EDITION 2

SHOULDER
PAIN
AX*

RENE CAILLIET, M.D./PAlM SERIES

UNIVERSITY OF CALIFORNIA
SAN FRANCISCO
LIBRARY
SHOULDER
PAIN
 Digitized by the Internet Archive
in 2012

http://archive.org/details/shoulderpaine2cail
 EDITION 2

SHOULDER
PAIN

RENE CAILLIET, M.D.

Chairman
Professor and
Department of Rehabilitative Medicine
University of Southern California
School of Medicine
Los Angeles, California

C3fc
19*/

F. A. DAVIS COMPANY • Philadelphia

37S0.1Q
Also by Rene Cailliet:

FOOT AND ANKLE PAIN

HAND PAIN AND IMPAIRMENT
KNEE PAIN AND DISABILITY
LOW BACK PAIN SYNDROME
NECK AND ARM PAIN
SCOLIOSIS
SOFT TISSUE PAIN AND DISABILITY
THE SHOULDER IN HEMIPLEGIA

Copyright © 1981 by F. A. Davis Company

Copyright 1966 by F. A. Davis Company

All rights reserved. This book is protected by
copyright. No part of it may be reproduced,
stored in a retrieval system, or transmitted in
any form or by any means, electronic, mechani-
cal, photocopying, recording, or otherwise,
without written permission from the publisher.

Printed in the United States of America

Library of Congress Cataloging in Publication

Data
Cailliet,Rene.
Shoulder pain.

Bibliography: p.
Includes index.
1. Shoulder —
Diseases. 2. Pain. I. Title.
[DNLM: 1. Pain—Therapy. 2. Shoulder
WE 810 C134s]
RC939.C36 1981 617'.572 80-27750
ISBN 0-8036-1613-9
 Preface

Pain in the shoulder region is exceeded in clinical frequency only by

pain in the low back and pain in the neck. Recent developments and
modifications of older concepts concerning shoulder pain, together
with the need for further clarification of associated disease syndromes,
have prompted this new edition.
The shoulder remains a complex functional unit with numerous
tissues capable of causing joint dysfunction. As in all musculoskeletal
systems, a thorough knowledge of functional anatomy is mandatory,
and the examiner must evaluate every aspect of this functional anat-
omy. Treatment must, therefore, be based on modification or correction
of these malfunctions. The shoulder joints, some eight or nine in
number, may all contribute to pain and dysfunction, thus methodical
examination, individually and collectively, of all these joints must be
performed.
When man began to assume the upright position, and his forelegs
became arms and hands, the shoulder and its arm components became
useful to place the hand in functional position and to acquire greater
mobility at the expense of stability. Due to this lack of stability, degen-
eration, damage, pain, and malfunction can result.
This new edition is meant to supplement the previous one. Its or-
ganization is basically the same in that functional anatomy is stressed,
and examination to determine any deviation from normal can be appre-
ciated. The patient's history and examination thus become meaningful,
and treatment evolves from this concept, based on physiologic princi-
ples.
New chapters have been added which involve the hemiplegic shoul-
der and the shoulder-hand-finger syndrome, both of which are seen
constantly in daily practice. The bibliography has been chosen to
update current references to the concepts postulated.

Rene Cailliet, M.D.

 Contents

Illustrations viii

Introduction xii

Chapter 1. Functional Anatomy 1

Glenohumeral Joints 4
Glenohumeral Capsule 6
The Suprahumeral Joint 9
Masculature of the Glenohumeral Joint 10
Glenohumeral Movement 17
Scapular Movement 22
Scapulohumeral Movement 26
Acromioclavicular and Sternoclavicular Joints 28
Composite Shoulder Girdle Movements 32
Biceps Mechanism 34

Chapter 2. Musculoskeletal Pain 38

Tendinitis: Attrition and Degeneration 38
Calcific Tendinitis 43
Bursitis 47
Diagnosis 48
Treatment 53

Chapter 3. Cuff Tear 74

Diagnosis 74
Arthrography 76
Treatment » 78

Chapter 4. Adhesive Capsulitis: The "Frozen Shoulder" 82

Diagnosis 84
Treatment 85

VI
Chapter 5. Neurologic Referred Pain 90
Cervical Nerve Root Pressure (Radiculitis) 90
Spinal Cord Tumor 93
Brachial Plexus Involvement 94
Scapulocostal Syndrome 95
Cervical Rib 101
Anterior Scalene Syndrome 103
Claviculocostal Syndrome 103
Pectoralis Minor Syndrome 104
Superior Pulmonary Sulcus Tumors 105
Suprascapular Nerve Entrapment 106
Dorsal Scapular Nerve Entrapment 106
Arteriosclerotic Occlusion 106

Chapter 6. Sympathetic Referred Pain 108

Pathophysiologic Mechanisms 110
Diagnosis 113
Etiology 119
Treatment 1 19
Psychiatric Aspects 122

Chapter 7. Traumatic Pain 125

Mechanism of Dislocation 126
Diagnosis of Dislocation 128
Treatment 130
Acromioclavicular Lesions 132
Diagnosis 134
Treatment 136

Chapter 8. Biceps Tendinitis and Tear 137

Pathology 138
Diagnosis 138
Treatment 139

Chapter 9. The Shoulder in Hemiplegia 140

Chapter 10. Visceral Referred Pain 148

References 151

Index 156

vn
 Illustrations

1. The joints of the shoulder girdle 2

2. The acromiocoracoid arch 3
3. Congruous-incongruous joints 5
4. The scapula 6
5. The glenohumeral synovial capsule 7
6. Capsular action during glenohumeral movement 8
7. The anterior capsule and the glenohumeral ligaments ... 9
8. The coracohumeral ligament 10
9. Rotator cuff insertion upon the humerus 11
10. Capsular-passive cuff support 12
11. Sites of muscular origin and insertion upon the scapula
and the humerus 13
12. The supraspinatus muscle and the infraspinatus muscle . 14
13. The subscapularis muscle 15
14. Circulation of the tendons of the cuff: the "critical zone" 16
15. Blood circulation 16
16. The deltoid muscle and its isolated function 17
17. The planes of arm movement, indicating the direction of
movement and the planes of movement in relation to the
body 18
18. Glenohumeral movement of arm abduction 19
19. Function of the suprasinatus muscle 20
20. Rotator cuff mechanism 21
21. Combined cuff and deltoid action upon the glenohumeral
articulation 22
22. Abduction angle of deltoid 23
23. Influence of humeral rotation upon abduction range of
the glenohumeral joint 24
24. Scapular musculature: rotators 25
25. Downward rotators of the scapula 26

Vlll
26. Pectoralis major 27
27. Scapulohumeral rhythm 28
28. Deltoid action upon the glenohumeral joint 29
29. Evolution of the acromioclavicular disk (meniscus) 30
30. Action of the coracoclavicular ligaments upon the
acromioclavicular joint 30
31. Scapular elevation resulting from clavicular rotation 31
32. The sternoclavicular joint 32
33. Muscles acting upon the clavicle 33
34. Accessory movement of the scapulohumeral rhythm other
than the glenohumeral movement 34
35. Biceps mechanism 36
36. Sites of tissue pain 39
37. Roentgenographic changes in shoulder dysfunction: cysts
in the tuberosities of the humerus 42
38. Stages of degeneration 43
39. upon glenohumeral range of motion
Postural effect 44
40. Natural sequence of calcific tendinitis 45
41. Evolution of the calcified tendinitis and formation of
"bursitis" 46
42. Subacromial bursa 48
43. Acute tendinitis and inflammation of contiguous tissues . 49
44. Trigger points 50
45. Mechanism by which irritation leads to functional
disability 51
46. Pendular exercise 53
47. Active pendular glenohumeral exercise 54
48. Technique of tendinitis-bursitis injection 56
49. Suprascapular nerve block 57
50. Exercises 58
51. Home exercise to increase shoulder range of motion 60
52. Exercise to stretch anterior capsule and increase posterior
flexion 61
53. Overhead exercise 62
54. Correct and incorrect use of "wall climbing" exercise .... 63
55. Scapular mobility exercises 64
56. Normal scapulohumeral motions 65
57. Subtle signs of shoulder limitation 66
58. Manipulation treatment of "involuntary" motion of the
glenohumeral joint 68
59. Rhythmic stabilization manipulation of the glenohumeral
joint 71
60. Schematic graph of rhythmic stabilization 72
61. Cuff tear 76

IX
62. Cuff tear 77
63. Injection technique for intra-articular arthrogram and
brisement treatment 78
64. Arthrogram 79
65. Proper spica cast for the torn cuff treatment 80
66. Schematic stages toward functional disability in the
painful shoulder 83
67. Periarticular case of the suprahumeral joint 85
68. Adhesive capsulitis 86
69. Component fibers of a cervical nerve 91
70. Foraminal opening variations 92
71. Foraminal closure in head rotation and lateral flexion .... 93
72. Regions of shoulder pain referral from cervical radiculitis 94
73. Cervical dorsal outlet 96
74. Levator scapulae "trigger" zone in postural fatigue
syndrome 98
75. Anterior view of prevertebral fascia and muscles 99
76. Standing scapular elevation exercises 101
77. Posture-scapular elevation exercises 102
78. Scalene anticus syndrome 104
79. Claviculocostal and pectoralis minor syndromes 105
80. Venous lymphatic pumps of the upper extremity 109
81. Sequences leading to "frozen" shoulder-hand-finger
syndrome Ill
82. Neuron pathways of pain 112
83. Sympathetic fibers in a segmental peripheral nerve and
pathways along the sympathetic nerve
afferent 114
84. Finger changes in the hand-shoulder syndrome 116
85. Normal flexion-extension of the metacarpophalangeal
joints 117
86. Hand patterns 118
87. Technique of stellate ganglion or brachial plexus block . . 121
88. Removal of finger edema 122
89. Antigravity treatment of the edematous extremity 123
90. The "five Ds" resulting from pain 124
91. Anterior capsule, glenohumeral ligaments, and avenue of
anterior shoulder dislocation 126
92. Four types of shoulder dislocation 127
93. Relationship of age of patient to mechanism of anterior
dislocation 128
94. Mechanism of dislocation: "hyperextension theory" 129
95. Intra-articular fracture in recurrent shoulder dislocation
("notch lesion of Hermodsson") 130
96. Kocher manipulation for closed treatment of dislocation .. 131
 97. Schematic brachial plexus 133
98. Mechanism of acromioclavicular separation 134
99. Immobilization of acromioclavicular separation: strapping 135
100. Biceps tendon tear 139
101. Mechanism of glenohumeral subluxation 141
102. Scapular depression 142
103. Spastic medial scapular muscles 142
104. Shoulder slings 143
105. Rood sling 144
106. Proposed design for prevention of subluxation 144
107. Wheel chair arm sling 145
108. Flexor synergy of the upper extremity 146
109. Visceral sources of "shoulder" pain 149

XI
 Introduction

The complaint of pain in the upper extremity can present a confusing

diagnostic problem to the practitioner and to the therapist. The upper
extremity includes the anterior and posterior angles of the neck, shoul-
der, arm, elbow, wrist, and hand. Pain can originate from these tissues
or may be felt in these tissues as a referred pain from other areas.
The outline appearing on pages 40 and 41 enumerates the major
causes of pain in the upper extremity. Obviously, exhaustive consid-
eration of all these causes is not possible in a single monograph. Since
the predominant causes seen in daily clinical practice belong in the
musculoskeletal system, these will be stressed.
Degenerative causes affecting the shoulder girdle and its numerous
joints cannot be completely differentiated from other causes of inflam-
mation or from trauma.
This examination is grounded in biomechanical physiology, which
classifies the glenohumeral joint as an incongruous joint. The congruity
which affords stability to a joint and limited motion also must be
studied in conjunction with incongruity, such as that of the glenohum-
eral joint, which permits excessive mobility and inadequate stability,
thus providing the basis for pain, degeneration, and dysfunction.
Terminology used in reference to the upper extremity, especially
with regard to theshoulder girdle, is vague, nonspecific, and arbitrary.
Many hackneyed terms have gained dignity of specificity but are
loosely employed, devoid of real meaning, and without physiologic
basis. As their use becomes well established, these meaningless terms,
invoking no pathomechanical concept, are bound to lead to inadequate
treatment and persistence of pain and disability. This text is intended to
furnish a sound functional pathophysiologic basis for understanding
pain and dysfunction of the shoulder.
The purpose of this new edition is to provide the clinician with a
sound basis for performing a significant history and a meaningful ex-

xn
amination, and for prescribing rational treatment for the patient who
complains of pain in the shoulder region, in the upper extremity as
related to the shoulder, or in the shoulder emanating from other por-
tions of the musculoskeletal system. Hopefully, better prescription for
treatment and better functional evaluations will result, and the physical
and occupational therapists who are assigned the responsibility of
providing treatment will have recourse to clearer and more reliable
guidelines.

