�
1 Non-mechanical
I
J 1
1 Dysfunction syndrome •
Local infiltrations: Triamcinolone Sclerosants
•
Posture?
•
Surgery
J 1
Lateral recess stenosis •
Nerve root blocks
Ir
Epidurals Nerve root blocks - -
Figure 59.1
I
Sclerosants
Desensitization of dural sleeve: •
1 Stenotic
Spinal stenosis
Spontaneous recovery
•
J
-
Treatment scheme for lumbosciatic pain.
the USA approached $81 billion. IS By 1995 the total cost to society of low back pain was more than $100 billionl6 and the economic loss 101.8 million workdaysY In the UK, the direct health care cost of back pain in 1998 was estimated to be £1632 million. However, this direct cost of back pain is insignificant compared to the cost of the production losses related to it, which was £10 668 million, making back pain one of the most costly conditions for which an economic analysis has been carried out.IS A substantial portion of low back care costs reflects expensive surgical therapy, when many patients could have been effectively treated if the above-mentioned less costly regimes had been tried first. Unfortunately, the average spinal surgeon is usually neither trained in nor knowledgeable about conservative spinal therapy. In fact, in some of the present state health care systems, surgery is routinely performed on almost all cases of low back pain (Burton:14 p. 105). This has been confirmed by Finneson, 19 who studied one series of 94 patients who had failed back surgery and found that in 81% the original surgery was not indicated.
MANIPULATION
INTRODUCTION Manipulation and traction are no exceptions to the rule that all medicine can be traced back to Hi ppocrates (400 Be). His methods of treating back disorders were practised in the following centuries by other famous physicians, for example Appolonius, Galen, Avicenna, Ambroise Pare, Percival Pott, Sir James Paget and many others. In China, the technique of manipulation was fully established during the Tang Dynasty (AD 618-907). Illustrations show that the ancient methods of manipula tion and apparatus traction did not differ very much from the methods of treatment practised nowadays in low back pain and sciatica (Fig. 59.2). M anipulation and traction are methods of reducing pain and disability caused by internal derangement of intervertebral cartilaginous structures. This treatment has undoubtedly come into existence from man's experi ence with those examples of lumbago, low back pain and
876 SECTION TEN - THE LUMBAR SPINE
C\H
Ladder treatment, 1 st century BC. H. Sch6me (ed) //Iustrierler [by Apollonius Citiensisj zu der Hippokrateischen Schrift. Teubner, Leipzig. ( By courtesy of Wellcome Trustees.) Figure 59.2:
Kommentar
sciatica that were relieved by a sudden twist or a fall. Schiotz and Cyriax20 described several examples in which patients reported such a sudden relief of symp toms after an unintentional movement. One of our colleagues reported a patient who recovered from her backache on falling down her own basement cellar steps. Undoubted ly such experiences have given rise to various and sometimes bizarre mechanical treatments in folk medicine, such as trampling on a patient's back, wrestling the back, striking the back with the weight of a steel bar or standing back-to-back ' weighing salt' (two persons stand back-to-back hooking their arms at the elbow; each person bends forward in turn, lifting the other from the floor). These measures seem non-specific and possibly harmful but SchiOtz commented : ' It seems justi fied to infer that methods found effective by the natives of parts of the world as far apart as Norway, Mexico and the Pacific Islands over many, many cen turies must be valid'. These primitive methods are also the models for more modern techniques of manipulation and traction taught and practised by trained doctors and therapists all over the world.
Although different methods and different theoretical concepts developed, this seemed not to matter much as all claimed their successes. Cyriax21 was convinced that in nearly all cases a similar mechanism is at work - a dis located fragment of disc returns to position or a protru sion is 'sucked back'. He also stated: 'Spinal manipulative methods of orthopaedic medicine are perfectly straight forward and possess an explicable intention directed to a factual lesion. They are based on the discovery of disc lesions as the primary cause of degenerative change and pain of spinal origin'. It is hard to believe that even nowadays many doctors still refuse to recommend manipulation of the back as the treatment of choice in nearly all cases of acute low back pain and sciatica. To avoid discussion of the topic of spinal manipulation is also unwise, since a significant number of their patients will have received or will be considering this form of treatment: in the USA in 1980, 120 million office visits were made to chiropractors.22 An increasing number of controlled clinical trials on well-delineated subgroups, which compare the results of manipulation to different forms of placebo therapy as well as to other forms of conservative management have been published .23-34 The positive effects of manipulation appear to occur either immediately after the manipula tion session or within the first 4-6 weeks of treatment.3S-37 DEFINITION OF MANIPULATION In orthopaedic medicine, spinal manipulation is defined as a method of conservative treatment by passive move ments, carried out with a single thrust or sustained pressure, in order to return a displacement to its proper position (see Ch. 5). During the thrust an audible click is often produced. This may accompany immediate relief of symptoms and signs, which supports the precision cif the diagnosis and selected therapy. There are different schools of thought in manipulation which derive from different attitudes towards spinal disorders. The theories on which manipulation is based include the reduction of disc protrusions,38,39 the correc tion of posterior joint dysfunction,40 the mobilization of blocked vertebral joints, 41-44 the reduction of nerve root compression,4s,46 the normalization of reflex activity47-so and the relaxation of muscles.sl The objective of the manipulative techniques dis cussed in this book is to alter the discodural or disco radicular interaction by moving a displaced cartilaginous rim away from sensitive structures. The method relies on two principles:
•
The lumbar spine is positioned in such a way thal>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
-
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.
-
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
-
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
-
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
R EF ER ENC ES 1 . Deyo RA. Treatment of low back pain. JAMA 1986;253: 1122-1123 2. Deyo RA. Conservative therapy for low back pain: JAMA Distinguishing useful from useless therapy. 1983;250:1 057-1062 3. Gilbert JR. Management of low back pain in family practice: a critical review. Can Fam Physician 1 986;32:1855-1861 4. Nachemson A. A critical look at conservative treatment for low back pain. In: Jayson M (ed) The Lumbar Spine and Low Back Pain. Pitman, London, 1 976
5. Koes BW, Bouter LM, Beckerman H, van der Heyden GJMG, Knjpschild PG. Oefentherapie bij rugkJachten. Een geblindeerd Ii teratuuronderzoek. Ned Tijdschr Fysiother 1 99 1;101(10):37-41 6. Martin PR, Rose MJ, Nichols PJR Russell PL, Hughes JG. Physiotherapy exercises for low back pain; process and clinical outcome. Int Rehabil Med 1980,8:34-38 7. Ponte OJ, Jensen Gl, Kent BE. A preLiminary report on the use of the McKenzie protocol versus Williams protocol in the treatment of low back pain. J Orthop Sports Phys Ther 1 984;6(2): 1 30-139
932 SECTION TEN - T H E L U M BAR SPI N E
8 . Weber H . Conservative management o f back pain: critical eval uation of conservative treatment programmes. Presented at the First European Congress on Back Pain, Current Concepts and Recent Advances, Helsinki, 1 986 9. Spitzer WOo Scientific approach to the assessment and manage ment of activity-related spinal disorders; a monograph for clini cians. Report of the Quebec Task Force on SpinaJ Disorders. Spille 1987;12(7)(suppl). 10. Mannion AF, Muntener M, Taimela S, Dvorak ). A randomized clinical trial of three active therapies for chronic low back pain. Spille 1 999;24(23):2435-2448. 1 1 . Cochrane T. Workillg Group Oil Back Paill. Department of Health and Social Security, London, 1 979. 12. Van Tu lder MW, Koes BW, Bouter LM et al Management of chronic nonspecific low back pain in primary care: a descriptive study. Spille 1 997;22:76-82. 13. Koes BW, Assendelft WJJ, van der Heijden GJ et at. Spinal manipu lation for low back pain; an updated systematic review of randomized clinical trials. Spille 1996;21:2860-2873. 1 4. Burton Cv. Gravity lumbar reduction. In: Kirkaldy-Willis WH (ed ) Mallagillg Low Back Pain. Churchill Livingstone, New York, 1 988:Chapter 19. 15. Annual costs of back pain approaching $81 billion. Millneapolis Tribulle, 21 August 1 986. 1 6. Frymoyer JW, Durett CL. The economics of spinal disorders. In: Frymoyer )W (ed ) The Adult Spille, Prillciples and Practice, 2nd edn. Lippi ncott-Raven, Phi ladelphia, 1997: 1 43-150. 1 7. Guo HR, Tanaka S, Halperin WE, Cameron LL. Back pain prevalence in US industry and estimates of lost workdays. Alii ] Public Health 1999;89(7): 1029-1 035. 18. Maniadakis N, Gray A. The economic burden of back pain i n the UK. Paill 2000;84(1):95-103. 19. Finneson BE. Low Back Paill, 2nd edn. Lippincott, Philadelphia, 1 980. 20. Schiotz EH, Cyriax ]. Manipulatioll Past and Present. Heinemann, London, 1975. 2 1 . Cyriax J. Textbook of Orthopaedic Medicille, vol I, Diagllosis of Soft Tissue Lesiolls. 8th edn. Baill iere Tindall, London, 1982. 22. Von Kuster T Jr. Chiropractic Health Care: A National Study of the
Cost of Educatioll, Service, Utilization, Number of Practicing Doctors of Chiropractic and Other Key Policy Issues. Foundation for 23.
24.
25.
26. 27. 28.
29.
30.
Advancement of Chiropractic Tenets and Science, Washington, 1 980. Macdonald RS, Bell CMJ. An open controlled assessment of osteopathic manipulation in non-specific low-back pain. Spine 1 990;15:364-370 Postacchini F, Facchini M, Palieri P. Efficacy of various forms of conservative treatment in low back pain, a comparative study. Neuro-Orthopedics 1988;6:28-35. Hadler NM, Curtis P, Gillings DB, Stinnett S. A benefit of spinal manipulation as adjunctive therapy for acute low back pain. A stratified controlled trial. Spine 1 987;12:703-706. Kuo P-F, Loh Z-c. Treatment of l u mbar intervertebral disc pro trusions by manipulation. c/in Orthop Rei Res 1 987;215:47-55. Arkuszewski Z. The efficacy of manual treatment in low back pain: a clinical trial. Manual Med 1 986;2:68-7 1 . Waagen G , Haldeman S, Cook G , Lopez D , D e Boer K. Short term trial of chiropractic adjustments for the relief of chronic low back pain. Mallual Med 1986;2:63-67. Farrell J P, Twomey LT. Acute low back pain. Comparison of two conservative treatment approaches. Med ] A ust 1 982;1: 160-164. Nwuga VCB. Relative therapeutic efficacy of vertebral manipu lation and conventional treatment i n back pain management. Alii ] Phys Med 1982;61(6):273-278.
3 1 . Hoehler FK, Tobis JS, Buerger AA. Spinal manipulation for low back pain. ]AMA 1981;245:1 835-1838. 32. Sims-Williams H, Jayson MI, Young SM, Baddeley H, Collins E. Controlled trial of mobilization and manipulation for patients with low back pain in general practice. BM] 2:1 338-1340. 33. Mathews JA, Yates DAH. Reduction of lumbar disc prolapse by manipulation. BM] 1969;3:696-697. 34. Henderson BS. The treahnent of lumbar intervertebral disc pro trusion. BM] 1 952;42:597-598. 35. Meade TW, Dyer S, Browne W, Townsend J, Frank AO. Low back pain of medlanical origin: randomized comparison of dliro practic and hospital outpatient treahnent. BM] 1 990;300(6737): 1431-1 437. 36. Meade TW, Dyer S, Browne W, Frank AO. Randomised com parison of chiropractic and hospital outpatient management for low back pain: results from extended follow up. BM] 1 995;311(7001):349-351. 37. Koes BW. Efficacy of manual therapy and physiotherapy for back and neck complaints. Dissertation, Rijksuni versiteit Limburg, Maastricht, 1992. 38. Cyriax ]. Textbook of Orthopaedic Medicine, vol I I, Treatlllellt by Mal1ipulation, Massage alld Treatlllellt, 1 1 th edn. Bailliere Tindall, London, 1984. 39. Maigne R. Orthopedic Medicine. A New Approach to Vertebral Manipulation (trans. WT Liberson). Thomas, Springfield, 1 972. 40. Mennell J. Back Paill. Diagllosis and Treailllel1t Using Mallipulative Therapy. Little Brown, Boston, 1960. 4 1 . Gillett H, Liekens M. Belgiall Chiropractic Research Notes. 10th edn. Brussels, 1973. 42. Lewit D. Man uelle Medizin illl Rah/JIell der lIIedizillischen Rehabilitation, 2nd edn. Johann Ambrosius, Leipzig, 1977. 43. Maitland GD. Vertebral Mallipulation, 3rd edn. Bu tterworths, London, 1973. 44. Schaefer R, Faye L. Motiol1 Palpatioll al1d Chiropractic Tec/mic. Prillciples of Dyllamic Chiropractic. The Motion Palpation Institute, Huntington Beach, 1989. 45. Olmarker K, Rydevik B, Holm S, Bagge U. Effects of experi mental graded compression on blood flow in spinal nerve roots. A vital microscopic study on the porcine cauda equina. ] Ort/rop Res 1 989;77(6):79-85. 46. Palmer DD. The Science, Art alld Philosophy of Chiropractic. Portland Printing House, Portland, 1910. 47. Janda V. Pain in the locomotor system - a broad approach. In: Glasgow E, Twomey L, Scull E et al (eds) Aspects of Mallipulative Therapy, 2nd edn. Churchill Livingstone, Melbourne, 1 985: 1 48- 1 5 1 . 48. Korr 1 M . The Neurobiologic Mechanisms ill Manipulative Therapy. Plenum Press, New York, 1978. 49. Lewit K. Manipulative Therapy in the Rehabilitation of the Locomotor System. Butterworth, London, 1985. 50. Herzog W, Scheel D, Conway PJ. Electromyographic responses of back and limb muscles associated with spinal manipulative therapy. Spine 1 999;24:146-153. 5 1 . Perl ER. Pain, spinal and peripheral factors. In: Goldstein M (ed) The Research Status of Spinal Manipulative Therapy. NINCDS Monograph No 15. DHEW Publication no. (NIH) 76-998, 1975. 52. Gonella C, Paris S, Kuhler M . Reliability i n evaluating passive intervertebral motion. Phys Ther 1 982;62:437. 53. Matyas TA, Bach TM. The reliability in selected techniques in clinical arthrometrics. Aust ] Physiother 1 985;1:1 75. 54. Potter N W, Rothstein JM. Intertester reliability for selected ' clinical tests of the sacro-iliac joint. Phys Ther 1 984;6:2. 55. Mootz RD, Keating JC, Kontz H P. Intra- and inter-observer reli ability of passive motion palpation of the lumbar spine. ] Manip Physiol Ther 1 989;12:440-445.
CHAPTER 59 - TREATMENT OF T H E L U M BAR SPI N E 933
56. Keating Je, Bermann TF, Jacobs GF et al Inter-examiner relia ,bility of eight evaluative dimensions of lumbar segmental abnormality. ] Manip Physiol Ther 1990;13:463-470 57. Panzer OM. The reliability of lumbar motion palpation. ] Manip Physiol Ther 1992;15:518-524 58. McKenzie R . The L U ll1bar Spine: Mechanical Diagnosis al1d Thempy. Spinal Publications, Waikanae, New Zealand,
1981 59. McKenzie R. A perspective on manipulative therapy. Physiothempy 1989;75(8):440-444 60. Szechenyi F, Csipo L, Kiss E. Epidurografiaral kirnutatott, torzios
extensioral
reponalt
agyeki
porckorongservek.
Ideggyogyaszati Szemle 1989;31:436 6 1 . Barbor R. Low backache BM] 1955;i:55 62. Fisk B. Manipulation in general practice. NZ Med ] 1971;74:172-175 63. Kleynhans AM. Complications of and contraindications to spinal manipulative therapy. In: Haldeman S (ed) Modern Developlllen ts in the Principles and Practice of Chiropractic. Appleton-Century-Crofts, New York, 1980 64. Livingston Me. Spinal manipulation causing injury. Br Col Med ] 1972;14:78-81 65. Jennet WB. A study of 25 cases of compression of the cauda equina by prolapse intervertebral discs. J Neurol Neurosurg Psychiatry 1956;19:109-11 6 66. Richard ) . Disk rupture with cauda equina syndrome after chiropractic adjustment. NY State Med 1967;67:2496-2498 67. Stoddard A. Manual of Osteopathic Technique. Hutchinson, London, 1959 68. Kostuik JP, Harrington I, Alexander D, Rand W, Evans D. Cauda equina syndrome and lumbar disc herniation. ] Bone ]oil/t SlIrg 1 986;68A:386-391 69. Dabbert 0, Freeman DG, Weis AI. Spinal meningeal hematoma, warfarin therapy and chiropractic adjustment.
]AMA 1970;214(11):2058 70. Fisk Jw. A Pmctical GlIide to Mmmgelllellt of the Painful Neck and Back. Thomas, Springfield, 1977 71 . Kirkaldy-Willis WH, Cassidy JD. Spinal manipulation in the treatment of low back pain. Can Falll Physician 1985;31:535-540 72. Morrison Me. The best back to manipulate? AliI! R Coli Surg ElIgI 1 984;66:52-53 73. Potter GE. A study of 744 cases of neck and back pain treated with spinal manipulation. ] Can Chiro Pmt Assoc 1977;21(4): 154-156 74. Kirkaldy-Willis WH, Cassidy JD. Effects of manipulation on chronic low back pain. Presented at a conference on manipula tive medicine in the management of low back pain, University of Southern California and the North American Academy of manipulative medicine, Oct 1978 75. Potter GE. Chiropractors [letter]. Can Med Assoc
] 1979;121:705-706 76. Livingston Me. Spinal manipulation causing injury. Br Col Med J 1972;14:78-81 77. Assendelft WJ, Bouter LM, Knipschild PG. Complications of spinal manipulation: a comprehensive review of the literature. ] Fam Pract 1996;42(5):475-480 78. Haldeman S, Rubinstein SM. Cauda equina syndrome in patients undergoing manipulation of the lumbar spine. Spille
1992;17(12):1469-1473 79. Bergquist-Ullman M, Larsson U. Acute low back pain in industry. Acta Orthop Scand 1977;170( suppl) :1-117 80. Buerger AA. A clinical trial of rotational manipulation. Pain abstracts 1 :248. Second World Congress on Pain, International Association for the Study of Pain, Montreal, Canada, 1978
81. Glover JR, Morris JG, Khosla T. Back pain. A random ized clin ical trial of rotational manipulation of the trunk. Br ] Illd Mcd 1 974;31 :59-64 82. Rasmussen GG. Manipu lation in the low back: a randomized clinical trial. Man Med 1977;1 :8-1 0 83. Mathews JA, Mills SB, Jenkins VM et al Back pain and sciatica: controlled trials of manipulation, traction, sclerosant and epidural injections. Br J RheulIlato/ 1987;26:416-423 84. Donelson R, Silva G, Murphy K. Centralization phenomenon: its usefulness in evaluating and treating referred pain. Spillc
1990;15:211 85. Krause M, Refshauge KM, Dessen M, Boland R. Lumbar spine 86. 87. 88. 89.
traction: evaluation of effects and recommended application for treatment. Manllal Thempy 2000;5(2):72-81 Pellecchia GL. Lumbar traction: a review of the literature. ] Orthop Sports Phys Tiler 1994;20(5):262-267 Lidstrom A, Zachrisson M. Physical therapy on low back pain and sciatica. Scand J Rehabil Med 1 970;2:37-42 Larsson U, Choler U, Lidstrom A et al Au to-traction for treat ment of l u mbago-sciatica. Acta Ort/lOp Scal/d 1 980;51:791 -798 Moret NC, Vanderstap M, Hagmeijer R et al. Design and feasi bility of a randomized trial to evaluate the effect of vertical traction in patients with a lumbar radicular syndrome. Mal/ual
Thempy 1998;3:203-211 90. Wilkins RH. Neurosurgical Classics. Johnson Reprint, New York, 1965. 91 . Cyriax J . Treatment of lumbar disc lesions. BM] 1950,ii:1434 92. Weber H. Traction therapy in sciatica due to disc prolapse. J Oslo City Hosp 1973;23:1 67-1 76 93. Weber H, Ljunggren AE, Wa lker L. Traction therapy in patients with herniated lumbar intervertebral discs. ] Oslo City Hosp 1 984;34:61-70 94. Worden RE, Humphrey TL. Effect of spinal traction on length of body. Archs Phys Med 1 964;45:318 95. Levernieux J. Tmction Vertebmle. Expansion Scientifique, Paris, 1960 96. Twomey LT. Sustained lumbar traction. An experimental study of long spine segments. Spine 1985;10(2):146-149 97. Bridger RS, Ossey S, Fourie G. Effect of lumbar traction on stature. Spine 1990;15(6):522-524 98. Troisier O. Les Aigies Discales et Ligmllentaires du Rachis. Masson, Paris, 1953 99. Tekeoglu I, Adak B, Bozkurt M, Gurbuzoglu N. Distraction of lumbar vertebrae in gravitational traction. Spil/e 1998;23(9): 1 061-1063. 100. Janke AW, Kerkow TA, Griffiths HJ, Sparrow EM, Iaizzo PA. The biomechanics of gravity-dependent traction of the lumbar spine. Spine 1997;22(3):253-260. 101. Lancourt JE. Traction techniques for low back pain.
J Musculoskel Med 1986;Apr23:44. 102. Guinet RJ, Hadler NM. Diagnosis and treatment of backache. Semin Arthritis Rheum 1 979;8:261-287. 103. Judovich BD, Nobel GR. Traction therapy: study of resistance factors, preliminary report on new method of lumbar traction.
Am J Surg 1957;93:108-114. 104. One! 0, Tuzlaci M, Sari H, Demir K. Computed tomographic investigation of the effect of traction on lumbar disc hernia tions. Spine 1989;14(1):82-90. 1 05. Fast A. Low back disorders: conservative management. Arch
Phys Med Rehabil 1988;69:880-891 . 1 06. Nachemson A, Elfstrom G . Intravital dynamic pressure measurements in lumbar discs. Scand ] Rehabil Med 1 970; 1(suppl):5-40.
107. Ramos G, Martin W. 1 994 Effects of vertebral axial decompres sion on intradiscal pressure. ] Neurosurg 1988;81(3):350-353.
934 SECTI O N T E N - T H E L U M BAR SPI N E
1 08. Chen YG, L i FB, Huang CD. Biomechanics o f traction for treat ment of lumbar disc prolapse. Chung Hua I Hsueh Tsa Chih 1994;74(1):40-42, 64. 109. Mathews JA. Dynamic d iscography: a study of lumbar trac tion. Arlll Phys Med 1968;9:275-279. n o. Burton ChV. Gravity lumbar reduction. In: Kirkaldy-Willis
W H (ed ) Mallaging Low Back Pain. Churchill Livingstone, Edinburgh, 1 988. 111 . One I 0, Tuzlaci M, Sari H et al. Annulus tears and interverte bral disc degeneration: an experimental study using an animal model. Spine ] 989;150:762-767. 112. Wyke BD. Electromyography in back-pain d iagnosis. Pain
Topics 1980;3:3. 113. Andersson GBJ, Schultz AB, Nachemson AL. Intervertebral disc pressure during traction. Scand J Rehabil Med 1983;9:88-91. 114. Quain MB, Tecklin JS. Lumbar traction: its effect on respiration. Phys Ther 1 985;65(9):1 343-1 346. 1 1 5. Meszaros TF, Olson R, Kulig K, Creighton 0, Czarnecki E. Effect of 1 0%, 30%, and 60% body weight traction on the straight leg raise test of symptomatic patients with low back pain. } Orthop Sports Phys Ther 2000;30(10):595-601 . 116. Van Wijmen PM. The use of repeated movements in the McKenzie method of spinal examination. In: Boyling JD, Palastanga N (eds) Grieve's Modern Manllal Therapy: The Vertebral Colllll1n, 2nd edn. Churchill Livingstone, Edinburgh,
1994:565-575. 1 1 7. Moss ] M . Cervical and lumbar pain syndromes. In: Boyling JD, Palastanga N (eds) Grieve's Modem Manual Therapy: The Vertebral Colllllln, 2nd edn. Churchill Livingstone, Edinburgh, 1 994:391-400. 1 1 8. Robinson MG. The McKenzie method of spinal pain manage ment. In: Boyling JD, Palastanga N (eds) Grieve's Modern Manual Therapy: The Vertebral Columll, 2nd edn. Churchill Livingstone, Edinburgh, 1994:753-769. 1 19. Long AJ . The centralization phenomenon. Its usefulness as a pred ictor of outcome in conservative treatment of chronic low back pain (a pilot study). Spine 1 995;20:2513-2521 . 1 20. McKenzie RA. The Lumbar Spine. Mechanical Diagnosis and Therapy. Spinal Publications, Waikanae, Wellington, NZ, 1981 . 121. McKenzie RA. Mechanical diagnosis and therapy for low back pain: toward a better understanding. In: Twomey LT, Taylor JR (eds) Physical Therapy of the Low Back. Churchill Livingstone, New York, 1987: 1 57-1 73. 122. McKenzie RA. A perspective on manipulative therapy.
Physiotherapy 1989;75:440-444. 123. Sicard A. Les injections medicamenteuses extradurales par voie sacro-coccygienne. CR Hebdomadaires Seances Mell1 Soc Bioi 1901 ;53:396-398. 124. Cathelin MF. Injection epidurale par Ie procede du canal sacre. CR Soc Bioi 1901;53:452. 1 25. Caussade G, Queste P. Bull Soc Med Hop Paris 1909;28:865. 1 26. Viner N. Intractable sciatica: sacral epidural injection. Can Med Assoc J 1925;15:630. 1 27. Evans W. Intrasacral epidural injection in the treatment of sciatica. Lancet 1930;Dec:1 225-1229. 128. Cyriax JH. Lumbago: the mechanism of dural pain. Lancet 1945;ii:427. 129. Cyriax JH. Epidural anaesthesia and bed rest in sciatica. BMJ 1961;1:20-24. 130. Kramer J. Biochemie der Zwischenwirbelscheiben. Wirbelsaule Forsch. Prax 1974;59:10. 1 3 1 . Adams M, Hutton We. The effect of posture on the flu i d content o f the l umbar intervertebral d isc. Spine 1 983;8:665-671 . 132. U rban JPG, McMullan JF. Swelling pressure of the lumbar
intervertebral discs: influence of age, spinal level, composition and degeneration. Spine 1988;13:1 79-187. 133. Cooper AB, Sharpe MD. Bacterial meningitis and cauda equina syndrome after epidural steroid injections. Call } Anaesth
1996;43(5 Pt 1):471-474. 1 34. Humphries Sv. Personal view. BM} 1973;ii:452. 1 35. Eriksson E. Atlas del' Lokalaniisthesie, 2nd edn. Springer, Berlin, 1980:138. 136. Price CM, Rogers PO, Prosser AS, Arden NK. Comparison of the caudal and lumbar approaches to the epidural space. Anll Rheull1 Dis 2000;59(11):879-882. 1 37. Ryder HW. Mechanism of change in cerebrospinal fluid pres sure following induced change in volume of fluid space. } Lab Clin Med 1953;41:428. 138. Lindahl O. Hyperalgesia of the lumbar nerve roots in sciatica. Acta Orthop Scand 1966;37:367. 139. Troisier O. Semiologie et Traitelllent des Algies Discales et Ligamentaires du Rachis. Masson, Paris, 1973. 1 40. Wiltse LL. Therapeutic caudal or epidural block for lower back or sciatic pain. JAMA 1980;243:369-370. 141 . Cyriax J H . Textbook of Orthopaedic Medicine, vol 1, 7th edn. Bailliere Tindall, London, 1978:513. 142. Bhatia MT, Parikh LCJ. Epidural saline therapy in lumbosciatic syndrome. ] Indian Med Assoc 1966;47(11):537-542. 143. Gupta AK, M i tal VK, Azmi RU. Observations on the manage 144. 1 45. 146. 147.
148.
ment of l umbosciatic syndromes (sciatica) by epidural saline. ] Indian Med Assoc 1 970;54:194-196. Revel M, Au leley GR, Alaoui S et al Forceful epidural injections for the treatment of lumbosciatic pain with post-operative lumbar spinal fibrosis. Rev RIll/III EngI 1996;63(4):270-277. Wall PO, Melzack R. Textbook of Pain. Churchill Livingstone, London, 1 984:240-25l . Coomes E N . A comparison between epidural anaesthesia and bed rest in sciatica. BM] 1961;1:20-24. Goebert WW, Jallo SJ, Gardner J, Wasmuth CEo Sciatica treat ment with epidural hydrocortisone. Scientific exhibit, Congress of American Society of AnestheSiologists, New York, Nov 1960. Knutsen 0, Ygge H. Prolonged extradural anaesthesia with bupivacaine at lumbago and sciatica. Acta Orthop Scalld
1 971;42:338-352. 149. Beliveau P. A comparison between epidural anaesthesia with and without corticosteroid in the treatment of scialica.
Rheumatol Phys Med 1971;11:40. 1 50. Yates OW. A comparison of the types of epidural injection commonly used in the treahnent of low back pain and sciatica.
Rheum RehabiI 1978;17(3):181-1 86. 1 5 1 . Mam MK. Results of epidural injection of local anaesthetic and corticosteroid in patients with lumbosciatic pain. ] Illdian Med Assoc 1995;93(1):17-18, 24. 1 52. Hauswirth R, Michot F. Sacral epidural anesthesia in the treat ment of l u mbosacral backache. Sclnveiz Med Wochenschr 1982;112(7):222-225. 1 53. Bush K, Hillier S. A controlled study of caudal epidural injec tions of triamcinolone plus procaine for the management of intractable sciatica. Spine 1991;16:572-575. 154. Ombregt L. Epidurale Lokale Anesthesie; Beoordeling na drie jaar gebruik. International Symposium on Low Back Pain, BSSOM, De Haan, Belgium, 12 June 1982. 1 55. Uhlenbrock 0, Arlinghaus J. Results of CT-guided periradicu lar pain therapy. 1997;166(6):528-534. 1 56. Viton JM, Peretti-Vi ton P, Rubino T, Delarque A, Salamofl N. Short-term assessment of periradicular corticosteroid injec tions in lumbar radiculopathy associated with disc pathology.
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 .
of low back pain and sciatic syndrome in disc disease or injury: results of a joint neurosurgical and orthopaedic project. Aust
NZ j Surg 1975;45:183-191. 167. Finnegan WI, FenIin JM, Marvel JP et al. Results of surgical intervention in the symptomatic m ultiply-operated back patient. j Bone joint Surg 1979;61A: 1077-1082. 168. Lutze M, Stendel R, Vesper J, Brock M. Periradicular therapy in lumbar radicular syndromes: methodology and results. Acta Neurochir (Wien) 1997;139(8):719-724. 169. Krempen JF, Smith BS. Nerve root injection. J Bone Joint Surg
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
1989;71B:684-686. 178. Bogduk N, Macintosh JE. The applied anatomy of the thoraco lumbar fascia. Spine 1984;9:164-170. 179. Rees WES. Multiple bilateral subcutaneous rhizolysis of segmental nerves in the treatment of the intervertebral disc syndrome. Ann Gen Prac! 1971;26:126-127. 180. Shealy CN. Facet denervation in the management of back pain and sciatic pain. c/in Orthop 1976;115:157-164. 181. Silvers HR. Lumbar percutaneous facet rhizotomy. Spine
1990;15:36-40. 182. Leong JCY, Luk KDK, Chow DHK, Woo CWO The biomechani cal functions of the iliolumbar ligament in maintaining stabil ity of the lumbosacral junction. Spine 1987;12:669-674.
183. Chow DHK, Luk KDK, Leong JCY and Woo CX. Torsional stability of the lumbosacral junction: significance of the ilio lumbar ligament. Spine 1989;14:611-615. 184. Yamamoto I, Panjabi MM, Oxlands TR, Crisco JJ. The role of the iliolumbar ligament in the lumbosacral junction. Spine
1990;15:1138-1141. 185. Hirschberg GG, Froetscher L, Naeim F . Iliolumbar syndrome as a common cause of low back pain: diagnosis and prognosis.
Arch Phys Med RehabiI 1979;60:415-419. 186. Naeim F, Froetscher L, Hirschberg Gc. Treatment of the chronic iliolumbar syndrome by infiltration of the iliolumbar ligament. West J Med 1982;136:372-374. 187. H ackett GS. Ligament and Tendon Relaxation Treated by Prolotherapy, 3rd edn. Thomas, Springfield, 1958. 1 88. Hackett GS, Huang Te, Raftery A, Dodd TJ. Back pain following trauma and disease - prolotherapy. Milit Med
1961;126:517-525. 1 89. Ongley MJ, Klein RG, Thomas AD, Dormak AD, Eek BC, Hubert LJ. A new approach to the treatment of chronic low back pain. Lancet 1987;July 18:143-146. 190. Klein R, Dorman T, Johnson C. Proliferant injections for low back pain: histologic changes of injected ligaments and objec tive measurements of lumbar spinal mobility before and after treatment. J Neural Orthop Med Surg 1989;10:123-126. 191. Wilkinson HA. The Failed Back Syndrome: Etiology and Therapy. Lippincott, Philadelphia, 1983. 192. Gildenberg PL, De Vau l RA. M a nagement of chronic pain refractory to specific therapy. In: Yomans JR (ed ) Neurological Surgery, 3rd e d n . Saunders, Philadelphia,
1990:4144-4165. 193. Klein RG, Eek Be, DeLong WB, Mooney V A randomized double-blind trial of dextrose-glycerine-phenol injections for chronic, low back pain. J Spinal Disord 1993;6(1):23-33. 194. Nordin M, Weiser S, Halpern N . The prevention and treatment of low back disorders. In: Frymoyer JM (ed) The Adult Spine. Raven Press, New York, 1991 :1642. 195. Association of Schools of Public Health. Proposed National
Strategies for the Prevention of Leading Work-Related Diseases alld Injuries. Part I, Association of Schools of Public Health, Washington DC, 1986. 196. Hall H, leeton JA. Back school. An overview with specific reference to the Canadian Back Education Units. c/in Orthop 1983;179:10-17. 197. Valkenburg HA, Haanen HCM. The epidemiology of low back pain. In: White AA III, Gordon SL (eds) American Academy of Orthopaedic Surgeons Symposium on Idiopathic Low Back Pain. Mosby, St Louis, 1982:9-22. 198. Vlaeyen JW, Smeets RI, Mulder HP et al Secundaire preventie v a n chronische l age rugpijn : Een gedragsgeorienteerde benadering. Ned Tijdschr Geneeskd 1993;137:1544-1549. 199. Nachemson A. The influence of spinal movements on the lumbar intradiscal pressure and on the tensile stresses in the annulus fibroslls. Acta Orthop Scand 1963;33:1 83. 200. Shah JS, Hampson WA, Jayson MIV The distribution of surface strain in the cadaveric l u mbar spine. J Bone Join t Surg
1978;60B:246-251 . 201. Krag M H , Seroussi RE, Wilder DG, Pope M H . Internal displacement distribution from il1 vitro loading of human thoracic and lumbar spinal motion segments: experimental results and theoretical predictions. Spine 1987;12: 1001-
1007. 202. Schnebel BE, Simmons JW, Chowning I, Davidson R. A digitiz ing technique for the study of movements of intradiscal dye in response to flexion and extension of the lumbar spine. Spine
1988;13:309-312.
936 SECTION TEN - T H E L U M BAR SPI N E
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
1989;7:122-1 31. 204. Peters T. Anthropometrische u n d physiologische Grundlagen
zur Gestaltung von Bii roarbeitssitzen. In: Grandjean E (ed) Sitting Posture. Taylor & Francis, London, 1969:48-56. 205. Kroemer KHE. Seating in plant and office. Am Industr Hyg
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
Assoc j 1971 ;32:633. 206. Burandt U, Grandjean E. Sitting habits of office employees. Ergonomics 1963;6:21 7. 207. Akerblom B. Anatomische und physiologische Grundlagen zur Gestaltung von Sitzen. In: Grandjean E (ed) Sitting Posture. Taylor & Francis, London, 1969:6-17. 208. Laurig W. Der Stehsitz als physiologisch gunstige Alternative zum reinen Steharbeitsplatz. Arbeitsmed Sozialmed Arbeitshyg 1969;4:219. 209. Cyriax jH. The Slipped Disc, 2nd edn. Gower Press, Epping, 1975. 210. Andersson BJG, brtengren R, Nachemson A, Elfstrom G.
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 .
C HAPTER 59 - TREATMENT OF THE L U M BAR S PI N E 937
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 .
THIS PAGE INTENTIONALLY LEFT BLANK
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
THIS PAGE INTENTIONALLY LEFT BLANK
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
-
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
-
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
-
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.
REFERENCES 1 . Healey LA. Polymyalgia rheumatica. In: McCarthy DJ (ed)
13. Mankin HI, Dorfman H, Lipiello L, Zarins A . Biomechanical
& Febiger,
and metabolic abnormalities in articular cartilage from human
2. Goldenberg DL, Cohen A S . Acute infectious arthritis. A review
14. Castors CW, Dorstewitz EL, Smith SF, Ritchie Je. Connective
Arthritis alld Allied Conditions,
9th
edn.
Lea
Philadelphia, 1979:68 1 .
osteoarthritic hips. J Bone Joint Surg 1970;52A:424-434.
of patients with non-gonococcal joint infections (with emphasis
tissue activation. I. The natu re, specificity and distribution of
on therapy and prognosis). JAMA 1976;60:369.
connective
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
activating
peptides.
Arthritis
Rheu m
1971;14:41-54.
15. Dingle JT, Saklatvala I, Hembry R, Tyler J, Fell HB, Jubb RW. A
cartilage
catabolic
factor
from
synovium.
Biochem
J
1979;184:1 77-180. 16. Christmann OD. Biomechanical aspects of degenerative joint disease. Clin Orthop 1969;64:77-85. 1 7. Pitsillides AA, Skerry TM, Edwards Je. Joint immobilization reduces synovial fluid hyaluronan concentration and is accom panied by changes in the synovial intimal cell populations. Rheumatology 1999;38(11) : 1 1 08-1 112. 18. Strange FSe. The Hip. Heinemann, London, 1965:226-262.
8. Visuri T. Stress osteopathy of the femoral head: 10 military recruits
19. Long W, Dorr LD, Healy B et al. Functional recovery of non
9. Radin EL, Martin RB, Burr DB, Caterson B , Boyd RD, Goodwin
20. Nakamura T, Susuki K. Muscular changes in osteoarthritis of the
followed for 5-11 years. Acta Orthop Scand 1 997;68:138-14 l .
e. Mechanical factors influencing cartilage damage. In: Peyron JG (ed) Osteoarthrosis. Currell t Clin ical and Fundamental Problems. CIBA-Geigy, Paris, 1986:90-99. 10. Byers PD, Contempomi CA, Farkas TA. A postmortem study of the hip joint. Am Rheum Dis 1 970;29:15. 11 . Meachim G, Emery I H . Cartilage fibrillation in shoulder and hip joints of Liverpool necropsies. J Anat 1973:116:6 l . 1 2 . Radin EL, Rose RM. Role of subchondral bone i n the initiation and progression of cartilage damage. Ciin Orthop 1 986;213: 34-40.
cementa! total hip arthroplasty. Ciin Orthop Rei Res 1993;288:73-77. hip and knee. Nippon Seikeigeka Gukki Zasshi 1 992;66(5) :467-475. 2 1 . Nillson BE, Danielsson LG, Jerker Hernborg SA. Clinical feature and natural course of coxarthrosis and gonarthrosis. Scand J Rheum SuppI 1980;(43 suppl) : 1 3-21 .
22. Robertsson 0, Wingstrand H , Onnerfalt R . Intracapsular pres sure and pain in coxarthrosis. J Arthroplasty 1995;10(5):632-635.
23. Bijl D, Dekker I, van Baar ME et al. Validity of Cyriax's concept capsular pattern for the diagnosis of osteoarthritis of hip and / or knee. Scand J RheumatoI 1998;27(5) :347-351 .
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
24. Janda V. Muscle Function Testing. Butterworths, London, 1983.
25. LG1wit K. Manipulative Therapy in Rehabilitation of the Locomotor System, 2nd edn. Butterworth Heinemann, Oxford, 1 99 1 .
50. Leroux JL, Denat B, Thomas E et al. Sacral insu fficiency fractures presenting as acute low back pain. Spine 1 993;8(1 6): 2502-2506.
26. Vogt L , Banzer W. Dynamic testing of the motor stereotype in prone hip extension from the neutral position. Clin Biomech
5 1 . Weber M, Hasler P, Gerber H. Insu fficiency fractures of the sacrum. Spine 1993;19(16):2507-2512.
52. Schmidek R, Smith DA, Kristiansen TK. Sacral fractures.
1997;12:122-127. 27. Bierma-Zeinstra S, Bohnen A, Ginai A, Prins A, Verhaar J .
Neuros u rgery 1984;15:735-746.
Validity of American College of Rheumatology criteria for diag
53. Kristiansen TK. Fractures of the sacrum and coccygodynia. In:
nosing hip osteoarthrosis in primary care research. J Rheumatol
Fryomer JW (ed) The Adult Spine. Raven Press, New York,
1999;26(5): 1 1 29-1133. 28. Ledingham
I,
Dawson S, Preston B, Milligan G, Doherty M.
Radiographic patterns and associations of osteoarthrosis of the hip. Ann Rheum Dis 1992;51(10) :1111-1116.
1991:2145-2148. 54. Mirra JM. Bone Tumours: Diagnosis and Treatment. Lippincott, Philadelphia, 1980:1 38-1 6 1 . 55. Shamahan MDG, Ackroyd C E o Pyogenic infections of the sacro
29. Cameron H, MacNab I . Observations on osteoarthritis of the hip
iliac joint. J Bone Joint Surg 1985;64B :605-608.
joint. Clin Orthop Rei Res 1975;108:31-40.
56. Dunn EJ, Bryan DM, Nugent JT, Robinson A. Pyogenic infec
of exercise therapy in patients with osteoarthritis of the hip or
57. Feldman JC, Menkes CJ, Weill B, Delrieu F, Delbasse F. Les
30. Van Baar ME, Dekker I, Oostendorp RA et al. The effectiveness knee: a randomized clinical trial. J Rheumatol 1 998;25(12):
sacro-iliites infectieuses. Etude multicentrique sur 214 observa tions. Rev Rhum Mal Osteoartic 1981;48:83-9 1 .
2432-2439. 3 1 . Van Baar ME, Assendelft WI, Dekker J, Oostendrop RA, Bijlsma JW.
tions of the sacro-iliac joint. Clin Orthop 1976;118 : 1 1 3- 1 1 7.
Effectiveness
of exercise
therapy
in
patients
58. Kerr R. Pyogenic sacro-iliitis. Orthopedics 1985;8(8):1 028-1034.
with
59. Hamdam J, Ashra M, Mallouch A, Usta H, Talab Y, Ahmad M.
osteoarthritis of the hip or knee: a systematic review of ran
Early diagnosis of septic arthritis of the sacroiliac joint by use
domised clinical trials. Arthritis Rheum 1999;42(7) : 1361-1369. 32. Solomon L, Schnitzler C, Browett O. Osteoarthritis of the hip,
of computed tomography. J Rheumato/ 1981;8:979-982.
60. Masri BA, Masterson EL, Duncan CPo The classification and
the patient behind the disease. Peyron J (ed) EpidemiologJJ of
radiographic evaluation of bone loss in revision hip arthro
Osteoarthritis. CIBA-Geigy, Paris, 1981:40-52.
plasty. Orthop Clin North Am 1998;2:21 9-227.
33. Dequeker I, Goris F, Uytterhoeven R. Osteoporosis-osteoarthro sis: anthropometric d istinctions. JAMA 1 983;249: 1 448-145 1 .
61 . Haenisch H . Arthritis dissecans de H u fte. Zentralbl Chir 1 925;52:999.
34. Kaltenborn F. Manual Mobilisation of the Extremity Joints, 4th edn.
62. Jacobs
35. Lewit K. Manipulative Therapy in Rehabilitation of the Locomotor
63. Streda A. Participation of osteonecrosis in the development of
Olaf Norlis Bokhandel, Oslo, 1989.
system, 2nd edn. Butterworth Heinemann, Oxford, 1991. 36. Mink AJF, ter Veer HJ, Vorselaars JACTh. Extremiteiten. Funktie onderzoek en Man uele Therapie.
Uitg,
Holkema, Houten, NL, 1990.
Bohn; Scheltema &
37. Janda V. Muscle Function Testing. Bu tterworth, London, 1983.
38. Lewit K. Manipulative Therapy in Rehabilitation of the Locomotor System, 2nd edn. Butterworth Heinemann, Oxford, 199 1 . 39. Kendall F, McCreary E. M uscles Testing a n d Function, 3rd edn.
B.
Epidemiology of traumatic and
non-traumatic
osteonecrosis of the head of the femur. Clin Orthop 1978;130:5. severe coxarthrosis. Acta Univ Coal (Med) (Praha) Monogr 46 1971 : 1 03-142. 64. Hungerford DS, Zizic TM. Pathogenesis of ischemic necrosis of the femoral head. Hip 1983;5:249-262. 65. Vreden SG, Hermus AR, van Liessum PA et al. Aseptic bone necrosis in patients on glucocorticoid replacement therapy. Netherlands J Med 1991;39:153-157. 66. Matsuo K, Horohata T, Sugioka Y et al. Influence of alcohol
Williams & Wilkins, Baltimore, 1983.
intake, cigarette smoking and occupational status on idio
conservative management. Manual Therapy 1999;4(3):127-135.
1 988;234:1 15-123.
40. Sims K. The development of hip osteoarthritis: implications for 41 . Kisner C, Colby L.
Therapeutic Exercise: Foundations and
Techn iques, 3rd edn. FA Davis, Philadelphia, 1996:68. ticosteroid on knee joints: a clinical investigation on primary gonarthrosis. J Jpn Orthop Assoc 1 978;52(3) :359-374. RL.
Early
failure
of
modern
cemented
osteonecrosis
of
the
femoral
hea d .
Clin
Orthop
67. Warner JJP, Philip JH, Brodsky GL, Thornhill TS. Studies of nontraumatic
42. Ishikawa K . A study of deleterious effects of intra-articular cor
43. Barrack
pathic
osteonecrosis;
manometric
and
histologic
studies of the femoral head a fter chronic steroid treatment: an experimental study in
rabbits.
Clin
Orthop
1 987;225:
128-140. stems.
68. Cruess RL. Osteonecrosis of bone. Current concepts as to
44. Herberts P, Malchau H. Long-term registration has improved the
69. Conklin I, Alderson PO, Zizic TM et al. Comparison of bone scan
] ArthroplashJ 2000;15(8) : 1 036-1050. quality of hip replacement: a review of the Swedish THR Register comparing 1 60,000 cases. Acta Orthop Scand 2000;71(2):111-12 1 . 45. Breusch SJ, Aldinger PR, Thomsen M , Lukoschek M, Ewerbeck
V. Anchoring principles in hip prosthesis implantation. II: Acetabulum components. Unfallchirurg 2000;103(12): 1 0 1 7-103 1 .