Xlll
CHAPTER 1

Functional Anatomy

The term shoulder joint requires elucidation. The common use of

the term joint referring to the glenohumeral joint, refers to only one of
,

the seven joints that form the shoulder complex. Since all the joints
comprising the complex are separately and collectively important in
normal function, and since impairment of one may cause impairment
of all, a collective term is desirable. The term shoulder girdle is pref-
erable if it enjoys the definition of "arm-trunk mechanism," "thor-
acic-scapular-humeral articulation," or "shoulder-arm complex."
The shoulder girdle is a composite of seven joints all moving syn-
chronously, each incumbent upon the other, with dysfunction result-
ing from the impairment of any of the participating joints. Rhythmic
movement of the arm upon the chest wall is totally dependent for its
mobility upon coordinated muscular action and for its stability upon
combined muscular and ligamentous structures.
When man became an erect individual, his arms, which in his quad-
riped state were his forelegs, gave up anatomical and functional sta-
bility in favor of mobility 7
. Consequently the shoulder girdle in man
has sacrificed stability for mobility which is the greatest of all the joints
of the body.
Analysis of total movement of the shoulder girdle proceeds best if
each joint is considered separately, rather than the total combined.
Admittedly, this separate approach is unphysiologic because the
shoulder complex functions by synchronous movements occurring
simultaneously in a smooth, integrated manner, which is aptly de-
scribed as the "scapulohumeral rhythm" by Dr. E. A. Codman. The 1

individual joint approach permits simplicity of inspection and evalua-

tion and facilitates ultimate integration into the complex.
The component joints of the shoulder girdle are shown in Figure 1.
These joints can be enumerated in reverse order from the legend of
Figure 1 beginning with the first and only attachment to the vertebral

1
FIGURE 1. The joints of the shoulder girdle: (1) glenohumeral; (2) suprahumeral; (3)
acromioclavicular; (4) scapulocostal; (5) sternoclavicular; (6) costosternal; (7) costo-
vertebral.

column. All other contiguous joints are extrinsic to the vertebral col-
umn.
The initial joint is the joint between the ribs and the vertebral body,
the costovertebral joint The next contiguous joint is the costosternal
.

joint, followed by the sternoclavicular joint The remaining. articula-

tion of the trunk portion of the girdle the scapulocostal joint. The
is

first three joints mentioned conform more to the accepted definition of

a joint in that they are unions of two bones that permit movement at
their junction. 2 The scapulocostal joint conforms only equivocally to
the definition: it is a gliding joint of the scapula with the rib cage
separated by muscles and a bursa.
The arm portion of the arm-trunk complex, at best an arbitrary divi-
sion, begins with the acromioclavicular joint. The sixth joint is the
suprahumeral joint which is also a functional joint rather than a true
,
 ACROMIOCLAVICULAR LIGAMENT
CORACOACROMIAL LIGAMENT

CORACOCLAVICULAR
LIGAMENTS

TRAPEZOID
CONOID ~
CORACOID

GLENOID LIP

Figure 2. The acromiocoracoid arch. The diagram depicts the shape of the glenoid
fossa and its relationship to the acromial process, the coracoid process, and the coracoa-
cromial ligament. In essence this diagram shows the socket of the glenohumeral joint
and also portrays the relationship of the suprahumeral joint.

joint.This "joint" refers to the relationship of the humeral head to the

overlying coracoacromial arch (Fig. 2). Although alluded to as a
"pseudo" joint, the relationship of this joint is extremely important in
the normal movement of the shoulder girdle and is an integral part in
many of the pathologic states.
The seventh joint commonly considered the shoulder joint is the
glenohumeral joint An additional articulation that has pathologic sig-
.

nificance but little functional importance is the biceps mechanism, a

gliding articulation of the biceps tendon within the bicipital groove.
Actually, the tendon does not glide within the groove, but stays fixed,
and the humerus glides along the tendon. This gliding motion occurs
during any and all movement of the shoulder joint. Flexing and
spinating the forearm upon the humerus, a biceps action, causes the
biceps tendon to become taut but not to glide or move within the
bicipital groove.
Each of the enumerated joints will be considered separately, then
the coordinated motion involving all these single actions will be
analyzed. Failure of any component movement will cause failure of
the composite movement of the shoulder girdle. The clinical exami-
nation inspects each movement as well as the complex movement.
Examination also reveals the defect in the mechanism that, coupled
with the history, gives a mechanical diagnosis and a rational treatment
aimed at restoring normal function to the impaired component and
restitution of the "scapulohumeral rhythm."

GLENOHUMERAL JOINTS
The glenohumeral joint, part 1 in Figure 1, may be termed the
scapulohumeral joint and the joint that is most commonly termed the
shoulder joint.
The glenohumeral joint is a classic example of an incongruous joint.
In a congruous joint the surfaces are symmetrical or parallel with the
concave surface, and the convex opposing surfaces are equidistant
(Fig. 3A). The convex surface is roundly cylindrical, whereas the in-
congruous joint's surfaces are oval.
In the congruous joints, rotation occurs about a fixed central axis.
Rotation of the inserting joint's surface occurs about this stationary
axis, and thus the muscles that move it have equal action upon the
moving part. This congruous joint relationship affords stability insofar
as the ball-socket relationship seats the head within the socket. The
capsule, also about a symmetrical joint, extends equally in all di-
rections during movement.
The incongruous joint, having a shallow concave surface that ar-
ticulates with a more convex and thus dissimilar surface, loses its
relationship. The incongruous joint is thus not in a ball-socket re-
lationship and is unstable. The convex portion of the joint does not
seat itself into the shallow concave portion (Fig. 3B).
Movement of the incongruous joint not rotation about a fixed axis,
is

but rather a gliding motion about a constantly changing axis of rota-

tion. The muscles thus must not only move the joint, but must also
afford it its stability. The capsule
of an incongruous joint must have
greater flexibility as extended further during the gliding activity.
it is

The glenohumeral joint is an example of an incongruous joint with

all the factors of this type of joint affecting normal movement and
contributing to pain and disability.
The scapula, the "shoulder blade" (Fig. 4), lies on the posterior
surface of the thoracic cage with its ventral surface concave, corre-
sponding to the convex surface of the rib cage. The only attachments
to the thorax and spinal column other than the acromioclavicular joint
are muscular.
The dorsal surface of the scapula is divided by the spine, a horizon-
tal bony ridge ending in a
that extends laterally past the glenoid fossa
bulbous end, the acromial process. This process overhangs the head
of the humerus, is the site of attachment to the clavicle (the acromio-
clavicular joint), and receives the fibers of the coracoacromial liga-
Figure 3. Congruous-incongruous joints. A. In a congruous joint the concave, convex
surfaces are symmetrical. The articular surfaces are equidistant from each other at all
points along their circumference (a = b = c = d, etc.). In rotation, movement occurs
about a fixed axis (A). Muscular action (M) is that of symmetrical movement about this
fixed axis and is needed for motion, not stability. The depth of the concave surface gives
the joint stability. The capsule (C) has symmetrical elongation. B. Incongruous joints
have asymmetrical articulatory surfaces. The concave surface is elongated and the con-
vex more circular, thus the distance between them varies at each point (g > f > e < h).
As the joint moves, the axis of rotation (A) shifts and joint movement is that of gliding
rather than rolling. Therefore, muscles must slide the joint and simultaneously maintain
stability. The capsule varies in its elongation at all levels of movement. The gleno-
humeral joint is an incongruous joint.

merit.The acromion and the coracoacromial ligament form part of the

arch overlying the suprahumeral joint (see Fig. 2).
The glenoid fossa, the female portion of the glenohumeral joint, is
located on the anterior superior angle of the scapula, midway between
and below the acromion and the coracoid process. The glenoid fossa is
a shallow, ovoid socket that faces anteriorly, laterally, and upward
(Fig. 4). The direction upward has clinical significance in furnishing
stability to theglenohumeral joint.
Surrounding the perimeter of the fossa, to deepen the cup, is a
fibrous lip known as the glenoid labrum. This lip, originally consid-
ered to be fibrocartilage, 2 contains no cartilage but is primarily fibrous
3
tissue, a redundant fold of the anterior capsule. This fold, and appar-
ently the labrum, disappears as the humerus is externally rotated.
There is marked discrepancy between the surface area and the
 Anterior
Posterior

Sagittal

FIGURE 4. The scapula. The posterior, anterior, and sagittal views of the scapula are
shown. The spine of the scapula seen on the posterior view divides the blade into the
supra- and infraspinatus fossae, from which originate the muscles that also hear these
names. The sagittal view is more graphically seen in Figure 2, which depicts the
relationship of the glenoid fossa to the overhanging acromial process and the medially
located coracoid process. Note the angle of the glenoid fossa, facing laterally, anteriorly,
and upward.

curvature of the glenoid fossa and the convex surface of the humeral
head. Only a small portion of the head of the humerus is in contact
with the fossa at any time. This incongruous joint relationship de-
mands a gliding joint movement rather than the hall-bearing type of
joint in the hip. This unstable but mobile relationship requires syn-
chronous muscular actions for its movements.

GLENOHUMERAL CAPSULE
The capsule of the glenohumeral joint is an extremely thin-walled,
spacious container that attaches around the entire perimeter of the
glenoid rim. A small portion of the epiphyseal line of the glenoid
extends within the capsule, which is the reason that osteomyelitis can
sometimes extend into the articular space.
As shown in Figure 5, the capsule arises from the glenoid fossa and
inserts around the anatomical neck of the humerus. There is a syno-
vial lining throughout that blends with the hyaline cartilage of the
 CORACOACROMIAL LIGAMENT

TRANSVERSE HUMERA
LIGAMENT
BICEPS TENDON
INVAGINATION
BICEPS TENDON

BICEPS TENDON

SYNOVIAL LINING
FOSSA ARTICULAR CARTILAGE
HUMERUS ARTICULAR CARTILAGE
SYNOVIAL FLUID

Figure 5. The glenohumeral synovial capsule. A. The spacious capsule covers the
entire humeral head. The invagination of the capsule accompanying the biceps tendon
down the bicipital groove passes under the transverse humeral ligament at the level of
the point of attachment of the pectoralis major muscle to the shaft of the humerus. The
subscapularis and subcoracoid pouches of the capsule contain synovial fluid and are in
direct continuity with the major capsule. These pouches are clearly seen in dye arthro-
grams. B. The intracapsular, extrasynovial invagination of the long head of the biceps
tendon as it proceeds to attach to the superior rim of the glenoid fossa. The synovial
lining attaches to the articular cartilage of the head of the humerus but attaches to the
glenoid fossa at a distance from the rim of the glenoid cartilage.

head of the humerus but fails to reach the cartilage of the glenoid fossa
(Fig. SB).
The long head of the biceps attaches to the superior aspect of the
glenoid fossa (see Fig. 2). It invaginates the capsule but does not enter
the synovial cavity. The biceps tendon is thus intracapsular but re-
mains extrasynovial. The capsule folds and incorporates the biceps
tendon down into the intertubercular sulcus of the humerus and ends
blindly at a site on the humerus opposite the insertion of the pectoralis
major muscle (Fig. 5A). 4
With the arm hanging loosely in a dependent position at the side,
the upper portion of the capsule is taut, and the inferior portion, the
axillary fold, is loose and pleated (Fig. 6). The opposite situation exists
when the arm is fully abducted. Here the inferior portion becomes
taut and the superior portion pleated. The tautness of the superior
capsule with the arm dependent prevents downward dislocation of
the arm, and the laxity of the capsule permits the gliding motion of the
glenohumeral joint.
Rotation of the arm around its longitudinal axis (turning the arm in
Figure 6. Capsular action during glenohumeral movement. The upper drawing de-
picts the "gliding" jointmotion between the head of the humerus and the glenoid fossa.
The arc of both joint surfaces differ and thus form an incongruous joint surface relation-
ship. The lower left drawing shows the arm dependent with the superior portion of the
capsule taut, which prevents downward movement. The lower right drawing shows the
arm abducted, which relaxes the superior portion of the capsule and causes the inferior
portion to become taut. In the half-abducted arm both superior and inferior capsules are
slack, which position is thus one of instability of the glenohumeral joint.

and out and and from the trunk, while dependent) has the same
to
effect of tautness and laxity upon the capsule, anteriorly and poste-
riorly. The anterior portion of the capsule is reinforced by the supe-
rior, middle, and inferior glenohumeral ligaments. These ligaments
are actually pleated horizontal folds of the anterior capsule in a fan-
shaped appearance in front of the glenohumeral joint. These fan-
shaped ligaments have a base attached on the humerus and converge
toward the glenoid rim, some distance in from the edge of the fossa, to
attach on the anterior superior portion of the glenoid and the adjacent
bone (Fig. 7).

There is a recess, a pouch, in the anterior capsule due to the loose-

ness of the capsule. The capsule is actually loose enough to permit the
humerus to be drawn as much as 3 cm from the fossa. An opening
usually exists between the superior and middle glenohumeral liga-
ments (folds), termed the foramen of Weitbrecht, which is merely

8
 SUMMtKlUK
SUPPERIOR )
MIDDLE I GLENOHUMERAL
-inferior/ LIGAMENTS
BICEPS
TENDON FORAMEN OF WEITBRECHT

GLENOID LABRUM

Figure 7. The anterior capsule and the glenohumeral ligaments. The glenohumeral
ligaments that reinforce the anterior joint capsule are mere folds of the capsule. Three
in number, they are fan-shaped, attach from the humerus, and converge toward the
glenoid rim. The foramen of Weitbrecht may be covered by a thin layer or may be open
as a communication between the joint space and the subscapular recess.

covered by a thin layer of capsule, or may be open as a communication

between the joint capsule and the subscapular recess. The anterior
pouch, due to capsular laxity and the foramen of Weitbrecht, assumes
significance in dislocations of the humerus. 5
Limitation of external rotation upon the glenoid fossa is also im-
posed by the coracohumeral ligament (Fig. 8). This ligament origi-
nates at the coracoid process of the scapula and attaches to the
humerus at the bicipital groove upon the bone and the ligament of the
biceps tendon. In active or passive external rotation of the humerus
this ligament acts to limit the extent of rotation. Constriction of this
ligament is considered to play a role in the "frozen shoulder," or
limited adhesive capsulitis.

THE SUPRAHUMERAL JOINT

The suprahumeral joint is not a joint in the true sense: an articula-
more or less moveable, between two or more bones. 6 The supra-
tion,
humeral joint is more a protective articulation between the head of the
humerus and an arch formed by a broad, triangular ligament connect-
ing the acromial process and the coracoid process (see Fig. 2).
The coracoacromial arch prevents trauma from above to the
glenohumeral joint or to the head of the humerus and also prevents
upward dislocation of the humerus. Its proximity to the humerus in its
inner aspect presents an obstacle to abduction of the humerus in the
 Figure 8. The coracohumeral ligament.

coronal plane (see Fig. 15). This will be discussed in the section on
composite shoulder girdle movements.
The suprahumeral articulation is bounded within by the glenoid
cavity, superiorly and slightly posteriorly by the acromial process,
anteriorly and medially by the coracoid process, and above by the
coracoacromial ligament. The humeral head lies under this hood.
Within the suprahumeral joint are found portions of the subacromial
bursa, the subcoracoid bursa, the supraspinatus muscle and its tendon,
the superior portion of the glenohumeral capsule, a portion of the
biceps tendon, and the interposed loose connective tissue. Many sen-
sitive tissues are enclosed within this small area. 7,8
As the arm abducts, the greater tuberosity must pass under the
coracoacromial ligament and not compress the enclosed tissues. The
movement requires fine muscular coordination, laxity of soft tissues,
and proper external rotation of the humerus. Impairment of any of
these factors can result in limited movement, pain, and disability.

MUSCULATURE OF THE GLENOHUMERAL JOINT

Five of the nine muscles related to the glenohumeral joint can be
considered the prime movers. The more complex in their movement
are those collectively known as the musculotendinous cuff muscles.

10
SUPRASPINATUS
INFRASPINATUS
TERES MINOR
SUBSCAPULARIS

FIGURE 9. upon the humerus. The conjoined tendinous insertion

Rotator cuff insertion
of the four rotator muscles that comprise the "cuff" is viewed anteriorly. The supra-

spinatus attaches to the greater tuberosity; the infraspinatus, immediately below it; and
then the teres minor. The subscapularis inserts upon the lesser tuberosity below the
cartilage of the head and medial to the bicipital groove. There is a sulcus through which
the biceps tendon emerges.

The important motions of the glenohumeral joint are performed by

these cuff muscles. Through their attachment to the humerus they act
as rotators and combine with the deltoid muscle to abduct the arm by
producing various combinations of force couples about the glenohu-
meral joint (Fig. 9).
The cuff muscles, especially the supraspinatus muscle, passively
support the dependent humerus in the person standing or sitting. The
arm at the glenohumeral articulation would dislocate downward out of
the socket if it were not for the cuff support and the angle of the
glenoid fossa (Fig. 10).
The rotator action of the cuff muscles relates to rotation around a
point located in the center of the head of the humerus in an arc of the
sagittal plane. This rotation differs from rotation around the long shaft
of the humerus, as in internal and external rotation of the arm.
The muscles comprising the rotator cuff are the supraspinatus,
infraspinatus, teres minor, and the subscapularis muscles.
The supraspinatus muscle originates from the supraspinatus fossa

11
FIGURE 10. Capsular-passive cuff support. Due to the orientation of the glenoid fossa
which faces forward, outward, and upward, the superior capsule, being taut in the
normal position, becomes more taut as the humeral head (A) descends. B depicts an
analogy of a ball rolling down an angled plane.

of the scapula above the spine of the scapula (Fig. 11) on its posterior
surface. It passes laterally under the coracoacromial ligament and at-
taches to the greater tuberosity of the humeral head (Fig. 12). The
greater tuberosity of the humerus is located lateral to the bicipital
groove. The supraspinatus muscle is innervated by the suprascapular
nerve C4 C5 C6
, , .

The infraspinatus muscle originates from the greater surface area of

the infraspinatus fossa of the scapula located below the spine of the
scapula. The muscle proceeds laterally to insert just below the at-
tachment of the supraspinatus muscle on the greater tuberosity. The
tendons of the supraspinatus, the infraspinatus, and the teres minor
merge into a conjoined tendon before attachment (Fig. 12). The infra-
spinatus muscle is also innervated by the suprascapular nerve C 4 C 5 , ,

c..
The teres minor muscle arises from the lateral portion of the axillary
border of the scapula (Fig. 11) and passes laterally and upward to
insert on the humerus immediately below the infraspinatus, on the
greater tuberosity. The teres minor receives a branch of the axillary
nerve as it proceeds to the deltoid muscle, C 5 and C 6 .

The subscapularis muscle (Fig. 13) is the most anterior and the most
medial muscle of the cuff. It originates from the entire anterior

12
 SUPRASPINATUS TRAPEZIUS

BICEPS - SHORT HEAD

. PECTORALIS MINOR

SUBSCAPULARIS
RHOMBOID
MAJOR
SERRATUS
ANTERIOR

origin

^ insert

DELTOID —

Figure 11. Sites of muscular -origin and insertion upon the scapula and the humerus.
All the muscles that perform shoulder girdle function are shown here. The stippled
areas indicate the places from which the muscles originate, and the hatched areas
represent spots upon which the muscles or their tendons insert.

(thoracic) surface of the scapulaand proceeds laterally to attach to the

lesser tuberosity of the head of the humerus. The lesser tuberosity is
located just medial to the bicipital groove (see Figs. 7 and 9). The
subscapularis muscle passes in front of the shoulder joint and is sepa-
rated from the neck of the scapula by a bursa. This bursa (see Fig. 5) is
a pouching of the synovial cavity of the shoulder joint. The muscle
receives its nerve supply from the upper and lower subscapular
nerves C 5 and C 6 9 .

There is an opening in the anterior portion of the cuff insertion upon

the humerus, located between the supraspinatus muscle and the sub-
scapularis muscle, through which the biceps tendon, its sheath, and an
invagination of the synovial cavity pass. This opening is reinforced by
the coracohumeral ligament (see Fig. 8), a ligament that proceeds from
the coracoid process and fuses into the anterior superior aspect of the
glenohumeral capsule. There is further reinforcement by the trans-
verse humeral ligament (see Fig. 5) that holds the biceps tendon in

13
FIGURE 12. The supraspinatus muscle and the infraspinatus muscle. Anterior view:
The supraspinatus muscle originates from the supraspinatus fossa of the scapula and
passes laterally under the coracohumeral ligament to attach upon the greater tuberosity
of the humerus. Posterior view. The infraspinatus muscle originates from the infra-
spinatus fossa and inserts upon the greater tuberosity just below the insertion of the
supraspinatus tendon. The combined action of these two muscles (insert) brings the
head of the humerus against the glenoid fossa in a slightly "downward" direction.

the biceps groove. The cuffs tendinous insertion is a conjoined ten-

don of all four cuff muscles: the supraspinatus, infraspinatus, teres
minor, and the subscapularis (see Fig. 9).
When tears occur in the cuff, they usually occur longitudinally in
the anterior portion of the cuff between the supraspinatus tendon and
the coracohumeral ligament at the critical zone. This critical zone
(Fig. 14) is the region of maximal tensile strength and is the area of
vascular anastamosis between the osseous vessels (arteries) and the
muscular vessels.

14
Figure 13. The subscapularis muscle. The subscapularis muscle originates from the
entire anterior surface of the scapula (see Fig. 11), the surface that glides against the
thoracic wall.The muscle extends laterally and attaches to the lesser tuberosity of the
humerus. Its tendon is the most medial of those forming the "cuff." Its action is to pull
the head of the humerus into the glenoid fossa and slightly downward.

The critical zone is so called because it is the site of degeneration

and cuff tear is usually relatively ischemic. When the arm is depen-
dent, hanging at the side, the cuff is under traction tension which
obliterates or compresses the blood vessels. When the arm is actively
abducting, the cuff muscles, especially the supraspinatus, are con-
tractingand thus placing traction upon the conjoined tendon. Either
during activity or during dependency the critical zone is ischemic. It
is apparent that in an average 24 hours of normal activity there is

ischemia during 12 to 18 hours. Only during recumbency is the cuff

hyperemic. This may explain why symptoms occur at night (Fig. 15)
(see Chapter 2).
The deltoid muscle (Fig. 16) arises anteriorly from the clavicle, lat-
erallyfrom the acromion, and posteriorly from the spine of the scapula
(see Fig. 9), and passes down in front of, lateral to, and behind the
shoulder glenohumeral joint. The fibers attach to the anterior lateral
area of the middle third of the humerus. The basic action of deltoid

15
 -SUPRASCAPULAR ARTERY
le
TENDON
(CRITICAL)
ZONE *- SUBSCAPULAR ARTERY

(ASCENDS THE
BICIPITAL GROOVE)

ANTERIOR CIRCUMFLEX
ARTERY

Figure 14. Circulation of the tendons of the cuff: the "critical zone." The tendons of
the "cuff" have a highly vascular zone at the anastomosis of the muscular vessels and
the osseous vessels. This "critical zone" is the portion with the greatest tensile strength
and is also the area that accumulates the calcium deposits; thus it is the site of cuff
ruptures. This zone is graphically shown, and the contributing vessels are identified.

PULL

ARTERY.

Figure 15. Blood circulation. Left Circulation to the rotator cuff. The arterial branch
:

from the anterior circumflex artery (ACA) enters from the bone. The suprascapular
(SSC) and the subscapular (SC) branches merge to enter from the muscle. The critical
zone of the tendon is an anastomosis which is patent when the arm is supported and
inactive. Right Traction upon the cuff from the dependent arm or from pull of the
:

contracting cuff muscle elongates the tendon and renders the critical zone (arrows)
relatively ischemic.

16
Figure 16. The deltoid muscle and its isolated function. The deltoid muscle originates
from the inferior aspect of the spine of the scapula and the protruding acromial process
(see Fig. 11). By its attachment into the humeral shaft, it has a direction of pull as
depicted by the arrow in the large figure. Its isolated action shown in the circle is that of
elevation, impinging the head of the humerus directly up under the coracoacromial
arch. As the head of the humerus is rotated, depressed, and adducted into the glenoid
fossa by the other cuff muscles, the deltoid becomes a powerful abductor.

contraction is elevation of the humerus along a line parallel to the

humerus and tends to force the humeral head up against the coraco-
acromial ligament (see insert, Fig. 15). When working in harmony
with the cuff muscles, the middle (lateral) fibers of the deltoid abduct
the arm in the coronal plane. The anterior deltoid fibers forward flex
in the sagittal plane while slightly internally rotating the humerus.
The posterior fibers extend the humerus posteriorly in the sagittal
plane and externally rotate the humerus (Fig. 17). The deltoid muscle
is innervated by the axillary nerve (C 5 and C 6 ).

GLENOHUMERAL MOVEMENT
Movement of the humeral head upon the glenoid fossa of the
scapula is intricate in that the greater articular surface of the humerus,
the male portion of the joint, is larger in area and is less convex than
the glenoid fossa, the female portion of the joint. Glenohumeral

17
 ORONAL PLANE

E LEVAT ION

ADDUCTION

FIGURE 17. The planes of arm movement, indicating the direction of movement and
the planes of movement in relation to the body. The body is viewed from above and
from the front. All arm planes are related to these two body positions.

movement is a gliding of two incongruous surfaces. Abduction of the

arm in the coronal plane is possible only by depression of the humerus
to pass under the coracoacromial arch (Fig. 18).
Glenohumeral movement requires simultaneous abduction of the
arm with depression of the humeral head. This complex movement
occurs by coordinated action of the musculotendinous cuff muscles
and the deltoid muscle. This motion is a part of the scapulohumeral
rhythm.
The deltoid muscle, by virtue of its attachment from the inferior
surface of the protruding acromial process and its attachment to the
lateral portion of the upper third of the humerus, elevates the humerus
along the line of the humeral shaft to butt the head of the humerus
against the coracoacromial hood (see Fig. 16).
This upward movement of the head of the humerus must be in-

18
FIGURE 18. Glenohumeral movement of arm abduction. The incongruity of the articu-
lar surface humerus and the surface of the glenoid fossa is shown.
of the head of the
Left: The greater tuberosity of the humerus impinging upon the coracoacromial liga-
ment if rotation is not accompanied by depression of the humerus. Right: Simultaneous
depression and rotation in a gliding motion permitting the greatei tuberosity to pass
under the coracoacromial hood during arm abduction.

clined toward the glenoid fossa and simultaneously rotated downward

to permit the greater tuberosity to pass under the coracoacromial
ligament. This permits the arm to abduct to the horizontal position.
The movement of rotation and fixation of the head of the humerus into
the glenoid fossa is performed by the action of the cuff muscles.
Of the cuff muscles the supraspinatus arises from the supraspinatus
fossa of the scapula and passes under the coracoacromial hood to at-
tach upon the greater tuberosity and pulls the head of the humerus
into the glenoid fossa. As its is slightly above the center of
line of pull
rotation (Fig. 19), it motion of the head of the humerus.
exerts rotatory
This rotation is considered by some to be minor, 10 but it is sufficient to
place the humerus into adequate abduction to permit the deltoid to
function. By pulling the head of the humerus horizontally, it also fixes
the head into the glenoid fossa. When viewed superiorly, the line of
pull is behind the linear axis of rotation of the humerus; thus the
supraspinatus muscle also externally rotates the humerus. This latter
action is important in the thorough motion required to place the arm
overhead.
Early studies of kinesiology maintained that the supraspinatus initi-
ated and acted during the first degrees of abduction with its maximum
11
activity exerted at 100° of abduction. This has been disproven.

19
 ANTERIOR VIEW

Figure 19. Function of the supra-

spinatus muscle. The anterior view
shows supraspinatus function abduct-
ing the arm in the coronal plane.
Viewed superiorly, this muscle exter-
nally rotates the arm. SUPERIOR VIEW

Electromyographic studies have shown the supraspinatus to act dur-

ing the entire abduction of the arm in the coronal plane. The function
of the supraspinatus is a quantitative one. Paralysis of the supra-
spinatus muscle by a selective nerve block permits the arm to move
through full range with minimal diminution of strength and endur-
ance. 12
In summary, the supraspinatus muscle acts in conjunction with the
other cuff muscles during glenohumeral movement to bring the head
into the glenoid fossa, exerting minimal rotatory action.
The remaining cuff muscles, the infraspinatus, subscapularis, and
the teres minor, by their origin and insertion, have more of a down-
ward pulland thus depress the head of the humerus in a downward
rotatory direction. In addition to being termed cuff muscles, they are
also called short rotators (Fig. 20). The subscapular muscle originates
from the entire thoracic surface of the scapula and inserts into the
lesser tuberosity of the humerus, having a similar action to the other

20
 SUP«4$P/N„
r(/J

Figure 20. Rotator cuff mechanism. The

supraspinous (supraspinatus) muscle pulls
the head of the humerus into the glenoid and
slightly rotates the humerus into abduction.
The infraspinous (infraspinatus) muscle also
rotates the head and slightly pulls it down.
The teres minor muscle pulls in a more
downward direction. The subscapular (sub-
scapularis) muscle pulls the head into the
glenoid, but its main rotatory action is to in-

ternally rotate the humerus about its lon-

gitudinal axis.

short rotators. The combined action of the cuff muscles pulls the hu-
jneral head into the glenoid fossa, depresses and rotates the head,
fixes it there, and assists the deltoid in its abduction action (Figs. 21
and 22).
The movement of the humerus at the glenohumeral joint
active
differs from its passive range and is influenced by rotation of the
humerus. The arm can be abducted passively to 120° with movement
exclusively at the glenohumeral joint. After 120°, abduction is blocked
by the humerus impinging upon the acromial process and the
coracoacromial ligament. Active abduction is possible only to 90°,
after which active abduction is possible only with simultaneous rota-
tion of the humerus that permits the greater tuberosity of the humerus
to pass posteriorly to the acromial process.
Only 60° of abduction is possible with the humerus in internal rota-
tion,due to the fact that the humerus, in internal rotation, impinges
much earlier upon the coracoacromial ligament than it does in exter-
nal rotation (Fig. 23). This explains the limited shoulder abduction in
patients who have a limited humeral rotation as a result of surgical
repair of recurrent shoulder dislocations.
Since the arm can be abducted and elevated fully overhead, an arc
of 180°, an additional 60° to the active 90° and passive 120° occurring at
the glenohumeral joint must occur. This motion results from rotation
of the scapula, adding an additional 60° to overhead elevation of the
arm. The combined movement of the humerus upon the scapula at the
glenohumeral joint and the scapula upon the thorax, in its simultane-
ous synchronous movement, conforms to the well-established scapu-
lohumeral rhythm. 1
Before discussing this total arm movement, the scapular phase of
the rhythm requires evaluation.

21
Figure 21. Combined cuff and deltoid action upon the glenohumeral articulation. Ab-
duction of the humerus along the plane H is the result of combined action of the
supraspinatus (Ssp) adducting the head into the fossa; the infraspinatus and subscapu-
laris (Isp and Ssc) adducting and depressing the head; and the deltoid (D) acting as an
abductor when working with these cuff muscles. The center of rotation (C) lowers
during this downward gliding motion.