46. Fran�ois F. Une nouvelle entite clinique: l a bursite ischiatique. Rev Rhum Mal Osteoartic 1 966;33:255-256. 47. Parks AG, Gordon PH, Hardcastle JD. A classification of fistula in-ano. Br J Surg 1 976;63 : 1 . 48. Golighter JC, Ellis M , Pissidis A G . A critique of anal glandular
etiology and pathogenesis. Clin Orthop 1986;208:31-39. and radiographic sensitivity in the detection of steroid-induced ischemic necrosis of bone. Radiology 1983;147:221-226. 70. Hungerford DS. Bone marrow pressu re, venography and core decompression in ischemic necrosis of the femoral head. In: The Hip: Proceedings of the Seventh Open Scien tific Meeting of The Hip Socieh;. Mosby, St. Louis, 1979:218-237. 71. Mitchell DG, Kressel HY, Arger PH et al. Avascu lar necrosis of the femoral head: morphologic assessment by MR imaging, with CT correlation. Radiology 1 986;161:739-742. 72. Robinson HJ, Hartleben PD, Lund G et al. Evaluation of mag
infection in the aetiology and treatment of idiopathic ano-rectal
netic resonance imaging in the diagnosis of the osteonecrosis of
abscesses and fistulas. Br J Surg 1967;54:977.
the femoral head. J Bone Joint Surg 1989;71A:650-663.
49. Denis F, Davis S, Comfort T. Sacral fractures: an important
73. Kukobo
T,
Taka tori Y, Ninpmiya S et al. Magnetic resonance
problem. Retrospective analysis of 236 cases. Clin Orthop
imaging and scintigraphy of avascular necrosis of the femoral
1988;227:67-8 1 .
head. MR [mag Scin tig ANFH 1 992;27:54-60.
1 022 SECTIO N TWELVE - T H E H I P A N D B UTTOCK
74. Halland AM, Klemp P, Botes 0 et al. Avascular necrosis of the hip in systemic lupus erythematosus: the role of magnetic
resonance imaging. Br J Rheum 1993;32:972-976.
graphy in the diagnosis of disorders of the hip. Clin Orthop Rei Res 1987;221 :238-24 1 . 1 0 1 . Toohey AK, LaSalle TL, Martinez S , PoUsson RP. Iliopsoas
75. Ficat RP, Arlet J. Ischemia and Necrosis of Bone. Williams & Wilkins, Baltimore, 1980.
76. Mitchell DG, Rao VM, Dalin.ka M K et al. Femoral head avascu
bursitis: clinical features, radiographic findings, and disease associations. Semin Arthritis Rheum 1990;20(1):41--47. 102. Fortin L, Belanger R. Bursitis of the iliopsoas: four cases with
lar necrosis: correlation of MR imaging, radiographic staging,
pain as the only clinical indicator. J Rheumatol 1995;10:
radionuclide
1971-1973.
imaging,
and
clinical
findings.
Radiology
103. O'Connor OS. Early recogn.ition of iliopectineal bursitis. Surg
1987;162:709-715. 77. Ficat RP. Idiopathic bone necrosis of the femoral head. Early 78. Gri ffiths HI. Etiology, pathogenesis and early diagnosis of ischemic necrosis of the hip. lAMA 1981;246:2615-2617. as trochanteric bursitis. Ann Rheum Dis 1990;49(9): 730-732.
bursitis
presenting
as
unilateral
femoral
nerve
palsy.
] Rheumato/ 1991;18(3):462--463.
80. Webber MM, Wagner J, Craign MD. Radionuclide patterns of
1 Nuc/ Med B ioi
the hip. Arthritis Rheum 1 971;14:105. 105. Letourneau L, Dessureault M, Carette S. Rheumatoid iliopsoas
79. Mandell BF. Avascular necrosis of the femoral head presenting
femoral head disease. Int
Gynecol Obstet 1933;57:674-684. 104. Samuelson C, Ward JR, Albo D. Rheumatoid synovial cyst of
diagnosis and treatment. J Bone Joint Surg 1985;67B:3.
106. Ginesty E, Dromer C, Galy-Fourcade D et al. Iliopsoas bursopathies. A review of twelve cases. Rev R/wYIl EI/gi
1 977;4:167.
8 1 . Steinberg ME, Brighton CT, Hayken GO, Tooze SE, Steinberg
1998;65(3) : 1 81-186.
DR. Early results in the treatment of avascular necrosis of the
107. Mallant MPJH, Mastboom WJB, De Backer GPM. Liesklachten
femoral head with electrical stimulation. Orthop Clin North A m
door bursitis iliopectinea. Ned Tijdschr Gelleeskd 1998;142(23):
1984;15: 1 63.
1328-133 l .
82. Atsumi T, Kuroki Y. Role of impairment of blood supply of the femoral head in the pathogenesis of idiopathic osteonecrosis.
Clin Orthop Rei Res 1 992;227:22-30. 83. Meyers M H . Osteonecrosis of the femoral head. Pathogenesis and long-term results of treatment. Clin Orthop 1 988;231 :51-6 1 . 84. Hopson CN, Siverhus SW. Ischemic necrosis of the femoral head: treatment by core decompression. J Bone Joint Surg
toid arthritis. Clin Exp Rheumato/ 1993;11(5):549-55l . 109. Weiner JR, Robinson ow. Pigmented villonodular synovitis of iliopectineal bursa. J Bone Joint Surg 1951;33A:988.
110. Binek R, Levinsohn M. Enlarged iliopsoas bursa; an unusual cause of thigh mass and hip pain. Clin Orthop 1987;224:158-163. 1 1 1 . Swezey RL. Pseudo-radiculopathy in subacute trochanteric bursitis of the subgluteus maxim us bursa. Arch Phys Med
1988;70A:1048-105 l . 85. Ennecking WF. The choice of surgical procedure i n idiopathic aseptic necrosis. In: Proceedings of The Hip Society VII. Mosby, St. Louis, 1979:238-243.
army recru its: implications of bone density, calcium intake, 88. Stoneham MD, Morgan NY. Stress fractures of the hip in Royal Marine recruits under training: retrospective analysiS. Br
1
Sports Med 1991;25(3): 1 45-148. 89. Tountas AA, WaddeLl JP. Stress fractures of the femoral neck. A report of seven cases. Clin Orthop 1986;210:1 60-165.
low back pain.
Scalld ]
1 1 4. Little H. Trochanteric bursitis: a common cause of pelvic girdle 115. Duthie RB, Bentley e. Trod1anteric bursitis (subgluteal bursa). In: Mercer's Orthopaedic Surgery, 8th edn. Edward Arnold, London, 1983:710. 116. Traycoff RB. ' Pseudotrochanteric bursitis': the differential diag nosis of lateral hip pain. ] Rheumato/ 1991;18(12):1810-1812.
90. Jones DL, Erhard RE. Diagnosis of trochanteric bursitis versus femoral neck stress fracture. Phys Ther 1997;77(1) :58-67.
1 1 7. Samson M, Lequesne M. Tendinites de la region de la hanche. Rev Prat 1991 ;14(18) : 1 667-1 671.
9 1 . Dome HL, Lander PH. Spontaneous stress fractures of the femoral neck. Am J Roen tgenoI 1985;144(2):343-347.
]0,
syndrome in
RheumatoI 1991 ;20:262-266. pain. Can Med Assoc J 1 979;120:456--458.
Nutr 1998;17(2) : 1 28-135.
92. Shin AY, Morin WD, Gorman
113. CoHee G, Dijkmans BAC, Vandenbroucke JP, Cats A. Greater trochanteric pain
Int J Sports Med 1995;16(8):563-567. 87. Cline AD, Jansen GR, Melby CL. Stress fractures in female
f Am ColL
Rehabil 1 976;57:387-390. 112. Spear 1M, Lipscomb PR. Noninfectious trochanteric bursitis and peritendinitis. Surg Clin North Am 1952;32:1217.
86. Batt ME, Timmerman LA. Hip pains in a recreational runner.
and exercise.
108. Generini S , Matucci-Cerinic M. Iliopsoas bursitis i n rheuma
118. Schipira 0, Menachem N, Scharf Y. Trochanteric bursitis: a common clinical problem. Arch Phys Med Rehabil 1986;67:
Jones SB, Lapinsky AS. The
superiority of magnetic resonance imaging in differentiating the cause of hip pain in endurance athletes. Am J Sports Med 1996;24:168-176.
815-917. 1 1 9. Raman 0, Haslock 1. Trochanteric bursitis: a frequent cause of 'hip' pain in rheumatoid arthritis. Ann Rheum Dis 1982;41:
602-603.
93. Dorfrnann H, Boyer T. Arthroscopy of the hip: 12 years of
120. De Windt VE, Verhaar J, Vanderlinden A, Duysings J. De oper ative behandeling van de bursitis trochanterica. Ned Tijdschr
experience. Arthroscopy 1999;15(1):67-76. 94. Allen WC, Cope R. Coxa saltans. The snapping hip revisited.
Geneeskd 1990;134:2167.
] Am Acad Orthop Surg 1995;3:303-308.
1 2 1 . Anderson TP. Trochanteric bursitis: diagnostic criteria and
labrum. Clin Orthop 1995;320 : 1 76-1 8 l .
122. Karpinsky MRK, Pigott H. Greater trochanteric pain syn
95. Kim YT, Azuma H. The nerve endings of the acetabular 96. Lage LA, Patel JV, Villar R N . The acetabular labral tear: A n arthroscopic classification. Arthroscopy 1996;12:269-272. ment. Clin Ort/wp 1995;311 :60-68. bular labral tears. Arthroscopy 1999;15(2) : 1 32-137. The
iliopsoas
trochanter
pain syndrome). Mayo Clin Proc 1 996;71(6):
565-569.
98. Farjo LA, Glick JM, Sampson TG. Hip arthroscopy for aceta SB.
drome. J Bone Joint Surg 1985;67B(5):762-763. 1 23. Shbeeb MI, Matteson EL. Trochanteric bursitis (greater
97. Fitzgerald RH J r. Acetabular labrum tears. Diagnosis and treat
99. Chandler
clinical significance. Arch Phys Med Rehabil 1958;39:617-622.
bursa
in
man.
124. Traycoff RB. 'Pseudotrochanteric bursitis': the differential diagnosis
A nat
Rec
1934;58:235. 100. Harper MC, Schaberg JE, Allen We. Primary iliopsoas burso-
of lateral
hip
pain.
J
Rheumatol
1991;18'(12):
1 810-1 812. 1 25. Schein AI, Lehrmann O. Acute trochanteric bursitis with calcification. Surgery 1941;9:771-779.
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
REFERENCES 1. Gullmo A, Buring K, Ekstrand J. Groin injuries in athletes. Proceedings, Swedish Sports Medicine Society, Karlstad, Sweden. 1977:10. 2 Renstrom P, Peterson L. Groin injuries in athletes. Br ] Sports Med 1980;14:30. 3 Mozes M, Papa MZ, Zweig A, Horoszowski H, Adar R. Iliopsoas injury in soccer players. BrJ Sports Med 1985; 19(3):168-170. 4. Ekstrand JS, GiIlquist J. Soccer injuries and their mechanisms: a prospective study. Med Sci Sports 1983;15:267-270. 5. Genety J, Brunet-Guedj E. Traumatologie du sport. Pratique Med. Courante, 2nd edn. Paris, 1980. 6. O'Donoghue OH. Treatment of Injuries to Athletes, 2nd edn. Saunders, Philadelphia, 1970:46�65. 7. Cyriax J. Textbook of Orthopaedic Medicine, vol II, Treatment by Manipulation, Massage and Injection, 11th edn. Bailliere Tindall, London, 1984. 8 Lotke PA. Soft tissue afflictions. Steinberg ME (ed) The Hip and Its Disorders. Saunders, Philadelphia, 1991:669-682. 9. Lieberman GM, Harwin SF. Pelvis, hip, and thigh. In: Scuderi GR, McCrum PD, Brwlo PJ (eds) Sports Medicine: Principles of Primary Care. Mosby, St Louis, 1997:306-335 10. Brosterhaus Dors FP, van Oyen JA. Obstructie-ilieus met pijnuin het been denk aan een hernia obturatoria. Ned Tijdschr Geneeskd 1993;137(43):2177-2179 11. Kling TF. Pelvic and acetabular fractures. In: Steinberg ME (ed) TIle Hip and its Disorders. Saunders, Philadelphia, 1991:173-197.
12. Butler JE, Eggert AW. Fracture of the iliac crest apophysis: an unusual hip pointer. Am] Sports Med 1975;3:192-193. 13. T heologis TN, Epps H, Latz K, Cole We. Isolated fractures of the lesser trochanter in children. Injury 1997;28:5-6, 363-364. 14. Khoury JG, Brandser EA, Found EM Jr, Buckwalter JA. Non traumatic lesser trochanter avulsion: a report of three cases. Iowa OrthopJ 1998;18:150-154. 15. Riedeberger J et al. Das Schrunbein-, Adduktorensyndrom bei Fussballspielern. Zentralbl ChiI' 1967;XCII:2655-2660. 16. Schiirer-Waldheim H, Wolner E. Der Leistenschmerz des Sportlers. Sportarzt 1969;20:482-486. 17. Spring R. Die chronische Leistenzerrung beim Spitzensportler und deren T herapie. Z Orthop Grenzgeb 1977;CXV:369-371. 18. Eismann HJ et al. Zur Atiologie, Symptomatologie, Differentialdiagnose, T herapie und Prophylaxe des Leistenschmerzes bei jugendIichen Fussballspielern. Med Sport 1972;12:80-84. 19. Adams RJ Chandler FA. Osteitis pubis of traumatic etiology. J BoneJoint Surg 1953;35A:685-696. 20. Cochrane GM. Osteitis pubis in athletes. Br J Sports Med 1971;5:233-235. 21. Merrifield HH, Consu RF. Ice hockey groin pulls. Am J Sports Med 1973;1:41-42. 22. Fricher PA, Taunton JE, Amman W. Osteitis pubis in athletes. Infection, inflammation, injury. Sports Med 1991; 12(4):266-279.
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.
THIS PAGE INTENTIONALLY LEFT BLANK
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
THIS PAGE INTENTIONALLY LEFT BLANK
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
THIS PAGE INTENTIONALLY LEFT BLANK
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.
RE FERENCES 1 . Fritz JM, Delitto A, Erhard RE, Roman M. An examination of the selective tissue tension scheme; with evidence for the concept of a capsular pattern of the knee. Phys Ther 1998;
78:1 046-1056. 2. Haslock I, Wright V. The arthritis associated with intestinal disease. Bull Rheum Dis 1 973;32:479. 3. Mielants H, Veys EM. Reiter's syndrome and reactive arthritis. New Engl ] Med 1 984;310:1 538. 4. Chandler GN, Jones DT, Wright V. Charcot's arthropathy fol lowing intra-articu lar hydrocortisone. BMJ 1959;1:952-953. 5. Ishikawa K. A study of deleterious effects of intra-articular cor ticosteroid on knee joints - a clinical investigation on primary gon-arthrosis. J Jap Orthop Ass 1978;52(3):359-374. 6. Balch HW, Gibson JMe, El-Ghobarey E et al. Steroid injections into knee. Rheumatol Rehab 1977;16:137. 7. Gray RG, Gottlieb NL. Intra-articular corticosteroids: an updated assessment. Clin Orthop ReI Res 1983;177:235-263. 8. Seedhom BB. Loadbearing function of the menisci. Physiotherapy
1976;62(7):223-226. 9. Smilie IS. Injuries of the Kllee Joint. Churchill Livingstone, Edinburgh, 1978. 1 0. Jackson JP. Degenerative changes in the knee after meniscec tomy. BM] 1968;2:525-527. 1 1 . Seedhom BB. Can footballers play well without their carti lages? Medisport 1 980;2:98. 1 2. Albi:ick S, Bauer G, Bohne WHo Spontaneous osteonecrosis of the knee. Arthritis Rheum 1968;9:705-733. 13. Aglieti P, Insall I N , Bussi R, Deschamps e. Idiopathic osteonecrosis of the knee. Aetiology, prognosis and treatment.
J Bone Joint Surg 1983;65B(5):588-597. 14. Rozing PM, De Jonge-Bok JM. Idiopathische osteonecrose van de mediale femurcondyl: een zeldzame oorzaak van pijn in de knie bij een oudere patient. Ned Tidschr Geneeskd 1983; 127(19) :809-81 1 . 15. Gunther KP, Scharf H P. Standardization o f roentgen diagnosis in coxarthrosis and gonarthrosis in clinical studies. Recommendations of the 1 st Working Circle of the DGOT. Z Orthop Ihre Grenzgeb 1997;135(3) : 193-196. 16. Griffin MR. Epidemiology of nonsteroi dal anti-inflammatory drug-associated gastrointestinal injury. Am J Med 1998; 104 ( su ppl 3):235-29S. 1 7. Jones A, Doherty M. Intra-articular corticosteroids are effective in osteoarthritis but there are no clinical predictors of response.
Anll Rheum Dis 1996;55:829-832. 18. Balazs E, Denlinger JL. Viscosupplementation: a new concept in the treatment of osteoarthritis. J Rheumatol 1 9 93 ;3 9( suppl) : 1 0-15.
19. Wobig M, Dickhut A, Maier R, Vetter G. Viscosupplementation with hylan G-F 20: a 26-week controlled trial of efficacy and safety in the osteoarthritic knee. Clin Ther 1998;20(3):410-423. 20. Lolunander LS, Dalen N, Englund G et al. Intra-articular hyaluronan injections in the treatment of osteoarthritis of the knee: a randomised, double blind, placebo controlled multi centre trial. Hyaluronan Mul ticentre Trial Group. Anll Rheum
Dis 1996;55(7):424-431 . 2 1 . Altman RD, Moskowitz R . Intraarticular sodium hyal uronate (Hyalgan) in the treatment of patients with osteoarthritis of the knee: a randomized clinical trial. Hyalgan Study Group.
J RheumatoI 1998;25(1l):2203-2212. 22. Frizziero L, Govoni E, Bacchini P. Intra-articu lar hyaluronic acid in the treatment of osteoarthritis of the knee: clinical and morphological study. Clin Exp Rheumato/ 1998;16(4):441-449. 23. Moskowitz RW. Hyaluronic acid supplementation. Curl'
Rheul7latol Rep 2000;2(6):466-471 . 24. Huskisson Ee, Donnelly S. Hyaluronic acid in the treatment of osteoarthritis of the knee. Rheumatology 1999;38(7):602-607. 25. Cyriax JH. Textbook of Orthopaedic Medicine, Vol I, 8th edn. Bailliere Tind all, London, 1 982:404.
26. Fletcher MR, Scott JT. Chronic monarticu lar synovitis. Diagnostic and prognostic features. AIlIl Rheum Dis 1 975;34:171. 27. Auquier L, Cohen de Lara A, Siaud JR. Devenir de 173 monoarthrites et monoarthropathies d' allure inflammatoire.
Rev Rhum 1 973;40:125. 28. Iguchi T, Matsubara T, Kawai K, Hirohata K . Clinical and his
29. 30.
31.
32.
33. 34. 35.
tological observations of monoarthritis. Anticipation of its pro gression to rheumatoid arthritis. Clin Orthop 1990;250:241-249. Jaffe HL, Lichtenstein L, Sutro CJ. Pigmented villonodular synovitis. A rch Path 1941;31:731-765. Wyllie Je. The stromal cell reaction of pigmented villonodular synovitis: an electron microscopic study. Arthr Rheum 1 969;12:205-214. D'Eshougues JR. Delcambre B, Leonardelli J et al. Hemarthrose du genou: par chondrocalcinose ou par synovite villonodu laire? Rev Rhum 1 976;43:309-310. Chappel R, Mortier G, Herregods P et al. Gepigmenteerde villonodulaire synovitis: een niet zo zeldzame oorzaak van rcidiverende haemarthrose van de knie. Tijdschr Gel1eeskd 1983;39(18) : 1 1 41-1144. Henry AN. Arthroscopy in practice. BMf 1977;i:87. Granowitz SP, Mankin HJ. Localized pigmented villonoduJar synovitis of the knee. f Bone ]oil1t Surg 1967;49A: 122-128. ' Cloud SR. Intra-articular thiotepa held effective in pigmented villonodular synovitis. American Rheumatology Association Western Region Meeting. Wellcome Trel1ds Rheum 1981;3(2).
CHAPTER 76 - DISO R D E RS OF T H E I N E RT STRU CTURES 1 097
36. Goss JA, Adams RF. Local injections of corticosteroids in rheu .matic diseases. I Musculoskeletal Med 1993;Mar:83-92. 37. Dieppe PA, Calvent P. Crystals and loint Disease. Chapman & Hall, London, 1983. 38. Moskowitz RW, Garcia F. Chondrocalcinosis articularis (pseudogout syndrome). Arch Intern Med 1973;132:87. 39. Caner JE, Decker JL. Recurrent acute arthritis in chronic renal failure treated by haemodialysis. Am I Med 1964;36:571. 40. PassIer J, Felli nger M, Seggl W. Der posttraumatische Hamarthros des Kniegelenkes-eine Indikation zur Arthroskopie.
Akt Tmulllato/ 1989;19:135-138. 41. Bomberg Be, McGinty TB. Acute hemarthrosis of the knee: indications for diagnostic a rthroscopy. Arthroscopy 1990;6(3):221-225. 42. Maffulli N, Binfield PM, King JB, Good CJ. Acute haemarthro sis of the knee in athletes. A prospective study of 106 cases. I Bone Joillt Surg 1 993;75B:945-949. 43. Dustmann HO. Knorpelveranderungen beim Hama rthros unter besonderen Beri.icksichtigiung der Ruhigstellung. Arch Orthop Ullfallchirurg 1971;71 : 1 48. 44. Convery FR. Experimental hemarthrosis in the knee of the mature canine. Arthritis Rheum 1976;19:59-67. 45. Cotta H, Puhl W, Niethard FU. Der Einfluss des Hamarthros auf den Knorpel der Gelenke. Unfal/chil" 1982;8:145-151. 46. Phelip X, Verdier JM, Gras JP et al. Les hemarthroses de l a chondrocalcinose articulaire. Rev Rhum 1 976;43:259-266. 47. Moskovich R, Parisien JS. Localized pigmented villonodular synovitis of the knee. Arthroscopic treatment. c/ill Orthop 1991;271:218-224. 48. Goldenberg DL, Reed JI. Bacterial arthritis. N Engl J Med 1985;312:764-769. 49. Meijers KA, Dijkmans BA, Hermans J et al. Non-gonococcal infectious arthritis: a retrospective study. J Infect 1987; 14:13-20. 50. Goldenberg DL, Cohen AS. Acute infectious arthritis: a review of patients with nongonococcal joint infections. Am J Med 1976;60:369. 51. Mielants H, Dhondt E, Goethals L et at. Long-term functional results of non-surgical treatment of common bacterial infec tions of joints. Scand ] RheUlllato/ 1981;11 : 1 0 1 . 52. Terry Ge, Tagert BE, Young MJ. Reliability of the clinical assessment in predicting the cause of internal derangement of the knee. Arthroscopy 1995;11:568-576. 53. Jeannopoulos CL. Observation of discoid menisci. I Bone ]oint
Surg 1950;32A:649-652. 54. Dickhaut SC, Delee JC The discoid lateral meniscus syndrome. J Bone loint Surg 1982;64A:1068-1073. 55. Woods GW, Whelan JM. Discoid meniscus. c/in Sports Med 1990;9(3):695-706. 56. Kobayashi A. Discoid meniscus of the knee joint. c/in Orthop Surg Ipll 1975;10:10-24. 57. Bullough PG, Vosburgh F, Arnoczky Sp, Levy 1M. The menisci of the knee. In: Insall J (ed) Surgery of the Kllee. Churchil l Livingstone, New York, 1984:135. 58. Poehling GG, Ruch DS, Chabon SJ. The landscape of meniscal injuries. c/in Sports Med 1990;9(3):539-549. 59. Weiss CB, Lundberg M, Hamberg P, De Haven KE, Gillquist J . Non-operative treatment of meniscal tears. J Bone ]oint Surg 1989;71A:8 1 l . 60. Satku K, Kumar J P, Ngoi SS. Anterior cruciate ligament injuries: to counsel or operate? I Bone loint Surg 1986;68B: 458--461. 61. Bray RC, Dandy DJ. Meniscal lesions and chronic anterior cruci ate ligament deficiency. J Bone loint Surg 1989;71B: 128-130. 62. Egner E. Knee joint meniscal degeneration as it relates to tissue fiber structure and mechanical resistance. Pathol Res Pmct 1982;173:310.
63. Smillie IS. The current pattern of internal derangements of the knee joint relative to the menisci. c/in Orthop 1 967;51 : 1 1 7 . 64. Hadfield G. Immobile meniscus syndrome. Proc R Soc Med 1966;59:117. 65. Noble J, Turner P. The function, pathology and su rgery of the meniscus. Clin Orthop Rei Res 1 986;210:62-68. 66. Fahmy NR, Williams E, Noble J. Meniscal pathology and osteoarthrosis of the knee. ] Bone Joint Surg 1983;65B:24. 67. Dandy DJ. Arthroscopic S u rgery of the Knee. Churchill Livingstone, Edinburgh, 1981 . 68. McGinty JB, Matza RA. Arthroscopy of the knee. Evaluation of an out-patient procedure under local anaesthetic. I Bone Joint Surg 1978;60A:787-789. 69. Casscells SW. Technology: a good servant but a bad master. Arthroscopy 1990;6(1):1-2. 70. Goodfellow J. 'He who hesitates is saved'. I Bone Joint Surg 1980;62B:1-2. 71. Noble J, Hambden DL. The pathology of the degenerate meniscus lesion. I Bone Joint Surg 1 975;57B: 1 80. 72. Noble J . Lesions of the menisci. I BOlle loint Surg 1977;59A:480. 73. Casscells SW The place of arthroscopy in the diagnosis and treatment of internal derangement of the knee: an analysis of 1000 cases. c/in Orthop 1980;151: 1 35. 74. Fitzgibbons RE, Shelbourne KD. 'Aggressive' nontreatment of lateral meniscal tears seen during anterior cruciate ligament reconstruction. Am I Sports Med 1 995;23(2):156-159. 75. Hargreaves DJ, Seedhom BB. On the 'bucket handle' tear: partial or total meniscectomy? A quantita tive study. I Bone loint
Surg 1979;61B:381. 76. Bourne RB, Finlay JB, Papadopoulos P, Andreae P. The effect of medial meniscectomy on strain distribution in the proximal part of the tibia. I Bone Joint Surg 1984;66B:143l . 77. Walker PS, Erkman MJ. The role of the menisci in force trans mission across the knee. c/in Orthop 1975;109:184-1 92. 78. Dandy DJ, Jackson RW The diagnosis of problems a fter meniscectomy. I Bone loint Surg 1975;57B(3):349-352. 79. Johnson RJ, Kettelkamp DB, Clark W, Leaverton P. Factors affecting later results a fter meniscectomy. I Balle loint Surg
1974;56A:712-729. 80. Noble J, Erat K. In defence of the meniscus: a prospective study of two hundred meniscectomy patients. I Balle Joint Surg 1980;62(B):6-11 . 8 1 . Floman Y, Eyre DR, Glincher MJ. Induction o f osteoarthrosis in the rabbit knee joint: biomechanical studies on the articular cartilage. c/in Orthop 1980;147:278. 82. Glosh P, Sutherland JM, Taylor TKF, Pettit GD, Bellinger CR. The effects of post-operative joint immobilization of articular cartilage degeneration, following meniscectomy. J Surg Res
1983;35:461. 83. Neyret P, Donell ST, Dejour D , Dejour H . Partial meniscectomy and anterior ligament rupture in soccer players; a study with a minimum 20 year follow-up. Am I Sports Med 1993;21:455-460. 84. Burke DL, Ahmed AM. Biomechanical study of partial and total medial meniscectomy of the knee. Trans Orlhop Res Soc
1978;3:9l. 85. Bourne R. Menisci distribute weight. Med PosI 1 980;16:29. 86. Dandy DJ. Early results of closed partial meniscectomy. BMI 1978;ii: 1 099. 87. Jackson RW, Dandy DJ. Partial meniscectomy. J Bone Joint Surg 1976;58(B):142. 88. McGinty ]B, Guess LF, Marvin RA. Partial or total meniscectomy. A comparative analysis. I Bone Joint Surg 1977;59A:763-766. 89. Northmore-Ball MD, Dandy DJ, Jackson RW Arthroscopic, open partial and total meniscectomy: a comparative study.
I Bone Joint Surg 1983;65B:400.
1 098 SECTI O N TH I RT E E N - T H E K N E E
90. Lyshom J , Gillquist J. Endoscopic meniscectomy - a follow-up study. Int Orthop 1981;5:265-270. 91. Hamberg P, Gillquist J, Lysholm J. A comparison between arthroscopic meniscectomy and modified open meniscectomy.
J Bone Joint Surg 1984;66B: 189-192. 92. Cassidy RE, Shaffer AJ. Repair of peripheral meniscus tears. A preliminary report. AIIl J Sports Med 1981;9:209-214. 93. De Haven KE. Peripheral meniscus repair. An alternative to meniscectomy. Orthop Trans 1 981;5:399-400. 94. Hennings C E o Arthroscopic repair of meniscus tears.
Orthopedics 1 983;6:1130. 95. Rosenberg TO, Scott SM, Coward DB et al. Arthroscopic menis cal repair evaluated with repeat arthroscopy. Arthroscopy 1986;2:14. 96. Barber FA, Stone RG. Meniscal repak an arthroscopic tech nique. J Balle Joint SlIrg 1985;67B:39-41. 97. Albrecht-Olsen PM, Bak K . Arthroscopic repair of the bucket handle meniscus. 10 failures in 27 stable knees followed for 3 years. Acta Orthop Scalld 1993;64:446-448. 98. Hamberg P, Gillquist j, Lysholm J. Suture of new and old periph eral meniscus tears. J Bone Joint Surg 1983;65A(2): 1 20-124. 99. Shelbourne KD, Porter DA. Meniscal repair. Description of a surgical technique. Am J Sports Med 1993;21(6):870-872. 100. Eggli S, Wegmuller H, Kosina J et al. Long-term results of arthroscopic meniscal repair: an analysis of isolated tears. Am } Sports Med 1995;23:715-720. 1 01 . DeHaven KE, Lohrer WA, Lovelock JE. Long-term results of open meniscal repair. Am J Sports Med 1995;23(5):524-530. 102. Bonnin Je. Cysts of the semilunar cartilages of the knee joint.
Br } Surg 1953;40:558-565. 1 03. Wroblenski BM. Trauma and the cystic meniscus: review of 500 cases. Injury 1973;4:319-321 . 104. Pisani AJ. Pathognomonic sign for cyst o f the knee cartilage.
Arch Surg 1947;54:188. 105. Tyson LL, Daughters TC Jr, Ryu RK, Crues JV 3rd. MRl appear ance of meniscal cysts. Skeletal Radial 1 995;24(6):421-424. ] 06. Lantz B, Singer KM. Meniscal cysts. Clin Sports Med 1 990;9:707-725. 107. Seger BM, Woods WG. Arthroscopic management of lateral meniscus cysts. Am } Sports Med 1986;14:105. 108. Pariesien JS. Arthroscopic treatment of cysts of the menisci. Clill Orthop 1990;257:154-158. 109. Tu disco C, Meo A, Blasucci C, Ippolito E . Arthroscopic treat ment of lateral meniscal cysts using an outside-in technique.
AIIl } Sports Med 2000;28(5):683-686. 110. Mitrovic 0, Stankovic A, Borda-Iriarte 0 et al. Resultats de l'examen autopsique des cartilages des genoux chez 120 sujets decedes en milieu hospitalier. Rev Rhum Mal Osteoartic 1987;54:15. Ill. MacNicol MF. The Problem Knee: Diagnosis and Management in tire You nger Patient. Heinemann, London, 1986. 1 1 2. Bradley J, Dandy OJ. Osteochondritis dissecans and other lesions of the femoral condyles. J Bone Joint Surg 1989;
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
-
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)
-
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
-
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
-
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
REFERENCES 1 . Hardy
MA,
The biology of scar formation. Phys Ther
23. Indelicato P, Hermansdorfer J, H uegel M. Nonoperative man
2. O'Donoghue DH. Surgical treatment of fresh injuries to the
agement of complete tears of the medial collateral ligament of the knee in intercollegiate football players. CLin Orthop
3. O'Donoghue DH. Treatment of acute ligamentous injuries of the
24. Mathieu P, Wybier M, Busson J, Morvan G. The medial
1 989;69: 1 0 1 4- 1 023.
major ligaments of the knee. I Bone Joint S u rg 1950;32A: 721-738.
1990;256: 1 74-177.
collateral
knee. Orthop Clin North Am 1 973;4:617. 4. Shelbourne KD, Nitz PA. The O'Donoghue triad revisited.
Combined knee .inj uries invol ving anterior cruciate and medial collateral ligament tears. A m ] Sports Med 1 991;19(5): 474-477. 5. Bomberg BC, McGinty JB. Acute hemarthrosis of the knee:
indications for diagnostic arthroscopy.
7.
8.
9. 10.
13.
14.
15.
Scalld 1982;168(suppl):42.
football: non-operative management of grade I and I I sprains.
Radial
(Paris)
clinical study. Acta Chir Scand 1938;81(suppl 53). 28. Schweitzer ME, Tran D, Deely DM, Hume EL. Medial collateral
ligament injuries: evaluation of multiple signs, prevalence and location of associated bone bruises, and assessment with MR imaging. Radiology 1995;194(3):825-829. 29. Tucker WE. Post-traumatic para-articular ossification of the medial collateral ligament of the knee. Br ] Sports Med 1969;4:212. 30. Frank G, Woo SL-Y, Amiel D et al. Medial collateral ligament
healing. A multidisciplinary assessment in rabbits. Am I Sports
Med 1983;11:379. 31 . Burri C, Helbing G, Spier W. Rehabilitation of knee ligament
injuries. In: The Knee. Springer, New York, 1978. 32. Steadman J. Rehabilitation of first and second degree sprains of
the medial collateral ligament. Am I Sports Med 1979;7(5): 485-493. 33. Montgomery J, Steadman J. Rehabilitation of the injured knee. Clill Sports Med 1985;4:333. 34. Cyriax JH. Rheumatism of Soft-tissue Injuries. Hamilton, London, 1947. 35. De Maeseneer M, Lenchik L, Starok M et at. 1998. Normal and
36.
37. 38.
1 6. Derscheld GL, Garrick JG. Medial collateral ligament injuries in Al ii ] Sports Med 1981 ;9:365.
A n ll
Med 1 996;21(2):147-156.
1972;54A:91 9-95 1 .
12.
knee.
27. Palmer I. On the injuries to the ligaments of the knee joint. A
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 I<;niegelenkes-Arthroskopische Abklarung del' Ursachen. Unfall
69. Jarvinen M, Kannus P. Quadriceps muscle atrophy and long
term recovery after knee ligament injury. Ann Chirurg Gynaecol 1987;76: 108-11 3 .
Chirurg 1982;8:159-169. 47. Noyes FR, Bassett RW, Grood ES, Butler DL. Arthroscopy in
70. Hughston JC, Andrews JR, Cross MJ, Moschi AM. Classification
acute traumatic haemarthrosis of the knee. J Bone joint S u rg
of knee ligament instabilities. J Bone joint S u rg 1976;58A(2):
1980;62A:687. 48. PassIer J,
Fellinger M, Seggl W. Der posttraumatische Hamarthros des Kniegelenkes - eine I n d i kation zur Arthroskopie. Akt Traumato/ 1989;19:135-138. 49. Hoaglund FF. Experimental haemarthrosis. j Bone joint S u rgery 1967;49A: 1 .
159-179. 71. Muhr G, Wagner M. Kapselbandverletzungen des Kniegelenks. Diagnostikfibel. Springel� Berlin, 198 1 . 72. Claes T, Martens M . D e voorste kruisband: Anatomie, Funktie
en Pathologie. Spectrum lnt 1 987;30(4) :1 . 73. Liljedahl 50, Lindvall N, Wetterfors J. Early diagnosis and treat
ment of acute ruptures of the anterior cruciate ligament. I Bone
50. Vahey TN, Meyer SF, Shelbourne KD, Klootwyk T E . M R
imaging of anterior cruciate ligament injuries. Magn Reson Imaging Ciill North Am 1994;2(3):365-380.
Joint S u rg 1 965;47A(8) : 1 503-1513. 74. Rubinstein RA Jr, Shelbourne KD, McCarroll JR, VanMeter CD,
Rettig AC. The accuracy of the clinical examination in the setting of posterior cTuciate ligament injuries. AII1 J Sports Med
5 1 . Sandberg R, Balkiors B. Partial rupture of the anterior cruciate
ligament - natural course. Ciill Orthop Rei Res 1987;220: 1 76-178. 52. Clancy WG, Ray JM, Zoltan DJ. Acute tears of the anterior cruciate ligament. Surgical versus conservative treatment. j Bone joint S u rg 1988;70A:1483-1488. 53. Buss DD, Min R, Skyhar et al. Nonoperative treatment of acute
anterior cruciate ligament injuries in a selected group of patients. Am j Sports Med 1995;23(2):1 60-165. 54. Fitzgerald GK, Axe MJ, Snyder-Mackler L. Proposed practice guidelines for nonoperative anterior cruciate ligament rehabili tation vf physically active individuals, J Orthop Sports Phys Ther
1 994;22(4) :550-557. 75. Bach BR, Warren RF, Wickiewicz TL. The pivot shift phenomenon:
results and description of a modified clinical test for anterior cruciate ligament insufficiency. Am J Sports Med 1988;16(6):571 . 76. Trickey E L . Ligamentous injuries around the knee. BMJ 1976;2:1492. 77. Clancy WG, Ray JM, Zoltan DJ. Acute tears of the anterior
cruciate ligament. J Bone joint S u rg 1988;60A:1483. 78. Kannus P. Non-operative treatment of grade II and grade I I I
sprains of the lateral ligament compartment of the knee. Alii j
2000;30(4) : 1 94-203. 55. Messner K, Maletius W. Eighteen- to twenty-five-year follow
up after acute partial anterior cruciate ligament rupture. Am j
Sports Med 1989;17(1):83. 79. Kal1.l1us P, Jarvinen M. Non-operative treatment of acute knee
ligament injuries. Sports Med 1990;9(4) :244.
Sports Med 1999;27(4) :455-459. 56. Matsumoto H, Seedhom BB, Sud a Y, Otani T, Fujikawa K. Axis
80. Shelbourne KD, Nitz P. Accelerated rehabilitation after anterior
location of tibial rotation and its change with flexion angle. Clin
cruciate ligament reconstruction. Am J Sports Med 1990;80:
Orthop 2000;371 : 1 78-182.
292-299.
57. Janousek AT, Jones DG, Clatworthy M, Higgins LD, Fu FH.
8 1 . Hughston JC, Eilers AF. The role of the posterior oblique liga
Posterior cruciate ligament injuries of the knee joint. Sports Med
ment in repairs of acute medial collateral ligament tears of the knee. J Bone joint S u rg 1 9 73;55A:923. 82. Sandberg R, Balkiors B, Nilsson B, Westin N. Operative versus non-operative treatment of recent injuries to the ligaments of the knee. A prospective randomized study. J BOlle joint S u rg
1999;28(6) :429-44 1 . 58. Keller PM, Shelbourne KD, McCarroll JR, Rettig AC. Non
operatively treated isolated posterior cruciate ligament injuries. Am j Sports Med 1993;3 : 1 43-- 1 53.
q, Bach BR. Current concepts review. Posterior cruci ate ligament. Am J Knee S u rg 1 990;3:143-153. 60. Hochstein P, Schmickal T, Grutzner PA, Wentzensen A . Diagnosis and incidence o f the rupture o f the posterior cruciate ligament. Unfallchirurg 1 999;102(10) :753-762. 61. Covey DC, Sapega AA. Current concepts review. Injuries of the posterior cruciate ligament. J Bone Joint Surg 1993;75A:1376--1 386. 62. Sonin AH, Fitzgerald SW, Friedman H et al. Posterior cruciate ligament injury: MR imaging diagnosis and patterns of injury. 59. Johnson
Radiology 1994;190(2) :455-458.
1987;69A:1120. 83. Cyriax J. Textbook of Orthopaedic Medicine, Vol II, Treatmellt by Manipulation, Massage and Injection, 11th edn. Bailliere Tindall,
London, 1 984. 84. Hughston Je. Complications of anterior cruciate ligament
surgery. Orthop Clin North A m 1985;16:237. 85. Buckley 5L, Barrack RL, Alexander AH. The natural history of
conservatively treated partial anterior cruciate ligament tears. Am J Sports Med 1989;17(2) :221 . 86. Barton T. Posterior cruciate ligament insufficiency. Sports Med
63. Shelbourne KD, Jennings RW, Vahey TN. Magnetic resonance
imaging of posterior cruciate ligament injuries: assessment of healing. Am J Knee Surg 1999;12(4) :209-213. 64. Duri ZA, Aichroth PM, Zorrilla P. The posterior cruciate liga ment: a review. Am J Knee Surg 1997;10(3): 149-164. 65. Shino K, Horibe S, Nakata K et at. Conservative treatment of isolated injuries to the posterior cruciate ligament in athletes. j BOlle Joint Surg 1995;77B(6):895-900.
1 984;1 :419-430. 87. Barton T, Torg J. Natural history of the posterior cruciate liga
ment deficient knee. A m j Sports Med 1985;13:439. 88. Longenecker 5, Hughston J. Long-term follow-up of isolated
posterior cruciate injuries. Am J Sports Med 1987;15:628. 89. Fowler P, Messieh S. Isolated posterior cruciate ligament
injuries in athletes. Am J Sports Med 1 987;15:553. 90. Dejour H. The natural history of rupture of the posterior cruci
66. Parolie JM, Bergfeld JA. Long-term results of nonoperative
treatment of isolated posterior cruciate ligament injuries in the athlete. Am J Sports Med 1986;14(1) :35-38. 67. Shelbourne KD, Davis TJ, Patel DV The natural history of acute, isolated, nonoperatively treated posterior cruciate ligament injuries. A prospective study. Am J Sports Med 1 999;27(3):276--283. 68. McDaniel WJ Jr. Isolated partial tear of the anterior cruciate ligament. Ciin Orthop 1976;115:209.
ate ligament. Rev Chirurg Orthop 1988;74:35. 9 1 . MacNicol MF. The Problem Knee. Diagnosis and Managel1lent ill the Younger Patient. Heinemcu1.l1 Medical, London, 1986. 92. Gerber
CH. Funktionelle Rehabil i tation nach komplexen Knieverletzungen. Wissenschaftliche Grundlagen u Praxis. Schweiz Zeitschr Sportmed 1 980;28:37-56.
93.
Hermans GPH, Rondhuis G. Kniebandreconstructies bij 'late' instabiliteit. Ned Tijdschr Fysioth 1981 ;2:34.
1 1 30 SECTI O N T H I RT E E N - T H E K N E E
94. Ahrendt E , Frenzel G. Erfahrungen i n der Diagnostik, Therapie u Rehabilitation bei Kreuzbandverletzungen. Med Sport 1982;5:145-149. 95. Managine RE, Noyes FR, DeMaio M. Sports Medicine Rehabilitation Series. Minimal protection programme: ad vanced weight bearing and range of motion after ACL reconstruction. Weeks 1-5. Orthopedics 1992;15(4):504-515. 96. DeMaio M, Noyes FR, Managine RE. Advanced muscle train ing after ACL reconstruction: weeks 6 to 52. Orthopedics 1 992;15(6):757-767. 97. Salter RB. The biologic concept of continuous passive motion of synovial joints. The first 1 8 years of basic research and its clinical application. Ciin Ort/wp 1 989;242:12-25. 98. Noyes FR, Barber D, DeMaio M, Managine RE. Early knee motion a fter open and arthroscopic anterior cruciate ligament reconstruction. Am ] Sports Med 1987;15:149-160. 99. Sachs RA, Daniel DM, Stone ML et al. Complications of knee ligament surgery. In: Daniel DM, Akeson WH, O'Connor JJ (eds) Knee Ligaments: Structure, Fu nction, Injury and Repair. Raven Press, New York, 1990:505-520. 1 00. DeMaio M, Noyes FR, Managine RE. Principles for aggressive rehabilitation after reconstruction of the anterior cruciate liga ment. Orthopedics 1992;15(3):385-392. 101 . Barber-Westin SD, Noyes FR, Heckmann TP et a/. The effect of exercise and rehabilitation on anterior-posterior knee dis placements after anterior cruciate ligament autograft recon struction. Alii J Sports Med 1999;27(1):84-93. 1 02. Spencer I, Hayes KC, Alexander IJ et al. Knee joint effusion and quadriceps inhibition in man. A rch Phys Med 1984;65:1 71-177. 1 03. Stokes M, Young A. Investigations of quadriceps inhibition. Implications for clinical practice. Physiotherapy 1984;70(11): 425-428. 104. Kennedy JC, Alexander II, Hayes KC et al. Nerve supply of the human knee and its functional importance. Am J Sports Med 1 982;10:329-335. 1 05. Fulkerson JP, Schutzer SF, Winters TF Jr et a/. Articular carti lage. In: Albright J A, Brand RA (eds) The Scien tific Base of
Orthopaedics, 2nd edn. Appleton & Lange, Norwalk, CT,
1987:347-371 . 106. Glasgow SG, Gabriel JF, Sapega AA et al. The effect of early versus late return to vigorous activities on the outcome of anterior cruciate ligament reconstruction. AI1I J Sports Med 1 993;21:243-248. 1 07. Shelbourne KD, Nitz P. Accelerated rehabilitation after anterior cruciate ligament reconstruction. Aln j Sports Med 1990;18:292-299. 108. Shelbourne KD, Klootwyk TE, Wilckens JH et a/. Ligament sta bility 2 to 6 years after anterior cruciate ligament reconstruc tion with au togenous patellar tendon graft and participation in accelerated rehabilitation program. A lii j Sports Med 1995;23:575-579. 109. Dodds JA, Keene JS, Graf BK et al. Results of knee manipula tions after anterior cruciate ligament reconstruction. Am J Sports Med 1 991;19:283-287. 110. Behrens F, Kraft EL, Oegema TR Jr et al. Biochemical changes in articular cartilage a fter joint immobilization by casting or external fixation. J Orthop Res 1 989;7:335-343. 1 1 1 . Arms SW. The biomechanics of the anterior cruciate ligament rehabilitation and reconstruction. Am J Sports Med 1984; 412:8-18. 112. Palmoski MI, Colyer RA, Brandt KD et al. Joint motion in the absence of normal loading does not maintain normal articular cartilage. Arthritis Rheum 1 980;23:325-334. 113. Ghosh F, Sutherland I, Bellenger C et al. The influence of weight bearing exercise on articular cartilage of meniscectomy joints. An experiment study in sheep. Ciill Orthop 1990; 252:101-113. 114. Ohkoshi Y, Yasuda K, Kaneda K et al. Biomechanical analysis of rehabilitation in the standing position. Am j Sports Med 1991;19:605--611 . 115. Sapega AA. Muscle performance evaluation in orthopedic practice. J Bone joint Surg 1990;72A:1 562-1574. 116. American Academy of Orthopedic Surgeons. Athletic Training and Sports Medicine, 2nd edn. AAOS, Parkridge IL, 1991 :724-750.