SCAPULAR MOVEMENT
The scapula moves in a gliding manner upon the thoracic wall at the
thoracoscapular articulation. Movement occurs at the distal end of the
clavicle, the acromioclavicular joint, by virtue of motion and rotation
of the clavicle. Motion of the scapula is primarily produced by two
muscles, the trapezius and the serratus anterior.
The broad fan-shaped trapezius muscle acts as three muscles (Fig.
24). The upper fibers of the trapezius originate from the ligamentum
nuchae in the lower cervical region, the posterior spinous processes of
the cervical spine, and the upper thoracic spine. They radiate laterally
and downward to attach to the upper margin of the medial and central
portion of the scapular spine. 13,14 The action of the upper trapezius
pulls the scapula upward and causes inward pivoting about the acro-
mioclavicular joint.
The middle fibers originate from the spinous processes of the upper
thoracic vertebrae, proceed laterally, and attach to the medial border

22
Figure 22. Abduction angle of deltoid. A. With the arm dependent, the deltoid line of
pull is along the line of the humerus and thus elevates the arm up against the acromion.
B. With slight abduction of the humerus the angle of the deltoid changes its pull to
abduction of the arm.

of the scapular spine. These middle fibers principally "fix" the

scapula during abduction of the arm. They must relax during forward
flexion of the arm-shoulder in the sagittal plane (see Fig. 17).
The lower fibers of the trapezius originate from the spinous proc-
esses of the lower thoracic vertebrae and attach to the medial portion
of the spine of the scapula. The isolated function of these fibers pulls
the medial border of the spine of the scapula down and in. The com-
bined action of the upper and lower trapezius fibers rotates the
scapula around the axis center of the acromioclavicular joint, de-
pressing the vertebral border, and elevating the glenoid fossa on the
outer portion. The trapezius is supplied by the spinal accessory nerve
(XI).
The is the other major muscle acting to rotate the
serratus anterior
scapula. This broad muscle originates from the upper eight ribs of the
anterolateral chest wall, anterior to the scapula, and runs posteriorly to
insert upon the medial (vertebral) border of the scapula. The heaviest
fibers attach upon the inferior border. The serratus is located in the

23
 E TERNALLY

INTERNALLY

ROTATED

FIGURE 23. Influence of humeral rotation upon abduction range of the glenohumeral
joint. A. Active abduction is possible to 90°, and an additional 30° can be gained pas-
sively if the humerus rotates externally approximately through a 90° arc. This abduction
range of 120° is possible because the rotation allows the greater tuberosity to pass
behind the acromion. B. With the arm internally rotated, the greater tuberosity im-
pinges against the coracoacromial arch and blocks abduction at 60°.

scapulocostal joint space between the scapula and the rib cage. Its
line of pull moves the scapula forward and, because it acts below the
axis of the acromioclavicular joint, acts as a rotator. The serratus mus-
cle is innervated by the long thoracic nerve formed by the anterior
branches of the roots of C 5 C 6 and C 7 (primarily C 6 ) before they enter
, ,

the brachial plexus.

The combined action of the upper trapezius, the lower trapezius,
and the serratus causes rotation of the scapula about the pivotal point
of the acromioclavicular joint and elevates the glenoid fossa.
Other muscles that act upon the scapula but are not involved in the
scapulohumeral rhythm can be mentioned briefly. Under the
trapezius are three muscles that attach to the vertebral border of the
scapula: the levator scapula, the rhomboid major, and the rhomboid
minor (Fig. 25). The levator scapula originates from the cervical trans-

24
Figure 24. Scapular musculature: rotators. The scapular muscles forming the rotator
phase of the scapulohumeral rhythm are shown with the upper trapezius fibers elevat-
ing the outer border of the spine, the lower fibers of the trapezius depressing the medial
border of the spine, and the serratus pulling the lower portion of the scapula forward
from its position under the blade. The combined action moves the scapula in orbit
around the acromioclavicular center of rotation (u, m, and 1 = upper, middle, and lower
trapezius; s = seratus anterior; SR = scapular rotation).

verse processes and proceeds downward and laterally to attach to the

superior angle of the scapula. The rhomboid minor is located immedi-
ately below the levator, originates from the lower cervical vertebra,
and attaches to the vertebral border of the scapula at the level of the
scapular spine. The rhomboid major, much broader than the above
muscles, originates from the upper thoracic vertebrae and inserts into
the remainder of the vertebral border of the scapula. They elevate the
medial aspect of the scapula and cause downward rotation of the
glenoid fossa by virtue of the rotation around the acromioclavicular
pivotal point. These three muscles receive their nerve supply from C 5
through the dorsal scapular nerve.
Downward movement of the glenoid fossa is aided also by the ac-
tion of the pectoralis major and the latissimus dorsi muscles acting
upon the scapula indirectly through their attachments upon the
humerus.
The pectoralis major has an extensive origin: from the sternal half of

25
 Glenoid
Downward
Movemen t

FIGURE 25. A. Downward rotators of the scapula. B. The muscles acting upon the
scapula directly to cause downward rotation of the glenoid fossa are the levator scapulae
(upper arrow), the rhomboid minor (middle arrow), and the rhomboid major (lower
arrow).

the clavicle, the sternum and costal cartilages of the second to the
seventh rib, and the abdominal muscles (Fig. 26). It in-
fascia of the
serts into the crest of the greater tuberosity and downward along the
humerus several inches. It is innervated by the medial and lateral
thoracic nerves. Its function is primarily to pull the arm down from an
overhead forward position, adducting the arms when held in front of
the body, and internal rotation of the humerus.
The latissimus dorsi is the broadest muscle of the back and thoracic
region. It originates from the spinous processes of thoracic 6 down-
ward to the crest of the ilium. It inserts to the crest of the lesser
tuberosity of the humerus. In its action it depresses the arm downward
and internally rotates it.

The musculature acting upon the clavicle also effects scapular mo-
tion and will be discussed later.

SCAPULOHUMERAL MOVEMENT
Abduction elevation of the arm in the coronal plane, from de-

26
Figure 26. Pectoralis major.
The pectoralis major has three
laminae: clavicular (C), manu-
brial (M), and a sternocostal (S-C)
bundle. All form the pectoralis
muscle but are considered to
have slightly separate functions.

pendency at the side of the body until fully extended overhead, with
palms facing each other, is a smooth, synchronous motion involving
every component of the shoulder girdle complex. Motion must be
smooth and effortless, requiring full range of motion at each joint and
well-coordinated muscle balance. The normal composite movement is
stressed because knowledge and recognition of the slightest imbal-
ance and restriction must be recognized to evaluate the pain pro-
ducing impairment of the shoulder.
The smooth, integrated movement of the humerus, the scapula, and
the clavicle has been well termed the "scapulohumeral rhythm" by
Dr. E. A. Codman, whose book, The Shoulder, is a monumental
study. 1
Of every glenohumeral
15° of abduction of the arm, 10° occurs at the
joint, and from rotation of the scapula upon the chest wall. This 2:1
5°
ratio of humerus to scapula exists throughout the entire abduction
range in a smooth, rhythmic pattern (Fig. 27). To reiterate, the scapula
can rotate 60°; the humerus, 90° actively and 120° passively.
The scapula rotates to maintain mechanical stability of the glenohu-
meral joint and efficiency of the deltoid muscle. The deltoid, as all
muscles, has greatest efficiency at its rest length (Fig. 28), the point
midway between its extremes of motion. The deltoid is at rest length
when the arm is dependent at the side. Abduction shortens the muscle,
and by 90° abduction with no scapular rotation, the extreme of contrac-
tion is reached. The deltoid then is barely able to support the arm.
Scapular rotation maintains optimum deltoid length throughout ab-
duction.
Full overhead elevation requires little or no deltoid support if the
scapula has fully rotated. At this point the glenoid fossa is directly
under the head of the humerus. Had there been no scapular rotation,

27
 S _ 3_0 _ 60 _ I

H 60 120 2

FIGURE 27. Scapulohumeral rhythm. The scapula and the humerus at position of rest
with the scapula relaxed and the arm dependent, both at position 0°. The abduction
movement of the arm is accomplished in a smooth, coordinated movement during
which for each 15° of arm abduction 10° of motion occurs at the glenohumeral joint and
5° occurs due to scapular rotation upon the thorax. The humerus (H) has abducted 90° in

relation to the erect body, but this has been accomplished by a 30° rotation of the
scapula and a 60° rotation of the humerus at the glenohumeral joint, a ratio of 2:1. Right:
Full elevation of the arm: 60° at the scapula and 120° at the glenohumeral joint.

the humerus could shear out of the glenoid fossa. This is a mechanism
of shoulder dislocation.
Scapulohumeral movement at the glenohumeral joint and the
scapulothoracic joint has been highlighted with "motion around the
axis of the acromioclavicular joint." This joint and the sternoclavicular
joint play a vital role in total arm motion.

ACROMIOCLAVICULAR AND STERNOCLAVICULAR JOINTS

The acromioclavicular joint is a plane joint connecting the outer end
of the clavicle with its convex facet to the anterior medial portion of
the acromial process. A fibrocartilaginous ring that resembles an
intra-articular meniscus may exist. At the age of 2 years no joint space
exists; the acromion and the clavicle are connected by a fibrocarti-
laginous bridge. At the age of 3 years, a joint space appears consisting
of two synovial cavities, one at the end of the clavicle, the other at the
acromial end, with an interposed disk between them (Fig. 29).
The disk becomes meniscoid by the second decade, and the articu-

28
 eng th.

Figure 28. Deltoid action upon the glenohumeral joint. The mechanical efficiency
afforded the deltoid action upon abduction of the humerus by the simultaneous rotation
of the scapula is shown in the length-tension relationship upon muscle. Muscle effi-
ciency is greatest at rest length and diminishes upon shortening. In the abducted arm
without scapular rotation, the deltoid shortens to a length of less tension (B). Simul-
taneous scapular rotation keeps the deltoid at rest length (A).

lar surfaces of the acromion and the clavicle become smooth and glis-
tening. After the second decade the disk and the articular surfaces
undergo rapid degenerative changes that are marked by the fourth
decade. 15
The acromioclavicular joint has a weak, relaxed capsule that is
reinforced by strong superior and inferior acromioclavicular ligaments
that prevent posterior displacement of the clavicle upon the acromion.
The clavicle is firmly attached to the scapula by the coracoclavicular
ligament (see Fig. 2). Two resilient fascicles, each called a ligament,
form the coracoclavicular ligament: the lateral trapezoid and the me-
dial conoid ligaments. The manner of attachment of these ligaments
prevent the scapula from rotating about the acromioclavicular joint
and, by its "strut" shape, maintains a constant relationship of the
scapula to the clavicle (Fig. 30),
The coracoclavicular ligament, by its attachments in a strut shape
was once considered instrumental in holding the scapula away from
the chest wall and giving stability to the acromioclavicular joint. This

29
Figure 29. Evolution of the acromioclavicular disk (meniscus). A. From birth to age 2
a fibrocartilage bridge joins the acromion to the clavicle (Ac to CI) with no joint space. B.
From age 3 to 4, cavities form to either side of what will become the meniscus (x). C. In
the firstand second decades the meniscus is already beginning thinning and fibrilla-
tion, which increases rapidly from age 20 on. D. In the sixth decade the meniscus may
be completely gone.

FIGURE 30. Action of the coracoclavicular ligaments upon the acromioclavicular joint.
The coracoclavicular ligament attaches the scapula to the clavicle. It is divided into two

resilient fascicles termed the trapezoid ligament and the conoid ligament. From the
coracoid they proceed upward and laterally to attach onto the undersurface of the
clavicle. Elevation of the clavicle without rotation maintains a constant relationship of
the scapula to the clavicle. The rotation of the scapula depresses the coracoid and thus
rotates the clavicle about its long axis. The left drawing depicts the scapula at rest with
the coracoclavicular ligaments viewed through the sagittal axis (dotted circle). The
middle drawing shows abduction of the clavicle along the coronal plane without rota-
tion. The right drawing shows full elevation of the clavicle, still displaying an un-
changed relationship of the scapula to the clavicle in this coronal plane. Motion through
this range must occur at the sternoclavicular joint (SCJ).

isnow disproven by the retention of stability after severence of this

ligament. Instability results only when there is severence of the cora-
coclavicular ligament and the superior acromioclavicular ligament. 16
As the scapula rotates to elevate the glenoid fossa, it rotates the
clavicle about its long axis through the attachment of the coracoclav-
icular ligaments to the outer end of the clavicle. The "crank" shape
of the clavicle elevates the outer end with no change in the angle of

30
 rfffftfr.

FULL CLAVICULAR
• ELEVATION
30°
3

rcffr^r / 180° HUMERUS

u / ELEVATION

NO CLAVICULAR"
ELEVATION
-Jv

.TIONAL SCAPULAR
TATION TO 60°

FIGURE 31. Scapular elevation resulting from clavicular rotation. The upper drawing
shows the elevation of the clavicle without rotation to 30°. The remaining 30° of scapular
rotation, which is imperative in full scapulohumeral range, occurs by rotation of the
"crank-shaped" clavicle about its long axis.

elevation at the proximal sternoclavicular joint. Rotation of the clavi-

cle occurs primarily in the overhead arm elevation above 90° abduc-
tion of the arm (Fig. 31). The first 30° of clavicular elevation occurs at
the sternoclavicular joint. The next 30° of elevation is the result of
rotation of the clavicle about its long axis.
The sternoclavicular joint is formed by the sternal end of the clavi-
cle attaching to the superior lateral portion of the manubrium of the
sternum and the cartilage of the first rib (Fig. 32). An articular disk
between the sternum and the clavicle forms two joint spaces. Anterior
and posterior sternoclavicular ligaments reinforce a loose fibrous cap-
sule, and an interclavicular ligament connects the two clavicles. Sta-
bility of the joint is imparted by the costoclavicular ligament, a strong
ligament that arises from the medial portion of the first rib and runs
laterally and obliquely to attach into the undersurface of the clavicle
(Fig. 32). This ligament stabilizes the clavicle against muscle action
(Fig. 33) and acts as a fulcrum for all motions of the shoulder girdle.

31
 INTERCLAVICULAR LIGAMENT
.STERNOCLAVICULAR LIGAMENT
CLAVICLE
COSTOCLAVICULAR

RIB 1

LAGE

XIPHOID

FIGURE 32. The The sternoclavicular joint is formed by the me-

sternoclavicular joint.
dial portion of the clavicle articulatingupon the manubrium sterni and also with the
cartilage end of the first rib. The ligaments that stabilize the joint are shown. The
fibroelastic disk, or meniscus, is shown in the insert. In spite of marked movement at
this joint in all shoulder girdle movements, arthritic changes are rare, mild, and rarely
disabling.

The sternoclavicular joint, in spite ofplane joint surfaces, acts

its

motions of the shoulder

like a ball-and-socket joint, participating in all
complex. In spite of its excess use, unlike the acromioclavicular joint,
degenerative changes occur late in life and are mild with minimal
functional impediment. 15

COMPOSITE SHOULDER GIRDLE MOVEMENTS

Movement of the shoulder girdle requires smooth, effortless, syn-
chronous movement of the glenohumeral joint and all the accessory
joints. Each has been individually considered; now the composite
movement can be related.
When the arm is raised in abduction, the humerus and the scapula

move in a rhythm so that for every 15° of total abduction of the arm, 10°
occurs at the glenohumeral joint, with a corresponding 5° of rotation of

32
 30°-40°

Figure 33. Muscles acting upon the clavicle. The major muscles acting upon the
clavicle are shown, their direction of pull indicated by arrows: scm = sternocleidomas-
toid; t = trapezius; d = deltoid; s = subscapulars; and pm = pectoralis major. The
gravity pull (h) of the arm itself is indicated as well. The muscles that act indirectly
upon the clavicle are not shown.

the scapula. The humerus will complete its full possible abduction
^>nly if it externally rotates during elevation to permit the greater
tuberosity to pass under and behind the coracoacromial ligament.
Only 60° of humeral abduction is possible with the arm internally
rotated. Only in the externally rotated position can the humerus ab-
duct actively to 90°, and be passively abducted to 120°. Combined
muscular action of the rotators and abductors performs this task (Fig.
34).
Full elevation of the arm overhead (180°) requires 60° of scapular
rotation to alter the angle of the glenoid fossa upon which the humerus
articulates. Scapular rotation results from the combined action of the
trapezius and serratus muscles. Because the coracoclavicular liga-
ments prevent scapular rotation in the coronal plane, the scapula
pivots about the acromioclavicular joint from rotation of the crank-
shaped clavicle and elevation at the sternoclavicular joint.
Motion of the sternoclavicular joint is possible in all planes. The
clavicle and the scapula are elevated by the trapezius and other acces-
sory muscles that attach to the clavicle. For every 10° of arm elevation,
4° of the elevation occurs at the clavicle. There is varying elevation of
the clavicle during the total arm elevation phase. Approximately 15° of
clavicular elevation occurs during the first 30° of arm abduction, and

33
 yo^

-o^oi

FIGURE 34. Accessory movement of the scapulohumeral rhythm other than the gleno-
humeral movement. Movement of the arm through all phases of abduction involves all
joints of the shoulder girdle in a synchronous manner.

Phase I : The resting arm: 0° scapular rotation (S); 0° spinoclavicular angle (SCA); 0°
movement at the sternoclavicular joint (SC); no elevation of the outer end of the clavicle
(C);no abduction of the humerus (H).
Phase II Humerus abducted 30°: the outer end of the clavicle is elevated 12° to 15°
:

with no rotation of the clavicle; elevation occurs at the sternoclavicular joint; some
movement occurs at the acromioclavicular joint as seen by an increase of 10° of the
spinoclavicular angle (SCA) formed by the clavicle and the scapular spine.

the clavicle has elevated to its final position as the arm reaches the
horizontal level (90° abduction).
Half of the scapular rotation (30°) thus has been reached by clavicu-
lar elevation. The remaining 30° occurs by rotation of the crank-
shaped clavicle exerting pull on the coracoid process through the
coracoclavicular ligaments. The clavicle rotates 45°, which raises the
clavicle and attached scapula an additional 30°. The greater part, if
its

not all the rotation, occurs in the arm elevation above the horizontal
position.

BICEPS MECHANISM

The biceps is anatomically and pathologically involved in the

shoulder girdle, but its kinetics is unrelated to glenohumeral move-
ment.

34
Figure 34 (continued).

Phase III : Humerus (H) abducted to 90° (60° glenohumeral, 30° scapular): the clavicle
is elevated to its final no rotation of clavicle has occurred (all movement is
position, 30°;
at the sternoclavicular joint);no change in the SCA.
Phase IV: Full overhead elevation (SH = 180°; H = 120°; S = 60°): outer end of the
clavicle has not elevated further (at the sternoclavicular joint), but the SCA has in-
creased (to 20°). Because of the and its "cranklike" form, the clavicle
clavicle's rotation
elevates an additional 30°. The humerus through this phase has rotated, but this has not
influenced the above degrees of movement.

The biceps two heads but a common tendon insertion

brachii has
into the tuberosityupon the inner aspect of the radius. The short
medial head originates from the coracoid process. The long head
originates from the superior lip of the glenoid fossa, proceeds lat-
erally,and angles 90° at the bicipital groove of the humerus, to pro-
ceed downward to the common tendon (Fig. 35).
By its attachment on the ulnar side of the radius, its action is
primarily supination of the forearm and secondarily elbow flexion. In
the upper arm region the biceps assists the anterior deltoid in forward
flexing the shoulder.
Motion of the biceps tendon does not occur in the unmoving bicip-
groove. There is motion in the bicipital groove only when there is
ital

movement of the glenohumeral joint. Maximum downward movement

35
 SHB

Figure 35. Biceps mechanism. The biceps brachii originates from two tendons: the
short medial head, from the coracoid process; and the long head, from the superior rim
of the glenoid fossa. The long head passes down into the bicipital groove in a fibrous
sheath between the tendons of the subscapularis and the supraspinatus tendon. The
small drawings at left depicit the movement of the humerus upon the biceps tendon. A.
The dependent hanging arm. B. Arm adducted, internally rotated, and extended, caus-
ing the ligament (dot) to move away from the transverse humeral ligament. C depicts
thedownward movement of the ligament (dot below the transverse humeral
) ligament
when the arm is abducted, externally rotated, and flexed forward.

of the tendon within the groove occurs when the arm is internally
rotated and is elevated in the forward flexion movement. When the
arm is flexed backward (extended) and abducted with the humerus
externally rotated, the biceps tendon has the greatest upward move-
ment within the groove (actually the biceps groove moves downward

36
and thus the tendon glides upward). As any glenohumeral movement
glides the tendon within the groove, free motion must exist to insure
normal scapulohumeral movement. The bicipital mechanism is
therefore essentially a passive action.
In severe deltoid paralysis, such as poliomyelitis, the biceps can
become a "trick" abductor of the arm by the external rotation of the
humerus. This lines up the belly of the biceps and the tendon in a
direct line to the point of origin at the supraglenoid fossa; thus the
biceps pull, with the humeral head held snugly in the fossa, weakly
abducts the arm mechanically.

37
CHAPTER 2

Musculoskeletal Pain

The causes of pain in the shoulder, as enumerated in the outline on

the following pages, are manifold. The most common cause of shoul-
der pain, constituting 90 percent of nontraumatic painful disabilities, is
a degenerative tendinitis. 17 Among the names given to this condition
and "frozen shoulder."
are bursitis, pericapsulitis, adhesive capsulitis,
The pathologic mechanism by which pain and dysfunction occur is
more significant than the label, and by recognition of the abnormality
of function that causes pain, rational treatment can be prescribed. The
site of tissue pain can be determined by clinical examination (Fig. 36).

TENDINITIS: ATTRITION AND DEGENERATION

Man's upright posture and his daily activities are wearing on the
supraspinatus tendons and the cuff-conjoined tendons. Gravity causes
traction stress upon the capsule and tendons of the hanging arms, and
movement of forward flexion and abduction cause friction and com-
pression between the head of the humerus and the overlying coracoa-
cromial ligament.
has been noted that work requiring heavy lifting is not mandatory
It

to cause shoulder pain from degeneration, but principally work with

the hands at or above acromium height places a greater load upon the
shoulders. This sustained position also causes sustained ischemia of
the cuff and compresses the tendon between the greater tuberosity
and the acromium 18 (see Fig. 15).
A
progressive degeneration of the cuff has been noted in people
unaware of pain or dysfunction. 2 In the fifth decade many cuffs are
noted to be pulling away from their sites of insertion with the cuff
showing signs of thinning and fibrillation. This thinning and degen-
eration are noted mostly within the "critical zone" (see Fig. 14), and
the incidence of slight tears in later years becomes more marked. As

38
Figure 36. Sites of tissue pain: (1) greater
tuberosity: attachment of supraspinatus
tendon; (2) lesser tuberosity; (3) bicipital
groove: tendon of long head of biceps;
(4) subacromial bursa; (5) acromioclavic-
ular joint; (6) glenohumeral joint and cap-
sule; (7) subdeltoid bursa.(Modified from
Steindler, A. The Interpretation of Pain in
:

Orthopedic Practice. Charles C Thomas,

Springfield, 111., 1959.)

the intensity of cuff degeneration becomes more apparent, some

wearing away of the tuberosities of the humerus can also be noted
(Figs. 37 and 38). This is evidently due to the deltoid action of eleva-
tion of the humerus up against the coracoacromial hood being unop-
posed by the depressing and rotating action of the cuff "rotators."
Absorption of the tuberosities must also find compression of the
bicipital tendon as the bicipital groove becomes shallow and dis-
torted, and even completely obliterated. The subacromial bursa (see
Fig. 40) is also caught between these compressive pressures, and the
bursal walls thicken and, when there is rupture of the tendon or inva-
sion by calcium, become distended. The inferior surface of the ac-
romion, from friction and pressure of the abutting humerus, becomes
eburnated and thickened.
Aging must be considered a significant factor in degenerative ten-
dinitis.Other factors, however, are also at play.
Itwas noted during the discussion on functional anatomy that in
abduction of the arm the humeral head must be depressed within the
glenoid fossa and glide downward to permit the greater tuberosity to
pass under the coracoacromial arch. The posterior part of the arch, the
acromion, is farther removed from the glenoid cavity than are the
coracoid and the ligament (see Fig. 2). The greater tuberosity does not
hit the acromion, but is constantly pressing against the ligament in
19
everyday activities requiring elevation and abduction of the arm.
Almost every daily arm activity involves some degree of abduction.
During abduction of the arm internal rotation decreases the active
and passive range of motion at the glenohumeral joint from 90° to 60°
(see Fig. 18). A "round-shouldered" posture will depress the glenoid
fossa and thus also depress the acromial arch and cause impingement

39
 OUTLINE OF THE CAUSES OF PAIN FELT
IN THE UPPER EXTREMITY

I. Musculoskeletal
A. Degenerative
1. Tendinitis, with or without calcific deposits
2. Cuff tear, partial or complete
B. Traumatic
1. Fracture
2. Dislocation
3. Acromioclavicular separation
4. Biceps tendon tear
C. Inflammatory
1. Rheumatoid arthritis
2. Gout
3. Infectious arthritis

D. Tumors
1. Bone
2. Soft tissue

II. Neurologic
A. Peripheral nerve
1. Root (cervical)
a. Spinal foraminal
(1) Spondylosis
(2) Herniated disk
(3) Traumatic
(a) Fracture
(b) Dislocation
b. Extramedullary tumors
2. Brachial plexus
a. Mechanical
(1) Neurovascular bundle compression
("cervical dorsal outlet syndromes")
(2) Scalene anticus syndrome
(3) Cervical rib
(4) Claviculocostal syndrome
(5) Pectoralis minor syndrome

40
 b. Trauma
(1) Traction or penetrating injuries
c. Inflammatory
(1) Brachial plexitis
d. Tumors
(1) Pancoast
(2) Adenitis

B Central nervous system

.

1. Intramedullary tumors
2. Syringomyelia

III. Vascular
A. Arterial
1. Occlusive: acute and chronic
a. Embolic
b. Vasospastic
c. Traumatic
d. Atherosclerotic
2. Aneurysm or fistula

B. Venous
1. Phlebitis

C. Lymph
1. Lymphedema

IV. Referred Visceral-Somatic Pain

A. Cardiac
1. Anginal pain
2. Hand-shoulder syndrome
a. Causalgia
B. Gallbladder
C. Diaphragmatic
D. Ruptured viscus

V. Articular

A. Degenerative
B. Inflammatory
C. Infectious
D. Metabolic

41
 CUFF
CYST

"VOLCANO
EFFECT

BICEPS
TENDON

Figure 37. Roentgenographies changes in

shoulder dysfunction: cysts in the tuber-
osities of the humerus. These are early
With wear and
x-ray evidence of attrition.
tear, the tuberosities become eroded,
causing a volcano appearance. The bicipi-
tal groove becomes shallow.

much sooner in arm motions. This can be verified by abducting the

arms in the coronal plane to overhead position in the erect posture,
then attempting the movement in a forced "slumped" posture. The
latter will impede abduction markedly. It can be noted that the
"slumped" posture internally rotates the arms, further impeding ab-
duction.
Aging impairs joint range of motion because of the altered position
of the scapula, and, in turn, because of the increased dorsal spinal
kyphosis from dorsal disk degeneration. In the forward and backward
lifting of the upper arm there is a decrease of 50° (from 240° in youth to
190° at age 70) and a similar decrease in abduction (166° in the young
and 1 16° at age TO). 20 This slumped posture due to aging is also manifest
in postural problems, occupational positions, and the postural depic-
tions of the emotions (Fig. 39). 21

42
 EBURNATION

SPUR

Figure 38. Stages of degeneration. Top The

:

tuberosities disappear and are replaced by

eburnated bone. Bottom: In addition to
hypertrophic change of the humeral head and
the acromion, there are changes in the acro-
mioclavicular joint, including spur formation.

CALCIFIC TENDINITIS
The pathogenesis and evolution of calcific tendinitis are shown in
Figure 40.
The earliest microscopic changes are hyaline degeneration of the
collagen in the tendon. There is disintegration of the nuclei and fur-
ther degeneration of the tendon fibers which fibrillate, loosen, and
ultimately separate. As they become pulverized between the grinding
surfaces of the acromioclavicular ligament and the head of the
humerus, they form small particles. When these particles are small,
they are not visible in roentgenograms. They are said to be present in
most people by age 35. 17
This debris consists primarily of calcium salts in a highly vascular
area, 22 contrary to the old notion that degenerative tendinitis occurs in
an avascular tendon. In the dry state this powder casts a dense x-ray
shadow. If the tendon is traumatized, the resultant hyperemia absorbs
the calcium, forming a liquid, chalky material under pressure within

43
<^
w^>

Cj^"
FIGURE 39. Postural effect upon glenohumeral range of motion. The upper drawings
show the erect, "good" posture of the young: the forward elevation and the lateral
abduction range of the arm is full and free; the coracoacromial ligament is elevated, and
the humerus can do its corrective external rotation to allow the greater tuberosity to pass
under the acromion. The lower drawings depict the dorsal kyphotic posture of the aged,
the depressed individual, or the occupational ly stressed person, in which the coraco-
acromial hood is lowered and the arm is internally rotated. Both of these factors cause
impingement of the humerus against the arch. Compression and attrition of the cuff
tendons result.

the tendon. On x-ray the appearance fades into a translucency. The

double arrows between the stages in Figure 40 indicate that many of
these stages are reversible. Engorgement may be followed by "chalk"
and conversely revert into the dry, "silent" inclusion. The "silent"
phase may be composed of particles so small as to be invisible on
x-ray.