CHAPTER CONTENTS Extensor mechanism
Ruptures of the quadriceps bellies Adherent vastus intermedius 1132 Tendinous lesions about the patella Rupture of the quadriceps tendon Lesions of the infrapatellar tendon Lesions of the insertion at the tibial Patellar fracture 1137 Patellofemoral disorders
1131 1132 1136 1136 tuberosity
Strained iliotibial band
1137
1138
Introduction 1138 Mechanical theory 1138 Neural theory 1139 Clinical examination 1139 Clinical manifestations 1141
Flexor mechanism
Disorders of the contractile structures
1131
EXTENSOR MECHANISM RUP TURES OF THE QUADRICEPS BELLIES
1143
1144
Hamstring strains 1144 Biceps tendinitis 1145 Lesions of the upper tibiofibular joint Lesions of the pes anserinus 1146 Strained popliteus muscle 1146 Lesions of the gastrocnemius 1147
1145
A muscular tear of one of the quadriceps bellies is a common disorder in sprinters and soccer players. An abrupt and vigorous contraction during a sprint breaks some of the muscle fibres and is felt as a sudden and painful 'giving way' at the front of the thigh. Alternatively, the muscular lesion may result from a direct contusion during contact (judo or football), known as'Charley Horse'. There may be little discomfort while the athlete is in the middle of the game and the thigh is warm; conse quently the extent of the injury is underestimated. The stiffness, disability and pain then set in late at night and the following morning the patient can walk only with a limp.l Clinical examination shows a normal hip and knee, although passive knee flexion is painful or both painful and limited depending on the size of the rupture. Resisted extension of the knee is painful and slightly weak. As a rule, the lesion is at mid-thigh level. The affected muscle belly is hard and tender over a large area. Sometimes a haematoma can be palpated. In serious lesions a space can be detected by palpation. This is par ticularly the case in major ruptures just above the supra patellar tendon, which occur mainly in patients over 40 years of age.2 In such cases there is not only pain but also weakness during resisted extension, and the patient is unable to straighten the knee actively over the last 30°. Development of myositis ossificans as a complication of a thigh contusion is not uncommon in adolescents and young adults.3 It occurs in 9% of quadriceps contusions and seems to be associated with five risk factors (knee motion less than 120°, injury occurring during football, previous quadriceps injury, delay in treatment greater than 3 days and ipsilateral knee effusion).4 Early diagnosis is important and is usually made with the help of sonography.5,6 There is no proper treatment but the lesion undergoes spontaneous cure within 2 years? Therapy with deep transverse massage is contraindicated. 1 13 1
1 1 32 S ECTI O N T H I RT E E N - T H E K N E E
Treatment
Initial haemorrhage may be reduced by elastic strapping and an ice bag over the lesion. Minor ruptures in the quadriceps muscle require the same treatment as muscular lesions elsewhere. As soon as the patient is seen, the lesion is infiltrated thoroughly with 50 ml of procaine 0.5%. From the next day on, deep transverse friction is given, followed by active isometric contractions with the muscle in a shortened position. When the rupture is major, operative suture may be advised, especially if the patient is an athlete with high functional demand on the knee extensors. It is then important that surgical treatment is undertaken as soon as possible. The patient sits with the knees outstretched. Flexion at the hips, together with a maximal extension of the knees induces a complete relaxation of the quadriceps. The phYSiotherapist stands at the patient's side. The correct level is sought. The fingers of one hand are placed deep to the affected fibres. The other hand can reinforce the palpating one. The thumbs are placed laterally to be used as a fulcrum. By flexion of the fingers, during an upward drawing movement, the phYSiotherapist drives all the fibres between fingers and femur (Fig. 78. 1 ). At the end of the movement, the fingers are slightly extended and brought back to the previous spot, under the lesion. The skin must move with the fingers. Since this is an extremely tiring technique, periods of rest must be built in to the treatment session, which lasts about 20 minutes. Technique: deep friction to the quadriceps muscle.
Figure 78.1
Friction in minor rupture of the quadriceps.
After the friction, active isometric contractions are done over 5-10 minutes. Again, this is carried out in a fully relaxed position, so that the contraction cannot exert any tension on the healing tissue (see Ch. 5). Treatment with deep friction and contractions is given daily for the first week and on alternate days from the second week onwards. In athletes, there is a significant tendency for the lesion to recur and the patient should not restart a training programme until a week after com plete clinical cure. In the meantime, treatment should continue. The training programme must be built up gradually over the following 3-4 weeks. ADHERENT VASTUS INTERMEDIUS
This condition occurs typically after a fracture of the femur. There is a gross limitation of flexion, whereas the other knee movements are all full range. Only surgical treatment can give an acceptable outcome. TENDINOUS LESIONS ABOUT THE PATELLA
The quadriceps tendon has a superficial and a deep layer. The superficial layer runs without interruption from the quadriceps muscle, over the patella to the tibial tuberosity. The deep layer inserts all around the patellar border, effectively making the patella a sesamoid bone in the tendon. Tendinous lesions therefore not only occur at the inferior aspect of the bone but also at the superior, medial and lateral borders. Tendinitis about the patella is a typical overuse phenomenon in sports in which the quadriceps mechanism is under severe and continuous stress, such as volleyball, basketball, cycling and high jump. It was first described by Sinding-Larsen in 19219 and Johansson in 1924.10 Kulundll and Feretti12 also reported cases of tendinitis at the upper border of the patella. Cyriax1 3 describes three possible sites: the upper border (suprapatellar tendinitis), the apex, the classical 'jumper's knee' (infrapatellar tendinitis) and at either side of the patella (tendinitis of the quadriceps expan sion) (Fig. 78.2). The lesion was uncommon until the mid-1 960s, when the syndrome of jumper 's knee became more and more frequent because of increased training and higher performance goals for athletes.14,15 In the last decade, these lesions have reached epidemic proportions. The history is obvious: during or after exertion, there is localized pain at the front of the knee. In mild examples there is probably only a little pain after activity, whereas in a severe case the pain forces the athlete to stop and pain at rest can also supervene. The patient also s!ates that walking upstairs or getting up from a chair is painful. The lesion can be classified by its symptoms into four stages (Table 78.1).11 ,1 6,1 7
C HAPTER 78
-
D I S O R D E R S OF T H E CONTRACTI LE STRUCTU R E S 1 1 33
Treatment
2 2 3
Figure 78.2 Localizations of quadriceps tendinitis (Cyriax:13 p. 408): 1, suprapatellar; 2, expansion; 3, infrapatellar.
Clinical examination shows a normal knee with a full and painless range of movement and normal ligamen tous tests. Only resisted extension is painful or uncom fortable. When the history suggests a slight quadriceps tendinitis, but resisted extension is negative, the patient should take part in a training session and be re-examined immediately thereafter; this will probably reveal a minor lesion. Palpation identifies the site. To make the deeper layers of the tendon accessible for the palpating finger, the patella must be tilted as much as possible (see p. 1134 and 1136). Conventional radiographic techniques are of no use in the diagnosis of quadriceps tendinitis. Ultrasonography, however, seems to have some value in staging the disorder.1 8-2o On magnetic resonance imaging (MRI), swelling of the tendon and changes of the intrasubstance signal may be present.21 However, the sensitivity and specificity of MRI is 75% and 29%, respectively. In younger patients with relatively mild symptoms, MRI does not show significant changes and in older, active patients changes may be present in asymptomatic knees.22
Table 78.1 Staging of quadriceps tendinitis17 Stage
Symptoms Pain after activity Pain at onset, disappearing during and reappearing after activity
III IV
Continuous pain, inability to perform Weakness due to rupture
Classically, treatment consists of rest, ice, taping and anti inflammatory drugs. If these measures are insufficient or fail to relieve the symptoms, surgery is usually advised. The patellar tendon is incised and the hyaline inflamma tory tissue (usually the middle portion of the patellar lig ament) is removed.23, 24 Clinical experience suggests that results are not uniformly excellent, with a success rate varying between 58% 12 and 78%.25 Sporting success is seen in about 50% of tenotomy patients, with a median time to return to preinjury level of activity of 10 months.26 However, most instances can be cured by deep trans verse friction or local infiltrations of triamcinolone at the tenoperiosteal border.27 At the upper border or the apex, infiltration with triamcinolone can be used safely and with very good results, providing the injection is exactly at the right spot, using a weak solution (10 m g / ml) and according to the general principles of infiltration. If the lesion is too expensive, deep transverse friction is pre ferred. If a small joint remains resistant to treatment, it can be subsequently infiltrated. Lesions of the quadriceps expansion at either side of the patella respond extremely well to deep transverse friction but infiltration is of no use at this site. Because relative rest is always the first measure in tendinous lesions, the patient should not return to athletics until complete remission of the lesion has been achieved. After successful treatment, and in order to prevent recurrence, it is important to detect the possible causes of the tendinitis (inappropriate or faulty training pro gramme or structural factors) and to correct these. Technique: deep friction to the suprapatellar tendon.
The patient sits on the couch with the knee completely extended and the hip flexed, so that the quadriceps muscle is fully relaxed. The patella must be tilted in such a way that the affected spot can be reached. This can be achieved by pressing the lower pole of the patella posteriorly with the web of the thumb or with thumb and index finger which steadies the bone and forces the upper border upwards and forwards. With the middle finger of the other hand the tender spot can now be sought more easily. It is important to move the finger as far as possible under the inclined patella in order to catch the tendinous fibres of insertion deep under the bone. Deep friction is performed pressing the tendon between the middle finger and the superior aspect of the patella (Fig. 78.3). The index finger is used to reinforce the middle finger. The thumb is placed as far distally as possible on the leg and used as a fulcrum. The friction is a to-and-fro movement of the whole forearm and hand, in a transverse direction over the tendinous fibres.
1 134 SECTION T H I RTEEN - T H E K N E E
Figure 78.3
Deep friction to the suprapatellar tendon.
Twenty minutes of really hard friction are needed to produce a good result, which is expected after 10-20 sessions. The patient sits with the knee outstretched and the hip flexed, so that the quadriceps is fully relaxed. The patella is fixed as described earlier. The upper edge of the patella is marked and the tender area identified. Usually it lies at the medial, less frequently at the lateral edge of the upper border and as a rule it is no larger than 1 or 2 cm. A spot is chosen about 1.5-2.0 cm above the centre of the affected area. A 3 cm needle, fitted to a 2 ml syringe is introduced at this spot and moved in the direction of the patella (Fig. 78.4). The more the patella is tilted, the better the needle can reach the affected area. The small injec tions are given only when the tip of the needle is felt to pierce tendinous structure and touch bone. Considerable resistance is felt during the injection. Caution is taken to infiltrate the whole tender area by the usual technique of fanwise insertions and withdrawals. Significant discomfort may be expected for a day or two. If, after 2 weeks, clinical examination still evokes pain, a second injection must be given. Two or three injections cure most patients. Technique: infiltration to the suprapatellar tendon.
Technique: deep friction to the quadriceps expansion.
Infiltration of the quadriceps expansion seems to have little therapeutic effect. Deep transverse friction is there fore the only appropriate approach. Full and lasting relief is always attained, providing the massage technique is correct. The patient once again sits with the knees outstretched and the quadriceps muscle fully relaxed. The therapist
sits level with the patient's knees. With the thumb of one hand, the patella is pushed distally and over towards the affected side. This allows the edge of the patella to project outwards. The little finger of the other hand is extended as much as possible. The ring finger, reinforced by the middle finger, is placed under the patellar edge in such a way that it presses upwards, squeezing the tendinous fibres against the posterior aspect of the patella. Caution is observed so as to bring the hand into full supination, which means that the operating finger is horizontal, with pressure being applied against the back of the projecting edge of the patella. A vertical finger only presses against the femur and no friction on the tenoperiosteal junction results. Hand and forearm are held in line with the tibia and friction is produced by a horizontal movement along the patellar edge (Fig. 78.5). Twenty minutes' friction, three times a week for 2-3 weeks, nearly always results in cure. Technique: deep friction to the infrapatellar tendon.
Infrapatellar tendinitis is by far the most common ten dinitis at the patella. The lesion lies over an area of 1-2 cm at the inferior pole of the patella. In order to make this area more accessible, pressure is exerted at the upper part of the patella, in the following manner. The physio therapist stands level with the extended knee. One hand is placed just above the patella, so that the web of the thumb can exert downwards pressure. This stabilizes the patella and tilts the apex upwards, so that the tender area can be sought with great accuracy. The friction is given with the middle finger of the other hand, reinforced' by the index finger. The thumb is placed as far proximally as possible on the thigh. The pressure is exerted upwards, so that the lesion becomes squeezed between finger and
CH APTER 78 - DISO RDERS OF T H E CONTRACTILE STRUCTU RES 1 13 5
Figure 78.4 Infiltration of the suprapatellar tendon. The patella i s tilted (small arrows) b y pressing on the inferior pole (large arrow).
bone (Fig. 78.6). Sometimes a large osteophyte can be pal pated at the apex; if so, it is important to investigate to which side of the osteophyte the tenderness is located. Friction is given by alternate adduction and abduction movements at the shoulder, which draw the finger strongly along the inferior border of the patella. Twenty minutes of friction on alternate days, for 10-20 sessions is sufficient for cure. If no improvement is seen after 10 sessions, the patient is referred for triamcinolone infiltration. The patient sits supine with the quadriceps relaxed. The ther apist presses with one hand on the superior border of the patella, in such a way that the inferior pole moves distally Technique: infiltration of the infrapatellar tendon.
and upwards. This makes the in£rapatellar tendon acces sible to the palpating finger. The exact location of the lesion is now identified, in the way described earlier. The lower pole must be palpated very carefully, to determine the exact borders of the lesion. As already mentioned, caution should be observed in locating the lesion when an osteophyte is present. Once the exact location is identified and the borders marked on the skin, a point is chosen 1.5-2 cm inferior to the midpoint of the affected area. A 3 cm, thin needle is fitted with a syringe, containing 2 ml of triamcinolone. With the patella remaining tilted, the needle is inserted at the identified point and moved upwards, through the infrapatellar tendon, until it hits bone (Fig. 78.7). It is important to reach the posterior aspect of the patellar
1 1 36 SECTION T H I RTEEN - T H E KNEE
Figure 78.6
Deep friction to the infrapatellar tendon.
After the injection the patient should be at relative rest for about 10 days. Usually, considerable discomfort is experienced for 24-48 hours. The patient is seen again after 2 weeks. If pain is still elicited by resisted extension, infiltration is repeated. Usually one to three injections are required to obtain total and lasting relief. Return to sport must be gradual, and a training pro gramme that does not impose too much strain on the quadriceps during the first few weeks is advised. An underlying biomechanical factor as the basis for a possi ble recurrence should be sought.28 Treatment of quadriceps tendinitis is summarized in Figure 78.8. RUP TURE OF THE QUADRICEPS TENDON
Figure 78.5
Deep friction to the quadriceps expansion.
apex, because most of the lesions lie deeply at the teno periosteal junction. The infiltration is now given by a series of small droplets along the inferior border. Considerable pressure has to be exerted on the syringe to push the fluid in. Care is taken to inject only when the tip of the needle is felt to hit bone.
Rupture of the suprapatellar quadriceps tendon is an uncommon injury. Most of the patients are elderly, and sometimes there is diagnostic confusion with other causes of inability to use the legs, such as a mild stroke.29 The mechanism of injury usually involves forced hyperflexion or rapid extension from a weight-bearing position.3D Pain, swelling, a palpable gap and inability to straighten the leg against resistance are the cardinal features. Treatment is operative repair. LESIONS OF THE INFRAPATELLAR TENDON
Tendinitis of the infrapatellar tendon (ligamentum patel lae) is unusual and occurs only in rheumatic disorgers. Inflammation of the peritendineum, with pain, thickening and coarse crepitus, can be found. Treatment consists of triamcinolone infiltration along the surface of the tendon.
CHAPTER 78
- DISORDERS
OF T H E CONTRACTILE STRUCT U R E S 1 1 37
All types Rest until complete remission has been achieved Prophylaxis Structural factors? Training?
Suprapatellar tendinitis One or two infiltrations with 10-20 mg of triamcinolone
Or deep transverse frictions 3 times a week, for 10-20 sessions
Quadriceps expansion Deep transverse friction 3 times a week for 6-10 sessions
Infrapatellar tendinitis
Cure
Smaller lesions
No response
Figure 78.8
Surgery
Treatment of quadriceps tendinitis.
Apophysitis
Figure 78.7
Infiltration of the infrapatellar tendon. The patella is pressed distally, which moves the inferior pole upwards (arrows).
A patellar tendon rupture may be caused by acute or chronic excessive traction force. 31 The tendon is then pulled from the lower pole of the patella. 32 Degenerative rheumatic disease may also give rise to ruphue of the infrapatellar tendon.33,34 Treatment is surgicaP5
Osteochondrosis of the tibial hlberosity, or Osgood Schlatter disease, occurs in boys between 10 and 15 years of age. 36 The typical symptoms are local pain during sports or during walking upstairs. The local tenderness makes kneeling impossible. 3? Clinical examination reveals local ache during resisted extension of the knee. Palpation shows an enlarged, tender and warm tuberosity. Radiography confirms the diagnosis and is important in differentiating the condition from more serious disor ders such as osteomyelitis, arteriovenous malformations and osteosarcoma.38 In Osgood-Schlatter disease, nothing other than reduction of athletic activity should be advised. Spontaneous recovery takes place in 2 years, often with a permanently enlarged tuberosity (knee knob).
LESIONS OF THE INSERTION AT THE TIBIAL TUBEROSITY
PATELLAR FRACTURE
Tenoperiostitis
Most patellar fractures are stellate fractures, occurring after a fall or a direct blow (dashboard injuries). During the last decade an increasing number of patellar fractures in association with total knee replacement have been described.39,40 Clinical examination shows warmth, a capsular pattern and a joint that contains blood. Resisted extension
This exceptional lesion sometimes occurs in athletes. Resisted extension of the knee is painful at the insertion of the infrapatellar tendon. Palpation reveals the exact spot at the tibial tuberosity. Friction can be tried but is not always very helpful, and treatment mostly consists of one or two infiltrations with a small amount of triamcinolone.
1 1 38 S E CTION T H I RT E E N - T H E K N E E
is markedly weak and painful. The combination of a gross articular pattern and marked quadriceps signs shows that the part of the quadriceps mechanism overly ing the knee joint must be at fault. Radiography confirms the diagnosis. In young patients an uncomplicated fracture heals quickly but early osteoarthrosis has to be expected.41 When accurate reduction and stable fixation cannot be achieved, partial or total patellectomy must be consid ered and seems to produce satisfactory results.42,43 Transverse fractures are uncommon except in an elderly person with an osteoporotic patella. After the trauma the patient can walk with pain and, because the capsule enclosing the patella is not ruptured, displace ment is avoided and therefore the disability is minor.44
PATELLOFEMORAL DISORDERS INTRODUCTION
Patellofemoral pain is a common condition. About 25% of the population will, at some stage in their lives, suffer from patellofemoral symptoms.45 There is no clear con sensus in the literahlre concerning the terminology, aeti ology and treatment for pain in the anterior part of the knee. The term 'anterior knee pain' is suggested to encompass all pain-related problems. By excluding anterior knee pain caused by intra-articular disorders, peripatellar tendinitis or bursitis, plica syndromes, Osgood-Schlatter disease and other rarely occurring con ditions, it is suggested that remaining patients with a clinical presentation of anterior knee pain could be diag nosed as patellofemoral pain syndrome (PFPS).46 The term chondromalacia patellae, although once used as an all-inclusive term for anterior knee pain, is now only accepted to describe pathological lesions of the patellar articular cartilage found at arthroscopy or arthrotomy. 'Chondromalacia patellae' as a diagnosis for anterior knee pain is made far too often.47,48 Stougard detected cartilaginous lesions at the posterior aspect of the patella in almost every knee joint at autopsy49 and Paar and Riehl observed damage to the patellar cartilage in almost every operated knee.50 The cause of patellofemoral pain is unknown. Currently, there are two theories to explain its origin: the mechanical and the neural theory.51
rounding the patella as the prime cause of patellar 'mal tracking'. The soft-tissue balance is particularly critical in the first 20° of knee flexion, where the position of the patella in relation to the femur is determined by the inter action of the medial and the lateral soft-tissue structures; after this 20° of motion, the patella engages the femur and the bony architecture becomes more important for the position of the patella relative to the femur.55 Any imbal ance in the soft-tissue structures in the first 20° of flexion will mean that the patella does not encounter the trochlea optimally, which may lead to undue stress on various tissues around the joint and thus to pain. The imbalance may be the consequence of multiple biomechanical defaults. Weakness of the vastus medialis obliquus is thought to be the single most important factor causing momentary patellar subluxation.56 Also the passive stabi lizing structures are usually more extensive and stronger on the lateral than on the medial side. Active stabilization is provided by the quadriceps muscle - on the lateral side the vastus lateralis and on the medial side the vastus medialis. The fibres of the vastus medialis are divided functionally into two compartments: the vastus medialis longus and the vastus medialis obliquus (VMO). The latter does not play a role in active extension of the knee but keeps the patella centred in the trochlea of the femur throughout knee extension.57 The VMO is the only active stabilizer of the patella (Fig. 78.9); therefore the timing and the amount of activ-
MECHANICAL THEORY
Most authors stress the importance of the congruency between the articular surfaces of the femur and the patella.52-54 During the last decade, much emphaSiS was given to the idea of the imbalance of the soft tissues sur-
Figure 78.9 Active medial stabilization is provided by the vastus medialis obliquus (VMO): 1, VMO; 2, patella.
C H APTER 78 - D I S O R D E RS OF T H E CONTRACT I L E STRUCTU R E S 1 1 39
ity in the VMO is critical to patellofemoral function and it is hypothesized that small changes in its activity may have considerable effects on the patellar position. 58 Electromyography (EMG) studies have revealed that, in patellofemoral pain sufferers, the VMO contracts at a significantly slower rate than the vastus lateralis, whereas in normal subjects the reflex response time of both muscles is equaJ.59,60 Other biomechanical factors that may contribute to the development of patellofemoral pain are tightness in the lateral structures, increased Q angle (see below, p. 1140) and faulty foot mechanisms.6l-63 In a retrospective study on 282 male and female students enrolled in physical education classes, Witvrouw et al found a significant cor relation between four parameters and the development of patellofemoral pain: a shortened quadriceps muscle, an altered vastus medialis obliguus muscle reflex response time, a decreased explosive strength and a hypermobile patella.64 NEURAL THEORY
The normal articular cartilage is aneural, so defects in the surface are not thought to produce pain. It has therefore been suggested that irritation of the subchondral bone produces the pain.65 Schneider et al could reproduce the typical pain sensation by raising intrapatellar pressure in about 40% of patients suffering from persistent patellofemoral pain. This subgroup was treated with a new method of intraosseous drilling and decompression. Of the patients so treated, 90% experienced pain relief more than 3 years postoperatively, which may indicate an osseous hypertension as a cause of the pain.66 Some authors have sought the origin of the pain in soft-tissue structures around the knee. Nociceptive nerve fibres and neural markers (S-100 protein, neurofilament protein, substance P and neural growth factor) have been demonstrated in the medial and lateral retinacula and in the infrapatellar fat pad.67,68 From the existing studies it can be concluded that both theories are complementary rather than exclusive: the neural factor precipitates the symptoms in patients with certain biomechanical anomalies who subject their knee to overuse. CLINICAL EXAMINATION
It is important to stress the fact that most anterior knee pains are not caused by patellofemoral disorders but stem from infra-, supra- or peripatellar tendinitis, or a coronary ligament lesion. A basic functional examination should therefore always be performed first (Box 78.1, p. 1141). However, if specific symptoms warrant, and the basic functional examination is totally negative, attention
must be directed towards any peculiarities found during inspection of the patella and surrounding tissues. Inspection on standing
Alignment of the lower extremity is evaluated first by observing the patient standing. Excessive varus or valgus of the extremities and internal femoral rotation are often associated with an extensor mechanism malalignment. Hyperextendable knees may also contribute to the devel opment of anterior knee pain. McConnell points out that shock absorption throughout the lower leg then comes from internal rotation of the femur, rather than from knee flexion.69
Inspection on sitting
Some of the most important observations are made with the patient in the sitting position, with the legs bent to 90°. The position of the patella is then assessed by viewing the knee from the lateral and the frontal aspect respectively. In a lateral view (Fig. 78. 10), the patella should be situated on the distal end of the femur, with the proximal patellar pole level with the anterior femur and the anterior surface of the patella in line with the tibial shaft. In 'patella alta', the upper border of the patella sits more on the anterior surface of the femur and 'faces towards the ceiling'. Viewing from the anterior, a nor mally positioned patella faces straight ahead (Fig. 78.11); 'outfacing' and 'infacing' patellae are easily recognized in this position. Attention is also directed to the alignment of the patella and the patellar tendon in relation to the tibial tuberosity and the tibial crest. The bulk and the level of insertion of the vastus medi alis obliquus muscle is then assessed. The patient is asked to hold both knees actively at 45° of flexion. Normally the
I' , ,/ ,/
,/ ';
/ ' /','
'
' ''
.
. � , ,.
'''.
' -.;.I
r,r ' ' '-
' /_ /., /,;... , .. , I/JI.//" '/ ' l / / / .. /
I
/
/ /.
�
.�
/ / / /
�
Figure 78.10 In a lateral view the proximal pole of the patella should be level with the upper thigh.
1140 S ECTION T H I RT E EN - T H E KN E E
Figure 78. 1 1 ahead.
Viewing from anterior, normally positioned patellae face straight
VMO is seen as a substantial muscle, arising from the adductor tubercle and medial intermuscular septum and inserting into the upper one-third to half of the medial patellar border. In the obese knee it is advisable to palpate along the inner border of the patella during active contraction in 45° of flexion. Inspection in the supine position
The knee is in almost full extension (a small cushion is placed in the popliteal fossa) and the quadriceps is fully relaxed. The position of the patella in relation to the femur is observed. In the obese knee it may be necessary to palpate the patellar borders with one hand and the femoral condyles with the other. Four components affect the patella statically and dynamically: lateral glide, mediolateral tilt, anteroposterior tilt and rotation. An optimal patellar position is one where the patella is parallel to the femur in the frontal and the sagittal planes and midway between the two condyles of the femur when the knee is flexed to 20°.69 The glide component is determined by measuring the distance from the mid-pole of the patella to the medial and lateral femoral epicondyles. The patella should be precisely in the middle. The amount of mediolateral tilt is detected by comparing the height of the medial patellar border with that of the lateral patellar border. The two borders should be level compared to the horizontal. The anteroposterior component evaluates the position of the inferior pole of the patella relative to the superior pole. A rotation of the patella is determined by examining the position of the long axis of the patella, relative to the long axis of the femur. Q angle Next the Q angle is measured. This is the angle at the centre of the patella between two imaginary lines, from the anterior superior iliac spine and from the tibial tuberosity to the geometric centre of the patella. A Q
Figure 78. 1 2
The normal Q angle is about 15°.
angle of up to 10° is normal in the male and up to 15° in the female (Fig. 78. 12). 70 Passive movements of the patella
Patellar mobility is best assessed on a knee flexed to ± 20° (the knee resting on a cushion or on the thigh of the examiner) and with the quadriceps completely relaxed. The examiner's thumbs are placed on the medial border of the patella and the index fingers on the lateral border as attempts are first made to push the patella laterally and then medially. Quantitating the degree of mobility can be done by dividing the width of the patella into four longitudinal quadrants (Fig. 78.13). In normal subjects, the patella cannot be displaced more than three quad rants laterally and should allow a medial shift over at least one quadrant. When the patella is moved in a medial direction, it should initially remain parallel to the femur and not tilt during the first quadrant of the movement. During lateral movement of the patella the examiner is not only looking for patellar mobility but also for any associated apprehension in the subject: as the patella tends to slip over the lateral condyle of the femur, the patient suddenly contracts the quadriceps muscle and draws the patella back. This sudden reflex would not happen if the patella was not apt to subluxate, and is typical for cases of subluxation.
C H A PT E R 78 - D I SO R D E R S OF T H E CONTRACT I L E STRUCTUR E S 1 1 4 1
Box 78.1 Clinical examination of the patellofemoral articulation -
Inspection standing Inspection sitting with the knees hanging over the border of the couch From anterior From lateral Contraction of the quadriceps at 45° of flexion Inspection in the supine position Position of the patella: four components Q angle Passive movements of the patella Mediolateral glide Apprehension Mediolateral tilt
Figure 78.13 Quantitating the degree o f mobility can be done b y dividing the width of the patella into four longitudinal quadrants.
Inspection during active movement
Close observation of the patella in relation to the femur is then continued during active contraction of the quadri ceps. The patella should be pulled directly superiorly or superiorly and slightly laterally. Excessive lateral displacement represents lateral overpull by the quadri ceps and has been referred to as the 'lateral pull sign' (Fig. 78.14).71
Active contraction of the quadriceps Active flexion of the knee
Further observation is made during active flexion of the knee. The patella should remain centred on the trochlea. A patella which was sitting slightly lateral on the trochlea at full extension should move medially to be centred on the trochlea as soon as the knee flexes. CLINICAL MANIFESTATIONS
From a clinical perspective, patellofemoral problems in the skeletally mature patient fall into three broad cate gories: patellofemoral instability (subluxation or disloca tion), patellofemoral pain with malalignment but no episodes of instability and patellofemoral pain without malalignment. 72 Recurrent dislocation and subluxation of the patella
Figure 78.14 Lateral pull sign: the patella moves laterally during contraction of the quadriceps.
Dislocation mostly affects girls and begins at puberty. The history is that of a knee suddenly and painfully giving way. The youngster falls to the ground and feels something is out of place at the lateral aspect of the knee. When the leg is straightened there is a loud click and extension becomes possible at once. For some days afterwards the knee swells and hurts, consequent upon traumatic arthritis. Sooner or later the incident recurs. More often there is a subluxation of the kneecap. The patient does not report the dramatic features described above but merely a 'catching' of the knee, followed by medial pain. The latter is caused by a tearing of the medial capsular structures and should be differentiated from lesions of the medial meniscus.?3 Clinical examination often reveals an enlarged fat pad and patella alta. There is a deficiency or atrophy of the vastus medialis obliquus. Some authors find a significantly decreased Q angle. 74 The lateral patellar
1142 S ECTION T H I RT E EN - T H E KN E E
Figure 78.1 5 Anatomical changes in recurrent subluxation o f t h e patella: 1, increased patellar mobility; 2, decreased Q angle; 3, outfacing patella; 4, vastus medialis deficiency; 5, fal pad enlargement.
mobility is increased (more than three-quarters of the width of the patella) and apprehension can often be provoked during glide mobilization of the patella (Fig. 78.15). Treatment
In acute or recurrent dislocation, surgical intervention is advised but only after puberty, when the epiphysis has closed. Good subjective results are to be expected in about 80% of patients,?5 In recurrent subluxation, the decision to operate should not be taken lightly because it has been demon strated that the long-term results continue to show an incidence of persistent instability and late patellofemoral arthrosis,?6-78 Arthroscopic release only gives a satisfac tory result in 40% of cases. 79 Treatment of patellofemoral instability should therefore be conservative, surgical interventions being reserved for patients who do not respond adequately. Conservative treatment consists of intensive functional vastus medialis rehabilitation together with the use of a brace (see treatment of PFPS, p. 1143).
Most patients with knee pain attributed to PFPS are young women. The common symptom is of a dull and vague aching behind the knee cap during and after phys ical activity, especially during body-weight loading of the lower extremities (walking up- or downstairs and squat ting). The knee is usually also sore in a sitting position and a few patients also have nocturnal pain.82 Routine clinical examination reveals nothing. There is a full and painless range of movement, with normal end-feels. Resisted extension is strong and painless. Inspection may reveal some typical abnormalities. Excessive varus or valgus position of the lower extremi ties is often associated with a malalignment of the patella. The position of the patellae is first assessed in the sitting position. Laterally tilted patellae (Fig. 78.16) appear to be looking up and over the examiner's shoulders toward the ceiling, the so called' grasshopper eyes' kneecap. The vastus medialis obliquus is then assessed by asking the patient to hold the knees actively at 45° of flexion. In patients with atrophy of the VMO muscle there is a visible and palpable lack of muscular tissue at the upper medial border of the patella. The Q angle is often increased in patients with PFPS. Another common finding is tightness of the inert lateral structures which make the patella tilt laterally: the medial border of the patella is higher than the lateral border, the undersurface of which is hard to palpate. Any attempt to push the patella medially results in more anterior tilting of the medial border. If the lateral structures are tighter more distally on the patella, it externally rotates and if the tightness is greater in the superior pole, the patella will internally rotate during lateral pressure. Slight tightness of the lateral structures is revealed by a decreased medial glide: a medial displacement of only one quadrant indicates a tight lateral retinaculum. Again the patella tilts laterally during the manoeuvre. Excessive lateral movement of the patella during active contraction of the quadriceps (the 'lateral pull sign') or during active extension of the knee in a sitting
Patellofemoral pain syndrome without subluxation
The source of pain in 'patellofemoral pain syndrome' cannot be adequately explained. The hypotheSis is that patients with PFPS have lateral displacement of the patella within the femoral trochlea. 80 This lateral 'malalignment' may result from a number of factors, including malalign ment of the lower extremity and/ or the patella, tight lateral soft-tissue structures and muscular imbalance of the lower extremity. All may lf, ad to areas of increased stress on the patellofemoral joint and pain.81
, I'
(
/
Figure 78.16
Laterally tilted patellae.
C HAPTER 78
Figure 78.17 Anatomical changes in PFPS: 1, decreased patellar mobility; 2, increased Q angle; 3, lateral tilted patella; 4, hypertrophied lateral bands.
position, indicates predominance of lateral forces. They are common findings in PFPS (Fig. 78. 17). The classical radiological examination techniques to visualize the patellofemoral articulation are the MerchantB3 and Laurin84 views whereby the joint surfaces are visual ized with the knee flexed to 45° and 30° respectively. MRI has also been found to be an accurate and reproducible method of measurement of the patellar tilt angle.85,86 Arthroscopy is of little value in the diagnosis of PFPS. The incidence of damaged cartilage in asymptomatic patients is so high that arthroscopy on its own cannot determine whether the symptoms should be attributed to chondromalacia. Hertel detected lesions of the articular surface of the patella in about 50% of routine arthro scopies.87 Paar and Schneider found clear damage to the cartilage in 67% of the joints in which they undertook arthroscopies.88 These two series establish that arthro scopic lesions occur far more frequently than do clinical manifestations and that overestimation of disease is a hazard if the diagnosis is based totally on the result of arthroscopy. Treatment
In a number of patients the condition seems to be self limiting, as demonstrated by Sandow and Goodfellow who reported spontaneous cure in more than 20% of anterior knee syndromes. Of 54 girls suffering from PFPS, only nine were permanently unable to participate in sports after a follow-up period of 4 years.89 Many different treatment protocols for PFPS have been described in the literature. It is clear that, if an abnormal tracking of the patella is believed to be the reason for the pain, the initial treatment must be to try to restore normal alignment. An optimal patellar position is achieved by
-
D I SO R D E RS OF T H E CONTRACT I L E STR U CT U R E S 1 1 43
stretching the tight lateral structures and by changing the activation pattern of the vastus medialis obliquus.55 Stretching is performed passively by the therapist. However, the most effective stretch to the shortened retinacular tissue is obtained by sustained low load, using tape, which facilitates a permanent elongation of the tissue. 90 Specific training of the vastus medialis includes timing and intensity of the vastus medialis obliguus relative to the vastus lateralis (VL). Ideally, the VMO should come in slightly earlier than the VL.60 This is mainly achieved during weight-bearing activities. It has been proposed that training causes changes within the nervous system that allow an individual better to coordinate the activities of muscle groups.91 Biofeedback machines are extremely useful to facilitate this process.92 Adding some hip adduc tion in training will also cause an increase in VMO activ ity relative to VL.93 If symptoms persist despite a conservative treatment programme, surgery may be indicated. An arthroscopic approach, with shaving of the affected area94 and / or lateral release of the lateral retinaculum are recom mended.95,96 Before deciding to operate, however, it is well to remember that the long-term results are not as good as might be hoped.97,98 Patellofemoral arthrosis
This can occur after a flake fracture of the articular surface of the patella.99 It is not clear whether chondro malacia patellae precedes osteoarthritic changes, because the anatomical location of the two conditions differs. Chondromalacia is most often found near the median ridge, whereas osteoarthrosis first appears on the very medial side of the patella.ll Erosion of the cartilage at the medial edge may start before the age of 20 and has been shown to be present in three-quarters of individuals by the age of 30. As in other localizations of osteoarthrosis, radio graphic signs do not always equate with symptoms. Sometimes the patient is aware only of grating or crack ing when walking upstairs. Alternatively the symptoms may be very similar to those in chondromalacia: anterior pain during walking upstairs, squatting or sitting with bent knees.1 °o Palpation during squatting reveals pain, together with 'crackling' and 'popping' sensations. Treatment depends on the severity of the symptoms and varies from doing nothing, using an infrapatellar brace to finally operative removal of the patella.
STRAINED I LIOTIBIAL BAND
The iliotibial band, a thick extension of the fascia lata, inserts at the tibial tubercle of Gerdy. The band lies
1 1 44 S ECTION T H I RT E EN - T H E KN E E
anterior to the flexion-extension axis o f the knee i n exten sion and posterior in flexion. The tensor fasciae latae, acting through the band, is thus a weak external rotator and extensor of the knee. Iliotibial band friction syn drome is an overuse injury usually seen in military per sonnel, cyclists and long-distance runners.101 Jones et al diagnosed iliotibial tract syndromes in about 17% of all knee syndromes reported in long-distance runners.I 02 During repetitive flexion-extension movements the tight band overrides and rubs on the prominent lateral epi condyle (Fig. 78.18). Friction occurs at, or slightly below, 30° of flexion.I03 This can produce either irritation and subsequent inflammatory reactions within the iliotibial tract itself or formation of a painful bursa between the band and the epicondyle.Io4, ] 05 While running, the athlete notices an increasing pain at the outer side of the knee which forces a stop. The pain is more intense when the foot comes in contact with the ground during running downhill or during decelera tion.1 06 In severe instances, the pain may be so sharp that walking with a normal gait becomes impossible. Examination reveals no abnormality of the joint but some discomfort is experienced when extension and lateral rotation are carried out against resistance. Sometimes a painful arc is found when the band slips over the lateral epicondyle at 30° of flexion. When the routine examination is negative, a simple confirmatory test may be done: in 90° of flexion, pressure is applied at the iliotibial band over the lateral epicondyle; as the knee is gradually extended, the epicondylar area becomes
painful at about 30° of flexion. IO? MR imaging may be useful in confirming the diagnosis. lOS-l1 O Treatment
Preventive measures include avoidance of excessive dis tance and hill running and a reduction in length of stride. In most cases, two to three infiltrations with tri amcinolone, deeply between band and epicondyle, are successful.lll Partial resection is advised in persistent lesions.
FLEXOR MECHANISM
When resisted flexion of the knee causes pain in the pos terior aspect of the thigh, the fault is in the hamstrings. Resisted internal and external rotation then differentiates between lesions of the medial hamstrings and of the biceps femoris. Should resisted flexion hurt at the knee, other possibilities arise. These are a strained popliteus muscle, a tendinitis at either origin of the gastrocnemius, a sprained posterior cruciate ligament or a lesion of the upper tibiofibular joint. HAMSTRING STRAINS
The hamstrings have a double function. They not only extend the thigh and flex the knee (concentric function) but also antagonize the quadriceps during knee exten sion in running (eccentric function). It is probable that a sudden change from stabilizing activity to an active func tion is the main reason for a hamstring strain.112-114 Lesions of the hamstrings are frequently seen in ath letes, rugby, football and soccer players.1 J 5--1l 7 Classically a strain occurs as a sprinter leaves the starting blocks or during a slide in soccer. The athlete feels a snap, immedi ately followed by pain and functional loss. In lesions of the muscle belly, straight leg raising is limited by pain because of muscle spasm. Prone-lying resisted knee flexion is painful. Resisted external or internal rotation can then distinguish between a biceps lesion or a lesion in the medial hamstrings. The short head of the biceps seems to be the most frequently strained.l1S,1l9 Sometimes there is a haematoma and the tender area is swollen.12o Treatment
Figure 78.18 A strained iliotibial band results from the band rubbing on the lateral epicondyle during repeated flexion-extension movements.
An elastic wrap and an ice bag should be applied imme diately after the incident. Minor lesions require the same treatment as do other muscular lesions. As soon as the patient is seen, whether this is the first day or after a week, the lesion is infiltpted with 50 ml of procaine 0.5%. The patient lies prone, the hip extended and the knee well flexed and supported by a pillow, so that the muscle belly is completely relaxed.
CHAPTER 78
The tender area is now identified, which may not be easy, because the lesion may be deeply situated, especially when the short head of the biceps is affected. From the next day on, daily deep transverse friction is given, together with isometric contractions, until the lesion is completely cured. Technique: deep friction to the hamstrings. The tech nique is very similar to the one used in quadriceps lesions but here the patient lies prone, with the hip extended and the knee passively flexed to 90°. This position produces a complete relaxation of the muscle belly. The therapist sits or stands level with the patient's limb. The fingers of one hand, eventually reinforced by the other hand, are placed deep to the affected part of the belly. The thumbs are positioned laterally on the femur and used as a fulcrum. An extension movement at the wrists moves the flexed fingers upwards and pulls on the fibres, which are felt to slip under the fingers (Fig. 78. 19). The effect of deep fric tion can be increased somewhat by a rotational move ment around the thumbs at the end of this movement. In that this treatment is extremely tiring, three periods of 5 minutes of friction over a total of 20 minutes is as much as is practicable.
-
D I SO R D E R S OF T H E CONTRACTILE STRUCTU R E S 1 1 45
After friction, electric or active isometric contractions should be given for about 10 minutes. The purpose is to expand the muscle transversely as much as possible, without strain on the healing fibres. This prevents intra muscular adhesions, often responsible for recurrent or chronic strains of the hamstrings.121 The possibility of recurrence is considerable if the patient goes back to ath letics too soon.122 Therefore treatment should continue with massage and electric contractions for a week after clinical cure is established. Return to sport should be pro gressive, with special care to 'warm up' adequately. Prophylaxis should also include progressive strength ening exercises and stretching before and after activity.123 BICEPS TENDINITIS
This usually occurs as an overuse lesion in athletes, Pain develops at the outer side of the knee. Functional exami nation is entirely negative except that resisted flexion hurts at the outer side. Resisted external rotation is also painful. Tenderness is found at the biceps tendon, usually at the tenoperiosteal insertion at the head of the fibula.124, 125 Treatment consists of deep transverse friction. Alternatively, an infiltration with 20 mg of triamcinolone can be used but this is only effective if the lesion occurs at the insertion. Technique: friction to the biceps tendon. The patient lies prone with the knee fully outstretched. The physiothera pist stands at the opposite side, level with the knee. The head of the fibula is easily identified. The index finger is placed on the tendon at the level of the lesion. Counterpressure is exerted with the thumb placed at the medial side of the knee (Fig. 78.20). Massage is now given by small alternating extension and flexion movements at the wrist, while the thumb is kept still. Twenty minutes, three times a week for 3-6 weeks may be required.
LESIONS OF THE UPPER TIBIOFIBULAR JOINT
Figure 78.19
Deep friction to the hamstrings,
Dislocations or fractures may occur after violent twists or direct blows, for example when a rider 's knee is caught between a tree and the horse.126 It is clear that the exam iner must be especially alert for these injuries, because they can lead to peroneal nerve palsy. A sprain of the upper tibiofibular ligament can develop after trauma to the ankle join t or as the result of repetitive strains. The findings on clinical examination are the same as in biceps tendinitis. Because contraction of the biceps pulls the fibula backwards on the tibia, resisted flexion and resisted external rotation hurt at the outer side of the knee
1 1 46 SECTION T H I RTEEN - T H E KN E E
Figure 78.20
Massage o f t h e biceps tendon.
(Fig. 78.21a). However, when the biceps tendon is exam ined for tenderness, none is found. Resisted flexion in almost full extension is also painless, because the fibular head is now pulling upwards instead of backwards and stress is no longer imposed on the tibiofibular ligaments (Fig. 78.21b). Also passive backwards movement of the fibular head elicits pain and the anterior tibiofibular liga ment is tender to the touch. Treatment is infiltration of the tender structure. One or two infiltrations with 20 mg of triamcinolone solution usually obtain permanent cure.
(a)
�.