44
CRITICAL Z

SILENT ENGORGEMENT BULGE

Figure 40. Natural sequence of calcific tendinitis. A. The relationship of the supra-
spinatus (cuff) tendon between the coracoacromial ligament and the head of the
humerus. B. The repetitive pressure from daily use and abuse. C. The degenerative
changes of the tendon in the "critical zone." The lower sequence follows the silent
asymptomatic phase in the sequence steps to that of symptomatic "bulging." Compres-
sion from whatever external cause results in engorgement via the tendon circulation.
The debris of the "silent" phase absorbs fluid, and the dry powder becomes chalk.
Further irritation and engorgement cause the chalk to expand, or bulge. The double
arrows signify that each phase is reversible.

The bulge phase presents a mechanical obstacle to smooth, pain-

free abduction so that abduction, at approximately 70°, will impinge
under the coracoacromial ligament. Pain will result from this in-
creased tendon tension from compression. If the arm can be carried
further in its abduction cycle, the bulge may pass beyond the ligament
and become painless Repeated abduction of the arm compres-
at 110°.
ses this bulge further and increases the engorgement. Further in-
creases of the bulge ensue, and a vicious circle results.
Rest or treatment may resolve this irritation and allow the inflam-
mation to resolve. A return to "chalk" stage or the silent phase, can be
expected. Increase of the bulge and concomitant engorgement will
result in rupture of the calcific mass out of the tendon in the various
directions and locations depicted in Figure 41.
The deposit may rupture superiorly and locate under the subdeltoid
bursa. The ruptured deposit is frequently only partially evacuated

(Fig. 41, parts 3 thus the relief of painful tension is temporary.

and 4);
It may recur repeatedly until there is complete evacuation in various

45
Figure 41. Evolution of the calcified tendinitis and formation of "bursitis." 1. The
normal relationship of the supraspinatus tendon (cuff) to the coracoacromial arch and
the head of the humerus; the intimate relationship of the subdeltoid bursa and the
glenohumeral joint. 2. The site of calcium deposit in the cuff tendon. 3. The "bulging"
calcium has been evacuated from the tendon into the subbursal space. 4. A partial
evacuation into the subbursal space with much debris remaining within the tendon.
5. Tendon evacuates, with rupture into the subdeltoid bursa. 6. "Dumbbell" intrabursal

invasion. 7. Adhesive bursitis in which there is thickening of the walls of the bursa and
adhesion between the superior and inferior surfaces.

other manners or the overlying bursa becomes adherent and thick-

ened (Fig. 41, part 7). The evacuated debris may work itself laterally
and distally and repose under the deltoid insertion at the upper lateral
aspect of the humerus, where it is no longer under tension nor an
impediment to abduction.
The subbursal evacuation of the deposit may elevate the floor of the
bursa and by pressure and irritation may rupture into the bursal sac.
The rupture evokes acute, severe pain followed by a dull, deep ach-

46
ing, depending on the direction the calcium moves within the bursa.
If the debris moves laterally and distally within the bursa (Fig. 41, part
5), the tenderness is felt at the lateral insertion of the deltoid, and the
arm moves more freely under the coracoacromial ligament impinge-
ment. If the debris divides into a "dumbbell" form within the bursal
sac, (Fig. 41, part 6) separated by the coracoacromial ligament, the arm
will neither fully abduct nor adduct. It will be held in a partial abduc-
tion position (30° to 45°), resisting any movement.
The repeated bursal sac inflammation from persistent pressure may
cause chronic thickening of the bursal lining, thickening of the bursal
fluid, and adherence of the bursal walls; and an "adhesive pericap-
sulitis" results (see Fig. 43). This leads to a form of "frozen shoulder,"
when it is remembered that the superior wall of the bursa is adherent
to the undersurface of the deltoid muscle and the inferior wall is
adherent to the cuff. Other concepts of the "frozen shoulder" will be
discussed later.
Erosion of the calcific mass inferiorly into the humerus is a possi-
bility. This is not shown in Figure 41. This development is not usually
visualized on x-ray study but is revealed at surgery when intractable
pain requires surgical intervention.
In a brief summary, therefore, it may be assumed that over a long
period of time, even normal use of the arm may produce considerable
wear and tear to the cuff muscles and their tendons. Occupational
factors, abuses of the arm, faulty posture, trauma, and emotional fac-
tors may hasten degenerative changes. Nature attempts to repair these
tissue changes of damage by scar and ultimately by calcium deposit.
So long as the deposit of debris remains within the tendon and under
no tension, the shoulder is painless and unrestricted. Sudden injury
precipitates the clinical picture of pain and impaired motion.

BURSITIS

Before proceeding further in the clinical discussion of tendinitis,

calcific or noncalcific, "bursitis" merits discussion.This term is most
frequently used when shoulder pain is considered.
Bursitis is rarely a primary condition. Most frequently it is sec-
ondary to degenerative lesions of the cuff and thus is a secondary
phenomenon. The intimate relationship of the walls of the subdeltoid
bursa, superiorly to the highly vascular and richly sympathetic nerve-
supplied subdeltoid fascia and inferiorly inseparably adherent to the
supraspinous portion of the cuff relates any pathology of the tendon to
pathology of the bursa. The subdeltoid bursa is essentially the inner
lining of the deltoid and the acromium and the outer layer of the cuff
(Fig. 42). Filled with a small amount of fluid, any movement of the

47
Figure 42. Subacromial bursa. The subdeltoid bursa is essentially the inner synovial
lining of the deltoidmuscle and the undersurface of the acromium. The outer layer of
the supraspinatus portion of the cuff is the inner layer of the bursa. In any movement of
the arm, the two layers of the bursa glide upon each other as the bursa deforms.

arm in abduction or forward flexion causes the two adjacent layers of

the bursa to glide upon each Any
adjacent inflammation of the
other.
tendon causes inflammation of the bursa. It is inconceivable that bur-
sitis could exist without tendinitis and vice versa.

DIAGNOSIS
In a person who must be assumed to have a relative degree of cuff
tendon degeneration, depending on age, posture, occupation, and
psychological makeup, and who has previously been asymptomatic,
onset of pain can occur after a particularly strenuous activity such as
painting a ceiling or working in an awkward posture for long periods
of time. Causes of acute precipitation of shoulder pain can include
immobilization of the arm in a plaster cast for any reason, working on a
tedious task in a slumped position, making sudden movements in an
abnormal direction, or performing normal movements, but in a mo-
ment of fear, tension, or anxiety.
The adage of causation of musculoskeletal pain applies. Pain can
result in any of three conditions: (1) abnormal strain on a normal
joint, (2) normal strain on an abnormal joint, or (3) normal stress
upon a normal joint when the joint is unprepared and graded for that

48
 .sdf

Figure 43. Acute tendinitis and inflammation of contiguous tissues. A. The tissues
contained between the rotator cuff(c) and its tendons (t), and the subdeltoid fascia (sdf)
lining the undersurface of the deltoid muscle (d). The subdeltoid fascia is rich in blood
vessels and sympathetic nerves which originate in the stellate ganglia. Between the
subdeltoid fascia and the fascia covering the cuff is loose connective tissue within
which is located the subdeltoid bursa (b). B. Acute bulging of the tendon compresses
and causes inflammation and swelling of the fascial tissues and the bursa. This is the
acute mechanical phase during which there is severe pain and mechanical limitation of
motion. C. The bulging of the tendon has subsided, but the resultant fascia and bursal
inflammation persists, causing stiffness of the shoulder. A can go to B then to C and
reverse through the entire phase back to A. The tendon remains frayed, and degenera-
tive changes remain.

particular activity. 21 As has been considered in Chapter 1, the con-

cept of a joint is a complex one. The movements of the glenohumeral
joint and all other accessory joints elevate and abduct the total upper
extremity in a smooth, effortless motion. The balance and synchro-
nization are so accurate that the slightest disturbance in muscular
activity, faulty joint direction or range, or external stress can upset the
scapulohumeral rhythm. Pain, dysfunction, and limitation of motion
can result.
Pain is the initial symptom and varies in intensity. The stress, the

49
Figure 44. Trigger points. Palpable "trigger points" during the examination reveal the
site of the pathology, corroborate the history, and indicate the type of therapy. 1. The
greater tuberosity and the site of supraspinatus tendon insertion. 2. Lesser tuberosity,
site of subscapularis muscle insertion. 3. Bicipital groove in which glides the bicipital
tendon. 4. Site of the subdeltoid bursa. 5. Glenohumeral joint space. 6. Acromioclavi-
cular joint. 7. Sternoclavicular joint.

degree of swelling of the tendon, and the pain threshold of the patient
can alter the intensity of pain. Pain is usually localized in the shoulder
region. In initial attacks it is localized in the anterior lateral aspect of
the glenohumeral joint in the vicinity of the greater tuberosity and the
overhanging acromial process. Associated local tenderness is frequent
(Fig. 43).
Pain, from the onset, is associated with limitation, if not total pre-

vention, of motion. Abduction is especially limited. Forward flexion

50
 Emotional Physical
Tension Trauma

IRRITATION

Infection Immobilization
i
PAIN

I
MUSCLE TENSION

Internal
Retained
Tissue Edema
Metabolites
Ischemia

INFLAMMATION
i
Fibrous Reaction

/ Limited Muscle Elongation

I Movement
Restricted Joint
I Tendon Function Limitation
\ Fascial Shortening
X
I
FUNCTIONAL DISABILITY

Figure 45. Mechanism by which irritation leads to functional disability.

51
and rotation also are usually markedly limited, with either active or
passive motion causing an aggravation of pain. The reason for pain has
already been noted. The offending swollen tendon contained within a
narrow space is compressed between the moving humeral head and
the overhanging acromial process and the coracoacromial ligament
and arch.
As was depicted in Figure 44, the hanging dependent arm causes
the critical zone of the conjoined cuff tendon to be ischemic, as does
the contracting cuff in the abducting arm. In the resting arm the zone
becomes hyperemic, especially when irritated. At this point the ten-
don is too swollen to pass between the greater tuberosity and the
acromium.
The fact that the resting arm (i.e., the arm that is not dependent or
actively abducting or forward flexing) allows the cuff to become
hyperemic probably explains the frequency and severity of nocturnal
pain in acute tendinitis.
"Shrugging" of the shoulder replaces smooth, effortless scapulo-
humeral motion. "Shrugging" implies movement of the scapular
phase of the rhythm without simultaneous glenohumeral movement;
thus the scapula "shrugs" (elevates). The arm, limited at the gleno-
humeral joint, does not abduct. External and internal rotation are
equally limited and painful, but "shrugging" here is not noted as there
is less rhythmical scapular associated movement in these particular

movements. The glenohumeral movement, in external and internal

rotation, is merely obstructed locally, and pain is felt locally. Move-
ment is restricted at that joint.
Rest and treatment at this point may cause the acute phase to sub-
side and full and pain-free motion to return. The swelling within the
tendon and the inflammation of the contiguous tissues can abate, and
movement between the humeral head and the overhanging arch re-
sumes. The swelling that occurs in the peritendinous tissues, within
the subdeltoid fascia, may persist and leave a relatively painless re-
stricted movement, a "stiffness." This impaired scapulohumeral
rhythm predisposes to further tendon irritation, degeneration, swell-
ing, and recurrence of "acute" tendinitis. A recurrent vicious circle
ensues. The pathomechanics sequence sets the rationale for proper
treatment.
Should repeated irritation occur, the tendon may increase in size
and may rupture its now liquid material out of the sheath to the sub-
bursal area or into the bursal sac (see Fig. 41). The pain now is more
severe and more constant, regardless of movement. This continuous,
deep pain is caused by the constant tension within these tissues held
within the confines of the narrow container. Any movement now is
prohibited both by mechanical obstruction and by pain and protective

52
Figure 46. Pendular exercise. The patient bends forward, flexing the trunk to right
angles. The involved arm is dangled without muscular activity of the glenohumeral
joint. The body actively sways, thus passively swinging the dependent arm in forward
flexion-extension, lateral swing, and rotation. The body can be supported by placing the
other arm upon a table or chair. The arm is passively swung. No weight is held in the
hand as this causes muscular contraction of the arm and the shoulder.

spasm. Restriction is in all ranges of glenohumeral motion, and the

"shrugging" mechanism is total.

If the material ruptures outwardly and downward into the lower

portion of the subdeltoid bursa, the pain and tenderness may be felt
lower in the arm, at the lateral upper third of the humerus, where the
deltoid inserts upon the humerus. Due to the residual subdeltoid fas-
cialand bursal inflammation, "stiffness" of the glenohumeral joint
remains, exhibiting a "stretch" type of pain.

TREATMENT
During the acute phase rest is desirable. A sling is frequently help-
Ice packs, rather than heat, are indicated during the acute phase,
ful.

which lasts for approximately 2 days. Heat appears to increase the

engorgement of the inflamed tissues within the suprahumeral space.
Ice decreases spasm, acts as a local cutaneous anesthetic, and has

53
 oc
^•Al )

©
Figure 47. Active pendular glenohumeral exercise. 1. The posture to be assumed to
permit the arm to "dangle" freely, with or without a weight. 2. The arm moves in
forward and back sagittal plane, in forward and backward flexion. Circular motion in the
clockwise and counterclockwise direction is also done in ever-increasing large circles.
3. The front view of the exercise showing lateral pendular movement actually in the

coronal plane. The lower right diagram shows the effect of gravity (G) upon the gleno-
humeral joint (ghj) with an immobile scapula (s). The p to p arc is the pendular move-
ment.