LESIONS OF THE PES ANSERINUS
These lesions are rare but are brought to mind if resisted flexion and internal rotation hurt at the inner side of the knee. Palpation usually reveals a tender spot at the inser tion of the semimembranosus. Deep transverse friction clears the symptoms. It is important to remember that part of the semimem branosus inserts through the posterior oblique ligament at the posterior border of the medial meniscus. In lesions of the posterior horn, pain on resisted flexion can there fore complicate the clinical picture. STRAINED POPLITEUS MUSCLE
Should resisted flexion and internal rotation hurt at the lateral or posterolateral aspect of the knee, the popliteus tendon or muscle is suspect (Fig. 78.22). The popliteus tendon originates from the lateral femoral condyle. It passes deeply to the lateral collateral
(b)
Figure 78.21 Resisted flexion at a right angle and in full extension differentiates between a lesion of the upper tibiofibular joint and the biceps tendon.
ligament, which it separates from the lateral meniscus.127 The tendon also attaches partly to the lateral menis cuS.128, 129 The muscle belly inserts with a broad and short tendon at the posterior aspect of the tibia, in the popliteal fossa. Although the muscle is a flexor and internal rotator of the leg, its main function is to prevent a sliding for wards of the lateral femoral condyle on the fixed tibia during the stance phase in walking or ruru1ing, especially
CH APTER 78
-
D I SO R D ERS OF T H E CONTRACTILE STRUCTUR E S 1147
Figure 78.23
Figure 78.22: Anatomy of the lateral aspect of the knee: 1, lateral collateral ligament; 2, biceps tendon; 3a, popliteus muscle; 3b, popliteus tendon.
in running downhill or descending stairs. 1 3O--1 3 2 This makes the popliteus an important active stabilizer of the lateral and posterolateral aspect of the knee joint and explains the frequency of popliteal lesions in long distance runners and downhill skiers. The prevention of forwards sliding is also a function of the posterior cruciate ligament (passive stabilizer) and a strained popliteus muscle can closely simulate a ligamentous strain of the posterior cruciate. Only a careful functional examination differentiates the two lesions. 1 33 Localization of the pain and palpation for tenderness further disclose the lesion to lie at the tendon or in the muscle belly. 1 34,1 35 Treatment
Tendinous lesions respond very well to one or two infiltrations with 10 mg of triamcinolone. Alternatively deep friction can be tried, both to the origin and body of the tendon, although the position of the affected structure makes access for the palpating finger very difficult. Lesions of the muscle belly respond only to deep friction. Technique: infiltration of the popliteus tendon. The patient lies supine, with the knee flexed to 900• The tendon is identified by careful palpation of the lateral
Infiltration of the popliteus tendon.
condyle. At the most prominent aspect two small bony projections can be palpated, with a groove running verti cally downwards between them. In this groove the origin of the popliteus tendon can easily be palpated and fol lowed until it disappears under the lateral collateral liga ment. If the origin is tender, 1 ml of triamcinolone should be infiltrated with the usual technique: the needle is brought in through capsule and ligament until it reaches bone (Fig. 78.23). A series of droplets is then injected at different areas, but only when the tip of the needle is felt to touch bone. If the body of the tendon is tender, the injection should be made around the tendon and not in the tendon itself. The patient adopts a prone position, with the knee slightly bent. The physiotherapist stands lateral to the patient's leg. One thumb, reinforced by the other, is placed on the affected spot, parallel to the muscular fibres (Fig. 78.24). Deep transverse friction is now given, by a supination movement of both arms, which makes the thumbs roll transversely over the muscle fibres. The direction of the movement is cranial and medial. Technique: deep friction to the popliteus muscle.
LESIONS OF THE GASTROCNEMIUS
Tendinous lesions at the origin of the gastrocnemii are very uncommon. We have only seen this lesion in cyclists. Diagnosis becomes obvious when not only resis ted flexion but also rising on tiptoes hurts at the back of the knee. After careful palpation, the tender area is infiltrated with triamcinolone; this usually gives a good result.
1 1 48 S E CTION TH I RTE E N - T H E K N E E
Figure 78.24
Deep friction to the popliteus muscle.
The differential diagnosis of resisted knee flexion is summarized in Figure 78.25.
Resisted flexion painful in 90°
Painless in almost full extension
�
+I
_ _ _
Resisted internal rotation
Medial hamstrings Pes anserinus (Medial meniscus?) Popliteus muscle
Resisted external ...._--+1 rrotation
Rising on tiptoes
Figure 78.25
Posterior cruciate Upper tibiofibular joint
�
Biceps muscle Biceps tendon Upper tibiofibular joint
+I Origin of gastrocnemius
_ _ _
Differential diagnosis of resisted knee flexion.
REFERENCES 1. Ryan AJ. Quadriceps strain, rupture and charley horse. Med J Sports 1969;1:106-11 1 . 2 . Funk FJ Jr. Injuries of the extensor mechanism o f the knee. Athletic Trail7ing 1975;10:141-145. 3. Young JL, Laskowski ER, Rock Me. Thigh injuries in athletes. Mayo Clil7 Proc 1993;68(11):1099-1106. 4. Ryan JB, Wheeler JH, Hopkinson WJ, Arciero RA, Kolakowski KR. Quadriceps contusions. West Point update. Am ] Sports Med 1991;19(3):299-304. 5. Peck RJ, Metreweli C. Early myositis ossificans: a new echo graphic sign. Clil7 RadioI 1 988;139(6):586-588. 6. Mel lerowicz H, Stelling E, Kefenbaum A. Diagnostic u l tra sound in the athlete's locomotor system. Br ] Sports Med 1 990;24(1) :31-39.
7. Sumiyoshi K, Tsuneyoshi M, Enjoji M. Myositis ossificans. A clinicopathologic study of 21 cases. Acta Paillol Jpll 1985; 35(5):1109-11 22. 8. Kalenak A et al . Treating thigh contusions with ice. Phys Sportsmed 1975;3(3):65-67. 9. Sinding-Larsen eMF, Kristiana MD. A hitherto unknown affec tion of the patella in children. Acta RadioI 1921 ;1:171-173. 10. Johansson S. Eine bisher anscheinend unbekannte Erkrankung der Patella. Z Ortllop Chirurg 1 924;43:82-87. 1 1 . Kulund O N . The Injured Athlete, 2nd edn. Lippincott, Philadelphia, 1988. 12. Ferretti A, Puddu G, Marianni PP, Neri M. The natural history of jumper's knee. Patellar or quadriceps tendinitis. lilt Ort/lOp 1985;8:239-242.
CH APTER 78 - D I S O R D E R S OF T H E CONTRACT I L E STRUCT U R E S 1149
13. Cyriax JH.
Textbook of Orthopaedic Medicine, vol I, Diagnosis of -Soft Tissue Lesions, 8th edn. Bailliere Tindall, London, 1982. 14. Schneider PG. Das Patellaspitzensyndrom. Dtsch Z Sportsl1ledizin 1981;2:27-35. 15. Colosimo AJ, Bassett FH. Jumper's knee. Diagnosis and treat
ment. Orthop Rev 1990;19(2):1 39-149.
39. Bourne RB. Fractures of the patella after total knee replace
ment. Orthop Clin North Am 1999;30(2):287-29l .
40. Harwin SF. Patellofemoral complications i n symmetrical total
knee arthroplasty. J Arthroplasty 1998;13(7):753-762.
4 1 . Larson RL, Singer KM. Patellar d isorders.
Clin Sports Med
1985;4(2).
16. Roels J, Martens M, Mulier JC, Burssens A. Patellar tendinitis
42. Jakobsen J, Christiansen KS, Rasmussen OS. Patellectomy, a 20
17. Blazina ME, Kerlan RK, Jobe FW, Carter VS, Carlson GJ.
43. Freuler F, Brunner Ch, Ruter A. Spatresultate bei operierten
18. Fornage B. L'Ultrasongraphie du tendon rotulien.
44. Klassen IF, Trousdale RT. Treatment of delayed and nonunion
(jumper's knee). Am j Sports Med 1 978;6:362-368.
Jumper's knee. Orthop Clin North Am 1973;4:665-678.
Ultra-sonore
Patellafrakturen. Hefte UnfaLlheilkunde 1975;120:68-75.
] Echogr Med
1983;4:145-149.
19. Fritschy 0, de Gautard R. Jumper's knee and ultrasonography.
Am j Sports Med
1988;16(6):636-640.
20. King JB, Percy OJ, Mourad K, Kumar SJ. Lesions of the patellar
ligament. j Bone joint Surg 1990;72B:46-48.
21 . Johnson DP, Wakeley CJ, Watt I. Magnetic resonance imaging
of patellar tendonitis. j Bone loint Surg 1996;78B(3) :452-457.
22. Shalaby M, Almekinders Le. Patellar tendinitis: the significance
of magnetic resonance imaging findings. Am ] Sports Med 1 999;27(3):345-349.
23. Krahl H. 'Jumper's Knee' - Athiologie, Differentialdiagnose
und Therapeutische Moglichkeiten. Orthopiide 1 980;9: 197.
24. Pierets K, Verdonk R, De Muynck M, Lagast J. Jumper's knee:
postoperative assessment. A retrospective clinical study. Knee
Surg Sports Traumatol Arthrosc
25. Van der Ent, Baere GAJ. Jumper's knee. In:
]aarcongres van de Nederlandse Orthopaedische Vereniging. De Medicus, Leiden, 1985: 145-165.
et al. Open and arthroscopic
patellar tenotomy for chronic patellar tendinopathy. A retro
spective outcome study. Victorian Institute of Sport Tendon
Study Group. Am ] Sports Med 2000;28(2) : 1 83-190.
27. Houbben R. La tendinite d u tendon rotulien chez Ie sportif par
Ie massage transversal profound. Memoires de fin d'Etude, Ecole
Provinciale
Belgium, 1989.
28. Petracic
B,
Superieure
Petracic
A.
de
Kinestherapie,
Fleron,
Insertionstendinopathie
des
Kniegelenkes bei Radsportlern in Abhangigkeit von der Korperposition sowie Schuhpedalenverbindung. Sportverletz
Sportschaden
1992;6(1) :29-3 1 .
29. McEachern AG, P Iewes JL. Bilateral simultaneous rupture of
the quadriceps tendon. I Bone joint Surg 1984;66B:250-252.
30. Levine
RJ.
Patellar tendon rupture. The importance of
timely recognition and repair. Postgrad Med 1996;100(2):
241-242,245-246. 31 . Rosenberg JM, Whitaker JH. Bilateral infrapatellar tendon
rupture in a patient with jumper's knee. Am J Sports Med 1991;19(1) :94-95.
32. Zernicke RF, Garhammer J, Jobe FW. Human patellar tendon
rupture: a kinetic analysis. I Bone loint Surg 1 977;59A: 1 79-183. 33. Julius A. Rupture of the quadriceps tendon.
Neth J Surg
1984;36:1 34-1 36.
34. Loehr JR, Welsh RP. Spontaneous rupture of quadriceps
tendon and patellar ligament during treatment for chronic
renal failure. Can Med Assoc 1983;129:254-256.
35. Kelly DW, Carter VS, Joke FW, Kerlan RK.
Patellar and
quadriceps tendon ruptures - Jumper's knee. Am J Sports Med 1984;12:375. 36. Osgood RB. Lesions of the tibial tubercle occurring during
adolescence. Boston Med Surg ] 1903;148:1 14-117.
37. Mital M. Osgood-Schlatter'S disease: the painful puzzler.
Sportsmed
of the patella. J Orthop Trauma 1 997;11 (3):188-194. 45. Fulkerson J, Hungerford D.
46. Thomee R, Augustsson J, Karlsson J. Patellofemoral pain
syndrome: a review of current issues. Sports Med 1 999; 28(4):245-262.
47. Abernethy PJ. Is chondropathy a separate clinical entity?
loint Surg
] Bone
1978;60B:205-212.
48. Radin EL. Anterior knee pain - the need for a specific diagno
sis. Stop calling it chondromalacia! Orthop Rev 1 985;14:128.
49. Stougard J. Chondromalacia of the patellae: incidence, macro
scopical and radiographic findings at autopsy. Acta Orthop
Scand
1975;46:809.
50. Paar 0, Riehl KO. Chondropathia patellae und trauma.
MUllch
1982;124(41):888.
5 1 . Sanchis-Alfonso V, Rosello-Sastre E,
Martinez-Sanjuan V.
PathogeneSis of anterior knee pain syndrome and functional
patellofemoral instability in the active young. Am I Knee Surg 1999;12(1) :29-40. 52. Insall J. Current concepts review - patellar pain.
Surg
1 982;64A: 1 47-15l .
53. McNally EG, Ostlere SJ, Pal C
I Bone ]oillt
et al. Assessment of patellar mal
tracking using combined static and dynamic MRI. Eur Radial 2000;10(7):1051-1055.
54. Reider B . The anterior aspect of the knee joint. ]
Bone joint Sflrg
1981;63A(3) :35 1 .
55. McConnell J . Management of patellofemoral problems.
Therapy
Mal/flal
1996;1:60-66.
56. Sakai N, Luo ZP, Rand JA, An KN. The influence of weakness
in the vastus medialis oblique muscle on the patel lofemoral
joint: an in vitro biomechanical study. Clin Biomech 2000; 15(5):335-339.
57. Lieb F, Perry J. Quadriceps function.
] Bone Joint Surg
1 968;
50A(8):1 535-1548.
58. Powers CM. Patellar kinematics, part I: the influence of vastus
muscle activity in subjects with and without patellofemoral pain. Phys Ther 2000;80(10):956-964.
59. Mariano P, Caruso J. An electromyographic investigation of
subluxation of the patella. I Bone joint Surg 1 979;61 : 1 69-1 7 1 .
6 0 . Voigt M , Weider D. Comparative reflex response times of the
vastus medialis and the vashls lateralis in normal subjects and
subjects with extensor mechanism dysfunction. Am J Sports
Med
1991;10:131-137.
6 1 . Luo Z P, Sakai N, Rand JA, An KN. Tensile stress of the lateral
patellofemoral ligament during knee motion. Am J Knee Surg 1997;10(3): 139-144.
62. Huberti HH, Hayes We. Patellofemoral contact pressure.
J Bone Joint Surg
1984;66A:715-724.
63. Ficat P, Ficat C, Bail1eux A.
Syndrome d'hyperextension
externe de la rotule. Rev Chirurg Orthop 1 975;61 :39-59.
Phys
1977;5(6) :60-73.
38. D'Ambrosia RD, MacDonald GL. Pitfalls in the diagnosis of
Osgood-Schlatter disease. Clill Orthop 1 975;110:206-209.
Disorders of the Patellafemoral loint,
2nd edn. Williams & Wilkins, Baltimore, 1990.
Med Wochenschr
1 999;7(4) :239-242.
26. Coleman BD, Khan KM, Kiss ZS
year follow-up. Acta Orthop Scand 1985;56:430-432.
64. Witvrouw E, Lysens R, Bellemans J, Cambier D, Vander
straeten G. Intrinsic risk factors for the development of anterior knee pain in an athletic population. A two-year
prospective study. Am ] Sports Med 2000;28(4):480-489.
1 1 50 S ECTION T H I RT E E N - T H E K N E E
65. lnsall J . 'Chondromalacia patellae': patellar malalignment syndrome. Orthop Clin North Am 1979;10:117-127. 66. Schneider U, Breusch SJ, Thomsen M et al. A new concept in the treatment of anterior knee pain: patellar hypertension
syndrome. Orthopedics 2000;23(6):581-586. 67. Witonski D, Wagrowska-Danielewicz M. Distribution of sub stance-P nerve fibers in the knee joint in patients with anterior
knee pain syndrome. A preliminary report. Knee Surg Sports
88. Paar 0, Schneider B. Vergleichende klinische und arthro scopische Untersuchung des Kniegelenkes bei Chondro
malacia patellae. Akt TratlmatoI 1989;19:142-146. 89. Sandow MJ, Goodfellow JW. The natural history of anterior knee pain syndrome in adolescent. ] Bone loillt Surg 1985; 67B:36-38. 90. Somes S, Worrell TW, Corey BCD. Effects of patellar taping on patellar position in the open and closed kinetic chain: a pre
68. Sanchis-Al fonso V, Rosello-Sastre E. Immunohistochemical
analysis for neural markers of the lateral retinaculum in
liminary study. J Sports Rehab 1 997;6:299-308. 9 1 . Sale D. lnfluence of exercise and training on motor unit activa tion. Exerc Sports Sci Rev 1 987;5:95-151 .
patients with isolated symptomatic patellofemoral mal align
92. Ingersoll C, Knight K. Patellar location changes following
ment. A neuroanatomic basis for anterior knee pain in the
EMG biofeedback for progressive resistive exercises. Med Sci
active young patient. Am J Sports Med 2000;28(5):725-731 .
Sports Exerc 1991;23(10):1122-1127. 93. Hodges P, Richardson CA. An investigation into the effective
Traumatol Arthrosc 1999;7(3): 177-183.
69. McConnell J . The management of chondromalacia patellae. A long term solution. Aust J Physiother 1986;2:215-233. 70. Carson W, James S, Larson L et al. Patellofemoral disorders.
Physical and radiographic evaluation. Part I: physical exami
nation. Clin Orthop 1984;185:165-177. 71 . Kolowich PA, Paulos LE, Rosenberg TD, Fansworth S. Lateral release of the patella: indications and contraindications. Am J Sports Med 1990;18:359-365.
ness of hip adduction in the optimization of the vastus medi
alis oblique contraction. Scand ] Rehabil Med 1993;25:57-62. 94. Ogilvie-Harris DJ, Jackson RW. The arthroscopic treatment of chondromalacia patellae. I Bone Joint SlIrg 1984;668:660-665. 95. O'Neill DB. Open lateral retinacular lengthening compared with arthroscopic release. A prospective, randomized outcome
study. ] Bone Joint Surg 1 997;79A(12):1759-1769.
72. Holmes SW Jr, Clancy WG Jr. Clinical classification of
96. Pidoriano AJ, Fulkerson JP. Arthroscopy of the patellofemoral joint. Clin Sports Med 1 997;16(1): 1 7-28.
1998;28(5):299-306. 73. Hughston Je. Subluxation of the patella. J Bone Joint Surg 1 968;50A:1003-1026. 74. Reider B, Marshall J, Warren R. Clinical characteristics of patellar disorders in young athletes. Am J Sports Med 1981; 9(4):270-274. 75. Vainionpaa S, Laasonen E, Silvenoinne T et al. Acute disloca
97. Biedert R, Friederich N. Femoropatellar pain syndrome: which
patellofemoral pain and dysfunction. J Orthop Sports Phys Ther
tion of the patella: a prospective review of operative treatment.
] Bone Joint Surg 1990;77B:366-369. 76. De Cesare WF. Late results of the Hauser procedure for recur rent dislocation of the patella. Clin Orthop 1979;140:137-143. 77. Crossby E, Insall Jw. Recurrent dislocation of the patella. A study of its pathology and treatment in 106 knees. J Bone Joint Surg 1976;58A:9-13. 78. Nikku R, Nietosvaara Y, Kallio PE, Aalto K Michelsson JE.
Operative versus closed treatment of primary dislocation of
the patella. Similar 2-year results in 125 randomized patients.
Acta Orthop Scand 1 997;68(5):419-423. 79. Dandy DJ, Griffiths D. Lateral release for recurrent dislocations of the patella. J Bone Joint Stlrg 1989;71B:121-125.
80. Merchant Ae. Classification of patellofemoral disorders.
Arthroscopy 1988;4:235-240. 8 1 . Ahmed AM, Burke DL, Hyder A. Force analysis of the patellar mechanism. J Orthop Res 1 987;5:69-85. 82. Paar 0, Bernett P, Huyer e. Experiences with patellar chon d ropathy: etiology, diagnosis and therapy. Int J Sports Med 1986;6:803-813. 83. Merchant
AC,
Mercer
RL,
Jacobsen
RH,
Cool
CR.
Roentgenographic analysis of patellofemoral congruence.
] Bone Joint Surg 1 974;56A:1391-1396. 84. Laurin CA, Dussault R, Levesque HP. The tangential X-ray investigations of the patellofemoral joint. Clin Orthop 1979;144:16-26. 85. McNally EG, Ostlere SJ, Pal C et al. Assessment of patellar mal tracking using combined static and dynamic MRI. Eur Radial 2000;10(7):1051-1055. 86. Pookarnjanamorakot C, Jaovisidha S, Apiyasawat P. The patel
lar tilt angle: correlation of MRl evaluation with anterior knee
pain. J Med Assoc Thai 1998;81(12):958-963. 87. Hertel E. Die artroskopische Diagnostik der Chondropathia Patella. Orthop Praxis 1980;6:522.
operation is still sensible? Ther Umsch 1996;53(10):775. 98. Federico DJ, Reider B. Results of isolated patellar debridement for patellofemoral pain in patients with normal patellar align
ment. Am ] Sports Med 1997;25(5):663-669.
99. Bandi W. Die retropatellaren Kniegelenkschiiden. Huber, Bern, 1982. 100. Munzinger U, Bubs L, Buchmalill R. Das femoropatellare Schmerzsyndrom. Orthopiide 1985;14:247. 101. Kirk KL, Kuklo T, Klemme W. Iliotibial band friction syn drome. Orthopedics 2000;23(11):1209-1214. 1 02. Jones SL, Bates BT, Osternig LR. Injuries to runners. Am ] Sports Med 1 978;6(2):40-50. 103. Orchard JW, Fricker PA, Abud AT, Mason BR. Biomechanics of iliotibial band friction syndrome in runners. Am ] Sports Med 1996;24(3):375-379. 104. Renne JW. The i l iotibial band friction syndrome. ] Bone ]oillt Surg 1975;57A:1110-1 1 1 1 . 105. Ekman EF, Pope T, Martin DF, Curl WW. Magnetic resonance imaging of iliotibial band syndrome. Am ] Sports Med 1 994;22(6):851-854. 106. Noble HB, Hajek HR, Porter M. Diagnosis and treatment of iliotibial band tightness in rUlillers. Phys Sports Med 1 982; 10(4):67-74. 1 07. Noble CA. Iliotibial band friction syndrome in runners. Am J Sports Med 1980;8(4):232-234. 108. Murphy BJ, Hechtman KS, Uribe JW et al. Iliotibial band fric tion syndrome: MR imaging findings. Radiology 1992;185(2): 569-571 . 1 09. Muhle C, Ahn JM, Yeh L et al. Iliotibial band friction syndrome: MR imaging findings in 16 patients and MR arthrographic study of six cadaveric knees. Radiology 1 999;212(1):103-110. 1 1 0. Nishimura G, Yamato M, Tamai K et at. MR findings in ilio tibial band syndrome. Skeletal RadioI 1 997;26(9):533-537. 1 1 1 . Orava S. Iliotibial tract friction syndromes in athletes. Br I Sports Med 1978;12:69-73. 1 1 2 . Cooper DL, Fair J. Trainer's corner. Hamstring strains. Phys Sportsmed 1978;6(8):104. 1 13. Mann RA. Biomechanics in running. In: Mack R (ed) American Academy of Orthopedic Surgeons' Symposium all the Foot alld Leg in Running Sports. Mosby, St Louis, 1982:1-9. '
C HA PT E R 78 - D I S O R D E R S OF T H E CONTRACTI LE STRU CT U R E S 1 1 5 1
114. Stanton P, Purdam e . Hamstring injuries i n sprinting - the ,role of eccentric exercise. J Orthop Sports Phys Ther 1989;10(9):343-349. 115. Lysholm J, Wiklander J. Injuries in runners. Am J Sports Med 1987;15:168-1 71. 116. McMaster W, Walter M. Injuries in soccer. Am J Sports Med 1986;6(1):293-299. 1 1 7. Askling C, Tengvar M, Saartok T, Thorstensson A. Sports related hamstring strains - two cases with d ifferent etiologies
and injury sites. Scand J Med Sci Sports 2000;10(5):304-307.
118. Burkett LN. Investigation into hamstring strains: the case of the hybrid muscle. Am J Sports Med 1975;3:5. 119. Garrett WE, Rich FR, Nikolaous PK, Volger JB. Computed tomography of hamstring strains. Med Sci Sports Exer 1 989; 21(5):506-514. 120. Clanton TO, Coupe KJ. Hamstring strains in athletes: diagno sis and treatment. J Arn Acad Orthop Surg 1998;6(4):237-248. 121 . Nikolaous PK, Macdonald BL, Glisson PR et al. Biomechanical and histological evaluation of muscle after controlled strain
inju ry. AIlI J Sports Med 1987;15(1):9-14. 122. Agre Je. Hamstring injuries. Proposed aetiological factors, pre vention, and treatment. Sports Med 1985;2(1):21-33. 123. Worel l TW, Perrin DH. Hamstring muscle injury: the influence of strength, flexibility, warm-up and fatigue. J Orthop Sports Phys TIler 1992;16(1):12-18.
124. David A, Buchholz J, Muhr G. Tear of the biceps femoris tendon. Arch Orthop Traum.a Surg 1 994;113(6):351-352. 125. Lokiec F, Velkes S, Schindler A, Pritsch M. The snapping biceps femoris syndrome. Ciin Orthop 1 992;283:205-206. 1 26. Ogden JA. Subluxation and d islocation of the proximal tibiofibular joint. J Bone Joint Surg 1 974;56A:145-154. 127. Harley JD. An anatomic arthrographic study of the relation ships of the lateral meniscus and the popliteus tendon. Am J Roentgeno/ 1977;128:1 8 1 . 1 28. Jones CD, Keene GC, Christie AD. The popliteus as a retractor of the lateral meniscus of the knee. Arthroscopy 1 995; 11(3):270-274. 1 29. Olson WR, Rechkemmer L. Popliteus tendinitis. J Am Podiatr Med Assoc 1993;83(9):537-540. 130. Barnett e, Richardson AT. The postural function of the pop liteus muscle. Ann Phys Med 1953;17:179. 1 3 1 . Peterson L, Pitman MI, Gold J . The active pivot shift: the role of the popliteus muscle. Am J Sports Med 1984;12:313. 132. Mann RA, Hagy JL. The popliteus muscle. J Bone Joint Surg 1977;59A:924-927. 133. Stainier P. Le muscle poplite. Cyriax Info 1991;3(1):5-7. 1 34. Mayfield GW. Popliteus tendon tenosynovitis. Am J Sports Med 1977;5:31 . 1 35. Hughston Je, Jackson KE. Chronic posterolateral rotatory instability of the knee. J Bone Joint Surg 1985;67A:35 1 .
THIS PAGE INTENTIONALLY LEFT BLANK
i;>ifferential diagnosis of lesions at the knee
Anterior knee
Disorder
Diagnosis
Treatment
Patellar bursitis
Inspection and palpation
Aspiration/infiltration or surgery
History of local blow
Aspiration
pain Subsynovial haematoma
Marked limitation of flexion Normal extension Suprapatellar tendinitis
Painful resisted extension
Deep friction or triamcinolone
Tenderness at the upper border Infrapatellar tendinitis
Painful resisted extension
Deep friction or triamcinolone
Tenderness at the lower pole Quadriceps expansion tendinitis
Painful resisted extension
Deep friction
Lateral or medial tenderness Infrapatellar tenosynovitis
Painful resisted extension
Triamcinolone
Crepitus Local tenderness Apophysitis
Boys between 10 and 15 years
Rest
Local pain and tenderness Recurrent dislocation
Attacks of collapsing, swelling
Brace
and anteromedial pain
Tape and training VMO
Positive apprehension test
(Surgery)
Decreased Q angle Patellofemoral pain syndromes
Dull pain, also during sitting
Tape and training VMO
Increased Q angle Hypertrophied lateral bands Crepitus during squatting Patellofemoral arthrosis
Anterior pain during walking
I nfrapatellar strap
upstairs Crepitus Sometimes pain during sitting Sprain of the anterior cruciate,
Trauma
anterior insertion
Acute stages: capsular
Triamcinolone
pattern Chronic stage: only a positive anterior drawer test Sprain of the posterior cruciate,
Trauma
anterior insertion
Acute stages: capsular
Triamcinolone
pattern Chronic stage: only a positive posterior drawer test
1153
1154 SECTION THIRTEEN - THE KNEE
Medial knee
Disorder
Diagnosis
Medial coronary ligament
History of rotation trauma
Treatment Deep friction or infiltration
Painful lateral rotation
pain
Local tenderness Medial collateral ligament
History of trauma Acute cases: capsular pattern
Acute: deep friction and mobilization
and local tenderness
or triamcinolone
Chronic cases: limitation in a
Chronic: manipulation after deep
non-capsular pattern
friction
Painful valgus and lateral rotation Plica mediopatellaris
Vague medial pain
Triamcinolone or arthroscopic
Sometimes twinges
section
Painful arc Local thickening and tenderness Loose body
Middle-aged
Manipulation
Twinges, usually on walking downstairs Non-capsular pattern Typical end-feel 'Sprain without a sprain' Medial collateral bursitis
Middle-aged
Aspiration and triamcinolone
Nocturnal pain Non-capsular pattern Painful valgus and external rotation Hardish swelling Medial meniscus
Locking/manipulative unlocking
Manipulation or surgery
Symptoms of sprained coronary ligament Medial quadriceps expansion
Pain during exertion
tendinitis
Resisted extension painful
Deep friction
Local tenderness Pes anserinus tendinitis
Resisted flexion and internal
Deep friction or triamcinolone
rotation painful Lateral knee
Lateral coronary ligament
Rotation trauma
Deep friction or infiltration
Painful internal rotation
pain Lateral collateral ligament
Lateral meniscus tear
Trauma
Deep friction or triamcinolone
Painful varus
(acute)
Locking and manipulative
Manipulation or surgery
unlocking Symptoms of sprained lateral coronary ligarnent Lateral meniscus cyst
Pain on standing
Puncture (or surgery)
Palpable bulge on extension Discoid rneniscus
Children or adolescents
Surgery
Symptoms of internal derangement Arthroscopic diagnosis Biceps tendinitis
Positive resisted flexion, also with an extended knee Positive resisted external rotation
Deep .friction or triamcinolone
CHAPTER 79
Disorder Upper tibiofibular sprain
Diagnosis
-
DIFFERENTIAL DIAGNOSIS 1155
Treatment
Painful resisted flexion,
Triamcinolone at the anterior
disappearing with the knee in
ligament
extension Popliteus tendinitis
Painful squatting and walking
Triamcinolone (origin)
downstairs
Deep friction (body)
Painful resisted flexion and internal rotation Iliotibial friction syndrome
Runners/skiers/cyclists
Infiltration or operative section
Sometimes painful arc at 30° Painful resisted extension and flexion Local tenderness Lateral quadriceps expansion
Painful resisted extension
Deep friction
Triamcinolone
tendinitis Posterior
Posterior cruciate ligament, tibial
Trauma
knee pain
insertion
Painful passive extension Painful posterior drawer test Painful lateral shearing
Anterior cruciate ligament,
Trauma
femoral insertion
Painful anterior drawer test
Popliteus muscle
Trauma?
Triamcinolone
Deep friction
Painful squatting and walking downstairs Medial collateral ligament
Trauma
Chronic stage: manipulation
Chronic stage: slight non-capsular pattern, passive external rotation and valgus Posterior capsular strain
Trauma: hyperextension strain
Triamcinolone
Chronic stage: only passive extension is painful Sometimes slight calcification on the radiograph Popliteal cyst
Slight limitation of flexion
Aspiration
Soft end-feel Palpation Lesions of the posterior horn of
Slight internal derangement at
meniscus
the back of the knee
Coronary strain at the posterior
Trauma: rotational injury
part
After the capsular pattern has
Prophylaxis or surgery
Deep friction
subsided: pain during internal or external rotation Palpation at the posterior part of the joint line Tendinitis of the origin of the
Painful tiptoe
gastrocnemii
Painful resisted flexion, and internal or external rotation
Deep friction or triamcinolone
1156 SECTION THIRTEEN - THE KNEE
Disorder
Diagnosis
Treatment
Traumatic arthritis
Trauma
Deal with the cause
Pain in the knee Capsular
No synovial thickening
pattern Monoarticular arthritis
Slow onset
Two intra-articular injections with
First swelling, then pain and
triamcinolone
finally slight capsular pattern Synovial thickening Haemarthrosis
Posttraumatic/haemophilial
Aspiration
spontaneous
Causative treatment
Severe and immediate pain, swelling and tenderness Rheumatoid and reactive
Polyarthritis
Intra-articular triamcinolone
arthritis
Biomechanical changes
Causative treatment
Synovial thickening Septic arthritis
Hyperacute arthritis
Aspiration and antibiotics
Swelling, redness, tenderness and gross articular pattern Gout
Hyperacute arthritis Analysis of joint fluid
Aspiration (Intra-articular triamcinolone) Causative treatment
Pseudogout
Hyperacute arthritis
(Intra-articular triamcinolone)
Calcification of cartilaginous
Aspiration
structures Analysis of joint fluid Osteoarthrosis
Pain during weight bearing
No conservative treatment
Cold joint
Surgery
No synovial thickening Crepitus Non-
Loose body complicating
Twinges
capsular
osteoarthrosis
Moving pain
pattern
Manipulation
Sprain without a sprain Osteochondritis dissecans
Teenager
Surgery
Sudden locking in extension Posttraumatic arthritis (Positive Wilson's sign?) Impaction of ruptured anterior
Trauma
cruciate
Positive anterior drawer test
Surgery
Limitation of extension Intra-articular adhesions
After surgery or an atypical
Manipulation
sprain Progressive and painless limitation of flexion Normal extension Posterior horn lesions of the
Slight twinges
menisci
Symptoms of internal derangement Slight limitation of flexion
Manipulation or surgery
SECTION FOURTEEN
The lower leg, ankle and foot
SECTION CONTENTS 80. Applied anatomy of the lower leg. ankle and foot 1159 Definitions 1159 The leg 1159 The ankle and foot 1161 Muscles and tendons 1166
The plantar fascia 1170 The heel pad 1170 81. Clinical examination of the lower leg. ankle and foot
1171
Referred pain 1171 History 1171 Inspection 1172 Functional examination 1173 Accessoryexamination 1179 82. Interpretation of the clinical examination
85. Disorders of the midtarsal joints The capsular pattern 1242 Subacute arthritis in adolescence Subacute arthritis in middle age 1181
83. Disorders of the lower leg
1185 Bone disorders 1185 Lesions of the plantiflexors 1186 Lesions of the dorsiflexors 1195 Lesions of the invertors 1197 Lesions of the evertors 1199 Disorders causing neurological weakness of the foot 1201
84. Disorders of the ankle and subtalar joints
Non-capsular patterns 1213 Immobilizational stiffness 1213 Loose body 1214 Painful conditions at the heel 1215 Plantar fasciitis 1215 Plantar fascial tear 1216 Heel pad syndrome 1216 Subcutaneous bursitis 1218 Subcutaneous nodules 1218 Ligamentous disorders - ankle sprains Inversion sprain 1219 Eversion sprain 1232
1205 The ankle joint 1205 The capsular pattern 1205 Rheumatoid conditions 1205 Haemarthrosis 1206 Osteoarthrosis 1206 Injection or aspiration technique of the ankle joint 1206 Non-capsular patterns 1206 Immobilizational stiffness 1206 Loose body in the ankle joint 1206 Other lesions with a non-capsular pattern 1207 The subtalar (talocalcaneal) joint 1211 The capsular pattern 1212 Rheumatoid disorders 1212 Subacute traumatic arthritis 1212 Osteoarthrosis 1213 Spasmodic pes planus 1213
1218
1241 1242 1243
Rheumatoid arthritis 1243 Non-capsular patterns 1243 Midtarsal strain 1243 Midtarsal ligamentous contracture 1246 Aseptic necrosis 1247 Navicular stress fracture 1247 Cuboid rotation 1248 Midtarsal arthrosis 1248 Lesions of the cuneiform-first metatarsal joint 1248 Osteoarthrosis 1248 Gout 1249 Loose body 1249 86. Disorders of the forefoot and toes The forefoot 1251
1251
Short first metatarsal bone 1251 March fractures 1251 Fractures of the fifth metatarsal 1252 Splay foot 1253 The first metatarsophalangeal joint 1253 The capsular pattern 1254 Gout 1254 Arthritis in adolescence 1254 Traumatic arthritis 1255 Arthrosis in middle age 1255 Rheumatoid arthritis 1255 Non-capsular patterns 1256 Metatarsalgia 1256
Sesamometatarsal lesions 1256 Hallux valgus 1256 The outer four metatarsophalangeal joints 1257 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 1259 Pressure on nerves in the forefoot
CHAPTER CONTENTS Definitions The leg
1159
1159
Anterolateral compartment 1160 Lateral compartment 1160 Posterior compartment 1160
The ankle and foot
Applied anatomy of the lower leg, ankle and foot
1161
The posterior segment 1161 The middle segment 1164 The anterior segment 1165
Muscles and tendons 1166 Plantiflexors 1166 Dorsiflexors 1167
Invertors (adduction-supination) 1168 Evertors (abduction-pronation) 1168 Intrinsic muscles 1169
The plantar fascia The heel pad
1170
1170
DEFINITIONS
The functional terminology in the foot is very misleading, because the same terms are often used for very different things. The following definitions and explanations are used here: • Plantiflexion-dorsiflexion
•
•
•
•
indicate movement at the ankle. Plantiflexion is movement downwards towards the ground, and dorsiflexion upwards towards the tibia. There is also a plantiflexion-dorsiflexion movement at the midtarsal joint. Varus-valgus: these movements occur at the subtalar joint. In valgus, the calcaneus is rotated outwards on the talus; in varus, the calcaneus is rotated inwards on the talus. Abduction-adduction: these take place at the midtarsal joints. Abduction moves the forefoot laterally and adduction moves the forefoot medially on the midfoot. Pronation-supination are also movements at the midtarsal joints. In pronation, the forefoot is rotated big toe downwards and little toe upwards. In supination, the reverse happens: the big toe rotates upwards and the little toe downwards. Sometimes the terms internal rotation and external rotation are used to indicate supination or pronation. Inversion-eversion: these are combinations of three movements. In inversion, the varus movement at the subtalar joint is combined with an adduction and supination movement at the midtarsal joint. During eversion, a valgus movement at the subtalar joint is combined with an abduction and pronation movement at the midtarsal joint.
THE LEG
The bones (tibia and fibula) together with the interosseous membrane and fasciae divide the leg into three separate compartments: anterolateral, lateral and posterior. They contain the so-called extrinsic foot muscles. Each compartment has its own blood supply and innervation. 1159
1160 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
ANTEROLATERAL COMPARTMENT
LATERAL COMPARTMENT
The muscles of the anterolateral compartment are the tib ialis anterior, the extensor hallucis and the extensor digi torum, which are all dorsiflexors. The tibialis anterior, however, is also an invertor. The muscles lie in a strong osteofibrous envelope, consisting of tibia, fibula, interosseous membrane and superficial fascia. The ante rior tibial artery (Fig. 80.1) is located at the anterior surface of the interosseous membrane. It supplies the muscles of the anterior compartment and continues at the dorsum of the foot as the dorsalis pedis artery. The nerve supply of the anterior compartment is from the deep peroneal nerve, a branch of the common peroneal nerve.
The lateral compartment contains the peronei longus and brevis muscles. These are strong evertors and weak plantiflexors. Blood supply is from the peroneal artery, a branch of the posterior tibial artery and nerve supply from the superficial peroneal nerve.
POSTERIOR COMPARTMENT The posterior compartment has a deep and a superficial part. The deep part consists of the tibialis posterior, flexor hallucis longus and flexor digitorum longus muscles. The tendons run behind the medial malleolus
2
(b)
5
6
'-""';I--,f-f1--4
10
9
(e)
---'\----.?-
-
+-
-
-
---,'---+-t--7+---
a
b
Figure 80.1 Transverse sections halfway down the leg (a) and at the malleoli (b). 1, tibialis anterior; 2, extensor hallucis longus; 3, extensor digitorum longus; 4, peroneus brevis; 5, peroneus longus; 6, flexor hallucis longus; , 7, flexor digitorum longus; 8, tibialis posterior; 9, soleus; 10, plantaris; 11, gastrocnemii; 12, anterior tibial nerve; 13, anterior tibial vessels; 14, posterior tibial neuromuscular bundle.
CHAPTER 80
to the inner aspect of the sole and to the toes. Hence they are invertors of the foot and flexors of the toes. They also act as weak plantiflexors of the foot. The muscles of the superficial part are both heads of the gastrocnemius, the soleus and the plantaris. The soleus and both gastrocnemii form the triceps surae which inserts - via the Achilles tendon - at the upper posterior aspect of the calcaneus. The plantaris muscle usually has a separate insertion, just medial to the Achilles tendon. This group of muscles acts as a very strong plantiflexor. The artery of the posterior compartment is the posterior tibial. The tibial nerve provides the nerve supply.
Figure 80.2
The three arches of the foot.
ANATOMY 1161
Forefoot
Midfoot
Ankle
THE ANKLE AND FOOT
The 26 bones of the foot create an architectural vault, sup ported by three arches and resting on the ground at three points, which lie at the corners of an equilateral triangle (Fig. 80.2). Ligaments bind the bones to provide the static stability of the foot. The dynamic stability of the vault is achieved by the intrinsic and extrinsic muscles. Three functional segments can be distinguished: fore foot, midfoot and ankle (Fig. 80.3). Each has its particular functions and specific disorders. The posterior segment (ankle) is the connection between foot and leg. It lies directly under the tibia and fibula and is connected to them by strong ligaments. This segment contains the talus (in the mortice between the fibula and the tibia) and the calcaneus. The middle segment (midfoot) contains the five tarsal bones and is the keystone in the plantar vault. Excessive stresses falling on the vault therefore influence the midfoot in particular. The anterior segment (five metatarsals and 14 pha langeal bones) takes the whole body weight during the 'heel-off' phase in walking or running. This specific func tion of the forefoot underlies pressure disorders at the plantar surface of the metatarsals and toes.
- APPLIED
Figure 80.3 The three segments of the foot: 1, phalanges; 2, metatarsals; 3-5, medial, intermediate and lateral cuneiforms; 6, navicular; 7, cuboid; 8, talus; 9, calcaneus.
THE POSTERIOR SEGMENT The talus is the mechanical keystone at the ankle (Fig. 80.4). It distributes the body weight backwards towards the heel and forwards towards the midfoot (medial arch of the plantar vault). The talus has no mus cular insertions but is entirely covered by articular sur faces and ligamentous reinforcements. It is also crossed by the tendons of the extrinsic muscles of the foot.
Ankle joint The superior surface and the two sides of the body of the talus are gripped between fibular and tibial malleoli, forming the ankle mortice. Stability of this tibiofibular mortice is provided by the anterior and posterior tibiofibular ligaments and the interosseous ligament.
Figure 80.4
The talus distributes the body weight to the heel and midfoot.
1162 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
Because the body of the talus is wedge shaped, with the wider portion anterior, no varus-valgus movement will be possible with an ankle held in dorsiflexion, unless the malleoli or the tibiofibular ligaments are damaged (Fig. 80.5). The normal movement of the ankle joint is planti flexion-dorsiflexion, through an axis that passes trans versely through the body of the talus. The lateral end of this axis goes through the lateral malleolus (Fig. 80.6). Hence, a normal plantiflexion-dorsiflexion movement does not influence the tightness of the calcaneofibular lig ament. At the medial end, however, the axis is placed under the tip of the medial malleolus and thus under the malleolar point of attachment of the medial ligaments. Here, the posterior fibres of the deltoid ligament will become taut on dorsiflexion and the anterior fibres on plantiflexion (Fig. 80.7).
Subtalar joint The subtalar or talocalcaneal joint consists of two separate parts, divided by the tarsal canal (Fig. 80.8), which is funnel shaped with the wide portion at its lateral end. The lateral end of the canal is easily pal pated in front of the fibular malleolus between talus and calcaneus, especially when the foot is inverted. The canal runs posteromedially, to have its medial opening just behind and above the sustentaculum tali. In the canal a strong ligament, the interosseous talocalcaneal ligament, binds the two bones. The main movement of the subtalar joint is a varus-valgus movement around an axis through the talus. This axis has a 45° angle to the horizontal and a 15° angle medial to a line drawn through the second metatarsal.
x
--t�-t---+� --
X'
Figure 80.6 Axis of plantiflexion-dorsiflexion (X-X'): 1, lateral malleolus; 2, talus; 3, calcaneus.
Anterior (a)
Medial
(b) Posterior
Figure 80.5
The body of the talus is wedge shaped with a wider anterior portion.
Figure 80.7 The anterior fibres of the deltoid ligament become taut during plantiflexion (a) and the posterior fibres during dorsiflexion (b).
CHAPTER 80
-
APPLIED ANATOMY 1163
3 7
6
.:�--.�./. �� (a)
Figure BO.B View of the plantar calcaneonavicular ligament from above, with the talus removed: 1, calcaneus; 2, posterior part of subtalar joint; 3, sustentaculum tali; 4, anterior part of subtalar joint; 5, tarsal canal; 6, interosseous talocalcaneal ligament; 7, plantar calcaneonavicular ligament; 8, dorsal calcaneocuboid ligament; 9, cuboid; 10, navicular (transsection).
Ligaments of ankle and subtalar joints 5
lateral ligaments. The anterior talofibular ligament is a
triangular structure, its base attached to the anterior margin of the fibular malleolus and the smaller insertion at the neck of the talus (Fig. 80.9), just behind the mouth of the sinus tarsi. The calcaneofibular ligament is a strong round band ruru1ing obliquely downwards and backwards from the apex of the fibular malleolus to the lateral surface of the calcaneus. The posterior talofibular ligament arises from the medial surface of the lateral malleolus and runs horizon tally and medially to insert at the posterolateral tubercle of the talus. Because the axis of plantiflexion-dorsiflexion runs through the origin of these ligaments (the tip of the fibula), they are not taut during these movements. The exception is the anterior talofibular ligament, the medial fibres of which originate higher up on the fibula. These become stretched at the end of the plantiflexion movement. The main function of the lateral ligaments is to prevent excessive varus movement, especially during planti flexion. In extreme plantiflexion, the mortice no longer stabilizes the broader anterior part of the talus; varus movement of the ankle is then possible. Medial ligaments. The deltoid ligament is a strong and thick ligament and has deep and superficial layers. The
2
(b)
Figure BO.9 Lateral and posterior ligaments of the ankle: (a) lateral view; (b) posterior view: 1, posterior talofibular ligament; 2, calcaneofibular ligament; 3, distal tibiofibular ligament; 4, anterior talofibular ligament; 5, posterior tibiotalar ligament; 6, tarsal canal.
first has fibres which run from the medial malleolus to separate parts of the talus (anterior tibiotalar and poste rior tibiotalar ligaments; Fig. 80.10). The second runs from the medial malleolus to the sustentaculum tali (tibiocalcanean ligament) and to the navicular bone (tibionavicular ligament). The inferior part of the ligamentous structures at the inner side of the ankle is the plantar calcaneonavic ular ligament, which runs from the sustentaculum tali to the inferior border of the navicular bone. This ligament also helps to form the talocalcaneonavicular joint (Fig. 80.8).
1164 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
Figure 80.10 Medial ligaments of the ankle: 1, anterior tibiotalar ligament; 2, posterior tibiotalar ligament; 3, tibionavicular ligament; 4, plantar calcaneonavicular ligament; 5, tibiocalcanear ligament.
THE MIDDLE SEGMENT There are five tarsal bones: navicular, cuboid and the three cuneiforms. They form a semi-rigid transverse arch, held together with the interosseous ligaments and the functional stirrup of the tibialis anterior and the peroneus longus (see Fig. 80.20). The middle segment is the keystone in the plantar vault. Its elasticity permits accommodation to uneven surfaces during walking. The joint between the posterior segment (talus and calcaneus) and the middle segment (navicular and cuboid) is the transverse tarsal or Chopart's joint; that between middle and anterior segment is the tarso metatarsal or Lisfranc's joint (Fig. 80.11). Functionally, all the articulations act as one structure. Therefore, Cyriax called them the midtarsal joint. Passive clinical testing evokes considerable movement in three possible direc tions: flexion-extension, pronation-supination and abduction-adduction.