54
reflex action in relieving pain. 23 It has
been shown that intramuscular
temperatures, at a depth of 3 cm, are not affected until after a 10-
minute cooling period. A 20-minute period causes adequate, although
not the final, cooling. Icing can be administered by means of a towel
enclosing ice chips, ice in a rubber bag, or ethyl chloride spray. The
spray, an explosive gas, carries some risks and is more difficult to
self-administer.
Immobilization of the shoulder should never be prolonged. Immo-
whether induced by the patient as a "fear of hurting"
bilization,
mechanism or by the iatrogenic factor in which the doctor or therapist
does not limit the duration of immobilization, tends inevitably to fi-
brous reaction. The mechanism by which immobilization, along with
factors of trauma, infection, or emotional tension, initiates fibrous re-
action and functional disability is shown in Figure 45.
Immobilization fosters internal tissue ischemia, retention of
metabolites, and edema. Since the major tissues about the shoulder
are muscular and therefore for normal nutrition must contract and
relax, be shortened and elongated, the mechanism of disability from
immobilization is apparent. Immobilization, whether self-induced or
medically advised, leads to disuse, which has been claimed to be a
causative factor in pericapsulitis or "adhesive" capsulitis. 24,25 Disuse
leads to muscular atrophy and to loss of capsular elasticity.
The limitation of motion of the shoulder is probably caused by pro-
liferative inflammation of the soft-tissue components of the periar-
ticular gliding tissues that ultimately lead to fibrosis. Immobilization
entails circulatory disorders leading to ischemia and secondary
metabolic changes of the connective tissue.
To prevent immobilization early in the treatment, active range of
motion exercises should be insitituted. "Early" means usually within
the first week and more frequently within the first 4 days. Insofar as
the motion of abduction-elevation causes impingement of the in-
flamed bursa and tendon between the acromial process and the
greater tuberosity of the humerus, this maneuver should be avoided.
An antigravity exercise in which impingement is minimized and
abduction avoided, yet in which motion of the glenohumeral joint is
is

achieved, is the Codman, or pendular, exercise. This exercise adds

traction to the glenohumeral joint, stretches the capsule, avoids active

abduction, and minimizes the "shrugging" scapular elevation im-
posed by gravity upon the erect posture.
As described by Codman, the pendular exercises are done passively
with the arm dangling. No muscular activity of the shoulder is exerted.
No weight is held actively in the hand, as any muscular contraction of
the hand, wrist, or upper arm will cause a co-contraction of more
proximal muscles. A weight held passively attached to the wrist may

55
FIGURE 48. Technique of tendinitis-bursitis injection. Left The anterior view depicts
:

shown by the arrow. The palpating finger can feel

the site of entrance of the needle, as
the overhanging acromial process and the bicipital groove. Injection is just lateral to the
sulcus at the greater tuberosity where the superspinatus tendon inserts. Right Viewed
:

from above, two directions of entrance are shown, with the arrow depicting that shown
in the anterior view.

be utilized to cause more pendular motion and more traction at the

shoulder. The arm is moved passively by the undulating body (Fig.

46).
The active pendular exercise is a modification of the Codman
pendular exercise and is undertaken as soon as pain and restricted
movement permits. The active pendular exercise is done in the same
body position, but the arm is actively swung in the pendular planes
(Fig. 47). A weight can now be held in the hand and be of increasing
weight. All planes of movement are indicated: forward, sideways and
circumduction, and with increasing amplitude of arc.
The exercise must be done properly. The patient bends forward at
the waist to achieve a right angle trunk flexion. Slightly bent knees
will decrease the low back and hamstring stretch pain. The head,
rested upon a firm object and resting upon the other hand, permits
relaxed movement and concentration upon the indicated movement of
the involved shoulder.
In this position the dependent arm dangles vertically. Pendular
motion is started (1) in a lateral medial plane ("out and in"); then (2) in

a sagittal plane forward and backward (up and down with the body
upright); then (3) in a gradually increasing circle; and finally (4)
clockwise then counterclockwise. The use of an iron has been advo-
cated as the weight since it is readily available in the home. A weight
is frequently desirable as it adds traction to the dependent arm and

widens the pendular cycle.

Movement must be consciously achieved at the glenohumeral joint,

56
Figure 49. Suprascapular nerve block. A. The anatomy and course of the suprascapu-
lar nerve, originating from C 5_6 . The motor nerve to the supraspinatus (SSp), and infra-
spinatus (ISp) and the sensory branches to the acromioclavicular joint and the shoulder
joint (jt) are shown. B,C. Bisection of a line drawn along the scapular spine with the site of
the groove and of needle insertion. D. The difference between direct nerve contact and
indirect (ID) by infusion along the posterior portion of the scapula below the supra-
spinatus muscle.

with effort and thought directed to minimize scapular movement. The

dependent arm adds traction, and the pendular movement causes
range of motion at the glenohumeral joint in a manner that does not
impinge the supraspinatus tendon.
As the range of motion increases and becomes less painful, heat can
be applied, usually by the third day. Moist heat is preferable and may
be applied by hot, moist towels kept warm by an electric pad or by
chemical (hydrocollator) packs. The latter are more expensive, but
they have the benefit of simplicity, more prolonged heat, and the

57
Figure 50. Exercises. A. Lying on back with elbows at the side, hands toward the
ceiling. External rotation attempted actively by the patient and passively by the
is

therapist. Resistance may be applied when range permits. This exercise can be per-
formed in the upright position against the wall. B. Similar exercise to A, but with
increasing abduction of the arm through positions 1 to 5. C. Hands behind head, the

movement is backward motion of the elbows, to the floor when supine and to the wall
when erect. This motion may be assisted by a therapist and may be resisted. D. "Push-
ups" from the wall performed in a corner. The exercise starts with hands at waist level;
then the hands "climb" until they are fully extended overhead, still apart. The anterior
capsule is stretched, as are the pectorals. Rhythm here is necessary. Avoid arching the
back and the neck.

freedom to actively move the arm during the application of the pack.
Pain from an acute shoulder tendinitis must be decreased to permit
mobilization of the glenohumeral joint. Correspondingly, pain must
be decreased to prevent immobilization, disuse, fibrosis, and all the
periarticular tissue changes that lead to a "frozen" shoulder.
Analgesics may be employed. The type differs with the experience
of the physician and with the previous experience of patient response.

58
Figure 50 (continued). E. With (between door frames) that is adjust-
a "chinning bar"
able, begin with the bar at face level and gradually elevate the bar, either by changing
the position in the door frame or by doing a deep knee bend. Ultimately the bar should
be above and behind the head. F. Similar to E, except that a "wand" or wooden dowel is
held by both hands. This exercise is more active than in E, the ultimate object being to
place the wand behind the head from a fully extended overhead position. Lateral mo-
tion with the arms overhead should attempt movement of arms behind the head. G.
Wand behind the back. In the illustration the wand is elevated by the right hand to
bring the left (involved) arm up behind the back, which stretches the anterior capsule
and the external rotators. H. Placing hands behind the back upon a table, parallel bars,
or sink, and doing deep knee bends.

Opiates, when used sparingly in the first few days, may be necessary.
Apprehension, which increases the muscle tension about the inflamed
shoulder, must be controlled by sedatives or tranquilizers. Muscle
relaxants are numerous on today's pharmaceutical market and all have
their advocates. It is a safe assumption presently that there is no one
effective muscle relaxant and that none is without some sedative ef-
fect.
Nonsteroidal anti-inflammatory drugs have great value during the
acute phase of tendinitis. They all have potential side effects that
should be known to the prescriber and guarded against. Usually daily
doses for 5 davs are effective. Occasionallv several "courses" of these

59
Figure 51. Home exercise to increase shoulder range of motion. Seated with arm
supported upon table, the patient moves forward and downward to increase range of
arm toward elevation. The forearm, bent at right angles, internally and externally ro-
tates, thus further increasing range. A weight can be held in the hand.

drugs are needed. Contraindications to the use of these nonsteroidal

anti-inflammatory drugs are well documented in the literature and by
the pharmaceutical houses.
Oral steroids may occasionally be indicated and valuable. Large
doses for brief periods of time are often of greater value than smaller
doses for longer periods. The indications are those of severe
symptoms and findings. The contraindications are those of using
steroids for any reason.
The use combined with a local anesthetic
of steroids by injection
agent very effective. Injection during the first days of an acute attack
is

is usually not indicated. The injection of an anesthetic agent may

relieve the acute pain, but the introduction of steroids at this stage is
questionable when noninvasive therapy most often is effective.
The rationale of local injection merits discussion. Insofar as the
pain-causing tissue is an inflamed, swollen tendon, already weakened
and degenerated, further trauma must be avoided. The further trauma
alluded to is that caused by the puncture of a needle, introduction of a

60
Figure 52. Exercise to stretch anterior capsule and increase posterior flexion. The
patient places both hands on a table behind the back and performs gentle deep knee
bends. This elevates arms (small arrow) and increases posterior flexor range of motion.

foreign substance, at best locally irritating, and the introduction of

further fluid into a confined area already containing excessive fluid.
The introduction of Novocain is for its anesthetic effect, and cor-
tisone, for its analgesic and anti-inflammatory effect. The amount of

fluid is that which is sufficient to separate the inflamed tissues and

decrease the formation of adhesions. If the tendon sheath or the ten-
don is entered, the enclosed debris, acting as a "bulging" sterile
abscess within the sheath, may be decompressed. If the bursa is en-
tered, the needle may decompress the inflamed contents of the bursa.
All the effects of needle insertion, properly done, are beneficial in that
the insertion instills anesthetic and anti-inflammatory solution in an
inflamed area and tends to decompress by incising a bulging, fluid
mass.
The technique of injection varies with the clinician. The author
prefers to use the anterior approach (Fig. 48). Anterior palpation of the
shoulder can easily reveal the overhanging acromial process below
which is a horizontal sulcus, below which the head of the humerus

61
Figure 53. Overhead With a pulley placed above the head the involved arm
exercise.
is By having the pulley slightly behind the head,
passively elevated by the normal arm.
the arm gets further range of motion to overcome one of the subtle signs of limitation.

and the bicipital grooves can usually be felt. Palpation is done with
the arm hanging at the side in a neutral position of rotation. A 2-inch,
24-gauge needle, attached to a 5 cc syringe, filled with 1 cc of 1 per-
cent procaine and 1 cc of injectable steroid (25 mg equivalent of in-

62
 ffTT^

right
Figure 54. Correct and incorrect use of "wall climbing" exercise. The wall climbing
exercise frequently is done improperly. The normal arm climbs with normal
scapulohumeral rhythm. When there is a pericapsulitis, the wall climb in abduction is
done with "shrugging" of the scapula and accomplishes nothing. The wall climb should
be started facing the wall and gradually turning the body until the patient is at a right
angle to the wall.

jectable steroid) under sterile technique, is inserted anteriorly at a site

just above the greater humeral tuberosity (above and lateral to the
biceps sulcus) and under the acromion. The needle goes straight back
and slightly upward in an attempt to go under the acromium. It is then
partially withdrawn and reinserted medially, to follow the supra-
spinatus tendon. A third reinsertion from partial withdrawal is slightly
outward under the tip of the overhanging process. This should infil-
trate the subdeltoidbursa if it is at all distended.
The of needle insertion should be carefully palpated by the
site
finger. The acromial process is easily identified. The biceps groove
may need internal and external rotation of the humerus to verify the
groove moving under the palpating finger. Downward traction upon
the arm may "open"
the joint slightly as a few degrees of backward
abduction will outline more clearly the protruding humeral tuberos-
ity.

After entering the skin and going through the deltoid muscle, the
clinician must exert care to prevent "hitting" bone and injecting into

63
 r&*

Figure 55. Scapular mobility exercises. Previous exercise mobilizes the glenohumeral
as well as the scapulothoracic articulations. Motion here is elevation, forward and
backward motion, then circumduction of the shoulder girdle. Motion here also in-
creases sternoclavicular and acromioclavicular range of motion.

the periosteum, which will inevitably give "after-injection" pain,

often as painful as the condition for which the injection is given.
Attempt at aspiration is done to avoid injection into a blood vessel, but
rarely is bursal fluid aspirated. Return of joint or bursal fluid should
not be the criterion for injecting the mixture of Novocain and injecta-
ble steroid.
Aspiration and irrigation of calcific deposits is not advocated by the
author and will not be described. This technique is well documented
in the literature. 26 Radiotherapy is advocated by some early in acute
bursitis. 27 The consensus appears to indicate more favorable results
from radiation therapy in the acute cases rather than in the chronic
(acute being cases within 10 days of onset of pain, and chronic, after 10
days), and in cases where diagnostic x-rays reveal fine-appearing cal-
cification rather than dense calcifications. In the author's opinion,
results from radiation therapy have been disappointing.
To relieve pain about the glenohumeral joint and institute early
active motion, a suprascapular nerve block extremely effective and
is

is relatively simple to perform. The nerve location is shown in Figure

49. The patient is seated with arms at his side. The spine of the
scapula is palpated and marked at its vertebral end and its acromial
end with a line connecting the two points. This line is bisected and
the outer half again bisected. Approximately 1.5 cm above the supe-

64
 (0^r\

cm^

Figure 56. Normal scapulohumeral motions: (1) normal stance with parallel sym-
metric shoulder girdles;(2) symmetric abduction with equal proportional glenohumeral
abduction and scapular rotation; (3) symmetric full overhead arm elevation; (4) posterior
arm flexion and internal rotation.

rior border of the spine at this point a Novocain wheal is made, and the
needle is inserted.
A 24-gauge 2-inch needle is used, connected to a 10 cc syringe
containing 1 percent Novocain and 25 mg injectable steroid (hydro-
cortisone). The needle is advanced slowly until bone is hit. If the
nerve is contacted, paresthesia radiating to the shoulder will be eli-
cited. If bone is hit, the needle is withdrawn half the distance and
reinserted laterally and medially until paresthesia is elicited. Once
the nerve is located, 5 cc of the solution is injected. A complete block
should alleviate the pain of the shoulder and produce weakness of arm
abduction and external rotation (paresis of the supraspinatus and
infraspinatus muscle).
The foregoing technique is aimed at a complete, though transient,
nerve block. Since the possibility exists of an overlying vascular bun-
dle, over or behind the notch, rather than to "hit" the nerve directly,

65
 rnrv >i
r

®— *

^mc

© -

Figure 57. Subtle signs of shoulder limitation: (1) shrugging with excessive scapular
rotation and limited glenohumeral abduction; (2) limited right arm overhead elevation
(arm away from head and ear); (3) limited posterior flexion and internal rotation (hand
fails to reach normal interscapular distance of reach); (4) limited external rotation of

right arm, done with flexed elbow; (5) overhead elevation of right arm limited in poste-
rior direction as compared with normal, viewed from side; (6) external rotation as
viewed from above; (7) with hands behind head, failure of right arm to fully extend
posteriorly.