Figure 80.11
Midtarsal joint: Lisfranc's (1) and Chopart's (2).
and navicular bones: the intermediate cuneiform is set back and forms a fork into which fits the base of the second metatarsal (Fig. 80.13). Hence, the second metatarsal moves only in a plantiflexion-dorsiflexion plane and forms the axis of rotation in the tarsometatarsal joint. The base of the third metatarsal rotates around the second, the fourth around the third, and the base of the fifth moves around the fourth. The base of the first metatarsal also rotates around that of the second. Apart from this rotational movement, the Lisfranc joint allows some abduction-adduction and considerable plantiflexion-dorsiflexion movements. The spec:'fic nature of the Lisfranc line has a particular consequence for planti-
Chopart's joint The calcaneocuboid joint, being semi-rigid, only permits some gliding movement. At the talonavicular joint, larger movements are possible in the three directions (flexion-extension, pronation-supination and abduc tion-adduction). This greater mobility is because the artic ular surface of the talar head is larger than the surface of the adjoining navicular bone, so permitting a gliding of the navicular bone along the surface of the talus (Fig. 80.12).
2
Lisfranc's joint The joint line is not a continuous one between the bases of the metatarsals and the anterior border of the cuneiforms
Figure 80.12
Mobility of the talonavicular joint: 1, talus; 2, navicular.
CHAPTER 80
Figure 80.1 4
-
APPLIED ANATOMY 1165
Calcaneocuboid ligaments.
THE ANTERIOR SEGMENT
Figure 80.13
Movements at Lisfranc's joint.
flexion-dorsiflexion: because the line of the tarso metatarsal joints rW1S obliquely (its medial end lies 2 cm anterior to its lateral end), dorsiflexion will include some adduction. Furthermore, the bases of the metatarsals have a cone-shaped form. During plantiflexion the heads of the metatarsals therefore do not move straight downwards but incline towards the axis of the foot and so increase the curvature of the anterior arch (Fig. 80.13). In contrast, extension of the metatarsals is followed by flattening of the arch. These relationships are of great importance in w1der standing the mechanism of splay foot.
Ligaments of the middle segment The architecture of the plantar vault is protected by strong plantar and interosseous ligaments. Some of these have particular clinical importance and play a role in a number of painful conditions at the midfoot. These liga ments are:
The metatarsal shafts and the tarsometatarsal joints form the transverse anterior arch of the plantar vault. Changes in the curvature of the anterior arch result from movements occurring in the tarsometatarsal joints. In a plantiflexed position the anterior part of the foot is hollowed, whereas in a dorsiflexed position it is flattened. In that the arch is spanned only by relatively weak inter metatarsal ligaments and by only one muscle, the trans verse head of the adductor hallucis, the plantiflexed position at the tarsometatarsal joints is of great impor tance in maintaining the curvature of the arch and in preventing flattening of the foot. The two pillars of the arch are in contact with the ground through the soft tissues: the head of the first metatarsal rests on the sesamoid bones, about 6 mm from the ground; the head of the fifth metatarsal bone lies 5 mm above the ground; the head of the second metatarsal bone is, at about 9 mm, the highest of the row; and those of the third and fourth take up an inter mediate position (Fig. 80. 15). The sesamoid bones are incorporated into the tendons of the flexor hallucis brevis and act as a fulcrum in its function. They also play a role in bearing the body weight. The base of the proximal phalanx articulates in a gliding manner upon the convex articular surface of the
• At the lateral aspect:
•
the lateral calcaneocuboid ligament (Fig. 80. 14), which can be easily palpated at the lateral joint line between calcaneus and cuboid, just above the peroneal tendons. This ligament is often damaged after an inversion sprain. At the medial aspect: the plantar calcaneonavicular ligament, which is of great importance in preventing excessive dorsiflexion-abduction movements at the midfoot and thus prevents a flattening of the medial anteroposterior arch (Fig. 80.10).
Figure 80.15
The anterior arch at the level of the metatarsal heads.
1166 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
(a) Figure 80.16 hallucis (b).
(b)
Gripping movement at the outer toes during contraction of the flexor digitorum (a) and pressing movement at the big toe during contraction of the flexor
metatarsal head, thus allowing a considerable range of plantiflexion-dorsiflexion movement. The first meta tarsophalangeal joint is normally capable of 30° of flexion and 90° of extension. The particular insertions of the flexor hallucis longus and the flexor hallucis brevis muscles to the proximal and distal phalanges of the big toe cause the toe to be pressed to the ground during the 'foot-off' phase of walking (Fig. 80.16b), which distributes the body load. In the outer four toes, the proximal phalanx is free from muscle insertions, because the insertions of the flexor digitorum longus and flexor digitorum brevis fall at the base of the distal and middle phalanges. Contraction of these muscles therefore produces a prehensile move ment in the forefoot (Fig. 80.16a).
and gastrocnemius muscles meet in the Achilles tendon. The anterior fibres of the soleus run further downwards along the tendon and the medial head of the gastroc nemius ends a little higher than the lateral. The strong Achilles tendon inserts at the posterior surface of the cal caneus (Fig. 80.18). A bursa lies between the upper part of the calcaneus and the anterior surface of the Achilles tendon. Sometimes a pathological subcutaneous bursa forms between the posterior aspect of the calcaneus and the skin. Because the insertion at the calcaneus is medial to the axis of rotation (BB') of the subtalar joint, the triceps surae is also a weak invertor of the foot. The other plantiflexor muscles - the tibialis posterior, flexor hallucis longus, flexor digitorum longus, and peronei - are rather weak. Although they can achieve
MUSCLES AND TENDONS
PLANTIFLEXORS All the tendons lying behind the axis AA' at the ankle (Fig. 80.17) are plantiflexor muscles (Table 80.1). In prac tice, however, the triceps (soleus and both gastrocnemii) generates almost all the strength of plantiflexion. The gastrocnemius originates by two heads, one at each femoral condyle. It spans two joints and is therefore not only a plantiflexor at the ankle but also a weak flexor of the knee. The soleus originates from the upper tibia and fibula, below the knee joint. Halfway down the leg, the soleus
A A --+��H'!Mtr- '
Table 80.1 The plantiflexors Peripheral nerve
Spinal innervation
Triceps
Tibial
S1-S2
Tibialis posterior
Tibial
L4/LS, S1
Peronei
Superficial peroneal
Flexor hallucis longus
Tibial
Flexor digitorum longus
Tibial
LS, S1 LS, S1 LS, S1
S' Figure 80.17 foot.
Functional pOSition of the tendons in relation to the axes of the
CHAPTER 80 - APPLIED ANATOMY 1167
Table 80.2 The dorsifiexors Peripheral nerve
Spinal innervation
Tibialis anterior
Deep peroneal
L4 (L5)
Extensor hallucis longus
Deep peroneal
L4, L5
Extensor digitorum longus
Deep peroneal
L4, L5
2 --If--t'3
Figure 80.1 8 Insertion of the Achilles tendon, and the relationship of the bursae to it: 1, Achilles tendon; 2, sub-Achilleal bursa; 3, subcutaneous bursa.
active plantiflexion of the foot after a rupture of the Achilles tendon, they can only do this when the foot is free and unsupported. An intact triceps muscle and Achilles tendon are necessary to stand on tiptoe. The main function of the tibialis posterior is inversion and the function of both the peronei is eversion: these muscles are discussed later. The flexor hallucis longus originates at the distal two thirds of the posterior surface of the fibula and at the interosseous membrane. It runs behind and under the medial malleolus, in a sulcus of the talus, under the sus tentaculum tali and along the inner border of the foot to insert at the base of the distal phalanx of the big toe. The flexor digitorum longus arises from the posterior aspect of the tibia, passes under the flexor retinaculum and behind the medial malleolus, to attach at the distal phalanges of the four outer toes. Because its tendons cross the tendon of the flexor hallucis longus from below at the midfoot, the function of the latter will be reinforced by the first. The three tendons at the medial malleolus run in a fibrous tunnel, formed by the tibia and the flexor retinac ulum. At this level they are covered by a tendon sheath. From anterior to posterior they are the tendons of the tib ialis posterior, the flexor digitorum longus and the flexor hallucis longus. The flexor hallucis longus is the only tendon of the three running behind the sustentaculum tali. This position seems to play a role in maintaining the medial arch. The long flexor tendon of the big toe acts on the sustentaculum tali as a string on a pulley, and pushes the medial arch upwards during contraction (Fig. 80.19).
Because the extensor hallucis longus and the tibialis anterior are situated at the medial side of the axis of rota tion (BB'), they act as supinators. The extensor digitorum longus, passing lateral to this axis, acts as a pronator. The extensor hallucis longus arises from the anterior surface of the fibula and the interosseus membrane, and passes across the anterior surface of the ankle to insert at the distal phalanx of the big toe. Its main function is extension of the big toe. It also assists in dorsiflexion of the foot. The extensor digitorum longus arises from the lateral condyle of the tibia and the anterior surface of the fibula. It runs anterior to the ankle, under the lateral half of the retinaculum extensorum digitorum, and divides into four tendons which run to the four outer toes. At its end, each tendon divides into a central slip that inserts at the base of the middle phalanx and two lateral slips insert ing at both sides of the distal phalanx. The strongest function of the extensor digitorum is dorsiflexion at the ankle. It is of course also the main extensor of the toes
��--4
3
DORSIFLEXORS The tendons lying in front of the axis AA' at the ankle (Fig. 80.17) are those of the dorsiflexor muscles: the tibialis anterior, extensor hallucis longus and extensor digitorum longus (Table 80.2).
Figure 80.19 The tendons at the medial malleolus: 1, tibialis posterior; 2, fiexor digitorum longus; 3, fiexor hallucis longus; 4, sustentaculum tali.
1168 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
but this function is only apparent when dorsiflexion at the ankle is counteracted by an antagonistic plantiflexion movement of the triceps surae. The tibialis anterior is a strong dorsiflexor but first of all an adductor and supinator of the foot. Its dorsiflexion function is only possible when adduction-supination is counteracted by contraction of the peronei muscles.
INVERTORS (ADDUCTION-SUPINATION) The tendons of the ankle lying medial to the axis BB' are those of invertor muscles (adduction-supination; Table 80.3). The two most important invertors are the tibialis posterior and tibialis anterior. The tibialis posterior originates from the posterior aspect of the tibia and fibula, runs behind the medial malleolus and inserts at the medial and plantar aspect of the tarsal and metatarsal bones. The most important insertion, however, is at the tubercle of the navicular bone (Fig. 80.20).
Because the tibialis posterior crosses the ankle, the sub talar and the transverse joints, it can act simultaneously on all three. The attachments to the other tarsal and metatarsal bones produce supination and are therefore very important in maintenance of the plantar vault. The tibialis posterior is also a weak plantiflexor. Through its fibrous plantar attachments at the bases of the metatarsals, it also provides a plantiflexion move ment at the midtarsal joints and therefore is responsible for supporting the anterior arch (see plantar movement at Lisfranc's joint). Congenital absence of these plantar attachments is therefore one of the causes of pes planus valgus. The tibialis anterior originates from the upper lateral half of the tibia and crosses the dorsum of the foot to insert at the medial aspect of the medial cuneiform. Because it lifts all the structures of the medial arch - first metatarsal, first cuneiform, navicular and talus - it is an adductor, dorsiflexor and supinator.
EVERTORS (ABDUCTION-PRONATION)
Table 80.3 The invertors Peripheral nerve
Spinal innervation
Tibialis anterior
Deep peroneal
L4,15
Tibialis posterior
Tibial nerve
L4,L5, S1
Extensor hallucis longus
Deep peroneal
L4, L5
Flexor digitorum longus
Tibial nerve
L5, S1
Flexor hallucis longus
Tibial nerve
L5,S1,S2
3
The muscles with tendons that lie lateral to the axis BB' act as evertors (abduction and pronation; Table 80.4). They are the extensor digitorum longus, peroneus tertius and peronei longus and brevis. The small peroneus tertius is absent in more than 10% of subjects and does not have any role in disorders of the foot. The most powerful ever tors are the peronei longus and brevis. They arise from the lateral aspect of the fibula, the longus more proximally than the brevis. Their tendons run together in a common synovial sheath behind the lateral malleolus and are held in place by the retinaculum peroneorum. The tendon of the peroneus brevis, running more anteriorly and superiorly, inserts at the lateral tubercle of the base of the fifth metatarsal (Fig. 80.21). It acts as a strong abductor but also produces pronation of the anterior half of the foot. The peroneus longus runs under the tendon of the brevis, along the lateral border of the foot. At the cuboid tubercle it turns obliquely medially and anteriorly to insert at the base of the first metatarsal and the first cuneiform bone (Fig. 80.20). The peroneus longus is not only an abductor-pronator and a weak plantiflexor of the foot, it also plays an important role in the dynamics of the plantar arches. The abduction-pronation function is obvious from the view shown in Figure 80.22. Table 80.4 The evertors
Figure 80.20 Plantar view of the insertions of tibialis posterior, and its relationship with the tendon of the peroneus longus. 1, attachment to the tubercle of the navicular bone; 2, attachments to the tarsal bones; 3, attachments to the metatarsals; 4, insertions of the peroneus longus tendon.
Peripheral nerve
Spinal innervajion
Peronei
Deep peroneal
L5,S1
Extensor digitorum longus
Deep peroneal
L4, L5, S1
CHAPTER 80
Figure 80.21
The peroneal tendons: 1, peroneus brevis; 2, peroneus longus.
-
APPLIED ANATOMY 1169
The intrinsic muscles are the main contributors to the muscular support of the arches of the foot. They also assist the function of the long (extrinsic) muscles. Only the intrinsic muscles of the big toe and the dorsal inter ossei are clinically important. The muscles of the big toe (flexor hallucis brevis, abductor hallucis and adductor hallucis) are inserted on the lateral aspect of the basal phalanx and into the two sesamoid bones articulating with the head of the first metatarsal. The medial sesamoid gives insertion to the abductor hallucis and to the medial portion of the flexor hallucis brevis. The lateral portion of the flexor hallucis brevis and the adductor hallucis insert on the lateral sesamoid (Fig. 80.23).
Dorsal interossei Plantiflexion is produced in two ways; directly and indirectly. Direct plantiflexion needs no further explanation, because the tendon runs behind the axis AA' (Fig. 80.17). To understand indirect plantiflexion, the action of the triceps must be considered. Contraction of the triceps plantiflexes the calcaneus and the lateral metatarsals, connected through the cuboid with the calcaneus. By coupling the medial with the lateral metatarsals, the peroneus longus allows the triceps to pull on all the metatarsals at one time. Another function of the peroneus longus is to accentu ate the curvature at the three arches of the plantar vault. Together with the plantar expansions of the tibialis pos terior, it provides an important muscular support of the transverse arch. In that it runs obliquely to the anterior and medial side, it also acts as a tightening device for the medial and lateral arches.
The four bipenniform dorsal interossei originate from the sides of the adjacent metatarsal bones, The muscle bellies fill the intermetatarsal spaces and their tendons attach to the bases of the proximal phalanges and to the dorsal digital expansions. The first interosseus inserts into the medial side of the second toe; the other three pass to the lateral sides of the second, third and fourth toes (Fig. 80.24). They abduct the toes away from the
INTRINSIC MUSCLES The sole of the foot contains a number of muscles that take origin and insert on the plantar aspect of the foot. Most arise from the calcaneus and the inferior part of the posterior segment and insert at or close to the phalanges.
2
Figure 80.22 Plantar view of the peronei in abduction-pronation: 1, peroneus brevis; 2, peroneus longus.
Figure 80.23 Intrinsic muscles of the big toe: Ab.H, abductor hallucis; FHB, flexor hallucis brevis; FHL, flexor hallucis longus; Ad. 1 and Ad. 2, adductor hallucis.
1170 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
Figure 80.25
Figure 80.24
Dorsal interossei of the foot.
axis of the foot (second row) and assist in flexion and extension movement of the toes.
THE P LANTAR FASCIA
The plantar fascia and its insertions.
dynamic forces during walking and running. The thick skin is connected with the periosteum of the calcaneus by large vertical fibrous septa, dividing the subcutis into separate compartments, filled with fat (Fig. 80.26). During compression these heel chambers are deformed and turn around the tuberosity of the os calcis. This deformation of the chambers together with the flow of the enclosed adipose tissue contributes to the shock absorption.
Another structure that plays an important role in main taining the longitudinal arches in the foot is the plantar fascia (Fig. 80.25). This multilayered fibrous aponeurosis originates at the medial tuberosity of the calcaneus and passes anteriorly to split into five fibrous bands, which attach to the digits in the following manner: each splits at the level of the corresponding metatarsophalangeal joint to allow passage of the short and long plantiflexor tendons and attaches at both sides of these joints and their ligaments. When the metatarsophalangeal joints are dorsi flexed during walking, the plantar fascia tightens and raises the longitudinal arch.
THE HEEL PAD
The heel pad is specifically constructed to function as an efficient shock absorber to attenuate the peaks of the
Figure 80.26 Coronal section of the heel demonstrating the heel pad; 1, calcaneus; 2, skin and subcutis; 3, chambers; 4, vertical septa.
CHAPTER CONTENTS
Clinical examination of the lower leg, ankle and foot
,
Referred pain
1171
Pain referred to the foot 1171 Pain referred from the foot 1171
History
1171
Inspection
1172
Functional examination 1173 Rising on tiptoe 1173 Tests for the ankle joint 1174
Ligamentous tests at ankle and foot Mobility of the subtalar joint 1175 Passive tests for the midtarsal joints Resisted movements 1178
Accessory examination
1179
1174 1176
REFERRED PAIN PAIN REFERRED TO THE FOOT Pain referred from other structures (hip, sacroiliac joint,
lumbar spine) is hardly ever experienced in the foot alone.
Most commonly it involves the foot and the ankle, with
or without other parts of the lower limb. Only when the
clinical examination of the foot is completely negative
and the patient states that the foot pain is unaltered by walking, does the question of referred pain arise.
PAIN REFERRED FROM THE FOOT Because the foot is a distally located part of the body,
there is very little referred pain from lesions of the foot
(following the principles of referred pain). Therefore pain
in foot or ankle usually points fairly accurately to the site
of the lesion.
HISTORY Although the main question is the actual problem - where
the pain is now - it is best to try to obtain a chronological account, as summarized in Box 81.1. In order to work out
Box
8 1. 1
Summary of history-taking
What is the actual complaint? Onset Trauma No trauma
Evolution Better Worse Ups and downs
Present complaints Site of pain Influence of movements Nocturnal pain Twinges Instability Swelling
1171
1172 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
the problem systematically, the questions asked should follow the order given below.
•
When did the pain start?
subacute or chronic?
• How did it start?
• Is the pain felt at the beginning, during or after exertion? •
Is the problem acute,
•
raised heel with a horizontal surface relieves the
Was there an injury or not?
stress on these affected tissues and therefore relieves
the pain.
Further questioning should establish whether there are
What was the mechanism? What were the symptoms at that time?
Disability?
Pain? Swelling?
• What was their evolution over the following days?
'twinges' or instability: •
always be differentiated from'giving way'. In a
•
Did the pain come on suddenly or gradually?
•
What brought the pain on?
twinge, there is only momentary pain and not a
feeling of instability. By the time the patient realizes
Nothing special? Overuse?
it, the pain has disappeared. A twinge is very often an
Sometimes there will be some evolution in degree and
indication of a momentary impaction of a loose body
localization of pain, swelling and functional disability
in the ankle or subtalar joint. If localized in the fore
during the weeks or months after the onset.
foot, it can be a symptom of Morton's metatarsalgia
The examiner should also find out what sort of treat
ment the patient has already had, and what the results were.
Wiwt has been the evolution since the onset?
No
change? Gradually worse or gradually better? Ups
and downs, with complete or no recovery between
attacks? Do changes depend on exertion? • What sort of treatments did you have? • •
• • •
Where do you feel the pain now? Posterior, middle or
anterior segment? Medial, lateral or all over the
in sports. Normal walking or even rmming on a flat
surface hardly ever causes a feeling of giving way. In
the occasional case where this does happen, it is the
result of neurological weakness of the peronei muscles, rather than of a ligamentous lesion.
INSPECTION Inspection is first made in a standing position. The shape
of the legs is evaluated: valgus or varus deformity are
checked. The normal intermalleolar distance should not
indicates a high degree of inflammation.
normal, with an outward pointing of the toes of about
Is there pain at rest or during the night? Pain at night
exceed 5 cm. A slight outward rotation of the tibiae is
Is there long-standing morning stiffness? This also
15°. Exaggeration of this outwards rotation can be caused
What brings the pain on? Is there any pain during
during walking and running.
suggests a serious inflammatory disorder.
normal walking or normal running? Can you
of the foot, walking or running will always be the pro
voking activities:
Is there equal pain on walking and standing?
Can you walk on uneven surfaces? Because walking
upstairs and downstairs demands a normal mobility of the ankle joint, it is worth asking if the patient
can do so without problems. •
Do you have the feeling of instability? If so, describe it.
Real instability of the ankle or foot is only important
joint(s)?
Because foot disorders cause pain during the function
•
•
What are the problems now?
participate in your former sports?
•
or sesamoiditis.
What were the results?
The actual complaints should be investigated further: •
Do you have twinges, and when? A twinge in the foot is
a very important symptom. It is a sharp and sudden pain, mostly occurring during walking. It should
If there was no injury:
•
Sometimes an in-built wedge relieves or aggravates
the pain. In Achilles tendinitis or plantar fasciitis, a
If there was an injury: •
Does the pain depend on the sort of shoes you wear?
Is the pain provoked by particular movements?
by short calf muscles and results in a restricted step The shape of the feet in a standing position is studied
next. At the calcaneus there can be a valgus or varus
deformity.
The longitudinal arch of the foot is then estimated: a
cavus deformity or a flat foot may be identified. At the midtarsal region the shape and the regularity of the
bones is inspected and, at the forefoot, special attention is paid to the existence of an insufficient anterior arch,
hallux valgus, claw toes, hammer toes or metatarsus inversus.
After inspection in the standing position, it is some
times advisable to check the patient's gait and the wear to the shoes.
CHAPTER 81 - CLINICAL EXAMINATION
Inspection in the supine-lying position gives informa
tion about contours, shape, atrophy, colour of the skin,
swelling, oedema, haematoma, the condition of the skin
and nails and the existence of callosities.
Sometimes a second inspection in a standing position
may follow the routine functional examination, when
special attention should be paid to:
1173
RISING ON TIPTOE This movement (Fig. 81.1) is used to test the plantiflexor mechanism of the foot. If rising on
tiptoe hurts and resisted eversion and inversion remain
painless, the triceps muscle must be at fault. Because
plantiflexion is almost entirely performed by the contrac tion of the triceps, tiptoe rising will, in particular, test the
• Change of the shape of the foot during weight
integrity of triceps, the Achilles tendon and its insertion
• Which part of the foot comes under abnormal strain.
weak, painless or painful is noted.
bearing, in relation to the shape when lying.
• Changes in the colour of the skin (redness on
suspension and pallor on elevation point to arterial
insufficiency).
on the calcaneus. Whether the movement is strong or If tiptoe rising is painful, the following test distin
guishes between the soleus and the gastrocnemius
muscles. The patient lies prone and plantiflexion of the
foot is resisted, first with the knee fully extended, then
with the knee bent to a rightangle. Flexing the knee relaxes
FUNCTIONAL EXAMINATION The foot is the most difficult moving part of the body to
examine because a great number of strong structures,
both the gastrocnemii muscles but does not alter the pull
at the soleus muscle. Hence abolition of the pain when
the muscle is tested during knee flexion incriminates the gastrocnemius muscle.
with little individual mobility, are condensed into a small
volume. To test each structure in turn without the help of a lever is a very difficult task and demands great techni cal and manual ability.
In the foot the clinical tests consist of 18 movements
o
(see Box 81.2). Other than rising on tiptoe the clini-
cal examination is performed in the supine-lying posi tion. Consecutively, the ankle joint, the subtalar joint, the
midtarsal joints, the ligaments and the muscles are tested.
Box
8 1.2
Summary of movements of the foot
Rising on tiptoe Two tests for the ankle joint Plantiflexion Dorsiflexion Three ligamentous tests Mortice test Inversion Eversion Two tests for the subtalar joint Varus Valgus Six tests for the midtarsal joints Plantiflexion Dorsiflexion Adduction Abduction Pronation Supination Four resisted movements Plantiflexion Dorsiflexion Inversion Eversion Figure 81.1
Rising on tiptoe.
1 174 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
If rising on tiptoe is weak, a neurological lesion can be
to relax the gastrocnemii. In this position, the movement
the cause. Apart from the upper motor neurone lesions,
is brought to a stop by stretching of the posterior capsule
the cornmon cause of painless weakness is a first and
the talus and the anterior margin of the tibial surface. The
peroneal atrophy and direct injury to the sciatic nerve,
second sacral root palsy.
Tiptoe rising is also very important in the diagnosis of
of the joint and by bony engagement between the neck of end-feel of normal dorsiflexion at the ankle is soft.
Achilles tendon rupture. If the plantiflexor muscles are
examined in the supine-ly ing position only,
active
plantiflexion is not found to be lost, because the flexor
hallucis longus, the flexor digitorum longus, the tibialis posterior and the peronei remain intact.
TESTS FOR THE AN KLE JOIN T The ankle joint is a simple joint, allowing, in normal
circumstances, only plantiflexion and dorsiflexion. The
range of movement is measured by estimating the angle joined by the longitudinal axis of the tibia and the
dorsum of the foot.
Plantiflexion o
Normally an ankle can be plantiflexed until the
dorsal aspect of the foot falls into line with the leg
(Fig. 81.2). Plantiflexion is limited by the engagement of
the heel via the Achilles tendon against the back of the
tibia. Therefore the normal end-feel is soft.
LIG AMEN TOUS TESTS AT AN KLE AND FOOT Lateral ligaments o
To test the outer structures of ankle and foot, the examiner performs a strong inversion movement
during full plantiflexion. Inversion produces a combina
tion of varus at the subtalar joint and adduction/ supina
tion at the forefoot. This test stretches all the structures at
the outer and anterior side: the lateral ligaments of the ankle, the subtalar joint and the midtarsal joints, together
with the tendons of the peroneal and the extensor digito
rum longus muscles.
Technique. The ipsilateral hand of the examiner fixes the
leg at the distal and medial side (i.e. the left hand of the examiner on the right leg of the patient). The contralateral
hand is placed on the midfoot, so that the heel of the hand rests at the fifth metacarpal bone and the fingers encircle
the medial border. The heel of the hand now presses the
foot downwards and inwards. Meanwhile supination is
performed by an upwards pulling of the fingers at the
Dorsiflexion o
Normally the ankle can be moved to reduce the
medial border (Fig. 81.3).
Because there are considerable differences between
angle between the dorsum of the foot and the tibia
individuals in the range of this movement, both sides
limited by the length of the calf muscles. Therefore
of movement, the pain and the end-feel. The normal
to less than 90°. Occasionally, the range of dorsiflexion is dorsiflexion is performed with the knee slightly bent so as
end-feel is soft.
(b)
(a) Figure 81.2
should be compared. A note is made of the range
Passive plantiflexion (a) and dorsiflexion (b).
CHAPTER 81 - CLINICAL EXAMINATION 1175
Figure 81.3
Testing the lateral ligaments.
Figure 81.4
Testing the medial ligaments.
talofibular or the calcaneofibular ligaments, this test will
Medial ligaments o
A combined test is used: full plantiflexion at the
also be positive. Differentiation should then be made using the anterior drawer test (see p. 1231).
ankle joint, together with valgus at the subtalar
Technique. The ipsilateral hand fixes the patient's leg at
These movements stretch the anterior and middle
hand is important, both to give counterpressure and to
ament and the calcaneonavicular ligament. At the outer
lateral hand grasps the foot at the heel and forces it
joint and abduction-pronation at the midtarsal joint.
portion of the deltoid ligament, the anterior tibiotalar lig
side, however, the posterior talofibular ligament can become painfully squeezed.
Technique. With the contralateral hand, the examiner fixes the patient's lower leg at the distal and lateral side.
The ipsilateral hand encircles the midfoot. The hand lies
on the first metatarsal and the fingers encircle the lateral
border. The hand forces the foot into plantiflexion and
valgus. Meanwhile the fingers provide a pronation move ment (Fig. 81.4).
The thick deltoid ligament and the architecture of the
midfoot make the foot very firm in this direction.
Therefore, not much movement is achieved during this
combined test. The normal end-feel is soft.
Tibiofibular ligaments
its inner side, just above the ankle. This position of the detect the click when pressure is released. The contra with a strong and quick thrust into varus (Fig. 81.5).
MOBILITY OF THE SUBTALAR JOIN T Varus and valgus In order to move the calcaneus on the talus, the examiner
must try to avoid any movement at the ankle joint.
Because the width of the trochlear surface of the talus is
smaller posteriorly than anteriorly, the medial and lateral surfaces of the body of the talus are gripped tightly
during dorsiflexion of the ankle. Therefore the ankle
must be forced into and kept in full dorsiflexion during varus-valgus movements. o
Technique. The heel is firmly grasped between the two hands, the fingers clasped behind the heel.
A strong varus movement applied to the talus held
Dorsiflexion is performed by traction on the heel (Fig.
between the two malleoli, so testing the integrity of the
little mobility, and because it is hardly possible to obtain
o
in a neutral position forces this bone as a wedge
81.6). Because the test involves a very strong joint, with
distal tibiofibular ligaments. In a normal 'mortice', the
any leverage, the examiner must keep the heel as steady
prevent separation of the tibia and fibula. When there is
possible to gain a good idea of the range of motion.
outwards, a circumstance that is detected by a palpable
Mobility should always be compared with the other side
strong tibiofibular and lateral collateral ligaments
ligamentous rupture or laxity, the fibula can be pressed
click when the tibia and the fibula engage after their
momentary separation. In a total rupture of the anterior
as possible. By swinging the upper half of the body, it is A normal varus-valgus range is between 20 and 45°.
and the normal end-feel is soft. The varus movement also
tests the integrity of the calcaneofibular ligament.
1176 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
Figure 81.5
Testing the tibiofibular ligaments (the 'mortice' test).
Pronation and supination also examine the inner and
PASSIVE TESTS FOR THE MIDTARSAL JOIN TS Flexion-extension, pronation-supination, abduction-adduction Because the middle segment of the foot consists of several
bones and joints, it is very difficult to assess isolated
movement at the various joints. Therefore Cyriax consid
ered the whole middle segment as one integrated struc ture - the midtarsal joint.
Because of anatomical characteristics, plantiflexion is
outer ligaments of the midfoot. Pronation tests the
plantar calcaneonavicular ligament, whereas supination
and adduction bring the calcaneocuboid ligament and
the ligaments between cuboid and fifth metatarsal under stress. o
Technique. First, the posterior segment (ankle and subtalar joints) must be stabilized. Therefore, the
examiner uses the contralateral hand to pull strongly on
often accompanied by some adduction and dorsiflexion
the heel and force it into valgus. The traction forces the
(a)
(b)
by some abduction (see p. 1164).
Figure 81.6
Varus (a) and valgus (b).
talus into the dorsiflexed position between both the
CHAPTER 81 - CLINICAL EXAMINATION 1177
malleoli, thus immobilizing the ankle joint, and the
dorsiflexion in the foot by a simple pronation-supina
valgus position fixes the subtalar joint.
tion movement of his arm. An adduction-abduction
thumb comes to lie under the metatarsal heads and the
movement of the wrist and pronation-supination by
position, the examiner can easily perform plantiflexion-
the range of movement varies considerably between
The ipsilateral hand encircles the forefoot, so that the
fingers at the dorsum of the metatarsal shafts. In this
movement is achieved by an adduction-abduction
a flexion-extension movement (Fig. 81.7). Although
(a)
(b)
(c) Figure 81.7
Extension and fiexion (a), abduction and adduction (b), pronation and supination (c).
1178 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
individuals, it is surprising how much movement the
muscles. In order to avoid a false result, it is absolutely
The end-feel in flexion-extension and in abduc
tion. Therefore a good immobilization technique is of
normal midtarsal joints allow.
tion-adduction is rather hard, whereas the end-feel in both
rotations is soft.
RESISTED MOVEMENTS Resisted tests are alway s performed in a neutral position.
No active movement of the joint is allowed. The examiner
tries to evoke pure isometric contractions of the tested
essential to keep the joint immobile during the contrac
great importance, especially when inversion and eversion are to be tested against resistance. o
eversion, the patient's leg is immobilized by the
examiner's ipsilateral hand, placed at the medial and distal end of the leg. The examiner uses the contralateral
hand to give counterpressure at the lateral border of the
foot (Fig. 81.8).
(a)
(b) Figure 81.8
Technique. To stabilize the foot during resisted
Resisted dorsiflexion and plantiflexion (a), and eversion and inversion (b).
CHAPTER 81
During resisted inversion the reverse is done: the
, contralateral hand fixes the leg at the distal lateral
-
CLINICAL EXAMINATION 1179
Cases with pain but a normal examination
It is possible for a foot to hurt and yet appear normal on
side and the ipsilateral hand, placed at the inner border,
clinical examination, probably because the momentary
Resisted dorsiflexion tests the tibialis anterior,
This happens particularly in athletes and ballet dancers
gives counterpressure.
extensor hallucis longus, extensor digitorum longus
and the peroneus tertius. o
The plantiflexor muscles tested are the triceps
stress of the manual testing is insufficient to evoke pain.
who get pain after exertion, i.e. after a strain far greater
than any examiner can impose on the foot by mere
clinical testing. In such cases, patients should get off the
surae, tibialis posterior, flexor hallucis longus,
couch to demonstrate in the standing position which
Resisted eversion tests the integrity of the peronei
during or after training or exertion, the patient is asked
flexor digitorum longus and peronei brevis and longus.
muscles but also the peroneus tertius and extensor digitorum longus.
Inversion against resistance tests the tibialis posterior
and anterior, together with the flexor and extensor hallucis longus, and slightly tests the triceps surae.
particular movements hurt. If the pain only appears
to return when the pain has been provoked.
Clinical examination of the lower leg, ankle and foot is
summarized in Box 81.3.
Box
81.3
Summary of clinical examination
History Inspection ACCESSORY EXAMINATION Valgus under dorsiflexion Forcing the heel into valgus and in dorsiflexion is the
only way to reproduce pain in cases of a traumatic
periostitis at the anteroinferior surface of the fibula.
Examination of the toes
Passive and resisted examination of the big toe and the
outer four metatarsophalangeal joints is performed when a lesion at the forefoot or at the toes is suspected.
Anterior drawer test This tests the integrity of the anterior talofibular ligament (see p. 1231).
Functional examination Rising on tiptoe Ankle joint Plantiflexion Dorsiflexion Ligamentous tests Mortice Lateral ligaments Medial ligaments Subtalar joint Varus Valgus
Midtarsal joints Plantiflexion Dorsiflexion Abduction Adduction Supination Pronation Resisted movements Plantiflexion Dorsiflexion Inversion Eversion
Accessory tests Combined movements Examination of the toes Instability tests
THIS PAGE INTENTIONALLY LEFT BLANK
Interpretation of the clinical examination of the lower leg, ankle and foot 1---------------..'" Haemarthrosis
L Rheumatoid-type arthritis L Osteoarthrosis
..------- Immobilizational stiffness ...------- Loose body in the ankle joint Interpretation of the clinical examination of the ankle
I-------_ Sprain of talofibular ligament Sprain of anterior tibiotalar ligament Achilles bursitis Dancer's heel Pinching os trigonum Anterior periostitis Sprain of posterior talofibular ligament Jumper's sprain Tennis leg Achilles tendinitis Achilles tenovaginitis Calcaneus apophysitis (Peroneus lesion) Flexor digitorum lesion Tibialis posterior lesion Flexor hallucis lesion
Resisted movements are positive
Achilles tendon rupture
Contractile structures
S1 root lesion Tibialis anterior lesion Extensor hallucis lesion Extensor digitorum lesion Tenosynovitis of dorsiflexors Myosynovitis of tibialis anterior Tight fascial compartment syndrome L4 root lesion
Tibialis anterior tendinitis Tibialis posterior tendinitis 'Shin splint' Rupture of tibialis posterior L4 (LS) root lesions Peroneal nerve lesion Tibial nerve lesion Peroneal tendinitis
Resisted eversion is positive
1181
1182 SECTION TWELVE - THE HIP AND BUnOCK
Ligamentous lesions
E
Interpretation of the clinical examination at the subtalar joint Arthritis
Tibiofibular ligament Deltoid ligament Jumper's sprain
1------------... Rheumatoid disorders
L Subacute traumatic arthritis L Arthrosis
'--____.... :1
E
�
Immobilizational stiffness Loose body Psychoneurosis
1--------------------------'1"" Plantar fasciitis Plantar fascial tear Heel pad syndrome Haglund's disease Subcutaneous bursitis
I------ Instability
Arthritis
Interpretation of the clinical examination of the midtarsal joints
E
�
Subacute arthritis in adolescence Subacute arthritis in middle age Rheumatoid-type arthritis
1---------"'11'"' Late stage of midtarsal strain Midtarsal ligamentous contracture Aseptic necrosis of navicular bone Navicular stress fracture Cuboid rotation
E
Ligamentous lesions Midtarsal strain Periostitis
------ Midtarsal
strain
CHAPTER CONTENTS Bone disorders
Disorders of the lower leg
11 B6
lesions of the plantiflexors
1186
Pain 1186 Weakness 1193 Short plantiflexor muscles lesions of the dorsiflexors
1193
1195
Pain 1195 Weakness 1196 lesions of the invertors
1197
Pain 1197 Weakness 1199 lesions of the evertors
BONE DISORDERS 1199
Pain 1199 Weakness 1200 Disorders causing neurological weakness of the foot
1201
Because this book covers 'non-osseous' lesions of the moving parts of the body, not much attention will be paid to bone disorders. For differential diagnostic reasons, however, it is as well to bear in mind that, if the patient complains of continuous localized pain, without special clinical findings during functional examination, the pos sibility of a bone disorder should be considered and a radiograph or a bone scan obtained. Paget's disease, metastases, primary bony tumours and osteomyelitis are possibilities. Children between the ages of 6 and 11 years who com plain of diffuse pain in the legs but with a normal clinical examination are very often regarded as suffering from 'growing pains'. Paediatricians' estimates of the fre quency of this diagnosis vary from 4%1 to 20%2 of all children. During recent decades, several hypotheses have been put forward but none gives a good explanation for the symptoms. As it occurs between the ages of 6 and 12, which is not the period of maximum rate of growth, 'growing' cannot be the real reason for the pain. Whatever the origin of the pain it disappears sponta neously and completely after the age of 12 years.3
LESIONS OF THE PLANTIFLEXORS
During rising on tiptoe, which is still the best test of integrity of the plantiflexor mechanism, the examiner notes if there is any pain or weakness. PAIN Tennis leg
This is the common term to describe a tear in the triceps. It occurs most often in the medial belly of the gastroc nemius muscle, usually some 5 cm above the musculo tendinous junction.4 The disorder was first described by Hood in 1884.5 For decades it has been regarded as a ruptured plantaris tendon6,7 but careful clinical examination of patients suffering from this disorder shows this to be false.8 1183
1 184 SECTION FOURTEEN - THE LOWER LEG, AN K LE AND FOOT
The history is quite simple. During a vigorous contrac tion, for example starting to sprint, pushing a car or lifting a heavy weight, the patient experienced a sudden severe pain in the calf. From that moment, the patient was unable to dorsiflex the foot during walking. Therefore, it was necessary to tiptoe on the affected side. Examination reveals pain during resisted plantiflexion but no weakness. In the supine-lying position, dorsi flexion at the ankle is found to be markedly limited when the knee is in the extended position but becomes normal when the knee is flexed. This implicates the gastrocnemius muscle, part of which is in spasm around the tear. The difference in range between a flexed and an extended knee in a disorder of the gastrocnemius muscle is another example of the constant-length phenomenon. Were the plantaris tendon ruptured, the foot would not be fixed in plantiflexion nor would resisted plantiflexion be painful. Palpation of the calf reveals the tender area in the medial gastrocnemius, with either swelling and haematoma if the lesion is recent or induration around the tear if it is old. After a severe rupture, it is possible to palpate the gap in the medial gastrocnemius. Ultrasonography is the imaging technique of choice to demonstrate size and grade of the lesion.9,l o Differential diagnosis. Although the diagnosis is obvious, it is as well to bear in mind some other possibilities.
Although the similar onset and localization of the pain can cause diag nostic confusion, if a proper clinical examination is done this condition should hardly be a problem. Weak resisted plantiflexion and no spasm during the passive dorsiflexion in a ruptured Achilles tendon contrast with the findings in tennis leg.11,12 If there is doubt a simple test can be done, as follows.13 The patient lies prone, the foot hanging over the edge of the couch. The examiner squeezes the calf muscles. If the Achilles tendon is intact, the foot moves into plantar flexion. When there is total rupture, no movement results.
A high rupture of the Achilles tendon.
Deep venous thrombosis in the calf muscles. Differential diagnosis from this condition is very important. Instances have been described of patients with tennis leg receiving anticoagulants, which aggravated their condition.14 The main historical difference is in the onset. In deep venous thrombosis the pain appears after immobilization or after sitting for a couple of hours,lS and not during a vigorous contraction of the calf muscles. Clinical examination does not show limited passive dorsiflexion, although passive dorsiflexion and resisted plantiflexion can be painful. The calf muscle and leg are swollen and the foot becomes oedematous because of obstruction to venous return. Palpation of the tender spot shows other differences: in thrombosis the whole calf muscle is painful to the touch
and sometimes a painful 'string' can be palpated deep within it. 1 6, 17 Rupture of a Baker's cyst. In long-standing rheumatoid arthritis of the knee, chronic distension with fluid can weaken the posterior ligaments and during exertion these can rupture. Sudden pain in the knee, followed by swelling of the leg and oedema of the ankle, strongly suggest venous thrombosis.18 Here the long-standing rheumatoid arthritis and the absence of an injury suggest the diagnosis, which can be confirmed by arthrography. Intermittent claudication. The history is characteristic: pain in one calf is brought on by walking and relieved by rest. Routine clinical examination reveals nothing. Diminished or absent pulsations at the dorsalis artery of the foot and posterior tibial artery may be found. Angiography confirms the diagnosis. Posterior compartment syndrome. The patient, usually a young man, reports an ache and swelling in the calf some hours after an unaccustomed exercise. Walking is uncom fortable and increases the swelling. Examination shows that rising on tiptoe is not difficult and is scarcely uncom fortable. The calf is diffusely swollen and the skin is red and warm to the touch. Passive dorsiflexion of the foot is severely limited by loss of elasticity of the calf muscles. Palpation reveals uniform tenderness of the whole calf muscle without any localized tender area.19 The symp toms result from muscle ischaemia, produced by increased tissue fluid pressure in the closed fascial com partment. The difference from the tennis leg is in the discrepancy between marked restriction of passive dorsiflexion and the almost painless tiptoe rising. Treatment is surgical division of the deep fascia. Referred pain to the calf. This is most frequently the consequence of a compression of the Sl nerve root, whether by a primary posterolateral protrusion of nuclear substance at the fifth lumbar level in a younger patient, or by a compression in a narrowed lateral recess in an older one. W hen these conditions are suspected, a careful history must be taken and a clinical examination of the lumbar spine must be performed. Positive findings during the lumbar examination, together with painless tiptoe rising, confirm the diagnosis.
Different types of treatment have been advo cated for tennis leg. Most authorities advise partial or total immobilization for small tears20 And surgical suture for serious ruptures.21 ,22 In our opinion, surgery for this condition is scarcely ever necessary and partial or total immobilizatio� by plaster cast or strapping is obsolete. When such treat ment is instituted, the formation of a chronic adherent
Treatment.
CHAPTER 83 - DISORDERS OF THE LOWER LEG 1185
scar is favoured, which results in disability lasting seve'ral months. The aim of treatment in muscle tears is to allow the torn fibres to heal in such a way that mobile and functional scar tissue is formed. If the normal enlargement of the muscle is impaired by adhesions, a self-perpetuating inflammation will be the result. Muscle belly lesions (tennis leg is an excellent example) therefore need a different and more functional approach. The aim must be to restore normal movement in the damaged muscle as quickly as possible. This can be done by combined treatment: aspiration and infiltra tion with local anaesthetic as soon as the patient is seen, followed by deep transverse friction and electrically stimulated or active contractions of the muscle during the following days. During the recovery period the muscle must be protected by a raised heel, which enables the patient to use the unaffected parts of the gastrocnemius without strain on the line of healing. Technique: infiltration. As soon as the patient is seen - whether it is the day of the accident or some weeks or months later -- local anaesthesia is induced at the site of the partial rupture. The patient lies prone, the knee slightly bent and the foot plantiflexed, to allow maximal relaxation of the muscle. The tender spot is located and gripped between thumb and index finger (Fig. 83.1). If there is any fluctuation an attempt is made to aspirate the haematoma. Having done that, 30-50 ml of procaine 0.5% is injected following the usual infiltration tech niques. Because the spot is never precisely localized (gentle pressure does not disclose tenderness in the deeper part of the muscle, whereas strong pressure is apt to hurt throughout the belly) and the gastrocnemius muscle is a large structure, up to 50 ml of a 0.5% solution may be required.
After the injection pain ceases and a much greater range of passive dorsiflexion at the foot becomes possible within a few minutes. This suggests that the previous limitation was the result of spasm of the muscle. The patient is encouraged to move the foot further up and down while lying on the couch. Never allow the patient to
stand up and to take weight on the affected leg after the injec tion, because this might lead to a further tear. A raised heel pad must be given before standing and walking. W hile the patient is practising the non weight-bearing movements, a cork pad should be made and fitted into the shoe. By taking the weight on the raised heel, the patient will be able to use the unaffected parts of the temporarily shortened muscle, without straining the healing breach. For the first few days, a heel pad of 3-4 cm may be needed. Thereafter, as treatment and cure proceed, the height is reduced until it becomes unnecessary. Raised heel.
Technique: friction and electric contractions. The day after the injection, the patient is given the first session of deep friction and electric stimulation to the muscle. The patient lies prone with the foot fully plantiflexed. The therapist sits at the level of the patient's leg. The fingers are placed at one side of the affected area and the thumb at the opposite side of the leg so as to give coun terpressure. The other hand eventually reinforces the pal pating one (Fig. 83.2). Transverse friction starts deeply. By drawing the fingers upwards over the affected area, the therapist feels the muscle fibres escape from the grip until only skin and subcutaneous tissue remain. In the second stage, the fingers are slightly relaxed and moved back wards into the previous deep position, where the same movement starts again. The procedure is continued for
I
f
Figure 83.1
Infiltra tion with local anaesthesia in tennis leg.
Figure 83.2
Deep friction to the gastrocnemius muscle.
1186 SECTION FOURTEEN - THE LOWER LEG, AN KLE AND FOOT
about 15 minutes. During friction the fingers do not move in relation to the skin - fingers and skin move as a unit over the muscle fibres. At first, massage is given gently. After 5-10 minutes, friction can be deeper and firmer but must always remain comfortable. After each session of massage, the muscle is given elec trical stimulation and active contractions for about 10 minutes with the knee in the flexed and the foot in the plantiflexed position. Deep friction prevents transverse scar tissue formation. Electrically stimulated contractions ensure expansion in the muscle belly without tension on the line of healing. Massage and electrical stimulation are given daily for the first few days and then three times a week, and for a week after symptoms cease, so as to prevent recurrences. The diagnosis and treatment of tennis leg is summa rized in Box 83.1. Results. When the patient is seen within the first few days of trauma and this scheme of treatment is followed, one can expect a restart of normal sports activities after 3 weeks. A patient who presents with a palpable gap in the muscle belly is sometimes referred for surgery. However, in our opinion, surgery is seldom required when a muscle belly is torn. This contrasts with a tendinous rupture say of the Achilles tendon - which often calls for surgical intervention.
condition and it then starts after some unaccustomed exertion or after a long walk in inappropriate shoes. Nevertheless, most often it occurs in long-distance runners, and it comes as no surprise that the increase in the number of people running during the past decades has been paralleled by an increase in the number of cases of inflamed Achilles tendon.24,25 During the Olympic games in Melbourne in the 1960s, Achilles tendonitis was so frequent among the athletes that it was called the 'Olympic disease'.26 The site of the lesion lies usually at mid-tendon. Occasionally, the strain occurs level with the upper border of the calcaneus or, very rarely, at the musculo tendinous junction. Achilles tendinitis is multifactorial and usually the outcome of a combination of anatomical and biomechanical characteristics, along with poor train ing technique.27 The most important aetiological factors are short triceps (decreased touchdown angle), poor stretching habits and increased plantar flexion peak torque.28, 29 Some authors suggest that there might also be a vascular factor furthering the condition.30,31 The arguments for a vascular origin are: •
•
•
Achilles tendonitis
Tendinitis of the Achilles tendon is chiefly a runner's problem.23 Non-sporting people can also suffer from this
Box 83.1
Summary of tennis leg
Diagnosis Acute onset L i m itation of dorsiflexion Pa i nful ti ptoe raise Typical localization of pa i n and tenderness
Differential diagnosis H i g h r u pt u re of the Ach i l les tendon Deep venous thrombosis R u pture of Baker's cyst Interm ittent claud ication Ischaemic contracture Referred pa i n
(51)
Treatment Infi ltration with local a naesthetic +
Heel pad
Deep friction d a i ly d u r i n g the fi rst week +
E l ectrica l ly st i m u lated and active contractions
Deep friction t h re e t i m es a week +
Electrica l l y sti m u lated and active contractions
The usual site of the lesion is at the junction of the two vascular systems of the tendon: the calcaneus and muscle tissue.32,33 Calcifications of the posterior tibial artery have frequently been seen during operations on Achilles tendinitis. The onset is sudden in most cases.
During the last decade, fluoroquinolone antibiotics have been implicated in the aetiology of Achilles tendini tis and subsequent tendon rupture.34-37 The history in Achilles tendinitis is quite simple. The patient states that the heel aches during or after walking or running (stage I). Sometimes there is pain at the begin ning of exertion, improving after a while and reappearing on fatigue (stage II). Alternatively, there is continuous and worsening pain during exercise (stage III). Sometimes the pain does not cease after the exertion but continues at rest (stage IV). As a rule, however, pain eases at rest and increases on running or walking. Nocturnal pain is absent. Clinical examination shows rising on tiptoe to be painful although in minor cases the pain is only evoked by repetitive tiptoe rising. The rest of the functional examination is completely negative except in lesions at the tenoperiosteal junction, where full plantiflexion hurts slightly in that this squeezes the affected part of the tendon between the posterior aspect of the tibia and the upper surface of the calcaneum. Because we advocate deep transverse friction as the most effective conservative treatment for this disorder and massage only acts where it is applied, the tendon
CHAPTER 83 - DISORDERS OF THE LOWER LEG 1187
should be palpated very carefully to discover all the tender areas, because there may be more than one. The lesion nearly always lies at the inner or outer, or both, aspects of the tendon. Sometimes the anterior surface is affected, almost never the posterior. Most of the lesions lie 2-6 cm above the tenoperiosteal junction -- the area of reduced vascularization.38 The morphological and macroscopic changes in the condition are not always the same. Observations during surgery have led to the description of two separate macroscopic types: •
•
Peritendinitis: the inflammatory changes are confined to the peritenon, which is thickened and shows inflammatory changes, with considerable connective tissue proliferation and adhesions between peritendineum and tendon.39 Tendinosis: this is characterized by inflammatory and degenerative changes in the tendon tissue itself.4o Sometimes partial ruptures of deeply situated fibres can be seen, with the superficial parts of the tendon remaining intact. Here there is a visible and palpable enlargement at the tendon from the structural changes of chronic fibrosis.41
Treatment.
There are a number of approaches.
Rest, raising the heel, application of ice and stretching.
These comprise most of the treatments proposed in the recent literature. All may produce some benefit. Relative rest and a raised heel are wise because they allow the con tractile structure to heal. Ice is a good anti-inflammatory device and stretching seems to play a preventive role after the tendinitis has healed. None of these therapies, however, addresses the problem of adhesions in and around the tendon, which are in our opinion the main reasons for the self-perpetu ating inflammation, causing the Achilles tendinitis. Steroid injection. Most authors state that injections with corticosteroids give disappointing results. First of all, the lesion is too extensive for thorough infiltrations but even if infiltration is successful it seems to be followed by relapses weeks or months later. Furthermore, because the local steroid is injected into a very poorly vascularized structure, this procedure can be dangerous, especially if the wrong dose and wrong infiltration technique are used.42 Several reports demonstrate a higher risk for tendon ruptures, following multiple and repeated steroid injections.43-47 However, it should be remembered that not just the product itself but the wrong technique and the wrong dosage have to be blamed for these disastrous outcomes. In Achilles tendinitis, the injection is never made into the body of the tendon but along the surface, between tendon and peritendineum. After the injection the patient should avoid all exercises during the first 10
days, after which a training programme can gradually be resumed. The injection can be repeated once if there is no cure after 2 weeks. If this procedure is followed and the correct technique as set out below is used, postinfiltration ruptures are not to be feared.48 Technique: injection. The patient lies prone on a couch. The foot is forced into dorsiflexion over the edge of the couch. This stretches the tendon, which facilitates the pal pation of the affected area. A 2 ml syringe is filled with 20 mg triamcinolone. A 5 cm needle is fitted and intro duced some 3 cm away from the lesion. It is pushed through the skin and moved either upwards or down wards, parallel to the tendon, until the tip reaches the distal edge of the lesion. A small injection is given while the needle is drawn back along the surface of the tendon (Fig. 83.3); the manoeuvre is repeated four or five times, each time a little to one side of the previous infiltration line. If the tip of the needle stays superficial to the tendon, no particular resistance to the plunger will be felt during the injection.
Operative treatment should only be considered in long-standing cases when rest and conservative treat ment (deep transverse friction) have failed. The surgical procedures performed depend entirely on the underlying pathological features. In simple peritendinitis, the crural fascia and the paratenon are split longitudinally from the musculotendi nous junction to the insertion on the calcaneus and adhe sions between the tendon and the sheath are released.49 In cases with focal tendinosis and partial rupture of the tendon, the diseased area of the tendon is excised and the tendon repaired by side-to-side suture of the remaining tendinous fibres.50 Where excision of the degenerated tissue disrupts the continuity of the tendon, the tendon is reconstructed and reinforced with the fascia of the gastrocnemius.51 If there is extensive tendinitis, excessive scar tissue is excised.52 Some authors claim better results if carbon fibres are implanted between the tendinous straps.53 Postoperative care involves between 1 and 4 weeks of non-weight bearing, followed by 1-4 weeks of partial to full weight bearing, depending on the severity of the lesion and the type of surgical intervention. Results are good to excellent in about 85% of cases.54,55 Surgery.
Deep friction to the Achilles tendon. This was intro duced more than 40 years ago by Cyriax56 and is, in our opinion, the best conservative treatment for the condi tion, provide it is given correctly: (a) at the right point, (b) with a good friction technique, (c) 20 minutes per session and (d) at regular intervals (three times a week). During the period of treatment the patient must take relative rest.
1188 SECTION FOURTEEN - THE LOWER LEG, AN KLE AND FOOT
depending on the extent of the lesion (' a' in Fig. 83.4). Slight pressure under the tendon is exerted and the hand is drawn upwards until the fingers slip towards the pos terior aspect of the tendon ('b' in Fig. 83.4). At the final stage of this, only skin remains between the two grasping fingers. The pressure is now slightly released and the fingers are pushed downwards until they lie at the start ing position ('a') and the whole procedure can be repeated. The cycle is repeated for about 15 minutes. During friction, fingers and skin are moved as a whole over the tendon. Should there be movement between the patient's skin and the therapist's fingers, the friction will be imparted to the patient's skin and, if vigorous, will very soon raise a blister. Friction must be given with sufficient transverse sweep, which means that the amplitude of the to-and-fro movements must be large enough to ensure that the frictional element is paramount. Only thus can effective separation of each fibre from its neighbour be ensured. Although deep friction to the Achilles tendon, espe cially at first, is uncomfortable for the patient, is should never be intolerably painful. The true art is to give enough friction without too much pressure. The fact that massage is painful is no guarantee that it is correctly given. Technique: friction to the anterior part of the tendon.
Figure 83.3 Steroid infiltration parallel to the surface of the tendon in Achilles tendinitis.
Technique: friction to the medial and lateral edge of the
The patient lies face downwards on a low couch, with the foot projecting just beyond the edge of the couch. The therapist sits at the foot and pushes the sole into dorsiflexion through a slight pressure of the con tralateral knee. At the right point the tendon is grasped between finger and the thumb, or two fingers and thumb, tendon.
This localization should always be sought in addition to other tender spots. The patient lies face downwards on the couch but further up the couch than in the previous technique, in order to allow a full plantiflexion position of the foot. The relaxed tendon then has good mediolatern1 mobil ity. With one thumb at the opposite side, the examiner pushes the tendon over sideways, as far as it will go. The anterior aspect of the opposite side of the tendon can now be reached with the tip of the ring finger of the other hand. The ring finger is reinforced by the long finger, while the little finger is kept out of the way in order not to disturb the pronation-supination move ment. This movement is carried out with the elbow flexed and with the finger, hand and forearm in a straight line with the patient's leg. Once again friction is given in two phases. First, the fingertip is placed deeply under the tendon with the forearm in a slightly pronated position ('a' in Fig. 83.5). Pressure is exerted in a dorsal and medial direction; meanwhile the arm moves in full supination, until the lateral fibres escape under the fingertip ('b' in Fig. 83.5). Caution is taken not to move the finger on the skin but rather to move the skin and the fingertip as a whole. Now pressure is slightly released and the fingertips re-placed in the former position ('a'), so that the whole procedure can be repeated. The to-and-fro movements are per-
CHAPTER 83
(a)
-
DISORDERS OF THE LOWER LEG 1189
(b)
(a)
Figure 83.5
(b)
Deep friction to the anterior aspect of the Achilles tend on.
Technique: friction to the tenoperiosteal insertion of the
A lesion at the tenoperiosteal insertion lies level with the upper surface of the calcaneus. As in the earlier technique, the tendon must be relaxed; therefore the patient moves upwards on the couch to bring the foot into full plantiflexion. The tendon is compressed between the therapist's fingers and the upper surface of the calcaneus. Using both hands, a circle is made round the heel with one index finger, reinforced by the other, at the lesion. Both thumbs cross at the plantar surface. Pressing downwards squeezes the tendon between the fingers and the calca neus. Deep friction is performed by moving the forearms in opposite directions. The amplitude of the movement must be large enough to reach the whole width of the tendon (Fig. 83.6).
tendon.
Figure 83.4
Deep friction to the medial and lateral ed ge of the Achilles tendon.
formed for 15 minutes. The fingers must not be allowed to glide on the skin, to avoid the formation of a blister. During the whole procedure, there must be sufficient sweep, which can be achieved by a good pronation supination movement at the elbow.
1190 SECTION FOU RTEEN - THE LOWER LEG, AN K LE AND FOOT
method of prevention but, in our experience, has no therapeutic value. Achilles tenovaginitis
Although the Achilles tendon does not have a sheath, inflammation can sometimes take place between the tendon and the peritenon and create a so-called teno vaginitis of the Achilles tendon. This can take two forms: rheumatoid and xanthomatous. Rheumatoid arthritis and ankylosing spondylitis. In these conditions, the contrast between the slight symp toms and the marked signs is striking. It should also be remembered that gout can sometimes affect the Achilles tendon. The main complaint is not, as in tendinitis, pain during contraction of the triceps but pain during local pressure -- catching the heel against the border of the shoe. Examination shows that rising on tiptoe is indeed merely uncomfortable rather than painful but the tendon is warm, swollen and very tender to the touCh.61 ,62 Local treatment consists of infiltration with 20 mg of triamci nolone between the sheath and the tendon. The technique is the same as described for Achilles tendinitis.
Figure 83.6
Deep friction to the insertion of the Achilles tendon.
Provided massage is given at the right point and the technique is adequate, the results of deep transverse friction are good. Usually a schedule of 15 minu tes, three times a week over 2--4 weeks, is required. In the meantime, the patient should not run or walk further than necessary. The only failures are in nodular scarring around an old partial rupture. Our experience is that Achilles tendinitis with macroscopic fibrous changes in the deep layers of the tendon often remains refractory to conservative treatment, whereas superficial lesions without palpable changes respond quite well to friction. Results of deep friction.
Prevention. Raised heels, shock-absorbing heels and cor rection of a valgus deformity are usually prescribed.57 Because the triceps is also a slight invertor, a valgus deformity must always be corrected to relieve excessive strain on the tendon.58 Although these measures are certainly beneficial, it must be remembered that they are prescribed only for prevention, because they do not provoke substantial and histological changes at the site of adhesions. Many authors pay much attention to the preventive value of stretching exercises before running.59,60 Although they may have such value, one must not over estimate the worth of stretching techniques when they are used as therapy in actual lesions. Stretching is a good
Xanthomatous tenovaginitis. The Achilles tendon is a common site for xanthomatous lesions. Similar swel1ings can be seen and palpated at the extensor tendons on the dorsum of both hands or occasionally on the tendons crossing the dorsum of the foot and on a line at the upper part of the ulna and tibia. Small nodules can also be seen in the upper eyelids. There is only slight discomfort during walking and tiptoe rising is painless. Both tendons can be seen to be thickened, and palpation reveals enlargement and diffuse nodularity. The nodules are painless to the touch. Treatment consists of restoring normal lipid metabo lism with clofibrate 1.5 g daily, or fenofibrate 300 mg daily.
Calcaneus apophysitis
Apophysitis of the calcaneus (Sever's disease, Osgood's disease) occurs in boys between 6 and 12 years of age and is often bilateral. The disorder has been classified among the general osteochondrosis syndromes, such as Legg Calve-Perthes disease at the hip or Osgood-Schlatter disease at the tibial tuberosity. The child complains of a sharp pain in the heel, occurring during contraction of the triceps. The pain starts suddenly, can last a couple of hours or days, and may disappear and reappear. Rising on tiptoe can be negative but the bone is usually tender to the touch. The radiological appearances are characteristic - 'slight fragmentation of the apophysis' - and confirm the diagnosis. Spontaneous recovery occurs in a yea; or two, often with the development of a slight permanent prominence on the posterior aspect of the calcaneus.63
CHAPTER 83
There is no treatment except relative rest, slightly . . ral smg the heel and inserting shock-absorbing heel pads in the shoe.64
WEAKNESS
Weakness of the plantiflexor mechanism is detected by the inability to rise on tiptoe. Apart from neurological lesions, which are discussed at the end of this chapter, the commonest cause of weak ness is a rupture of the Achilles tendon, most frequent in athletes over 30 years of age.65 The tear lies in the 'critical zone of poor vascularization' which is 2-6 cm above the calcaneal insertion.66 It is surprising that this simple and easy to detect condition very often remains undiagnosed for a time. Between 30 and 41% of Achilles tendon ruptures remain undiagnosed for more than 2 weeks.31,67,68 The history is typical. During a sudden contraction for example starting or during a sprint, lifting a heavy object or pushing a car - the patient hurts the heel. There is a snap, followed by a dull pain in the heel. This eases fairly quickly but, from this time on, the patient finds that only hobbling on a flat floor is possible. Alternatively, there may have been no sudden contraction of the triceps but a severe elongation caused by an excessive and sudden dorsiflexion at the ankle. When the patient lies on the couch, the clinical exami nation reveals little. There is usually no haematoma or visible thickening. Passive movements are painless. An alert examiner will probably detect an excessive range of dorsiflexion. In the supine, non-weight-bearing position, resisted plantiflexion remains possible because the plan taris, flexor hallucis longus and flexor digitorum muscles still contract. Rising on tiptoe, however, immediately reveals the diagnosis. The squeeze test is also positive: the patient lays prone with both feet suspended over the edge of the couch; compressing the triceps surae causes plantiflexion of the foot when the tendon is intact but not when it is ruptured. 1 3 Differential diagnosis
The differential diagnosis from tennis leg is quite simple. In a patient with a minor tear in the medial gastroc nemius muscle, there is pain in the calf and the foot is fixed in plantiflexion. This contrasts very strongly with the absence of pain, the inability to plantiflex against resist ance and the excessive dorsiflexion range at the ankle that are characteristic of a rupture of the Achilles tendon. Although the history of sudden pain and disability may suggest a sprained ankle, a rupture of the Achilles tendon will not be missed if the clinical examination is executed properly.
-
DISORDERS OF THE LOWER LEG 1191
Treatment
There is still controversy concerning the best treatment for Achilles tendon ruptures. It appears that a satisfactory outcome may be achieved with either non-operative or operative treatment but surgical repair appears to provide better functional capacity69 with better scores of strength, power and endurance7o-n and lower re-rupture rates. The advantages of the conservative approach are that there are no risks of anaesthesia, infection, skin adhe sions and sural nerve injury.73,74 Reports in the literature indicate that in active, young, very-demanding individu als, surgical repair should be considered, with non surgical treatment reserved for elderly or sedentary patients.75-77 However, conservative treatment can also be considered in athletically active patients as treatment should always be individualized to the concerns and health of the patient.78,79 There is no single, uniformly accepted surgical tech nique for Achilles tendon repair. Most acute ruptures have been treated successfully with excision of the devitalized tendon tissue and simple end-to-end suture. However, various augmentation procedures, such as reinforcement of the suture with a triceps surae tendon tip-over graft, have been combined with simple suture with satisfactory . . . 10 mirumize the comp1 ications typically ou tcomes.80 -82 'r associated with open surgery, percutaneous techniques to repair the ruptured Achilles tendon have been advocated and the results are reported to be promising, although no� without failures and complications.83 Several recent studies have reported functional benefits of early postoperative tendon mobilization in well-motivated patients, in that treatment results are determined not only by the method of repair but also, and perhaps more importantly, by the early postopera tive functional rehabilitation.84 Conservative treatment consists of 8 weeks in a plaster cast with the foot in equinus position, followed by the use of a 2.5 cm heel for an additional 1 or 2 months.85,86 The thickened and enlarged scar tissue resulting after conser vative treatment can be massaged twice a week for 2-3 months. The fibrous swelling at the point of the rupture never seems to disappear, however, and some residual disability can be permanent. It can be concluded that the treatment of choice in the athletically active patient is primary surgical repair.87 Conservative treatment is chosen in middle-aged or less active patients.88 SHORT PLANTIFLEXOR MUSCLES
Short calf muscles, resulting in equinus deformity, are among the most common complications in children with cerebral palsy.89 Sometimes shortening of calf muscles is an isolated finding and may easily be overlooked.
1192 SECTION FOURTEEN - THE LOWER LEG, AN KLE AND FOOT
History
Usually the parents bring the child's gait to attention. They notice that the youngster turns the feet outwards during walking or running, adopting a 'Chaplin' style of moving. Because the child cannot dorsiflex the ankle joint during walking, the feet must be turned outwards to take off. As this is not the best technique for running, the child will run conspicuously slower than healthy peers. Sometimes the parents also notice that the child tends to tilt backwards on standing. The poise around the centre of gravity is incorrect, which leads to muscular fatigue. Therefore the child will complain that prolonged standing is tiring. Clinical examination
This shows the dorsiflexion range at the ankle joint to be painlessly limited to the horizontal line. In the literature, the description is often 'equinus to 90°'. Complications
Because the patient cannot adequately bear weight on the heels, midtarsal hypermobility and later painful strain will result. This very often occurs, especially if there is, as is common, a plantaris deformity of the forefoot compli cating the short calf muscles. Taking too much weight on the forefoot, as is the case in shortened calf muscles, eventually results in chronic metatarsalgia and strain of the plantar fascia.9o
(a)
Treatment Younger patients. The midtarsal joints, together with the plantar fascia and the forefoot must be protected. Therefore the heel must temporarily be raised by a hori zontal surface. The child is taught to do stretching exer cises for soleus and the gastrocnemii, several times a day, for 2-6 months. These lengthen the calf muscles so that the raised heel on the shoe can be discarded. The soleus muscle is stretched in the following way. The child performs knee flexion exercises and tries to keep the heels on the ground (Fig. 83.7a). Once this can be done without problems, leaning more and more forwards is encouraged so as to stretch the soleus further. To stretch the gastrocnemii muscles the child stands in front of a wall, with feet fully dorsiflexed and knees extended, the heels remaining on the ground. Leaning forwards, strongly keeping one knees in full extension, then takes place (Fig. 83.7b).
The same treatment can be tried but the process of stretching the calf muscles is tedious and tends to fail. Here, the shortening can only be compensated by raising the heel of the shoe. Alternatively, surgery can be advised.
Adults.
(b)
Figure 83.7 Stretching of the left soleus (a) and left gastrocnemii (b).
CHAPTER 83
LESIONS OF THE DORSIFLEXORS PAIN
If resisted dorsiflexion of the foot elicits pain, a resisted movement of the hallux, and then of the toes, identifies the offending muscle: tibialis anterior, extensor hallucis longus or extensor digitorum longus. Further palpation then discloses the precise localization, which can be at the muscle, the tendon or the tenoperiosteal insertion. Lesions of the muscle bellies respond equally well to local anaesthesia and deep friction (Box 83.2). Three injec tions, each of 10-30 ml of procaine 0.5%, at weekly inter vals usually give good results. Friction is given according to the general principles that it should be deep, trans verse, with sufficient sweep on a relaxed muscle, three times a week for 6-10 sessions. Lesions of the tendons respond to deep friction, on a stretched tendon, three sessions a week, for 6-10 sessions. Lesions at the tenoperiosteal junction respond to deep transverse friction and to infiltration with 10 mg of tri amcinolone.
-
DISORDERS OF THE LOWER LEG 1193
sheath and deep friction have equally good results. In rheumatic conditions, infiltration is the only method of symptom relief. Myosynovitis of the tibialis anterior muscle. The only parallel condition in the body is myosynovitis of the bellies of the abductor pollicis longus and the extensors pollicis muscles in the forearm. The lesion occurs as an overuse phenomenon in skaters, skiers and long distance runners. It has also been described in army recruits, after a long march in unaccustomed heavy boots.91 Resisted dorsiflexion hurts above the front of the ankle. Painless resisted dorsiflexion of the big toe and outer toes points to the tibialis anterior muscle but palpation fails to reveal any tenderness in the anterior tibial tendon itself. If the palpating finger moves upwards to the musculotendinous junction, a painful area is detected close to the bone. If the foot is moved gently up and down, crepitus may be felt. Treatment consists of deep transverse friction, which solves this problem very quickly: two to four sessions at intervals of 2 days usually give lasting relief. Technique: deep transverse friction to the tibialis anterior
Special conditions Ischaemic contracture or adherence of the extensor hal
The muscle may develop ischaemic con tracture or become adherent after a fracture at mid-tibia. This results in a constant-length phenomenon. Each time the foot is plantiflexed, the shortened extensor hallucis muscle extends the big toe which is forced against the tip of the shoe. This may result in extreme soreness of the big toe. The treatment is tenotomy level with the first metatarsophalangeal joint. lucis longus.
Tenosynovitis of the extensor digitorum longus or the
This rare condition occurs level with the ankle and is usually a sequel of a sprained ankle. Sometimes it is seen as a rheumatoid condition. Apart from pain, a localized swelling can be seen and occasion ally crepitus can be felt. In traumatic tenosynovitis, infiltra tion with 1 ml of triamcinolone between the tendon and extensor hallucis longus.
Box 83.2 Summary of treatment of lesions of the dorsiflexors Muscle Either
10-30
m l procaine
0.5%
Or deep friction 3 times a week,
Tendon Deep friction
3
ti mes a week,
Tenoperiosteal junction Either
1
ml tria mcinolone
Or deep friction
3
The therapist sits opposite the patient. With one hand the foot is brought into full plantiflexion and ever sion in order to stretch the muscle. The thumb of the other hand is placed at the medial aspect of the leg and the fingers on the lesion (Fig. 83.8). The thumb is used as a fixed point and the fingers move in a transverse direc tion over the anterior aspect of the anterior tibial muscle. To allow sufficient sweep, the movement is conducted by an adduction movement of the shoulder. muscle.
(10
10
10 sessions sessions
mg/ml)
times a week,
10 sessions
The disorder may resemble intermittent claudication but the patient is much younger and phYSically active. After some exertion, for instance kicking a football for about 10 minutes, voluntary dorsiflexion becomes impossible and what seems like a drop foot develops. This is accompa nied by vague pain at the front of the leg and sometimes by pins and needles over the dorsum of the foot and the inner four toes. After a short rest, the muscle recovers and pain and weakness disappear. When examined at rest, nothing special is revealed: dorsiflexion is strong and painless and the arterial pulsations are normal. In long standing cases, it is sometimes possible to palpate fascial hernias over the front of the leg.92 The symptoms result from increased tissue fluid pres sure in the closed fascial compartment which is formed by the tibia, the fibula, the interosseous membrane and the anterior fascia (Fig. 83.9). During exercise, muscle volume may expand 20%, from both increased blood flow and capillary filtration.93,94 If the superficial fascia is not lax enough to accommodate the greater volume, the Tight fascia syndrome of the anterior compartment.
1194 SECTION FOU RTEEN - THE LOWER LEG, AN K LE AND FOOT
Figure 83.9
Figure 83.8 Deep friction to the tibialis anterior muscle.
intramuscular pressure rises to levels that compress the anterior tibial artery. This produces relative muscle ischaemia and therefore temporary paralysis and pain. The swelling may also trap the superficial peroneal nerve at its exit through the fascial foramen at mid-leg and cause paraesthesia in the outer foot. After some minutes' rest, blood flow recovers and symptoms resolve. Because the patient is asymptomatic between occurrences and not chronically disabled, some authors prefer the suffix 'recurrent' rather than 'chronic' to identify anterior compartment syndromes.95 However, if the minute vessels in the belly of the muscle themselves gradually become silted up with cells, the disorder may become irreversible.96 The diagnosis is made on the typical history and the negative findings during clinical examination. When there is doubt, pressure in the anterior compartment before and after exertion can be measured.97,98 It is gener ally accepted that serious consideration should be given to decompression of the affected compartments if a dif ference of less than 30 mmHg between the diastolic and systolic tissue pressures can be measured.99,1 00 Acu te and severe anterior compartment syndromes may develop after a tibial fracture" ol or a direct blow.1 02
The anterior compartmen t (colour indicates the fascia).
Within a few hours, pain at the mid-leg becomes intense and is not relieved by immobilization. The overlying skin sometimes becomes shiny and warm. Together with the palpable tenderness, this may give the false impression of cellulitis. To make this error is a disaster for, if the diagnosis is not made at once and the fascia divided immediately, ischaemic necrosis will ensue. Complete paralysis with a permanent drop foot will then result. There are also documented cases of bilateral compartment syndrome with permanent drop foot complicating surgery of long duration in the lithotomy posi tion.' 03 Treatment. Apart from altering the patients' activities or training programmes, surgery seems to be the only effec tive treatment for recurrent compartmental syndromes. The surgical procedure consists of a subcu taneous fasciotomy.104-106 In acute cases, surgical decompression must be per formed as soon as possible. As in a strangulated inguinal hernia, the motto is: 'operate before sunset or sunrise'. l D7 Sheridan and Matsen1 08 found that fasciotomy performed within 12 hours of the onset of the compartment syn drome resulted in normal function in 68% of cases. However, in those decompressed after 12 hours, only 8% recovered normal function.
WEAKNESS
Weakness of dorsiflexion is always the result of neuro logical lesions that are discussed at the end of this chapter.
CHAPTER 83
-
DISORDERS OF THE LOWER LEG 1195
T echnique: friction to the upper part of tibialis posterior.
LESIONS OF THE INVERTORS PAIN
The main invertor muscles are the anterior (1) and poste rior (2) tibialis muscles (Fig. 83.10). The flexor hallucis longus and the triceps are weak invertors as well. Posterior tibial tendinitis is usually caused by overuse, which occurs frequently in a valgus deformity at the subtalar joint. 1 09 Resisted inversion of the foot hurts and dorsiflexion does not. Because the tibialis posterior has an additional function in stabilizing the hindfoot during rising on tiptoe, this test may also be painful. Palpation then discloses whether the lesion lies at the insertion on the navicular bone, at the tendon (distal or proximal to or under the medial malleolus), at the muscle belly or at the proximal musculotendinous junction. Sometimes the tendon sheath rather than the tendon is inflamed, causing a tenosynovitis. This occasionally occurs in rheumatoid arthri tis. Tendinitis usually recovers with a few sessions of massage but the valgus deformity at the heel must be corrected in order to prevent recurrences. Pain resulting from overuse secondary to a valgus deformity will never be relieved unless a combined approach of deep friction and correction of the valgus deformity by a support at the heel is used. In rheumatoid tenosynovitis, 10 mg of triamcinolone is injected between the tendon and its sheath. Deep friction techniques
The technique differs according to the site of the lesion: above or under the medial malleolus. In both instances, the patient lies on the couch with the hip in external rota tion so that the inner surface faces upwards.
The therapist sits lateral to the patient's foot. With the contralateral hand the foot is fixed in dorsiflexion. Because the tendon lies deeply between the posterior aspect of the tibia and the tendon of the flexor digitorum longus, the proper spot can only be reached if the prona tion-supination technique is used. The middle finger of the ipsilateral hand, reinforced by the index finger, is thus laid flat on the affected part of the tendon, just behind the edge of the tibia (Fig. 83.11). The ring and little fingers are kept extended. The fingers, the wrist and the forearm are brought into line with the tibia. The friction is imparted by a supination movement, which is continued until the tendon escapes from the finger. Pressure is then some what released and the finger returned to the original position by pronation. This alternating pronation-supination movement is continued for about 20 minutes. Usually 10 sessions, three times a week, suffice to clear up the condition. T echnique: friction to the lower part of tibialis posterior.
The patient's foot is dorsiflexed and the therapist sits level with the affected foot. The thumb of the contralat eral hand is placed at the lateral side of the foot. The tips of one or two fingers are placed on the affected length of the tendon, just beyond it. Friction is now given by an extension movement at the wrist (Fig. 83.12) using the thumb as a fulcrum. The fingers ride over the whole width of the tendon until the latter escapes form the pres sure. By flexion of the wrist and without losing contact with the skin, the fingers are then moved to the original position, behind the tendon, and the whole procedure is repeated. Friction is continued for 20 minutes, twice a week, for l or 2 weeks. Shin splints
Figure 83.10 Tendons and inserti ons of the main invertor muscles: 1 , tibialis anteri or; 2, tibialis p osteri or.
Pain at the posterior medial edge of the tibia in athletes and long-distance rum1ers is usually called shin splints. Few conditions have caused as much controversy. The term has been used to cover a variety of conditions, such as stress fractures, llO-l12 periostitis and soft tissue inflammation.113 The American Medical Association sub committee for classification of sports injuries restricts the name shin splints to the musculotendinous lesions of the tibialis posterior muscle.114 Orava and Puranenll 5 state that the pathogenesis can be explained by increased pressure in the fascial com partment of the deep flexor muscles from prolonged exercise, and cite the curative effect of fasciotomy to support their view.11 6 The disorder appears as an overuse phenomenon in runners. The patient complains of pain - usually a dull aching discomfort - at the medial tibial border during and after running.91
1196 SECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
Figure 83.1 1 Deep friction to the upper part of the tibialis muscle: (a) starting position; (b) end of the movement.
Figure 83.12
Deep friction to the lower part of the tibialis posterior.
CHAPTER 83 - DISORDERS OF THE LOWER LEG 1197
Clinical examination shows little pain during resisted inversion of the foot. Palpation reveals tenderness and sometimes induration at the musculotendinous junction of the tibialis posterior muscle, usually between its upper and medial thirds. Differential diagnosis must be made from a stress frac ture. Here, pain is elicited by sharply striking the heel or the bone is tender to direct pressure. During the initial weeks, a stress fracture is not visible on a plain radi ograph ll7 but can be detected with ultrasoundYs In cases of doubt a bone scintigram can be obtained that easily distinguishes an inflammatory shin splint from a stress fracture.119,120
rises and the body weight is imparted to the ball of the foot. With a rupture of the TPT, however, the initial varus movement at the heel is impossible and the patient rises up with the heel in valgus or does not get up onto the ball of the foot at al].125 Conservative treatment includes a medial heel wedge and a longitudinal arch support. Surgical treatment must be considered when the patient is young and active. A plantaris or extensor tendon graft may be used to bridge the defect. Recently, the transfer of the flexor digitorum longus tendon into the sheath of the tibialis posterior has been used for larger defects.126. l 27
The condi tion responds effectively to a series of ses sions of deep transverse friction. Good results have also been obtained with weekly infiltrations of procaine (10-20 m!) over 3 consecutive weeks. For a stress fracture, only rest is effective. A 6- to 8week pause in training is usually necessary.
LESIONS OF THE EVERTORS
WEAKNESS
Neurological lesions are discussed at the end of this chapter. Weak resisted inversion is often caused by a rupture of the tibialis posterior tendon (TPT), secondary to a combi nation of degenerative changes and trauma.12l It is usually located in a cri tical zone with a low degree of vasculari ty, posterior to the medial malleolus.122 Rupture of the TPT does not initially cause pain and usually the patient cannot recall an acute trauma. The main symptom that draws attention to the possibility is a gradual deformity of the foot. The triad of deformity appearing during weight bearing is: • • •
Valgus deformity of the heel Loss in height of the medial longitudinal arch Abduction of the forefoot, which is detected by the 'too many toes sign' :123 more of the lateral toes are seen on the affected side when the patient is inspected from behind.
A rupture of the tibialis posterior tendon thus leads to a progressive, unilateral, acquired flat foot, with increasing valgus of the heel, plantar flexion of the talus and sub luxation of the talonavicular jOint. l 2l,124 It is difficult to detect a weakness of the tibialis poste rior during manual testing, because the synergistic action of the other invertors of the foot substitutes for the power of the ruptured muscle. Weakness of the tendon is best detected during rising on tiptoe. This test has a typical normal sequence. First the TPT is activated, which inverts the foot and locks the heel. Then the triceps muscle pulls on the now rigid calcaneus, the heel
PAIN T endinitis
If there is pain on resisted eversion of the foot, the per oneal muscles are at fault. Peroneal tendinitis is usually a simple overuse phenomenon in runners and skaters, 1 28,129 although it may also appear as a complication of anl
Sometimes patients complain of a slight pain, together with a snapping feeling at the outer side of the ankle, during certain movements. The reason is a loosening of the peroneal tendons in the groove of the posterior surface of the fibula. They slip forwards over the mallleolus when the ankIe is dorsiflexed and 'jump back' during plantiflexion.132 This 'snapping ankIe' is usually not painful, merely uncomfortable. Sometimes, however, it is the origin of a super-imposed tendinitis. Non-surgical treatment should always be instituted first and consists of holding the tendons reduced in their anatomical positions while the superior peroneal retinac ulum heals by scarring.133 If considerable discomfort remains, surgery can be advised. Different methods of repair have been described.134, 1 35 Usually a new retinacu lum is constructed behind the lateral malleolus or the cal caneofibular ligament is transposed to the la teral side of the peroneal tendons.136 'Snapping ankle'.
Mucocele. A mucocele can form in the sheath of the tendon. It results in localized swelling and can be associ ated with a considerable ache. The diagnosis is obvious,
1 1 98 SECTION FOURTEEN - THE LOWER LEG, AN KLE AND FOOT
because the swelling is located in the sheath and can be made to fluctuate upwards and downwards along the malleolus by digital pressure. Treatment is aspiration. Because the viscous fluid has a high density, the aspira tion is difficul t to perform unless a wide-bore needle and a large syringe are used. Sometimes up to 50 ml of fluid can be removed. If there is pain, 1 or 2 ml of triamci nolone are injected into the now empty synovial space. Sometimes this procedure has to be repeated after a year or so. Peroneal spasm. This is not an intrinsic disorder of the peroneal muscles but results from arthritis of the talocal caneal and mid-tarsal joints. If the arthritis is cured, the spasm disappears immediately.
T reatment of tendinitis
Peroneal tendinitis is seldom sufficiently localized to be treated by steroid injection. However, it responds very well to deep transverse massage. T echnique:
deep friction above and u nder the malleolu s . 137
The patient lies supine, with the leg medially rotated. The therapist sits at the opposite side. The foot is brought into inversion: this stretches the tendon. Two or three fingertips of the therapist's ipsilateral hand are now placed on the tendon. The fingers are slightly flexed, thereby pressing the tendon against the fibular shaft. The thumb is placed at the medial side of the lower leg or ankle to provide counterpressure (Fig. 83.13). Friction is given by a to-and-fro movement at the forearm, during which the fingers ride over the tendon. The friction is in two phases: an active phase
during which the tendon is pressed and pulled and a relaxed phase during which the fingers are placed in the previous position to re-start the movement. Three sessions a week over 2-4 weeks may be required. During the treatment the patient should avoid exercise but complete rest is not required. The results are uniformly good. T echnique: deep friction level with the malleolus. The therapist sits by the patient's foot, facing it. The foot is held in inversion and plantar flexion produced by slight pressure of the ipsilateral hand. The therapist holds the contralateral hand and forearm in line with the leg. The middle finger, reinforced by the index finger, is placed in the sulcus, behind the peroneus tendon (Fig. 83. 14). Friction is started with the finger behind the tendon. Pressure is exerted and, by a supination movement of the forearm, the tendon is pressed anteriorly until it escapes from the finger and slips backwards. The now supinated hand is manoeuvred back to the pronated position behind the tendon, where the movement re starts. Friction is imparted by rotating the forearm in full supination and full pronation for about 15 minutes. Three sessions a week over 3-4 weeks are usually sufficient to cure the lesion.
WEAKNESS
Weakness of the peronei usually results from neurologi cal lesions. Differential diagnosis between posterior and anterior leg pain is summarized in Box 83.3.
cd Figure 83.13
Deep friction to the peroneal tendons under the malleolus.
Figure 83.14
Deep friction to the peroneal tendons level with the malleolus.
CHAPTER 83
80'S 83.3
Leg pain : differential diagnosis
Posterior leg pain Te nnis leg
Anterior leg pain Myosynovitis of the t i b i a l i s anterior
Ach i l les te n d i n itis at the
Shin s p l i nts
musculotendi nous j u nction Deep venous thrombosis
Stress fractu re
Rupture of Baker's cyst
Ti g ht fasc i a l compartment
I nterm ittent claud ication
Lesion of a dorsiflexor muscle b e l l y
Ischaemic contracture of the
L 3 , L 4 referred pa i n
calf m uscles LS-S2 refered pain
DISORDERS CAUSING NEUROLOG I CAL WEAKNESS OF THE FOOT
Weakness of the calf muscles is best detected by asking the patient to stand on one foot and to rise on tiptoe. Slight weakness can only be identified by repetitive rising on tiptoe, comparing one leg with the other.
-
DISORDERS OF THE LOWER LEG 1 1 99
Dorsiflexion, eversion and inversion are tested in the supine-lying position. As described in Chapter 81, it is very important to give strong counterpressure, with the leg in a neutral position. Normally the extrinsic muscles of the foot are very strong and their pull cannot be overcome by the examiner 's force. Both sides should be compared. In central or upper motor neurone lesions, the weak ness is gross and distributed over different muscles and muscle groups (Table 83.1). In lesions of the nerve root (sciatica caused by disc protrusion), the distribution is segmental. There is or there has been considerable pain in the respective derma tomes before the appearance of the weakness. Although the weakness can be significant, especially if two consecutive nerve roots are involved, it is almost never complete. In lesions of a peripheral nerve, the weakness follows the normal afferent distribution of the nerve. Very often the pain appears silently, without previous pain in the innervated area. Because the peripheral nerves in the lower limb behave in the same way as a nerve trunk, paraesthesia will only appear when pressure on the nerve is released and not during the actual period of compression (see release phenomenon in Ch. 7) . 1 38, 1 39
Table 83.1 Innervation of neurological weakness of the foot Muscle
Segmental innervation
Peripheral nerve
Tibialis anterior Extensor digitorum longus Extensor hallucis longus Peronei Tibialis posterior Flexor digitorum longus Flexor hallucis longus Triceps surae
L4 (LS) L4, LS L4, LS LS, S1 L4, LS LS-S1 LS-S1 S1 , S2
Deep peroneal Deep peroneal Deep peroneal Superfcial peroneal Tibial Tibial Tibial Tibial
REFEREN CES 1. Naish JM, Appley J. "Growing pains". A clinical study of
nonarthritic limb pain in children. Arch Dis Child 1951;26: 134-140. 2. Oster J. Nielsen A. Growing pains - a clinical investigation of a 3. 4.
S. 6.
7. 8.
school population. Actn Paedintr Scand 1972;61:134-140. Baxter MP, Dulberg C. "Growing pains" in childhood. A pro posal for treatment. J Pediatr Orlhop 1988;8:402-406. Miller A. Rupture of the musculotendinous juncture of the medial head of the gastrocnemius. Am J Sports Med 1977;5:191-193. Hood WP. On lawn-tennis leg. LanceI 1884;i:728-729. Gilcreest EL. Ruptures and tears of muscles and tendons of the lower extremity. JAMA 1993;100:1 53-160. Cornwell HE, Allredge RH. Ruptures and tears of tendons and muscles. Alii J Surg 1937;35 :22-33. Golding D. Tennis leg. BMJ 1 969;4:243.
9. Gaulrapp H. "Tennis leg": ultrasound differential diagnosis and
follow-up. Sporlverlelz Sporlschaden 1999;13(2):53-58. 10. Bianchi S, Martinoli C, Abdelwahab IF, Derchi LE, Damiani S.
Sonographic evaluation of tears of the gastrocnemius medial head ( " tennis leg" ). J Ultrasou n d Med 1998;17(3 ) : 1 57-162. 1 1 . Werken van der C, Marti RK. Rupturen van de Achillespees. Ned Tijdschr Geneeskd 1980;124:1321-1322. 12. Visser
JD.
Achillespeesruptuur.
Ned
Tijdschr
Gel1eeskd
124: 1 340-1342. 1 3 . Thompson TL, Doherty J H . Spontaneous rupture of tendon of
Achilles, a new d i agnostic clinical test. J Traull1a 1 962;2: 126-129. 14. Gauer EF, During M, Muller W. Die proximate Ruptl.lf im
Triceps surae, eine typische, aber oft verkannte Verletzung. Chirurgie 1976;236-240.
1200 SECTION FOURTEEN - THE LOWER LEG, AN K LE AND FOOT
15. 16. 17. 18. 19. 20. 21 . 22. 23.
Scurr JH, Coleridge-Smith PO, Hasby JH. Deep venous throm bosis: a continuing problem. BMI I 988;297:28. Lambie JM, Mahaffy RG, Barber DC et al. Diagnostic accuracy in venous thrombosis. BM] 1970;ii:142-143. Kakkar W, Howe CT, Fiance C, Clarke MB. Natural history of postoperative deep vein thrombosis. Lancet 1969;ii:230-232. Baker W M . Chronic synovial cysts 1 887; Report. St Bartholomew's Hospital, London. Cyriax JH. Textbook of Orthopaedic Medicine. Vol. I, 8th edn. Bailliere Tindall, London, 1982. Colson J HC Armour WJ. Sport Injuries and their Treat/llent. Stanley Paul. London, 1975. Franke K. Trnlllllatologie des Sports. Thieme, Stuttgart, 1980. Dlirig M, Schuppiser JP, Gauer EF, Muller W. Spontaneous rupture of the gastrocnemius muscle. Illjury 1977;9: 1 43-145. Biedert R. Beschwerden im Achillessehnenbereich. Atiologien und therapeutische Oberlegungen. Unfall Chirurg 1 99 1 ;
Daniel U, Skeoch MD, Spontaneous partial subcutaneous rup tures of the tendo Achilles. Am I Sports Med 1981;9(1 ) : 1 35-137. 44. Bedi S, Ellis W. Achilles tendon ruptures. AIIIl Rheul1l Dis 43.
1970;29:494. 45.
Devereaux MD, Lachmann SM. Athletes attending a sports injury clinic - a review. Br I Sports Med 1983;17:137-142. 25. Kvist DR, Jarvinen M. Zur Epidemiologie von Sportverletzungen und Fehlbelastungsformen. Patienten ana lyse einer Sportmedizinischer Pol iklinik. Med Sport 24.
46. 47.
30. 31 . 32. 33.
tendinitis.
Orthop
Ciin
North
Reinschmidt C, Nigg BM. Influence of heel height on ankle joint moments in running. Med Sci Sports Exerc 1995;27(3):410-416. Lemaire M, Miremad C Combelles F. Tendinite du tendon d' Achille du sportif. Med Sport 1981;55:6. Zuinen C. Ruptures du tendon d' Achille. Med Sport 1980;54:6. Logengren C, Lindholm A. Vascular distribution in the Achilles tendon. Acta ChiI' Scand 1 958;116:491-495. Schmid t-Rohlfing B, Graf J. Schneider U, Niethard Fo. The blood supply of the Achilles tendon. lnt Orthop 1 992;
Schepsis AA, Wagner C, Leach R. Surgical management of Achilles tendon overuse injuries. Am ] Sports Med 1994;5:611�19. 52. Nelen G, M artens M, Burssens A. Surgical treatment of chronic Achilles tendinitis. Am J Sports Med 1989;17:754-759. 53. Jenkins DHR, Forster IW, McKibbin B, RaJis ZA. Induction of tendon and ligament formation by carbon implantation. ] Balle
54.
Leach RE, Schepsis AA, Takai H. Long-term results of surgical management of Achilles tendinitis in runners. Ciill Orthop
55.
Maffulli N, Testa V, Capasso G, Bifulco G, Binfield PM. Results of percutaneous longitudinal tenotomy for Achilles tendino pathy in middle- and long-distance runners. AIIl ] Sports Med
56.
Cyriax JH. Textbook of Orthopaedic Medicine, vol. I I . Treat/llent by Mallipulatioll, Massage and injectioll. Bailliere Tindall, London,
57.
Subotnick SI. Orthotic foot control and the overuse syndrome.
58.
James SL, Bates BT. Ostering LR. Injuries to runners. Am ] Sports
1992;282:208-21 2 .
1997;25(6) :835-840.
1986.
Physician Sportsmed 1975;3(1):75-79. Med 1978;6(2) :40-50. 59.
792-795.
63. 64. 65. 66.
67.
1 984;12:1 79-1 84. 68.
Rev Rhul1I 1971 ;38:373-38l .
Shrier I, Matheson GO, Kohl HW. Achilles tendonitis: are corticosteroid injections useful or harmful? Ciill ] Sport Med 1996;6(4) :245-250.
Rask MR. Achilles tendon disease owing to rheumatoid disease. ]AMA 1978;239(5) :435-436.
Am ] Sports Med 1988;16:61 6-623.
Auquier L, Siaud JR. Tendinites nodulaires du tendon d' Achille.
Gerster JC, Vischer TL, Bennanin A, Fallet GH. The painful heel. Anll Rheum Dis 1977;36:343-349.
62.
Clement DB, Taunton JE, Smart GW. Achilles tendinitis and peritend initis. Etiology and treatment. A m J Sports Med
Wiktorsson-Moller M, Oeberg B, Ekstrand J, Gillquist J. Effects of warming up, massage and stretching on range of motion and muscle strength in the lower extremity. Am J Sports Med 1983;11:249-252.
61.
Lewis JR, Gums JG, Dickensheets DL. Levofloxacin-induced bilateral Achilles tendonitis. A n n Phannacother 1 999;33(7-8):
Casparian JM, Luchi M, Moffat RE, Hinthorn D. Quinolones and tendon ruptures. South Med ] 2000;93(5):488-491 . 38. Smart JW, Taunton JE, Clement DB. Achilles tendon disorders in runners - a review. Med Sci Sports Exerc 1980;4:231-243. 39. Kvist MH, Lehto MU, Jozsa L et al. Chronic Ach.illes paratenon itis: an immunohistologic study of fibronectin and fibrinogen.
Moller MHC Ekstrand J, Oeberg BE, Gillquist J. Duration of stretching effect on range of motion in lower extremities. Arch Phys Med RehabiI 1985;65:171-173.
60.
37.
42.
Read MT, Motto SG. Tendo Achillis pain: steroids and outcome.
Ankle S u rg 1 995;34(3):294-300.
Plwl"/nacoI 1999;48(3) :433-437.
41.
Mahler F, Fritschy D. Partial and complete ruptures of the Achilles tendon and local corticosteroid injections. Br ] Sports
Br J Sports Med 1 992;26(1 ) : 1 5-21 .
16(1):29-3l .
McGarvey WC, Singh 0, Trevino SG. Partial Achilles tendon ruptures associated with fluoroquinolone antibiotics: a case report and literature review. Foot Ankle Int 1996;17(8) :496-498. 35. van der Linden PO, van de Lei J, Nab HW, Knol A, Stricker BH. Achilles tendinitis associated with fluoroquinolones. Br ] Ciin
40.
Krahl H, Plaue R. Sehnenrupturen nach Cortisoninjektionen.
Schepsis AA, Leach RE. Surgical management of Achilles ten dinitis. Am ] Sports Med 1987;15(4) :308-3 1 5 . 5 0 . Saxena A. Surgery for chronic Achilles tendon problems. J Foot
Am
34.
36.
Gelleeskd
49.
1 994;25(1) : 1 77-1 82. 29.
Tijdschr
Med 1992;26(1):7-14. 48.
1999;31 (10):1 374-1 381 .
Achilles
Ned
Joint S u rg 1977;59B:53-57.
Riede 0, Franke J. Zur Rontgendiagnostik und Behandlung der Peritendinitis Achillae. Med Sport 1968;2:41-43. 27. McCrory J L, Martin OF, Lowery RB et al. Etiologic factors asso ciated with Achilles tendinitis in runners. Med Sci Sports Exerc M W.
Achillespeesruptuur.
Med Sport 1971;11 :264.
1 980;20:375-378. 26.
Scioli
JD.
51.
94(10):531-537.
28.
Visser
1 980;124(32) : 1 344-1 347.
69.
Rodman Gp, McEwen C, Wallace SL. Primer on rheumatic diseases. lAMA 1976;224(suppI5):67�8, 1 1 6-1 1 7. Taunton J. McKenzie D, Clement D. The role of biomechanics in the epidemiology of injuries. Sports Med 1988;6:1 07-120. Jozsa L. The role of recreational sport activity in Achilles tendon rupture. Am ] Sports Med 1989;3:338-343. Shields CL, Kerlan RK, Jobe FW, Carter VS, Lombardo SJ. The Cybex II evaluation of surgically repaired Achilles tendon rupture. Am I Sports Med 1978:6(6) :369-372. Kennedy R, Inglis J, Malcolm L. Late reconstruction of the Achilles tendon. ] Bone Joint S u rg 1979;61A(6) :653-658. Rodineau J. La Rupture du tendon d' Achille. Pratique Medicale, .. 27 J uin 1982. Majewski M, Rickert M, Steinbruck K. Acl1illes tendon rupture. A prospective study assessing various treatment possibilities. Orthopade 2000;29(7):670-676.
CHAPTER 83
Inglis AE, Scott WN, Sculco TP, Patterson AH. Ruptures of the .tendo Achillis: an objective assessment of surgical and non surgical treatment. J Bone Joint S u rg 1976;58A:990. 71. Jacobs 0, Martens M, Van Audekercke R. Comparison of con servative and operative treatment of Achilles tendon rupture.
70.
94. 95. 96.
Am J Sports Med 1978;6:107.
Percy EC, COlmochie LB. The surgical treatment of ruptured Achilles tendon. Am ] Sports Med 1978;6:132. 73. Stein SR, Leukens CA. Closed treatment of Achilles tendon ruptures. Orthop Clin North Am 1976;7:24 1 . 74. Fruensgaard S, Helmig P, Riis J, Stovrin.g JO. Conservative treatment for acute rupture of the Achilles tendon. i n t Orthop 72.
1992;16(1):29-3 1 .
Nistor L. Surgical and non-surgical treatment of Achilles tendon rupture. J Bone Joint Surg 1981 ;63A:394. 76. Carden OJ. Rupture of the calcaneal tendon: the early and the late management. J Bone joint S u rg 1987;69B:416-420. 77. Popovic N, Lemaire R. Diagnosis and treatment of acute rup tures of the Achilles tendon. Current concepts review. Acta
97.
98.
99.
75.
Orthop Belg 1999;65(4) :458-471 . 78.
Lo IK, Kirkley A, Nonweiler B, Kumbhare DA. Operative versus nonoperative treatment of acute Achilles tendon ruptures: a quantitative review. Clin j Sport Med 1 997;7(3): 207-2 1 1 .
Gorschewsky 0 , Vogel U, Schweizer A, van Laar B. Percutaneous tenodesis of the Achilles tendon. A new surgical method for the treatment of acute Achilles tendon rupture through percutaneous tenodesis. Injury 1999;30(5):315-321 . 80. Ralston EL, Schmidt ER. Repair o f the ruptured Achilles tendon. j Trauma 1971;11(1):15-2l . 8 1 . Winter E, Weise K, Weller S, Ambacher T. Surgical repair of Achilles tendon rupture. Comparison of surgical with conser vative treatment. Arch Orthop Trauma S u rg 1998;117(6-7): 79.
364-374.
Zell RA, Santoro VM. Augmented repair of acute Achilles tendon ruptures. Foot Ankle Int 2000;21(6):469-474. 83. Mertl P, Jarde 0, Van FT, Doutrellot P, Vives P. Percutaneous tenorrhaphy for Achilles tendon rupture. Study of 29 cases. 82.
Buchgraber A, Passier H H . Percutaneous repair of Achilles tendon rupture. Immobilization versus functional postopera tive treatment. Clin Orthop 1997;341 : 11 3-122. 85. Lea RB, Smith L. Non-surgical treatment of tendo Achilles rupture. j Bone joint Surg 1972;54A:1394. 86. Angermann P, Hovgaard D. Chronic Achilles tendinopathy in athletic individuals: results of nonsurgical treatment. Foot Ankle [nt 1999;20(5):304-306.
Singer K, Jones D. Soft tissue conditions of the ankle and foot. In: Nicholas J, Hershman E (eds) The Lower Extremity and Spine in Sports Medicine. Mosby, St Louis, 1 986:418-425. 88. Fruensgaard S, Helmig P, Riis J, Stovring JO. Conservative treatment for acute rupture of the Achilles tendon. In t Orthop Fontenrose A, Miller J, Hallum A. Physicians' and physical therapists' evaluation of cerebral-palsied children for Achilles tendon lengthenjng. Oev Child Neural 1 984;26:208-21 4. 90. Heim M, Blankstein A. Congenitla short Achilles tendon. 89.
1974;114:379-384.
Verleisdonk EJ, van den Helder C), Hoogendoorn HA, van der Werken C. Good results of fasciotomy in chroni c comparhnent syndrome of the lower leg. Ned Tijdsch r Geneeskd 1996;140(50):25 1 3-251 7.
Wiggins H . The anterior tibial compartment syndrome. A com plication of the Hauser procedure. Ciin Orthop 1 975;113:90-94. 102. Leach RE, Corbett M. Anterior tibial compartment syndrome in soccer players. Am J Sports Med 1979;7(4). 103. Duflo F, Allaouchiche B, Mathon L, Chassard D. Bi lateral ante rior tibial compartment syndrome from prolonged surgery in the lithotomy position. Ann Fr Anesth Reanim 1999;18(7):779-782. 104. Echtermeyer V, Muhr G, Oestern HJ, Tscherne H. Chirurgische Behandlung des Kompartiment-Syndroms. Unfallheilkunde 1982;85 : 144-152.
Blackman PG. A review of chronic exertional compartment syndrome in the lower leg. Med Sci Sports Exerc 2000;32(3 sup p l ): S4-S 1 0 . 106. Schepsis AA, Gill SS, Foster TA. Fasciotomy for exertional anterior compartment syndrome: is lateral compartment release necessary? Am J Sports Med 1 999;27(4) :430-435. 107. Swierstra JCc, Klasen HJ. Het tibialis anteriorsyndroom. 1 05.
Geneeskd Sport 1970;2(3) :45-46. 108.
Sheridan GW, Matsen FA. Fasciotomy in the treahnent of the acute compartmental syndrome. j Bone joi n t S u rg 1976;
109.
Conti SF. Posterior tibial tendon problems in athletes. Orthop
58A: 1 1 2-115.
Clin North Am 1 994;25(1): 1 09-1 21 .
Devereaux MD, Parr GR, Lachman SM et al. The diagnosis of stress fractures in athletes. ]AMA 1984;252:531-533. 1 1 1 . Batt ME, Ugalde V, Anderson MW, Shelton DK. A prospective controlled study of diagnostic imaging for acute shin splints. 110.
Med Sci Sports Exerc 1 998;30(11 ) : 1 564-1 571 . 112.
Anderson MW, Ugalde V, Batt M, Gacayan J. Shin splints: MR appearance in a preliminary study. Radiology 1 997;204(1):
113.
Jackson
1 77-180.
D.
Shinsplints:
an
update.
Phys
Sports
Med
1 978;6:51-61.
American Medical Association. Sta ndard Nomenclature of Athletic Injuries. American Medical Association, Chicago, 1976. 1 1 5 . Orava S, Puranen ]. Athlete's leg pains. Br J Sports Med 1979; 114.
13;92-97. 116.
Orthop Rev 1992;21 (1):105-107.
O'Donoghue DH. Treatment of injuries to Athletes, 3rd edn. Saunders, Philadelphia, 1976. 92. Vei th RG, Matsen FA, Newell SG. Recurrent anterior compart mental syndromes. Physician Sportsmed 1980;8(11 ). 93. Arai M, Endoh H . Blood flow through human skeletal muscle, during and after contraction. Tohoku J Exp Med 91.
Schissel DJ, Godwin J. Effort-related chronic compartment syn drome of the lower extremity. Mil Med 1999;164(11) :830-832. Reneman RS. The An terior and Lateral Compartmellt Syndrome of the Leg. Mouton, Hague, 1968 : 1 76. Harman W. Significance of local vascular phenomena in ischaemic necrosis in skeletal muscle. Am ] Path 1948;24:625. Mubarak SJ, Hargens AR, Owen CA et al. The wick catheter technique for measurement of intra-muscular pressure. A new research and clinical tool. ] Bone Joint S u rg 1976;58A: 1 0 1 6-1020. Pedowitz RA, H a rgens AR, Mubarak SJ, Hershuni D H . Modified criteria for the objective diagnosis of chronjc com partment syndromes of the leg. Am j Sports Med 1990;18:35-40. McQueen M. Acute compartment syndrome. Acta ChiI' Belg
101.
87.
1992;16(11) :33-35.
DISORDERS OF THE LOWER LEG 1201
1998;98(4 ) : 1 66-170. 1 00.
Rev Chir Orthop Reparatrice Appar Mot 1999;85(3):277-285. 84.
-
Detmer DE. Chron.ic shin splints. Classification and manage ment of medial tibial stress syndrome. Sports Med 1986;3(6): 436-446.
Prather Je Nuzynowitzi ML, Snody AJ et al. Scintigraphic findings in stress fractures. ] Bone Joint S u rg 1977;59A:896. 118. Gilaldi M. Comparison between radiography, bone scan and ultrasound in the diagnosis of stress fractures. Milit Med
1 1 7.
1 984;149:459-461 . 1 19.
Holder LE. Radionuclide bone-imaging in the evaluation of bone pain. J Bone Joint S u rg 1982;64A: 1391-1396.
1202 SECTION FOURT E E N - THE LOWER LEG, ANKLE AND FOOT
120.
Zwas ST, El kanovitch R, Frank G. Interpretation and classification of bone scintigraphic findings in stress features.
130.
J Nucl Med 1 987;28(4):452-457.
131.
Mann RA, Thompson F. Rupture of the posterior tibial tendon, causing flat foot. J Bone Joint S u rg 1985;67A:556-561 . 1 22. Frey Cc, Shereff MJ. Tendon injuries about the ankle in athletes. Ciill Sports Med 1988:7:103-1 18. 123. Johnson KA. Tibialis posterior tendon rupture. Ciin Orthop Rei 121 .
Res 1983;117 : 1 40-147. 124.
Funk DA, Cass JR, Johnson KA. Acquired adult flat foot sec ondary to posterior tibial tendon pathology. J Bone Joint Surg
1 25.
Johnson KA, Strom DE. Tibialis posterior tendon dysfunction.
132. 133. 134.
148-150.
1986;68A:95-102. 135.
Ciin Orthop 1989;239: 1 96-206. 1 26.
Hansen ST, Clark W. Tendon transfer to augment the weakened tibialis posterior mechanism. JAMA 1 988;78: 309-402.
Mendicino SS, Qu ilm M. Tibialis posterior dysfunction: an overview with a surgical case report using a flexor tendon transfer. J Foot S u rg 1989;28:154-157. 1 28. Sammarco GJ. Peroneal tendon injuries. Orthop Ciin North Am 1 27.
1994;25 ( 1 ) : 1 35-145. 1 29.
Jackson MA, Gudas CJ. Peroneus longus tendinitis: a possible biomechanical etiology. J Foot S u rg 1982;21(4):344-348.
Anderson E. Stenosing peroneal tenosynovitis symptomatically simulating ankle instability. Am J Sports Med 1987;157:258-260. Sammarco GJ, DiRaimondo cv. Chronic peroneus brevis tendon lesions. Foot Ankle 1989;9(4) : 1 63-170. McLennon JG. Treatment of acute and chronic luxations of the peroneal tendons. Am J Sports Med 1980;8:422-436. Stover CN, Bryan DR. Traumatic di location of the peroneal tendons. Am J S u rg 1962;103:180-186. Martens MA, Noyez JF, Mulier Ie. Recurrent dislocation of the peroneal tendons. Results of rerouting the tendons under the calcaneofibular ligament. Am ] Sports Med 1986;14(2): Das De S, Balasubramaniam P. A repair operation for recurrent dislocation of peroneal tendons. ] Bone Joint S u rg 1985; 67B(4):585-587.
Poll RG. Duijfjes F. The treatment of recurrent dislocation of the peroneal tendons. J Bone Joint S u rg 1984;66B(1) :98-100. 137. Bisschop P, Deconinck R, Ombregt L, Van de Velde T. Workbook for the Cyriax Course in Orthopaedic Medicine. Belgian Scientific Society of Orthopaedic Medicine, 1986. 138. Guarantors of Brain. Aids to the Examination of the Peripheral Nervous System. Bailliere Tindall, London, 1986. 139. Brugger A. Die Erkrankungen des Bewegungsapparates und seines Nervensystems. Gustav Fisher, Stuttgart, 1980. 136.
Disorders of the ankle and subtalar joints
CHAPTER CONTENTS The ankle joint
1205
The capsular pattern 1205 Rheumatoid conditions 1206 Haemarthrosis 1206 Osteoarthrosis 1206 Injection or aspiration technique of the ankle joint Non-capsular patterns 1206 Immobilizational stiffness 1206 Loose body in the ankle joint 1206 Other lesions with a non-capsular pattern The subtalar (talocalcaneal) joint
1207
THE ANKLE JOINT
1211
The capsular pattern 1212 Rheumatoid disorders 1212 Subacute traumatic arthritis 1212 Osteoarthrosis 1213 Spasmodic pes planus 1213
The ankle is a very simple j oint, allowing only plantiflexion-dorsiflexion movement. Normally the foot comes into a straight line with the lower leg during plantiflexion and can be moved to less than a right angle during dorsiflexion (Fig. 84. 1 ).
Non-capsular patterns 1213 Immobilizational stiffness 1213 Loose body 1214
--;:: "�""'-,-�� �
THE CAPSULAR PATTERN
Painful conditions at the heel 1215 Plantar fasciitis 1215 Plantar fascial tear 1216 Heel pad syndrome 1216 Subcutaneous bursitis 1218 Subcutaneous nodules 1218 Ligamentous disorders - ankle sprains Inversion sprain 1219 Eversion sprain 1232
1206
The capsular pattern of the ankle joint is slightly more limitation of plantiflexion than of dorsiflexion (Fig. 84.2). 1218
Figure 84.1
The normal range of plantiflexion (upper) and dorsiflexion (lower).
Plantiflexion
Dorsiflexion
Figure 84.2 The capsular pattern at the ankle joint. 1 203
1 204 S ECTION FOURTEEN - THE LOWER LEG, ANKLE AND FOOT
In patients with short calf muscles, however, dorsiflexion ceases before the extreme of the possible articular range is reached, which raises the question of whether limita tion is capsular or non-capsular. In such a case, a clinical diagnosis of arthritis at the ankle rests entirely on the end-feel. Limitation of plantiflexion with a hard end-feel indicates an arthritis. If ful l dorsiflexion cannot be reached because of short calf muscles, a softer end-feel is detected.
RHEUMATOID CONDITIONS Rheumatoid conditions, so often affecting the other tarsal joints, are not found in the ankle joint. If it does become inflamed, this occurs only after a long evolution of the rheumatoid disease. Exceptions are psoriatic arthritis and gout which are not uncommon at this joint. In an acute arthritis without apparent precipitating cause, a gout attack must always be suspected, especially if the patient is a middle-aged man. Gout attacks the ankle joint in almost 50% of all gout patients. } It responds very well to one or two injections with 20 mg of triamcinolone.
triamcinolone may help but should not be repeated too often for fear of further destruction of the joint from steroid arthropathy. If the symptoms warrant and the condition worsens, arthrodesis is the only satisfactory outcome and is usually acceptable, provided the patient is fitted with ade quate shoes that permit walking without difficulties.
INJECTION OR ASPIRATION TECHNIQUE OF THE ANKLE JOINT Technique. This is a simple procedure. The patient lies in the supine position, the knee bent and the foot flat on the couch, which forces the ankle into some plantar flexion. The medial malleolus and the tendon of the tibialis ante rior are easily identified. The trochlea tali is found by flexing and extending the talus under the tibia. A 4 cm needle is introduced between the medial malleolus and the tibialis anterior tendon, just under the edge of the tibia (Fig. 84.3). The tip lies intra-articularly when i t strikes cartilage.
HAEMARTHROSIS IMMOBILIZATIONAL STIFFNESS Haemarthrosis of the ankle is not uncommon in ankle sprains. It occurs after a direct trauma, for example in soccer players. A capsular pattern at the ankle joint after an inversion sprain or a direct trauma always suggests haemarthrosis. Because blood is a strong irritant to carti lage and provokes early arthrosis, it should be evacuated a t once. A radiograph of the talus and I or a magnetic resonance image (MRI) must be taken to exclude osteo chondral fracture.2
Limitation of both plantiflexion and dorsiflexion often occurs after long-standing immobilization of the ankle. Only strong and daily mobilization of the joint will afford benefit. Traction and translation techniques can be of great value in the treatment of this post-immobilization stiffness.4 Some authors report increased motion and pain relief after arthroscopy. 5
LOOSE BODY IN THE ANKLE JOINT OSTEOARTHROSIS Osteoarthrosis is often the result of shearing strains, for instance after a mal-union of a tibiofibular fracture. Early arthrosis has also been reported after aseptic necrosis of the talus.3 In sports in which repeated and severe sprains of the ankle occur, such as rugby, football and judo, osteoarthrosis is common and often early. Clinical exam ination shows a capsular pattern with a hard end-feel . Sometimes ligamentous ossifications are visible o n the radiograph and confirm the clinical diagnosis. The best conservative treatment is to fit the patient's shoe with a higher heel, which enables walking without much dorsiflexion at the ankle joint. However, conserva tive treatment of painfu l osteoarthrosis is seldom satisfac tory. Sometimes one or two injections of 20 mg of
A loose body with an osseous nucleus is well known as a result of transchondral fracture (osteochondritis disse cans) of the dome of the talus. In most of the cases, the aetiology is inversion sprain. 6,7 The diagnosis is made from the radiograph or CT, and symptoms may warrant surgery. However, when there is only a loose cartilagi nous fragment without an osseous nucleus, radiographs are negative, and the diagnosis must be made almost entirely on the history. The patient complains mainly of twinges in the ankle during walking. This seems to happen especially when the foot is plantiflexed, for instance on walking down stairs. The twinge is sudden, unexpected and pre'vents continuing walking. When the foot is shaken, the disabil ity disappears and walking can continue. There may be
CHAPTER 84
-
D ISORDERS OF THE ANKLE A N D SU BTALAR J O I NTS 1 205
with the negative clinical and radiographic findings should always remind the examiner of the possibility of a loose body in the ankle joint.
DIFFERENTIAL DIAGNOSIS The differential diagnosis is between a loose body in the subtalar joint (p. 1 2 1 4 ), distal tibiofibular ligament deficiency (p. 1 230), a snapping peroneal tendon (p. 1199 ) o r an unstable ankle ( p . 1 229).
TREATMENT Treatment is manipulation. The aim is to shift the piece of cartilage into a position within the joint where it can no longer subluxate. This manipulation is performed several times at one session. It is impossible to evaluate the imme diate result because the usual clinical criteria, so useful in the assessment of loose bodies in other joints, are com pletely absent here. The patient is reassessed a week after manipulation, to determine whether the frequency of twinges has changed . If no improvement results and if the diagnosis is maintained, a Root's shoe can be tried: the anterior wedge to the heel enables the patient to walk without the foot reaching full plantiflexion.
Figure 84.3
Injection of the ankle joint.
several twinges on one day, or none for weeks. Between the bouts of twinges, no pain or disability is reported. Sometimes the patient states that the symptoms appeared after a severe sprain of the ankle; sometimes no previous trauma is remembered. Examination does not reveal anything because the sub luxation is only momentary, nor does the radiograph because the fragment is cartilaginous. Diagnosis is impossible if the typical history is over looked. Twinges during plantiflexion of the foot, together
Technique: manipulation. The patient lies supine on the couch, the heel exactly level with the edge. An assistant grasps the upstretched hands of the patient, to apply counter-traction during the manipulation (illustrated in Fig. 84.4). The contralateral hand is pl aced under the heel. Because it is the fulcrum, it must be protected from the hard edge of the couch by a thick foam-rubber pad. The ipsilateral hand encircles the foot from the medial side in such a way that the fifth metacarpal bone of the manipu lator comes into contact with the neck of the patient's talus. The thumb is placed at the plantar side in order to press the foot upwards in slight dorsiflexion. The manip ulator now leans back, pulling as hard as possible with the uppermost hand. Levering around the fixed heel, a strong circumduction movement is carried out, clockwise for the right foot and anticlockwise for the left foot. During this manoeuvre, the assistant provides counter traction. The circumductory movements are repeated several times during the same session. The result cannot be assessed until a week later.
OTHER LESIONS WITH A NON-CAPSULAR PATTERN Although plantiflexion and dorsiflexion at the ankle joint show a full range of movement, they can be painful at the
1 206 SECTION FOURTEEN - THE LOWER LEG, ANKLE A N D FOOT
Figure 84.4 Manipulation for a loose body in the ankle joint: starting position (upper), manipulation (lower left) and detail (lower right). For further information, see p. 1207.
end of range, showing that a structure is pinched or stretched.
SPRAIN OF THE ANTERIOR TIBIOTALAR LIGAMENT This is an uncom mon Injury, caused by a pure plantiflexion stress. The chronic aching that results from this type of trauma may last for many years and is never severe unJess the patient is, for example, a rugby or soccer player and needs full and painless p lantiflexion mobility at the ankle joint. Kicking a heavy ball from underneath is especially painful. Examination shows that full passive plantiflexion hurts at the front of the ankle, all the other movements, including resisted dorsiflexion of the toes, being painless. The tender spot at the front of the ankle can easily be defined if the tendons of the
dorsiflexors of the toes are pushed away. The anterior tibiotalar ligament is a very thin structure and therefore is difficult to inject. However, friction is extremely effective in this condition. The main difficulty is pushing the tendons away to reach the thin sheath of tissue joining the talus and the tibia. Three to six sessions of deep transverse friction normally suffice for cure. In soccer p layers, new bone may form on the upper surface of the talar neck, as a result of traction at the insertion of the ligament. This has been called 'soccer ankle'. 8 The diagnosis is made from the radiograph. If pain persists, the bone spurs may be removed surgically.
ACHILLES BURSITIS If the b ursa, normally found between the Achilles tendon, the upper surface of the calcaneus and the tibia
CHAPTER 84
-
DISORDERS OF THE ANKLE A N D SU BTALAR J O I NTS 1 207
The only effective treatment is one or two infiltrations with triamcinolone. This stops the tenderness immediately but the mechanism of the disorder must be explained to the patient so that he or she can take care to avoid the causative trauma. The soccer player has to adopt another technique in kicking the ball from underneath and the dancer must take care not to 'overpoint' the foot.
Figure 84.5 The Achilles bursa.
Technique: infiltration. The patient adopts a prone-lying position, the foot over the edge of the couch. The poste rior articular margin of the tibia lies approximately 2 cm above the line joining the tips of the malleoli. A 2 ml syringe is filled with a steroid suspension and fitted with a fine needle, 4 cm long. The Achilles tendon is pushed medially (Fig. 84.6). The needle is inserted vertically downwards, lateral to the Achilles tendon, 2 cm above
(Fig. 84.5), becomes inflamed then pain will be elicited when it is squeezed between the posterior side of the tibia and the upper surface of the calcaneus at the extreme of passive plantiflexion.9, 10 Full plantiflexion evokes pain, this time at the back of the heel. Rising on tiptoe remains negative, thus excluding the Achilles tendon as a cause. Palpation reveals a tender spot anterior to the tendon, close to the superior border of the calcaneus.11 Achilles bursitis responds extremely well to one or two injections of triamcinolone. The tender spot is identified, at the lateral or medial side, just in front of the Achilles tendon. Two ml of a 10 mg / ml triamcinolone solution are introduced into the area, following the normal rule of infiltration: over a three-dimensional space and with several insertions and withdrawals. The whole procedure is repeated after 2 weeks if the condition is not com pletely cured by then.
DANCER'S HEEL (POSTERIOR PERIOSTITIS) This is a bruising of the periosteum at the back of the lower tibia. The lesion lies at the junction of the cartilage and periosteum and is caused by pressure from the upper edge of the posterior surface of the talus. It happens in ballet dancers who, during training, develop a hypermo bility in plantiflexion at the ankle joint, usually as a result of pointe work. The repetitive engagement of talus against the posterior tibial edge induces periosteal bruising.12-14 Sometimes the condition results from one vigorous plantiflexion strain such as when a soccer player kicks the ball from underneath. The patient complains of pain at the back of the heel during plantiflexion. Clinical examination reveals an excessive range of movement and pain is reproduced by forced plantiflexion of the ankle. Dancer's heel must be differentiated from Achilles bursitis. In the latter the end feel is soft, giving the impression of pinching some tissue, whereas in a dancer's heel the end-feel is normal.
Figure 84.6 Infiltration of dancer's heel.
1 208 SECTION FOURTE E N - THE LOWER LEG, ANKLE A N D FOOT
the line connecting the malleoli. The difficult part of the whole procedure is now to palpate with the tip of the needle and feel for the line at which bone (tibial peri osteum) gives way to articular cartilage. The infiltration is now made by placing a line of little droplets all along and just above this cartilaginoperiosteal border.
PINCHING OF THE OS TRIGONUM Posterior ankle pain d uring extreme plantiflexion can also be caused by a periostitis of the os trigonum. This accessory bone, located just behind the talus, is found in about 10% of the population. 15 Sometimes the ossicle is fused to the talus and is then called Stieda's process. With extreme plantiflexion, such as in ballet or soccer, the os trigonum may be pinched between talus and tibia and produce periostitis and pain.16 The clinical diagnosis is made when a posterior pain during passive plantiflexion is seen in combination with slight limitation of plantiflexion movement and a hard end-feel. Diagnosis can be confirmed by a MRI examinationP Sometimes a painful outcrop can be palpated in the posterior triangle. Martin 18 noted that this not only reduced dorsiflexion mobility but that painfully resisted plantiflexion of the big toe was also present. This is caused by fibrosis of the flexor hallucis longus tendon in the fibro-osseous canal behind the talus. Treatment is infiltration with triamcinolone. If pain persists, surgical removal can be considered.
ANTERIOR PERIOSTITIS The converse of a dancer 's heel is a periostitis at the ante rior margin of the tibia. This is caused by pressure of the anterior lip of the tibia on the talar neck during an extreme dorsiflexion movement at the ankle. 19 The typical injury inducing this lesion is a gymnast landing flat on the feet but with the knees bent so that the ankle is forced into extreme dorsiflexion. The result is immediate pain at the front of the ankle. The sharp component of the pain disappears but the lesion does not completely heal, leaving the patient with pain during extreme dorsiflexion movements. In ballet dancers, repeated and extreme dorsiflexion necessitated by the demi-plie position can lead to periostitis of the anterior tibial lip.2o,21 Examination shows a full range of movement with pain at the front of the ankle during extreme dorsiflexion. In mild cases, the pain will be evoked only when the foot is dorsiflexed during weight bearing (squat with the feet flat on the ground ). Treatment is one infiltration with triamcinolone, along the anterior tibial margin. This is within the reach of a palpating finger and therefore the infiltration is easy to perform. The results ate good. In recurrent cases the
Figure 84.7 The posterior talofibular ligament.
patient is referred for arthroscopic removal of the bony impingement.22
SPRAIN OF THE POSTERIOR TALOFIBULAR LIGAMENT Sprain of the posterior talofibular ligament (Fig. 84.7) is rare. The diagnosis is difficult to make if the examiner is not aware of the possibility of this lesion being present. The only painful movement during the routine functional examination is passive eversion of the foot during full plantiflexion - a movement performed to test the anterior fasciculus of the deltoid ligament. If the pain is postero lateral instead of anteromedial, it is obvious that a tissue is being pinched rather than stretched and the condition can be considered. The treatment of choice is an injection of triamcinolone into the tender ligament; one injection gives lasting relief. Although deep transverse friction can be used, it is very difficult to reach the lesion with the tip of a finger.
JUM PER'S SPRAIN (LATERAL PERIOSTI TIS) This is one of the classic lesions of high jumpers. Before the athlete takes off to jump, the foot is forcefully twisted in valgus and dorsiflexion. Apart from lesions at the inner side of the ankle (strain of the deltoid ligament and elon gation of the tibialis posterior tendon), compression at the outer side can result. During this extreme movement, the superolateral aspect of the anterior margin of the calca neus can impinge against the inferior and anterior edge of the fibula and produce bruising, which results in a traumatic periostitis.23 Sometimes the impingement leads
CHAPTER 84
-
D ISORDERS OF THE A N K LE A N D SUBTALAR J O I NTS 1 209
to chronic inflammation of the talofibular ligament, result ing in hypertrophic scar tissue.24 Examination reveals nothing if only the standard func tional tests are performed. When the possibility of this lesion is suspected, combined dorsiflexion-valgus move ment is performed to reproduce the pain (Fig. 84.8). If this manual stress is not sufficient to elicit the usual pain, the patient is asked to stand, squat with the foot flat on the ground and twist the heel into valgus. Palpation reveals localized tenderness at the anterioinferior surface of the fibula. One or two injections of triamcinolone bring total relief, provided the athlete avoids repeating the same trauma. Normally a slight inner wedge (0.5 em) within the shoe is needed, which prevents further bruising of the fibula during 'take-off'. Those patients refractory to conservative treatment require arthroscopic debridement.25,26 Disorders of the ankle joint are summarized in Table 84. 1 . Figure 84.8 Accessory test in jumper's sprain.
THE SUBTALAR (TALOCALCANEAL) JOINT The subtalar joint allows movement in two directions only: varus and valgus. Motion takes place around an
axis through the talus (Fig. 84.9), the axis being at 1 5° medial angle to a line drawn through the calcaneus and the second metatarsal.
Table 84.1 Summary of disorders of the ankle joint
Capsular pattern
Non-capsular patterns
Lesion
Symptoms
Signs
Treatment
Haemarthrosis
Trauma Nocturnal pain
Capsular pattern Warmth/fiuid
Aspiration
Rheumatic arthritis
Pain/morning stiffness
Capsular pattern
Triamcinolone
Osteoarthrosis
Pain on weight bearing
Capsular pattern Crepitus
Mobilization Higher heel Arthrodesis
Immobilizational stiffness
After plaster immobilization
Li mitation of plantifiexiondorsifiexion
Mobilization
Loose body
Twinges
Full range/no pain
Manipulation
Sprain of the anterior tibiotalar ligament
Anterior pain
Pain at full plantifiexion
Deep friction
Achilles bursitis
Posterior pain
Pain at full plantifiexion Soft end-feel
Triamcinolone
Dancer's heel
Posterior pain
Pain at full plantifiexion Hypermobility
Triamcinolone Surgery
Periostitis os trigonum
Posterior pain
Pain/limitation of plantiflexion
Triamcinolone
Anterior periostitis
Anterior pain
Pain at full dorsifiexion
Triamcinolone
Sprain of posterior talofibular ligament
Posterolateral pain
Pain at full plantifiexion and eversion
Triamcinolone Surgery
Jumper's sprain
Anterolateral pain
Pain at full dorsiflexion and eversion
Triamcinolone
1 2 1 0 SECTION FOURTEEN - THE LOWER LEG, ANKLE A N D FOOT
case of an acute joint inflammation, gout should not be forgotten.
TREATMENT valgus
varus
Figure 84.9
Normal varus and valgus movement at the subtalar joint.
'THE CAPSULAR PATTERN 1.:.1:,...._ ,'--�,.,� •
.f.
"
•
•
•
,,""---'
____
....�_t.:
The capsular pattern (Fig. 84.1 0 ) is progressive limita tion of varus with, in the end, fixation in valgus. The valgus position is maintained by spasm of the peronei muscles.
RHEUMATOID DISORDERS In addition to the limitation of movement towards varus by muscle spasm, local heat is present and synovial thick ening can be palpated . Very often, the midtarsal joint is affected as well (see p. 000). In rheumatoid arthritis, the arthritis is often accompanied by the characteristic changes in other joints. The possibility of a n early ankyl osing spondylitis should be kept in mind when a young patient presents with arthritis of the subtalar joint. In the
Valgus
Figure 84.10
The capsular pattern at the subtalar joint.
Apart from the causative treatments for rheumatoid dis orders, triamcinolone injected into the joint relieves the pain very quickly and, even if the range of movement does not increase, the patient can enjoy some comfort for months or even years. If the pain reappears after a short interval, it is not wise to continue the injections. Technique: injection. A 2 ml syringe is filled with steroid suspension and fitted with a thin 2 cm needle. Because there may be muscle spasm, the joint is fixed in valgus to create room to insert the needle from the medial side, which must be done just above the sustentaculum tali and parallel to the joint surface. The index finger of the palpating hand is placed at the lateral end of the sinus tarsi (Fig. 84. 1 1 ). The needle is moved in the direction of and slightly anterior to the palpating finger. Usually it meets bone after 1 cm. The needle must then be manoeu vred until it is felt to slip in further without resistance. The tip then lies within the anterior chamber of the joint, and 1 ml of the suspension is injected. The needle is then partly withdrawn and reinserted in a 45° posterior direc tion, where it enters the posterior chamber, and the remaining 1 ml is injected.
SUBACUTE TRAUMATIC ARTHRITIS Sometimes recovery after a serious varus sprain at the ankle is unduly delayed by pain and limitation of move ment in the ankle and midfoot. Examination reveals that the limitation of varus movement is caused by a spasm of the peroneal muscles. Usually the midtarsal joint is also affected. Palpation sometimes reveals warmth over the subtalar and midtarsal joints. Untreated, this condition can last for months or even years. Very often a wrong diagno sis of posttraumatic adhesions is made. If the limitation of varus movement at the talocalcaneal joint, together with the muscle spasm and the warmth are missed, such patients will probably be treated by mobilization, or even manipulation, which aggravate the condition. Patients suffering from this condition are often regarded as mentally unstable but it should be remem bered that in psychological disorders with projection to the foot, the heel is always fixed in varus, not in valgus. Treatment consists of two injections of 20 mg triamci nolone into the joint, at an interval of 2 weeks. If this treatment fails, the joint is immobilized for several ' months in plaster, which is done in as much varus posi tion as possible, sometimes after blocking the peroneal nerve.
--------�--
CHAPT E R 84
-
�
DISORDERS OF THE AN KLE A N D SU BTALAR J O I NTS 1 2 1 1
Figure 84.11 Injection of the subtalar joint (upper). Direction of the needle in relation to the palpating finger in the lateral opening of the sinus tarsi (lower).
OSTEOARTHROSIS This is a common disorder after an intra-articular fracture of the calcaneus. Diagnosis is made when a typical hard end-feel is detected, in the context of a previous fracture. The pain is incurable by conservative measures, including intra-articular injections. Persistent pain after an intra-articular fracture can only be relieved by arthrodesis.
SPASMODIC PES PLANUS This is discussed on page 1 292.
IMMOBILIZATIONAL STIFFNESS Marked limitation of movement at the talocalcaneal joint can result from plaster immobilization for tibiofibular fractures. There is a stiff joint, with an equal limitation of varus and valgus and without muscle spasm. The joint is in mid-position, whereas in arthritis it fixes in valgus. Capsular thickening and warmth are absent. Treatment consists of manual mobilization, which is technically difficult, for there is no lever, and the small size of the calcaneus affords very little purchase. Sometimes many months of repeated forcing will be
1 2 1 2 SECTI O N FOURTE E N - T H E LOWER LEG, ANKLE A N D FOOT
If an impaction of a loose body in the subtalar joint is suggested by a history of twinges or if repeated attacks of sudden fixation in valgus are mentioned, reduction must be attempted at once. Very often it succeeds immediately but the cartilage fragment is seldom permanently moved into a position from which it no longer subluxates. It is therefore wise to repeat the manipulation several times at intervals of a few days. If no permanent relief is obtained and the signs warrant it, arthrodesis is advised.
Figure 84.12
Mobilizalion for immobilizational stiffness of the subtalar joint.
necessa ry. Restoration of a full range is not always essen tial, because slight limitation of range of movement is still compatible with good function.
Technique: manipulation. The patient lies prone, pulling up at the upper edge of the couch until the dorsum of the foot engages the lower edge. This forces the foot into slight plantiflexion. The manipulator stands behind the patient and locks both hands around the heel, so that the crossed fingers are placed between the dorsum of the foot and the edge of the couch. The fingers are protected by a thick layer of foam. The thumbs are crossed at the dorsum of the calcaneus. In order to exert the utmost pos sible traction, the feet are placed against the legs of the couch and the body leans backwards. The elbows stay in line with the calcaneus, the abdomen close to the patient's foot (Fig. 84.1 3). The traction produced by the
Technique: mobilization. The patient lies face upwards on the couch. The therapist stands at the patient's foot. The fi ngers are clasped behind the heel and the calcaneus is grasped as strongly as possible between the palms of the hands. The elbows are brought forwards in order to dorsiflex the foot. This position (Fig. 84. 12) immobilizes the talus in the mortice. Mobilization is performed by swinging the body from one side to the other. This forcing must be repeated for 10 to 20 minutes at each session, and with the greatest possible vigour.
LOOSE BODY The patient experiences painful twinges, usually pro voked by walking on uneven surfaces, which may suggest instability of the ankle or an unstable mortice. Alternatively, the patient may have sudden attacks of pai nful fixation in valgus, provoked by a spasm of the peronei muscles. Clinical findings depend on when the examination is undertaken. If the patient has twinges only during certain movements, clinical examination is negative. If the patient presents during an attack of fixation, the typical valgus deformity and muscle spasm is found. Differential diagnosis from an articular disorder then depends entirely on the history because, in the case of a loose body, the patient states that pain and fixation are intermittent rather than permanent.
Figure 84.13
Manipulation for a loose body in the subtalar joint.
CHAPTER 84 - DISORDERS OF THE A N K LE A N D SU BTALAR J O I NTS 1 2 1 3
Table 84.2 Summary of disorders of the subtalar joint
Capsular pattern
Lesion
Symptoms
Signs
Treatment
Rheumatoid arthritis
Slow onset Other localizations
Warmth Capsular thickening Muscle spasm
Triamcinolone
Osteoarthrosis
After fracture
Hard end-feel
Arthrodesis
Subacute traumatic arthritis
Previous trauma
Muscle spasm Warmth
Triamcinolone Immobilization
Spasmodic pes planus
Youngster Little pain
Muscle spasm and midtarsal localization
Relief of weight bearing and support
Immobilizational stiffness
Plaster immobilization
Limitation of varus/valgus
Mobilization
Loose body
Twinges or fixation
Nothing or capsular pattern
Manipulation
Non-capsular patterns
Fixation in varus
Psychoneurosis
body weight is reinforced by a pronation movement of both forearms. Varus-valgus movements are forced at the joint by repea tedly swinging the shoulders from one side to the other. During the whole procedure, the patient is told to maintain the pulling position and not to allow any downwards movement of the body. Disorders of the subtalar joint are summarized in Table 84.2.
PAINFUL CONDITIONS AT THE HEEL Sometimes the patient has a clear history of pain at or about the heel but there are no findings on clinical examination. If the complaints consist of twinges, attention is drawn to the possibility of a loose body either in the ankle joint or in the subtalar joint. If mention is made of a feeling of giving way, instability of the ankle should be suspected. The pos sibility of referred pain from a Sl structure (Sl nerve root or sacroiliac joint) should also be kept in mind. However, if the patient has constant pain during standing and walking but there are no signs on clinical examination, pinching of inflamed tissue underneath the heel can be the cause.
PLANTAR FASCIITIS Plantar fasciitis is the most common d iagnosis for pain in the inferior aspect of the heel. It primarily afflicts the middle aged and elderly. It is more common among middle-aged athletes where it accounts for about 1 0% of running injuries. The diagnosis is relatively easy to establish because of the typical presentation. A patient suffering from an overstrained plantar fascia complains of localized pain at the inner aspect of the sole during weight bearing. The first steps taken after si tting or lying are especially
painful. Except when caused by an inflammatory condi tion, the lesion is usually an overuse phenomenon, occurring in the presence of pred isposing anatomical, biomechanical or environmental factors that put too much strain on the plantar fascia.27,28 The condition seems to be more common in people with a valgus deformity, because this fl attens the foot and puts more strain on the fascia.29 Short calf muscles can also be the cause of an overstrained fascia. In this condi tion, the Achilles tendon tends to pull the heel upwards during standing, which stresses the longitudinal arch and the fascia.3D Functional examination of the foot and the ankle is negative. The only positive sign is the detection of a point of deep tenderness, usually situated at the anteromedial portion of the calcaneus - the origin of the plantar fascia. Exceptionally, the tenderness is not at the tenoperiosteal junction but in the body of the fascia, between its origin on the calcaneus and the forefoot. Ultrasound examina tion can objectively confirm the clinical diagnosis31-33 but is usually not needed. Traction spurs, coming forward at the anterior border of the calcaneus, are commonly seen on radiographs and traditionally have been implicated as the cause of the painful heeP4 However, there is no relation between the spur and pain. The cause of the pain is the plantar fascial tendinitis resulting from excessive tension. The presence of a spur does not determine whether or not the patient has symptoms, because a spur is very often not found i.n patients with obvious signs and symptoms of plantar fasciitis. Therefore a radiograph is of no particular assis tance in the d iagnosis of plantar fasciitis.
TREATMENT The classical conservative treatment methods range from the application of a heel cup, heel cushion, walking cast
1 2 14 S ECTION FOURTEEN - T H E LOWER LEG, AN KLE A N D FOOT
(a )
(b)
Figure 84.14 The upper surface of the shoe heel should not be sloping (a) but should be flat (b).
and steroid injection to rest, ice and anti-inflammatory drugS.35 Recently some good results have been reported with the application of a dorsiflexion night splint (ankle splinted in neutral position and the toes in dorsiflexion) over 1-2 months.36,37 We have found the combination of alleviating the strain on the plantar fascia and one or two localized infi ltrations with triamcinolone to be effective in almost every case of plantar fasciitis. The most important measure to alleviate tension on the p lantar fascia is to raise the heel horizontally by 5-1 0 m m, which will drop the forefoot during weight bearing. This has a double effect: first, it shortens the distance between meta tars us and calcaneus and therefore directly relieves the fascia from strain; second, it removes the tension on the Achilles tendon and therefore indirectly relaxes the tension on the fascia. A high heel can afford i mme diate relief, provided the upper surface is horizontal and not wedge shaped as is the case in women's shoes (Fig. 84. 1 4); in the latter, a wedge that is thicker anteriorly is placed in the shoe to render the upper surface of the heel horizontal. Sometimes this simple orthotic measure does not suffice, and triamcinolone must be injected into the inflamed tissue. However, this must always be followed by use of a raised heel. Strengthening of the short plantiflexor muscles also affords a good active protection against further overstretching of the plantar fascia. Results of the infiltration depend entirely on its accu racy. It is extremely important to localize exactly the site and the extent of the lesion before the needle is intro duced. Palpation and infiltration should therefore be done with great care. Some authors even suggest placing the needle under ul trasound guidance38,39 although this is seldom really necessary. In the exceptional case that conservative treatment fails, the patient is sent for operative plantar fascia release: The results in terms of symptomatic relief are generally good.4o If an abnormal valgus position of the heel is present, a small inner wedge should be built in as well.41 ,42 Technique: injection. The patient lies prone on the couch, the knee flexed to a right angle. The therapist stands level wi th the foot. One hand encircles the heel, the thumb is
placed on the painful spot. A 2 ml syringe is filled with triamcinolone and a needle (4-5 cm long) is fitted to it. A point is chosen along the medial border of the fascia, about 3 cm distal to the lesion. The reason for inserting the needle so far away from the lesion is that the skin overlying the tender spot is too thick to be sterilized. Furthermore, if an oblique approach is made, the needle is thrust in, in the same direction as the fascial fibres, and points directly at the tenoperiosteal junction. The patient's foot is held in dorsiflexion, either with the dorsum of the injecting hand or by an assistant. This position renders the plantar fascia taut and creates more room for the needle, which aims towards the palpating thumb on the tender spot. After traversing the resistant fascia, it touches bone (Fig. 84. 15). The affected area at the tenoperiosteal border is now infiltrated. This is a very painful injection. The severe pain will last 24-48 hours and the patient must be warned that it may be impossible to stand or to walk during that time. The patient is re-examined after 14 days. If the condition has not completely resolved, a second injection is given. Combined with a raised heel, the results of the injection are uniformly good. Alternatively, tenotomy of the fascial origin at the heel under local anaesthesia may be required.43 This minor operation is followed by a couple of days' bed rest and exercises for the short plantiflexor muscles of the foot.
PLANTAR FASCIAL TEAR Like a ruptured Achilles tendon, a plantar fascial tear occurs mostly in middle-aged athletes.44 The presentation is a sudden pain in the midfoot during a sprint or a jump. There is an area of ecchymosis on the sole.45 Palpation reveals a tender and swollen area at the medial plantar aspect of the foot.46 Immediate treatment is reduction of the haematoma and swelling by ice and elevation. Strapping, together with strengthening exercises of the foot muscles, is given to support the medial arch. Deep friction to prevent adherent and painful scarring is applied as soon as possi ble. Full recovery occurs in 3-4 weeks.
HEEL PAD SYNDROME Inflammation of the heel pad between the calcaneus and the skin of the heel is also called superficial plantar fasci itis.47 The heel pad (Fig. 84. 16) consists of fatty tissue and elastic fibrous tissue, enclosed within compartments formed by fibrous septa; these connect the skin of the heel with the calcaneal periosteum . The fat pad acts as a shock absorber.48 It can become inflamed after a direct
C HAPTER 84
Figure 84.15
DIS O R D E RS OF T H E ANKLE A N D SU BTALAR J O I NTS 1 2 1 5
Injection i n plantar fasciitis.
blow or repeated minor injuries.49 The pain is felt all over the posterior part of the sole, especially during weight bearing. Examination shows nothing in particular except uniform tenderness over the whole inferior surface of the heel . It was recently demonstrated that the affected heel pad in plantar heel pain syndrome was stiffer under light pressure than the heel pad on the painless side and it was
Figure 84.16
-
Localization of tenderness in heel pad syndrome
hypothesized that this was caused by the changed nature of chambered adipose tissue.50
TREATMENT The measures that are so effective in treating plantar fasciitis, such as raising the heel and injecting steroid, are of no value in this condition. However, effective treat ment is injection of 10 ml of a local anaesthetic into the pad between the surface of the calcaneus and the superficial fascia. Technique: injection. The patient lies prone, with the knee flexed to a right angle. The physician stands at the foot, and encircles the heel with one hand. A 10 ml syringe is filled with procaine 0.5% and fitted to a needle 5 cm long. The needle is thrust in horizontally between calca neus and skin (Fig. 84.17). The tip of the needle is then moved some centimetres until it lies at the centre of the heel. The solution is injected there and diffuses over the whole area, forming a l arge, tense swelling. Significant pressure is needed to force in the last millilitre. The condition starts to improve after a few days. The patient should have another injection a week later, if
12 1 6 SECTI O N FOURTEEN - THE LOWER LEG, ANKLE A N D FOOT
Figure 84.17
Injection in heel pad syndrome.
necessary. It is astonishing how a couple of injections with anaesthetic cures patients who have suffered months or years of persistent and intractable heel pain.
SUBCUTANEOUS BURSITIS There is not an anatomical bursa between the posterior aspect of the calcaneus and the skin, but in some cir cumstances a bursa may form, particularly when narrow and ill-fitting shoes are worn, especially if they are curved in at the upper posterior edge. 51 Friction of the hard border against the calcaneus results in an adventi tious bursa. Chronic irritation will thicken the walls of the bursa and also the overlying skin. Palpation reveals a very tender spot at the posterior and upper surface of the calcaneus or at the lower extent of the Achilles tendon. The bursa is usually visibly inflamed and may contain some fluid. An excessive prominence of the bursal projection on the posterosuperior aspect of the calcaneus in combination with a swollen and painful bursa is called Haglund's disease.52 The initial treatment is to alter the back of the shoe and introduce a rubber pad at the lower half of the back of the calcaneus, which keeps the upper half away from the pressing edge. If this does not succeed, the bursa can be drained by aspiration followed by infiltration of 10 mg of triamcinolone. If such conservative treatment does not succeed, excision may be advised. The results of surgery are satisfactory, provided a dequate bone has been resected. 53,54
SUBCUTANEOUS NODULES At the posterior aspect of the calcaneus, nodules may form in the subcutaneous fascia and can cause severe pain when they are pinched between the calcaneus and the back of the shoe. Examination reveals small, tender nodules at the lower posterior border of the heel. They are the size of a rice grain and can be felt slipping to and fro under the palpating finger. Sometimes only one nodule can be palpated. The initial approach to treatment is to provide shoes with a gap posteriorly, al though this is not always acceptable to the patient. Division of the nodules by sub cutaneous tenotomy under local anaesthesia gives very good results and is easy to perform.
LIGAMENTOUS DISORDERS - ANKLE SPRAINS 'Sprained ankle' is the general name for a variety of trau matic lesions to the posterior segment of the foot. It is a very common sports injury. Several conditions are so described, varying from a simple strain of the ligaments to avulsion fractures and fractu re-dislocations. Sometimes only one structure is injured, sometimes severa1.55 In this book, there will not be a discussion of bony lesions or of fractu re-dislocations. H owever, it is important not to miss these during a routine clinical
CHAPTER 84
-
D ISORDERS OF T H E AN KLE A N D SU BTALAR J O I NTS 1 2 1 7
examination. The di agnosis should then b e confirmed by'radiography. Sprained ankles have been classified according to the causative stress (varus-valgus), the tissue damaged (liga ment, tendon or bone) or the degree of damage (grade I, II or III) and the time elapsed since the causative accident (acute, subacute or chronic) (see Box 84. 1 and Tables 83.3 and 83.4). The severity of a sprain involving a ligament is usually expressed in grades: grade I - slight over-stretching and elongation of the fibres without macroscopic disruption of their integrity; grade II - a severe sprain with a partial rupture of the ligament; grade I I I - total rupture. Clinically, the degree of damage is always hard to evalu ate, especially shortly after injury. Even technical investi gations, such as stress radiographs, arthrograms and tenograms, do not always provide an accurate diagnosis. Therefore a classification into grades is not used in this book.
INVERSION SPRAIN This is by far the commonest sports injury. In Holland 150 000 cases occur each year, 56 a quarter of all acute sports injuries. 57 Maehlum and Daljord58 found that of 4673 patients treated for sports injuries at an Oslo emer gency clinic, 1 6% had an inversion sprain. Soccer, basket ball and cross-country running are especially plagued by these injuries. 59,6o
MECHANISM The origin of an inversion sprain is usually an indirect force produced against an inverted and plantiflexed foot when the weight of the body forces the talus to rotate61 and twists the forefoot into supination and adduction. Hirsch and Lewis62 demonstrated that a rotational force of only 5-8 kg can produce a rupture of the anterior talofibular ligament. The site of the lesion will depend largely on the degree of plantiflexion during inversion63,64 (Fig 84. 18): • If the ankle is in the neutral position or slightly dorsiflexed during the excessive varus movement, the calcaneofibular ligament is damaged. • If the ankle is plantiflexed during the varus stress, the talus becomes involved in the movement and undergoes a medial rotation. This imposes the greatest stress between talus and fibula and the anterior talofibular ligament becomes stretched. • When not only do the ankle and subtalar joints undergo indirect violence but the midtarsal joints and the forefoot are also twisted into full plantiflexion, with supination and adduction, the stress tends to fall
Figure 84.18
Mechanism of inversion sprains: varus and supination in increasing
plantifiexion.
•
on more distally localized structures such as the calcaneocuboid ligament, the insertion of the short peroneal tendon at the fifth metatarsal bone or the cuboid-fifth metatarsal joint. During complete plantiflexion of the ankle, with slight or no varus movement, the anterior tibiotalar ligament or the tendons of the extensor digitorum longus may be damaged.
Most authors only mention the talofibular and calca neofibular ligaments.65,66 Very often, however, lesions of the calcaneocuboid ligament and tendinous lesions of the peronei and the long extensor of the toes result from an ankle sprain. It is very important to note that i n most cases of sprained ankle, a combination of lesions occurs. The coz monest association is a sprain of the fibular collateral lig ament together with the calcaneocuboid ligament. Injury to all these structures may be correctly described by the patient as a ' sprained ankle'. It is important to realize that, after a so-called varus sprain, not only ligamentous but also osseous lesions can occur. The most frequent lesions are fractures of both malleoli (Fig. 84.20): at the lateral malleolus a traction fracture, at the medial malleo lus a compression one. An avulsion fracture of the base of the fifth metatarsal is also not W1common. It is obvious that, if history or examination suggests a fracture, a plain radiograph must be taken. Decision rules for plain X-rays have been developed the so-called 'Ottawa rules'. A plain X-ray of ankle and foot should be asked for if the patient is over 60 years of
1 2 1 8 SECTION FOURTEEN - T H E LOWER LEG, ANKLE A N D FOOT
Table 84.3 Classification according to time since accident
Box 84. 1 Classification according to the site of the lesion (in order of descendi ng frequency67.68 - see Fig. 84. 1 9) -
1 2
F i b u l a r o r i g i n of a nterior talofi b u l a r l iga ment F i b u l a r orig i n of a nterior calcan eofi b u l a r l i gament
3
Ta l a r i nsertion of anterior talofi b u l a r l i g a ment
4 5
Lateral fi bres of calcaneocuboid l igament
6
Anterior t i b i otalar l ig a ment
Peroneal tendons
Stage
Time
I Traumatic inflammation
24-48
II Repair period
48
I I I Adherent scar tissue
>6
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).
-
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
-
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
-
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
REFE�ENCES 1. Dieppe PA, Calvent P. Crystals and Joint Disease. Chapman &
Hall, London, 2. Sijbrandij FS, Posttraumatic the talotibial
1982:145.
van Gils AP, Louwerens JW, de Lange EE. subchondral bone contusions and fractures of joint: occurrence of 'kissing' lesions. Aln J
Roelltgello/ 2000;175(6) : 1 707-1 710. 3. Trauth J, Blasius K. Die Talusnekrose und ihre Behandlung. Akt Traul/lato/ 1988;18:1 52-156. 4. Mink AJF, ter Veer HJ, Vorselaars JAC Extremiteiten, Functie ollderzoek ell IIlGll uele therapie. Bohn Scheltema and Holkema,
Utrecht/ Antwerp, 1990:454-46 1 . 5. Palladino SJ, Chan R. Adhesive capsulitis of the ankle. J Foot Surg 1987;26(6):484-491 .
27. Cornwall MW, McPoil TG. Plantar fasciitis: etioogy and treat
ment. J Orthop Sports Phys Ther 1999;29(12):756-760. 28. Quaschnick MS. The diagnosis and management of plantar
fasciitis. Nurse Pract 1996;21(4):50-54. 29. Katoh Y, Chao EY, Morrey BF. Objective technique for evaluat
ing painful heel syndrome and its treatment. Foot Allkle 1 983; 3:227. 30. Warren BC Anatomical factors associated with predicting
plantar fasciitis in long distance runners. Med Sci Sports Exec 1984;16:60. 3 1 . Tsai WC, Chiu MF, Wang CL, Tang FT, Wong MK. Ultrasound
evaluation of plantar fasciitis. Scand j Rheul11atol 2000;29(4): 255-259.
6 . Berndt AL, Harty M . Transchondral fractures (osteochondri
32. Kamel M, Kotob H. High frequency ultrasonographic findings
tis dissecans) of the tal us. ] Bone joint Surg 1959;41A(6):
in plantar fasciitis and assessment of local steroid injection. ] Rheumatol 2000;27(9):21 39-2141 . 33. Theodorou OJ, Theodorou SJ, Kakitsubata Y et al. Plantar fasci itis and fascial rupture: MR imaging findings in 26 patients supplemented with anatomic data in cadavers. Radiographics 2000;20: Spec 5181-5197. 34. Bassiouni M. Incidence of calcaneal spurs in osteoarthrosis and rheumatoid arthritis, and in control patients. Ann Rheum Dis
988-1 016. 7. Zinman C, Wolfson N, Reis NO. Osteochondritis dissecans of the
dome of the talus; computed tomography scanning in diagnosis and foLlow-up. J Bone Joillt Surg 1988;70A(7): 1017-1019. 8. McMurray TP. Footballer's ankle. ] Bone ]oillt Surg 1950; 328 :68-69. 9. Lohrer H. Seltene Ursa chen und Differentialdiagnosen der
Achillodynie. Sportverletz-Sportschaden 1992;5(4) : 1 82-185. 10. Hintermann B, Holzach P. Die Bursitis subachillea - eine
biomechanische Analyse und Klinische Studie. Z Orthop Ihre Grellzgeb 1992;130(2) :114-119. 11. Frey C, Rosenberg Z, Shereff MJ. The retrocalcaneal bursa:
anatomy and bursography. Foot Ankle 1992;13:203-207. 12. Hardaker TW Jr. Foot and ankle injuries in classical ballet dancers. Orthop Ciin North Am 1 989;20:621-627. 13. Quick R. Ballet injuries; the Australia experience. Ciin Sports Med 1983;2:507. 14. Demarais Y. Lesions articulaires micro-traumatique du pied 15. 16. 1 7.
18.
chez Ie danseur. Sci Sport 1986;1:331-361 . Johnson RP, Collier BD, Carrera GF. The os trigonum syn drome. Use of bone scan in the diagnosis. ] Trauma 1984;24:76 1 . Karasick 0, Schweitzer ME. The os trigonum syndrome: imaging features. Am ] Roen tgenoI 1996;166(1):1 25-129. Bureau NJ, Cardinal E, Hobden R, Aubin B. Posterior ankle impingement syndrome: MR imaging findings in seven patients. Radiology 2000;215(2) :497-503. Martin BF, Posterior triangle pain: the os trigonum. J Foot Surg 1 989;28(4):312-318.
19. Parker JCH, Hamilton WG, Patterson AH, Rawles JG. The
anterior impingement syndrome of the ankle. j Trauma 1 980; 20:895-898. 20. Kleiger B. Anterior tibial talar impingement syndrome in
dancers. Foot Allkle 1982;3:69. 21. Van Dijk, Marti R, Besselaar P. Aandoeningen van het beweg ingsapparaat bij ballet. Geneeskd Sport 1985;18:52-63. 22. Branca A, Di Palma L, Bucca C, Visconti CS, Di Mille M . Arthroscopic treatment o f anterior ankle impingement. Foot Ankle Jilt 1997;18(7)41 8-423. 23. Renstrom PA, Konradsen L. Ankle ligament injuries. Br J Sports Med 1997;31(1):1 1-20. 24. Jacobson KE, Liu SH. Anterolateral impingement of the ankle. J Med Assoc Ga 1992;81(6):297-299. 25. Ferkel RD, Karzel RP, Del Pizzo W, Friedman MJ, Fischer SP.
Arthroscopic treatment of anterolateral impingement of the ankle. Alii j Sports Med 1991;19(5) :440-446. 26. Kim SH, Ha KI. Arthroscopic treatment for impingement of the anterolateral soft tissues of the ankle. J Balle Joint Surg 2000; 828(7):1019-1021.
1 965;24:490. 35. Gill LH, Kiebzak GM. Outcome of nonsurgical treatment for
plantar fasciitis. Foot Ankle Int 1996;17(9):527-532. 36. Powell M, Post WR, Keener J, Wearden S. Effective treatment
of chronic plantar fasciitis with dorsiflexion night splints: a crossover prospective randomized outcome study. Foot Ankle Int 1 998;19(1):10-18. 37. Batt M, Tanji JL, Skattum N . Plantar fasciitis: a prospective
randomized clinical trial of the tension night splint. Ciill J Sports Med 1996;6:1 58-162. 38. Kane 0, Greaney T, Bresnihan B, Gibney R, FitzGerald O.
Ultrasound guided injection of recalcitrant plantar fasciitis. Am Rheum Dis 1998;57(6):383-384. 39. Tsai WC, Wang CL, Tang FT et al. Treatment of proximal
plantar fasciitis with ultrasound-guided steroid injection. Arch Phys Med Rehabil 2000;81 (10):1416-142 1 . 4 0 . Davies M S , Weiss G A , Saxby T S . Plantar fasciitis: how
successful is surgical intervention? Foot Ankle I n t 1999; 20(12) :803-807. 4 1 . Bates BT, Osternig LR, James MS, James LS. Foot orthotic
devices to modify selected aspects of lower extremity mechan ics. Am J Sports Med 1979;7:338. 42. Kwong PK, Kay 0, Voner RT, White MW. Plantar fasciitis. Mechanics and pathomechanics of treatment. Ciill Sports Med 1 988;7: 119-126. 43. Du Vries HL. Heel spur (calcaneal spur). Arch Surg 1957; 74:536-542. 44. Leach RT, Herrick S. Rupture of the plantaris fascia in athletes. j Bone Joint Surg 1 978;60A:537-539. 45. Ahstrom JP. Spontaneous rupture of the plantar fascia. Am I Sports Med 1988;16:306-307. 46. Kulund
O N . The Injured A thlete, 2nd edn. Lippincott, Philadelphia, 1988. 47. Cyriax J H . Textbook of Orthopaedic Medicine, vol. 1, Diagnosis of Soft Tissle Lesions, 8th edn. Bailliere Ti ndall, Lond on, 1982:433. 48. Jahss MH, Michelson JD, Desai P et 01. Investigations into the
fat pad of the sole of the foot: Anatomy and histology. Foot Ankle 1992;15 :233-242. 49. Bazzoli AS, Pollina FS. Heel pain in recreational runners. Phys Sportsl11ed 1989;17(2):55-6 1 .
1 236 S ECTIO N FOURTEEN - T H E LOWER LEG, AN KLE A N D FOOT
50. Tsai WC, Wang CL, Hsu TC, Hsieh FJ, Tang FT. The mechani
cal properties of the heel pad in unilateral plantar heel pain syndrome. Foot Ankle Int 1999;20(10) :663-668. 5 1 . Biedert R. Beschwerden im Acrullessehnenbereich. Aetiologien und therapeutische uberlegungen. Unfallchirurgie 1991;94(10): 531-537. 52. Stephens MM. Haglund's deformity and retrocalcaneal bursi
tis. Orthop Clill Nortll Am 1994;25(1):41-46. 53. Lehto MU, Jarvinen M, Suominen P. Chronic Achilles peri tendinitis and retrocalcanear bursitis. Long-term follow-up of surgically treated cases. Knee Surg Sports Traumatol Arthrosc 1 994;2(3): 1 82-185. 54. Sella FJ, Caminear DS, McLarney EA. Haglund's syndrome. J Foot Ankle Surg 1998;37(2): 1 1 0-114. 55. Boruta PM, Bishop JO, Braly WG, Tullos HS. Acute lateral
ankle ligament injuries: a literature review. Foot A 'lkle 1 990;11 (2) : 1 07-1 13. 56. De Bie RA, Hendriks HJM, Lenssens AE et af. KNFG-richtlijn
Acuut Enkelletsel. Ned Tijd Fysiotherapie 1998;108(1): suppl. 57. Ent FWC van der. Lateral Ankle Ligament Injury. Proefschrift,
Rotterdam, 1984. 58. Maehlum S, Daljord OA. Acute sports injuries in Oslo: a one
year study. Br J Sports Med 1984;18:181-185. 59. McMaster WD, Walter LM. Injuries in soccer. Am J Sports Med 1978;6:354-357. 60. Ekstrand J, Tropp H. The incidence of ankle sprains in soccer. Foot Ankle 1990;11:41-44.
76. De Lacey GJ, Bradbrooke S. Rationalising requests for X-ray
examination of acute ankle injuries. BMJ 1979;i:1 597-1598. 77. Vargish T, Clarke WR, Young RA, Jensen A. The ankle injury.
Indications for the selective use of X-rays. Injury 1983; 14:507-512. 78. Dunlop MG, Beattie TF, White GK, Raab GM, Doull R1.
Guidelines for selective radiological assessment of iJ1Version ankle injuries. BMJ 1986;293:603-605. 79. Van Ray HAM, Zeegers AVCM, Oostvogel HJM, Van der Wekken C. De waarde van het Rontgenonderzoek bij supi natieletsels van enkel en voet. Ned Tijdschr Geneeskd 1990; 134:1541-1 544. 80. Hoogenband CR, Moppes FI. Clinical diagnosis, arthrogra
phy, stress examination and surgical girding after inversion trauma of the ankle. Arch Orthop Tra u rn a Slirg 1984; 103: 1 1 5- 1 1 9 . 8 1 . Sanders
HWA, Betekenis van rontgenologische onder zoeksmethoden voor de diagnostiek van (laterale) enkelband laesies. Ned Tijdschr Geneeskd 1976;120:2053-2059. 82. Moppes FI van, Hoogenband CR van den. Diagnostic and Therapeutic Aspects of Inversion Trauma of the Ankle Joint.
Crouzen, Maastricht, 1982. 83. Fussell ME, Godley DR. Ankle arthrography in acute sprains. Clin Orthop 1973;93:278-290. 84. Nilsson S. Sprains of the lateral ankle ligaments. Part II. A con
trolled trial of different forms of conservative treatment. J Oslo City Hasp 1983;33:13.
6 1 . Lindstrand A. Lateral lesions in sprained ankle - a clinical and
85. Evans GA, Frenyo AD. The stress-tenogram in the diagnOSis of
roentgenological study with special reference to the anterior instability of the talus. Medical Dissertation, Lund University, Sweden, 1976. 62. Hirsch C, Lewis J. Experimental ankle-joint fractures. Acta
ruptures of the lateral ligament of the ankle. J Bone Joint Slirg
Orthop Scand 1965;36:408.
1979;618:347-351. 86. Black A, Brand R, Eickelberger MR. An improved technique
for evaluation of ligamentous injury of severe ankle sprains. Am J Sports Med 1 987;6:276-282.
63. Stephens MM, Sammarco GJ. The stabilizing role of the lateral
87. Kitaoka HB, Lee MD, Morrey BF, Cass JR. Acute repair
ligament complex around the ankle and subtalar joints. Foot
and delayed reconstruction for lateral ankle instability: twenty-year follow-up study. J Orthop Trauma 1997;11(7):
Ankle 1992;13: 130-136. 64. Wright IC, Neptune RR, van den Bogert AJ, Nigg BM. The
influence of foot positioning on ankle sprains. J B iornech 2000;323(5):513-519. 65. Brostrom L. Sprained ankles. I Anatomic lesions in recent
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
raphy a fter supination trauma of the ankle. Skeletal Radial 1998;27(5):256-261 . 69. McConkey J P. Ankle sprains, consequences and mimics. Med Sports Sci 1987;23:39-55. 70. Stiell IG, Greenberg GH, McKnight RD et al. Decision rules for
the use of radiography in acute ankle injuries. Refinement and prospective validation. lAMA 1993;269(9):1127-1132. 7 1 . Stiell IG, Greenberg GH, McKnight RD et al. A study to develop clinical decision rules for the use of radiography in acute ankle injuries. Ann Emerg Med 1992;21(4):381-390. 72. Akeson WH, Amiel D, Abel MF et al. E ffects of immobilization on joints. Clin Orthop 1987;219:33. 73. Enst W van. Distorsies van het enkelgewricht. Geneeskd Sport 1968;1:55-62. 74. Landeros 0, Frost HM, Higgins Cc. Post-traumatic anterior
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
treatment in lateral ankle sprains. Scand J Rehabil Med 1986;18:17-2 1 . 89. Roycroft S, Mantgani A B . Treatment o f inversion injuries of
the ankle by early active management. Physiotherapy 1983; 69:355-356. 90. Freeman MAR. The etiology and prevention of functional
instability of the foot. J Bone Joint Surg 1965;47B:678-685. 91. Speeckaert MTC. De behandeling van latera Ie enkelbandlae
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
eren of niet? Ned Tijdschr Geneeskd 1986;130(11):480-484. 94. Staples OS. Result study of ruptures of lateral ligaments of the
ankle. Clin Orthop 1972;85:50-58. 95. Ruth CJ. The surgical treatment of injuries of the fibular collat
eral ligament of the ankle. J Bone Joi"t Surg 1961;43A:229-239. 96. Caw D, Craft IL, Howells JB, Shaw Pc. Diagnosis and treat
ment of injury of lateral ligament of the ankle joint. Lancet 1 964;ii:720-723. 97. Klein J, Rixen D, Tilling T. Funktionelle versus gipsbehandlung
bei der frischen aussenbandruptur des oberen sprunggelenks. Unfallchirurgie 1991 ;94:99-104.
'
98. Brink PRG, Rum1e WC, Wever J. De functionele behandeling
van rupturen van de laterale enkelband. Ned Tijdschr Geneeskd 1988;132(15):672-676.
CHAPTER 84 - DISORDERS OF THE AN KLE A N D SU BTALAR J O I NTS 1 237
99. Klein J, Hoher J, Tilling T. Comparative study of therapies for fibular ligament rupture of the lateral ankle joint in competi tive basketball players. Foot Ankle 1993;14:320-324. 100. Moller-Larsen F, Wethelund 0, Jurik AG et at. Comparison of three different treatments for ruptured lateral ankle ligaments. Acta Orthop Swnd 1988;59(5):564-566. 101 . Sommer AM, Arza D. Functional treatment of recent ruptures of the fibular ligament of the ankle. [nt Orthop 1989;13:157-160. 102. Konradsen L, Holmer P, Sondergaard L. Early mobilizing treatment for grade III ankle ligament injuries. Foot Ankle 1991 ;12(2):69-73. 103. Kaikkonen A, Kannus P, Jarvinen M. Surgery versus functional treatment in ankle ligament tears. A prospective study. Clin Orthop 1996;326:194-202. 104. Eiff MP, Smith AT, Smith GE. Early mobilization versus immo bilization in the treatment of lateral ankle sprains. Am J Sports Med 1994;22(1):83-88. 105. 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. 106. Karlsson J, Eriksson BI, Sward L. Early functional treatment for acute ligamentous injuries of the ankle joint. Scand J Med Sci Sports 1996;6(6):341-345. 107. Peterson L, Althoff B, Renstrom P. Reconstruction of the lateral ligaments of the ankle joint. Proceedings of the First World Congress of Sports Medicine Applied to Football, Rome, Italy, Febr 1979:141 . 108. Cass JR, Morrey BF, Katoh Y, Chao EY. Ankle instability: com parison of primary repair and delayed reconstruction after long-term follow-up study. Clin Orthop 1985;198:1 1 0-117. 109. Safran MR, Zadlazewski JE, Benedetti RS, Bartolozzi AR, Mandelbaunm R. Lateral ankle sprains: a comprehensive review part 2: treatment and rehabilitation with emphasis on the athlete. Med Sci Sports Exerc 1 999;31(7 suppl):S438-S447. 110. Cyriax JH. Textbook of Orthopaedic Medicine, vol. II, Treatment by Manipulation, Massage and Injection, 11th edn. Bailliere Tindall, London, 1984:8. 111. Larsen E. Taping the ankle for chronic instability. Acta Orthop Swnd 1984;55:551-553. 112. De Carlo MS, Talbot RW. Evaluation of ankle joint proprio ception following injection of the anterior talofibular ligament. J Orthop Sports Phys Ther 1986;8:70-76. 113. Oostendorp RAB. Functionele instabiliteit na het inversie trauma van enkel en voet: een effectonderzoek pleisterban dage versus pleisterbandage gecombineerd met fysiotherapie. Geneeskd Sport 1987;20(2):678-685. 114. Boy tim MJ, Fismer DA, Neumann L. Syndesmotic ankle sprains. Am j Sports Med 1991;19(3):294-298. 115. Dehne E. Die Klinik der frischen und habituellen Adduktionssupinationsd istorsion des Fusses. Deutsch Z Chirurg 1 933;242:40-61 . �
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.
THIS PAGE INTENTIONALLY LEFT BLANK
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.
REFERENCES 1. Breithaupt HS. Zur pathologie des Menschlichen Fusses. Med Ztg 1855;XXIV:169-175. 2. Stechow. Sussodem und
Rontgenstrahlen. Dtsch Mil-Aeztl.
Zeitung 1897;XXVI. 3. Morris
JM, Bli ckenstaff LD. Fatigue Fractures. Thomas, Springfield, 1967. 4. Hardaker WT Jr. Foot and ankle injuries in classical ballet dancers. Orthop Clin North Am 1989;20:621-627. 5. O'Malley MJ, Hamilton WG, Munyak J, DeFranco MJ. Stress fractures at the base of the second metatarsal in ballet dancers. Foot Ankle Tnt 1996;17(2):89-94.
6. Chowchuen P, Resnick D. Stress fractures of the metatarsal
heads. Skeletal RadioI1998;27(1):22-25. 7. Estourgie RJA, Blok W. Marsfracturen. Ned Tijdschr Geneeskd 1981;125:86-87. 8. Cyriax J H . Textbook of Orthopaedic Medicine, vol 1, Diagnosis of Soft Tissue Lesiolls, 8th edn. Bailliere Tindall, London, 1982. 9. Holder LE. Radionuclide bone-imaging in the evaluation of
bone pain. I Bone ,oint Surg 1982;64A:1391-1396.
10. Gaeslien GE. Early detection of stress fractures, using 99mTc_
polyphosphate. RadiologtJ 1976;211:235-236. 11. Nitz A, Scoville CR. Use of ultrasound in early detection of
stress fractures of the medial tibial plateau. Mil Med 1980;145:844-846. 12. Ros HP. Ultrageluid als screeningsprocedure bij stress-frac
tmen. Ned Tijdschr Fysiother 1985;95(10):206-209. 13. Gilaldi M et at. Comparison between radiography, bone scan
and ultrasound in the diagnosis of stress fractures. Mil Med 1984;149:459-461.
JJ. Treatment strategies for acute fractures and non unions of the proximal fifth metatarsal. j Am Acad
14. Rosenberg GA, Sferra
Orthop Surg 2000;8(5):332-338. 15. Hetherington VJ, Carnett J, Patterson BA. Motion of the first
metatarsophalangeal joint. I Foot Surg 1989;28(1):13-19.
16. Joseph J. Range of motion of the great toe in men. j Bone'joint Surg 1954;36B:450-457. 17. Stokes TAF, Hutton WC,
Stott J R . Forces acting on the metatarsals during normal walking. I Anat 1979;129:579-590.
CHAPTER 86 - DI SORDERS OF THE FOREFOOT AND TOES 1 2 59
1 8. Shereff MJ, Begjiani FJ, Kummer FJ. Kinematics of the first
metatarsophalangeal joint. J Balle ]oillt Surg 1986;68A:392-398. 19. Dieppe PA, Calvent P. Cryslals and Joinl Disease. Chapman & Hall, London, 1982. 20. Seegmiller JE. The acute attack of gouty arthritis. Arlhrilis RheulII 1 965;8:714. 21. Yu TF, Gutman AB. Principles of current management of
primary gout. Alii ] Med Sci 1 967;254:893. 22. Gast LF, Cats A. Geneesmiddelen tegen Jicht. Ned Tijdschr Gweeskd 1 988;132(40) :1827-1831.
45. Irvin LM, Witt CS, Zielsdorf LM. Lesions of the metata rso
phalangeal joints. J Fool Surg 1985;24(3):256-262. 46. Grace DL. Sesamoid problems. Fool Ankle Clin 2000;5(3):609-{)27. 47. Oloff LM, Schulhofer SO. Sesamoid complex disorders. Clill Podialr Med Surg 1996;13(3):497-513. 48. Chomeley JA. Hallux valgus in adolescents. Proc R Soc Med 1958;51:903. 49. Root MC, Orien Wp, Weed JH. Norl1lal alld Abnorl1lal FUllclion of the Fool: Clinical Biomechanics, vol 2. Clinical Biomechanics, Los
Angeles, 1977.
23. Klinenberg J R, Goldfinger S, Seegmiller JE. The effectiveness of
50. Kelikian H. Hallux Valgus and Allied Deformilies of Ihe Forefool and
the xanthine oxidase inhibitor allopurinol in the treatment of gout. Ann Inlem Med 1 965;62:639. 24. Goodfellow J. Aetiology of hallux rigidus. Proc R Soc Med
51. Myerson MS, Badekas A. Hypermobility of the first ray. Fool
1965;59:82 1 . 25. Smith RW, Katchis SO, Ayson LC. Outcomes in hallux rigidus
patients treated nonoperatively: a long-term follow-up study. Fool Ankle 1111 2000;21(11):906-913. 26. Mann RA, Clanton TO. Hallux rigidus: treatment by cheilec
tomy. ] Balle Joilll Surg 1988;70A:400--406.
27. Love TR, Whynot AS, Farine I. Keller athroplasty: a prospective
review. Fool Allkle 1988;8:46-54. 28. Hamilton WG, Hubbard CEo Hallux rigidus. Excisional arthro
plasty. Fool A llkle Clill 2000;5(3):663-671. 29. Southgate J), Urry SR. Hallux rigid us: the long-term resul ts of
dorsal wedge osteotomy and arthrodesis in adults. J Fool Ankle Surg 1997;36(2):136-140. 30. Coker TP, Arnold JA, Weber OL. Traumatic lesions of the
metatarsophalangeal joint of the great toe in athletes. Am J Sporls Med 1 978;6:326-334. 3 1 . Clanton TO, Butler JE, Eggert A. Injuries to the metatarso
phalangeal joint of the great toe in athletes. Am J Sporls Med 1978;6:326-334. 32. Rodeo SA, O'Brien S, Warren RF el al. Turf-toe: an analysis of
metatarsophalangeal joint sprains in professional football players. Am J Sports Med 1990;18:280-285. 33. Clanton TO, Ford JJ. Tu rf toe injury. Clin Sports Med 1994;13(4):731-741. 34. Camasta CA. Hallux limittls and hallux rigid us. Clinical exam
ination, radiographic findings, and nattlral history. Clin Podialr Med Surg 1996;13(3):423--448. 35. Zollinger H. Hallux rigidus and its treatment. Ther Umsch 1991;48(12):832-835. 36. Mink AJF, ter Veer HJ, Vorselaars JA. Exlremiteiten; Funclie ollderzoek en Manuele Thernpie. Bonn Scheltema and Holkema,
Utrecht, 1990:184--49 l . 3 7 . Smith RW, Joanis TL, Maxwell PD. Great toe metatarso phalangeal joint arthrodesis: a user-friendly technique. Foot Ankle 1992;13(7):367-377. 38. Richardson EG. Halucal sesamoid pain: causes and surgical
treatment. J A m Acad Orthop Surg 1999;7(4):270-278. 39. McBryde AM Jr, Anderson RB. Sesamoid foot problems in the
athlete. Clin Sports Med 1988;7(1):51-60. 40. Karasick D, Schweitzer ME. Disorders of the hallux sesamoid
complex: MR features. Skelelal Radial 1998;27(8) :411--418. 41. Taylor JA, Sartoris OJ, Huang GS, Resnick OL. Painful condi
tions affecting the first metatarsal sesamoid bones. Radiographics 1993;13(4):817-830. 42. Axe MI, Ray RL. Orthotic treatment of sesamoid pain. Am J Sporls Med 1 988;16(4):411--416. 43. Van Hal ME, Keene JS, Lange TA, Clancy WG Jr. Stress fractures
of the great toe sesamoids. Am ] Sports Med 1982;10:122-128. 44. Abraham M, Sage R, Lorenz M. Tibial and fibular sesamoid
fractures on the same metatarsal: a review of two cases. J Fool Surg 1989;28:308-311.
Metalarsalgia. Saunders, Philadelphia, 1 965:4. Ankle Clin 2000;5(3):469--484. 52. Glasoe WM, Allen MK, Saltzman CL. First ray dorsal mobility
in relation to hallux valgus deformity and first intermetatarsal angle. Fool Ankle Inl 2001 ;22(2):98-1 01 . 53. Tanaka Y, Takakura Y, Sugimotor K el al. Precise anatomic configuration changes in the first ray of the hallux valgus foot. Fool Ankle InI 2000;21(8):651-656. 54. Greensburg GS. Relationship of hallux abductus angle and first
metatarsal angle to severity of pronation. ] Alii Podialr Assoc 1976;69(1):29. 55. Mann RA, Coughlin MJ. Hallux valgus and complications of
hallux valgus. In: Mann RA (ed) Slirgery of Ihe Fool, 5th edn. Mosby, St Louis, 1986:65. 56. Schoenhaus HO, Cohen RS. Etiology of the bunion. ] Fool Surg 1992;31(1) :25-29. 57. Johnson KA. Chevron osteotomy of the first metatarsal: patient
selection and technique. Conlemp Orlhop 1 981;3:707. 58. McBride ED. A conservative operation for bunions. ] Bone Joinl Surg 1 928;10:735. 59. M i tchell CL el al. Osteotomy buniectomy for hallux valgus. J Bone Joinl Surg 1958;40A:4. 60. De Doncker E, Kowalski C. Le pied normal et pathologique.
Notions d'anatomie, de physiologie et de pathologie des defor mations du pied. Acla Orlhop Belg 1970;36:4-5. 61. Weil LS. Scarf osteotomy for correction of hallux valgus. Historical perspective, surgical technique, and results. Fool Ankle Clin 2000;5(3):559-580. 62. Zembsch A, Trnka HI, Ritschl P. Correction of hallux valgus.
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
REFERENCES 1. Cyriax JH. Textbook of Orthopaedic Medicine, vol I, 8th edn.
5. Aszmann OC, Delion ES, Dellon AL. Anatomical course of the
Bailliere TindaLl, London, 1982. 2. Nakano KK. Sciatic nerve entrapment: the piriformis syndrome.
lateral femoral cutaneous nerve and its susceptibility to com pression and injury. Plast Recontr Surg 1977;100(3):600-604. 6. Hospodar Pp, Ashman ES, Traub JA. Anatomic study of the lateral femoral cutaneous nerve with respect to the ilioinguinal surgical dissection. J Orlhop Trauma 1999;13(1):17-19. 7. Surucu HS,TanyeIi E, Sargon MF, Karahan ST. An anatomic study of the lateral femoral cutaneous nerve. Surg Radiol Anal
Musculoskeletal Med 1987;4:33-37. 3. Asbury AK, Fields HL. Pain due to peripheral nerve damage: a
hypothesis. Neurology 1984;34:1587-1592. 4. Tasker RR, Tsudat T, Hawrylyshyn P. Clinical neurophysiologi
cal investigation of de-afferentation pain. Adv Pain Res T her 1983;5:713-738.
1997;19(5):307-310.
CHAPTER 88 - NERVE LESIONS OF THE LOWER LIMB
8. Grossbard GD. Meralgia paraesthetica after Perthes' disease.
1269
34. Mondelli M, Reale F, Cavallaro T. Neuroma of the sural nerve as
a complication of stripping of the small saphenous vein. Surg
f Bone Joint Surg 1981;63B:572. 9. Macnicol MF, Thompson WJ. Idiopathic meralgia paresthetica.
NeuroI1997;48(4):330-332. 35. Mountney J, Wilkinson GA. Saphenous neuralgia after coronary
Clin Orthop 1990;254:270-274.
artery bypass grafting. Eur J Cardiothorac Surg 1999;16(4):
10. King BB. Meralgia paraesthetica: report of five cases. Am J Surg 1941;52:364.
440-443.
11. Weikel AM, Habal MB. Meralgia paraesthetica: a complication
36. Seror P. Sural nerve neuropathy (external saphenous) linked to
of iliac bone procurement. Plas! Reconstr Surg 1977;60:572. 12. Boyce JR. Meralgia paresthetica and tight trousers [letter].
a disease of the small saphenous vein. Apropos of 5 cases. ] Mal Vasc 2000;25(2):128-131. 37. Brugger A. Die Erkrankungen des Bewegungsapparates und seines
JAMA 1984;251:1533. 13. Deal CL, Canosa JJ. Meralgia paraesthetica and large abdomens.
Nervensystems. F isher, Stuttgart, 1982. 38. Vloka JD, Hadzic A, April E, Thys DM. The division of the
Ann Intern Med 1982;96:787. 14. Segers M, Vandendriessche G, Vanderstraeten G. Meralgia
paresthetica. Med Phys 1986;9:281-285. 15. Streiffer RH. Meralgia paresthetica.
Physician
39.
16. Warfield CA. Meralgia paresthetica: causes and cures. Hasp
40.
Am
Fam
1986;33(3):141-144. Pract 1986;21(2):40A, 40C, 401-415. 17. Jiang Guo-Xiang, Xu Wei-Dong, Wang Al-Hao. Spinal stenosis
41.
with meralgia paraesthetica. J Bone Joint Surg 1983;70B: 42.
272-273. 18. Trummer M, Flaschka G, Unger F, Eustacchio S. Lumbar disc
herniation mimicking meralgia paresthetica: case report. Surg
Am J Sports Med 1990;18:108.
Neural 2000;54(1):80-81. 19. Eriksson E. Atlas dey Lokalaniisthesie. Springer, Berlin, 1980:108. 20. Keegan JJ, Holyoke EA. Meralgia paraesthetica. An anatomical
and surgical study. ] Neurosurg 1962;19:341. 21. Ivins GK. Meralgia paresthetica, the elusive diagnosis: clinical experience with 14 adult patients. Ann Surg 2000;232(2):
44. Leach RE, Purnell MB, Saito A. Peroneal nerve entrapment in
runners. Am J Sports Med 1990;17:287-291. 45. Aydogdu S, Cullu E, Arac N, Varolgunes N, Sur H. Prolonged
peroneaJ nerve dysfunction after high tibial osteotomy: pre- and postoperative electrophysiological study. Knee Surg Sports Traumatol Arthrosc 2000;8(5):305-308.
281-286. 22. Ecker AD, Woltman HW. Meralgia paresthetica: a report of one
hundred and fifty cases. JAMA 1938;110:1650. presenting
as
unilateral
femoral
nerve
palsy.
J RheumatoI1991;18(3):462-463. 24. Holm P, Roehr C. An important complication of anticoagula
tion therapy: a case presentation. South Dakota J Med 1985;
47. Dellon AL. Deep peroneal nerve entrapment on the dorsum of
the foot. Foot Ankle 1990;11(2):73-80. 48. Akyuz G, Us 0, Turan B et al. Anterior tarsal turulel syndrome. Electromyogr Clin Neurophysiol 2000;40(2):123-128. 49. Borges LF, Hullett M, Selker DJ, Welsh K. The anterior tarsal
tunnel syndrome. J Neurosurg 1981;54:89-92.
38:5-8. 25. Young MR, Norris JW. F emoral neuropathy during anticoagu
lant therapy. Neurology 1976;26:1173-1175. 26. Nusselder FA, Franke CL. Uitval van de nervus femoralis ten
gevolge van bloeding bij gebruik van anticoagulantia. Ned Tijdschr Geneeskd 1990;134:808-811. 27. Ebraheim NA, Mekhail AO. The infrapatellar branch of the
saphenous nerve:
46. Vastamiiki M. Decompression for peroneal nerve entrapment. Acta Orthop Scand 1986;57:551-554.
23. Letourneau L, Dessureault M, Carette S. Rheumatoid iliopsoas
bursitis
43.
sciatic nerve in the politeal fossa: anatomical implications for popliteal nerve blockade. Anesth Analg 2001;92(1):215-217. Hollinshead WHo Anatomy for Surgeons: The Back and Limbs, vol 3. Harper & Rowe, Philadelphia, 1982;800-802. Moller BN, Kadin S. Entrapment of the common peroneal nerve. Am J Sports Med 1987;15:90-91. W hite J. The result of traction injuries to the common peroneal nerve. J Bone Joint Surg 1968;50B:346-350. Togrol E. Bilateral peroneaJ nerve palsy induced by prolonged squatting. Mil Med 2000;165(3):240-242. Ekelund EL. Bilateral nerve entrapment in the popliteal space.
50. Marinacci AA. Neurological syndromes of the tarsal tunnels. Bull Los Angeles Neural Soc 1968;33:90-100. 51. Gessini L, Jandolo B, Pietrangeli A. The anterior tarsal syn
drome: report of four cases. J Bone Joint Surg 1984;66A:786-787. 52. Krause KH, Witt Ross A. The anterior tarsal tunnel syndrome. J Neural 1977;217:67-74.
an anatomic study. J Orthop Trauma
53. Tibrewall SB, Goodfellow JW. Peroneal nerve palsy at the level
28. Aszmann OC, Ebmer JM, Dellon AL. Cutaneous innervation of
54. Styf J. Diagnosis of exercise-induced pain in the lower leg. Am J
the medial ankle: an anatomic study of the saphenous, sural, and tibial nerves and their clinical significance. Foot Ankle Int
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
ated with plantarflexion-inversion ankle sprains. Clin Podiatr Med Surg 2000;17(2):361-369, vi-vii. 57. Sridhara CA, Izzo KL. Terminal sensory branches of the superficial peroneal nerve: an entrapment syndrome. Arch Phys Med RehabiI1985;66:789-791. 58. Styf J. Entrapment of the superficial peroneal nerve. Diagnosis
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
336-337.
Foot Ankle Int 1999;20(9):576-582.
(posterior tibial) nerve. Neural Clin 1999;17(3):593-615.
1270 SECTION FIFTEEN - NERVE LESIONS
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
1990;72A(3):453-454. 66. Radin EL. Tarsal tunnel syndrome.
Ankle Soc 1988;Jul:436-439.
Clin Orthop 1983;181:
167-170.
1981;63A:96-99. 77. Ward pJ, Porter ML. Tarsal tunnel syndrome: a study of the
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
nerve?
AI1I
J
Sports
Med
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
THIS PAGE INTENTIONALLY LEFT BLANK
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
REFERENCES 1 Wyke B. The neurology of low back pain. In: Jayson MIV (ed)
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.
THIS PAGE INTENTIONALLY LEFT BLANK
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
THIS PAGE INTENTIONALLY LEFT BLANK
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