66
the solution is placed under the supraspinatus muscle against the face
of the scapular supraspinatus fossa, and allowed to seep along this
plane to the nerve. The result is slowed but as effective. 28
As the acute episode subsides, full recovery must be achieved and
recurrence prevented if possible. The "stiff" shoulder and its com-
plications must be prevented. This is possible primarily by active
exercise. There are advocates of both active exercise and of passive
exercise, the latter being equated with manipulation as a treatment
modality. Both aspects of treatment are efficacious and merit consid-
eration in the treatment armamentarium of the painful stiff shoulder.
In summary, the object of treatment is to accomplish full range of
pain-free motion of the entire shoulder girdle throughout its range.
Pain noted in abduction of the arm has been attributed to mechani-
cal impingement of the cuff tendons and their contiguous tissues be-
tween the humerus and the coracoacromial ligament. Corrective ex-
ternal rotation of the humerus during abduction must occur to move
the greater tuberosity posteriorly and thus clear the acromion during
abduction. External rotation is thus the key movement in a full-range,
pain-free shoulder action. Maintaining or regaining free external rota-
tion is the prime purpose of the postacute phase of treatment.
Elevation of the arm in the sagittal plane is possible with much less
probability of impingement which constitutes the first phase of exer-
cise, already discussed under pendular exercise. Since the humeral
head must "depress" at the glenohumeral joint to permit abduction,
this movement is facilitated by the traction aspect of the pendular
exercise. Motion, considered by some to be "involuntary" motion, 29
may require passive (assistive), even forceful, assistance by a therapist
or doctor. This will be discussed later.
External rotator exercises may accompany the pendular exercise or
follow shortly thereafter. Only the most effective and the simplest
exercises will be discussed; they will be described in the legends
under the drawings, rather than in the text.
Exercises are classified as (1) passive (assistive), in which motion of
a joint is performed for the patient; (2) active, in which the effort is
solely that of the patient; (3) active assisted, in which there is a com-
bination of the two; and (4) active resistive, where the active effort of
the patient is resisted mechanically by equipment or resisted manu-
ally by a therapist. All the exercises illustrated (Fig. 50)can be mod-
ified into any of these categories. 29
Individual exercises are shown in Figures 51 through 55. These
can be given to patients for implementation in their home
illustrations
exercise program.
Passive and active unresisted exercises are essentially intended to
increase range of motion. Resistance is applied to increase muscular

67
Figure 58. Manipulation treatment of "involuntary" motion of the glenohumeral joint.
A. Elevation of the head of the humerus against the glenoid fossa. Pressure along the
shaft of the humerus, with the other hand preventing elevation of the scapula, causes
the humerus to elevate, thus stretching the superior capsule. B. Anterior and posterior
motion of the head of the humerus against the glenoid. Three points of contact must be
applied. One hand mobilizes the humerus while the other hand "fixes" the scapula.
The elbow or forearm is fixed by the therapist's body or elbow.

strength and endurance. Active assistive exercises that involve a sec-

ond party may vary from forced motion to manipulation.
Exercises should be performed smoothly and with concentration.
The patient must understand the purpose of the exercises so that his
effort is specific and he avoids substitution of movement. Some sen-
sation, even to the point of discomfort, is bound to occur, but it should
never be violent, nor should it leave residual pain and increased
disability. A patient who fails to feel some sensation of ''stretch,"
however, is bound not to improve, or at least will reach a plateau of
improvement that is never surpassed. Exercises must be done re-
peatedly, frequently, and correctly. To paraphrase Watson-Jones,

68
 fpr^

(f^^r

Figure 58 (continued). C. Lateral motion of the head of the humerus away (in separa-
tion) from the glenoid. One hand of the therapist pulls at a right angle to the shaft of the
humerus while the scapula and the elbow are "fixed." D. Traction to separate the head
of the humerus from the glenoid while abducting and gradually externally rotating the
arm. Counterre si stance (fixation) is applied against the axillary border of the scapula.

"Successful treatment of the stiff shoulder is best summarized in two

words, active exercise." 30
Tolerance of pain or even of discomfort is a human variable and
must be considered in the decision of prescription of exercise. In
passive people, exercise may be necessary longer than in energetic,
well-motivated patients. The combination of disuse and prolonged
immobilization in a person with a periarthritic personality 31 will fre-
quently lead to Si frozen shoulder.
A certain number of patients will not improve or will fail to improve
past a certain plateau despite intensive adequate treatment. In a por-
tion of these patients the shoulder range of motion remains grossly

69
and visibly limited. Pain persists during the achieved range of motion
but most often when further range is attempted.
There are patients, however, who feel they have gained full range of
motion and the examiner may, on cursory examination also feel they
have regained full range of motion. Pain persists. Often these patients
retain limitation that is barely perceptible. They exhibit the subtle
signs of shoulder pericapsulitis or peritendinitis. These subtle signs
must be sought for in every patient who has gained increased range of
motion yet continues to have pain (Figs. 56 and 57).
These subtle signs include the following:

1. In overhead elevation of the arms the involved arm fails to reach

the ear as does the normal arm.
2. In overhead elevation the involved arm does not go as far poste-
riorly(behind the head) as does the normal arm.
3. With arms at the side external rotation of the involved arm does
not rotate outwardly as far as does the normal.
4. In reaching behind the back and attempting to touch the thoracic
spine between the shoulder blades the involved arm does not
reach the same point as does the normal arm.

Upon finding these subtle signs in a symptomatic patient, exercises

performed by the patient without assistance will no longer be effec-
tive. Assistive exercises now are indicated. Mobilization, manipula-
tion, and active assistive exercises of the rhythmic stabilization type
are of value.
The rationale of manipulationis that certain involuntary move-

ments of the shoulder girdle can be accomplished through their range

of motion only by assistance and force. These movements must be free
before active motion is possible. The indications for manipulation
must be specific and the techniques of manipulation concise and pru-
dent. Careful clinical examination must be supplemented by recent
x-ray studies. In periarticular lesions, manipulation treatment has ra-
32
tionale, whereas articular lesions frequently contraindicate it.

The involuntary' movement33 may be summarized as (1) movement

of the humeral head upward upon the glenoid fossa up under the
coracoacromial hood; (2) forward movement of the head of the
humerus upon the glenoid; (3) backward movement of the humeral
head upon the fossa; (4) downward motion of the humerus upon the
glenoid; and (5) combination of the above motions. All these motions
are apparently aimed at stretching the glenohumeral capsule and re-
leasing adhesions.
Manipulation technique cannot be fully discussed in this text, but
based on training, close supervision by a trained person, and
skill,

70
 r s

/
FIGURE 59. Rhythmic stabilization manipulation of the glenohumeral joint. While the
patient applies isometric contraction of the glenohumeral joint to "prevent motion," the
therapist attempts to move the arm in abduction external rotation, then reverses to
adduction internal rotation. Traction (t) is constantly applied. Motion by the therapist is
smooth and gradually increasing then decreasing in force and amplitude, with the
patient resisting it with equal force. After one cycle at a specific range of abduction, the
arm is passively abducted and externally rotated to a further point, and the cycle is
repeated.

sound fundamental knowledge of anatomy must precede its applica-

tion (Fig. 58). Insofar as leverage is a component of the force applied,
it behooves the manipulator to use the utmost gentleness and care.

Extreme force is never necessary, 34 and abrupt movements must be

avoided.
Manipulation may be done with or without anesthesia. There are
advocates of both schools of thought, and there are ardent critics who
condemn manipulation under anesthesia as both dangerous and fu-
35
tile. It behooves the physician caring for shoulder problems to be

informed of the pros and cons, the indications and contraindications,

and the techniques. Judgment regarding their use then can follow the
individual's choice.
Prior to manipulation or immediately after the treatment, the sub-
deltoid bursal area should receive an injection of an anti-inflammatory
steroid, an anesthetic agent, and hyaluronidase. 36 37 The steroid in the
'

injected solution allays post-manipulation pain and inflammation, thus

minimizing fibroplasia and adhesions.

71
 JOINT
MOTION

"- T D
s*\s % , P
~_ r^'* / v,
1

V
i
. ''
/ <

// v« / / '
\'
/ *
'
c / *
i
' / '
\ / \
•

/'I 1
/' \ ' /' \'
/
/

\
/ /
o
"0 / \ / i /
i
/
i /
-D /
1
I
/ » 1 /
/ /
/• p / , i
/ / , REST
I' /• ; /,'
c / /

> "
o i
1 » 1 1 i / • \ f
t- - u 1
, / 1 > / i //
3
u> TJ '
/
Z
H
\ \
\_iy."
/,'
\yj
V-^- W-'
\*s"
z '
w

TIME

Figure 60. Schematic graph of rhythmic stabilization. The solid line (T) indicates the
increment of force applied to the shoulder by the therapist in alternating abduction then
adduction, immediately followed by opposing force from patient (P) to prevent joint
motion (0°).

The increase of motion and decrease of pain permit immediate

post-manipulation exercises which are imperative. Active, passive, and
active assisted exercises to maintain the gained range of motion and to
increase further range must be instituted, supervised, and continued.
Intra-articular injection of an anesthetic agent combined with a
steroid, as will be discussed as "infiltration brisement" in Chapter 4
(see also Fig. 63), is of great value to decrease pain and increase
mobility utilizing manipulative techniques. The performance of an
arthrogram (for diagnosis or for therapy) may be necessary to ascertain
that the injected material is in the joint space. Through this arthrogram
needle a solution of an anesthetic agent (10 cc of 5.0 percent Novocain,
lidocaine, or Marcaine) and a steroid are injected into the capsule.
This injection decreases the pain during and after the manipulation
and increases the range of motion. This results in better patient cooper-
ation to exercise. This injection can also precede and enhance the
benefit of mobilization or "rhythmic stabilization," as it does not de-
crease voluntary motion.
The author has used effectively a technique of rhythmic stabiliza-
tion, one that combines active exercises with prudent, controlled ma-
nipulation (Fig. 59). 38 The arm, held firmly and with traction, applied
manually along the shaft of the humerus, is passively moved in all

72
quadrants of glenohumeral movement. Each movement, foretold by
the therapist, is resisted by the patient, causing an isometric contrac-
tion of the periarticular muscles but no significant active movement of
the joint. After momentary isometric resistance to movement in one
direction, the therapist attempts movement in the opposite direction,
which the patient immediately resists (Fig. 60).
The back-and-forth passive movement, resisted by an equal force
from the patient and done rhythmically, loosens the joint, causes mus-
cular contractions that improve strength and endurance, and improves
local blood supply. After a series of alternating contraction-relaxation
motions, the arm is passively brought to a further point of increased
range of motion, and the rhythmic stabilization is done at this newly
gained range.
The constant application of traction upon the arm increases the in-
voluntary range of motion. The fulcrum created by the position of the
therapist and the alternating effort of the patient mobilizes the
glenohumeral joint in all the other involuntary motions. The patient's
active participation allays much of his fear of "forceful, painful stretch
by the therapist/' The need for anesthesia and the encouragement of
the postmanipulation effort are therefore minimized.

73
CHAPTER 3

Cuff Tear

Rupture of the rotator cuff is much more frequent than was previ-
ously suspected. Originally, this diagnosis was considered only in
people engaged in strenuous occupations who sustained violent
trauma, usually a fall. At autopsy tears are frequently noted in people
in their early forties who had no previous shoulder complaints.
A minor stress can easily cause a partial or complete tear to a tissue
already weakened by degenerative changes. The tissues that tear are
enclosed in a small, compact area between the overhanging coracoa-
cromial arch and the gliding humeral head. These tissues are exposed
to daily postural, vocational, and traumatic stresses; and in later years,
due to a diminishing blood supply, they become more friable.
Nearly all cuff tears occur in the anterior portion of the cuff and are
marginal (i.e., close to the point of attachment). Central tears can occur
as a linear tear between the tuberosity and the musculotendinous
junction, or they can exist along the bicipital groove. Tears can be
partial or complete in varying degrees.

DIAGNOSIS
A most often in men 40 to 50 years of age
history of cuff tear occurs
engaged hard manual work or experiencing unusual motion, as in
in
recreational sailing. The incidence of "tearing" usually follows a rela-
tively minor injury. The insult may be a fall on the outstretched arm,
causing a tear from the arm being "thrown" forward to protect against
the fall or the impact against the arm forcing the head of the humerus
to penetrate the anterior superior aspect of the cuff. Abduction of the
arm without the proper rotatory mechanism can impinge the cuff
against the coracoacromial arch and cause a tear. Tears can be iat-
rogenic from forceful manipulation tearing an already degenerated
cuff. Overhead movements of the arm, such as in plastering, painting

74
ceilings, or closing overhead garage doors, may be the tearing stress;
but frequently no specific history of trauma or unusual stress can be
elicited.
The history is usually of an acute, severe pain described as a "tear-
ing" pain followed by a 6- to 12-hour pain-free interval. This pain-free
interval is followed by a gradual return of pain of increasing severity,
lasting 4 to 7 days.
Incomplete cuff tears clinically resemble the signs and symptoms of
supraspinatius tendonitis. The pathologic reason for this is that the
torn fibers retractand "bunch" up, causing an enlargement similar to
that of the tendonitis (Fig. 61). Because there are still some intact
fibers of the supraspinatus muscle that can assist in abduction and
place the humerus in a position to allow the deltoid to act, abduction
of the arm is possible, albeit with (1) some pain, (2) some limitation,
and (3) an occasional "catch" during the process of abduction. The
scapulocostal rhythmn is not impaired.
Resisting abduction and external rotation may produce pain that
unresisted movement will not elicit, but this is not diagnostic. Ten-
derness over the site of the tear is prevalent, and, since the tear occurs
most frequently in the supraspinatus portion of the cuff, the tender-
ness is palpated over the greater tuberosity (see Fig. 44). Occasionally,
in very thin persons, a rent in the tendon can be palpated. Diagnosis of
an incomplete tear may be made on clinical manifestations, but ar-
thrography may be needed for confirmation.
In a complete tear the patient is unable to initiate abduction. The
loss of active abduction is caused by the failure of the cuff (especially
the supraspinatus) to initiate humerus abduction that places the del-
toid into a functional position. Pain may be severe and be considered
to be the cause of limited abduction. Even passive abduction may be
limited due to pain and confuse the examiner. Early recognition is
therefore often difficult.
Injecting an anesthetic agent into the suprahumeral area (see Fig.
48) can remove the pain and relieve the reflex spasm that immobilizes
the glenohumeral movement. With relief of pain and spasm clearer
diagnostic findings verify the tear. No active abduction is now evi-
dent. The patient merely "shrugs" due to scapular motion, but there is

no glenohumeral motion (Fig. 62). 39

The deltoid muscle contracts in spite of the absence of resultant arm
abduction, indicating that the axillary nerve is intact and that failure to
abduct is not due to nerve damage. If the arm is passively abducted by
the examiner, placing the humerus in slight abduction, the arm can be
held abducted. By passively placing the arm in abduction, the deltoid
now can function as the major abductor.
Because the cuff is not functioning, the head of the humerus is not

75
 TORN FIBERS

Figure 61. Cuff-tear. Above: Site and di-

rection of partial cuff tear. Below: Retraction
of torn cuff fibers forms a thickening of the
cuff, thus resembling the thickening of ten-
dinitis.

firmly seated into the glenoid fossa, and thus the glenohumeral joint is

not stable. Any downward pressure upon the abducted arm causes it to
"drop." The inability of the patient to actively abduct the arm, to
actively hold the arm in the abducted position upon the arm being
passively placed in abduction and the "drop arm test" upon exerting
downward pressure upon the abducted arm, is diagnostic of a com-
plete cuff tear. Arthrography will confirm the presence of a tear and
verify whether the complete or incomplete.
tear is

Paresis of the deltoid muscle, due to a peripheral nerve injury to the

axillary nerve (C 5 C 6 ) must always be kept in mind when abduction
,

weakness of the deltoid results after an injury. 40

ARTHROGRAPHY
Contrast dye study of the glenohumeral joint is a safe and simple
test that has conclusive value in determining the presence and com-
pleteness of a cuff tear. Normally there is no communication of the
articular cavity with the subdeltoid bursa. Communication of the
bursa with the articular cavity is abnormal and indicates pathologic
rupture (Fig. 62). The subscapular bursa normally communicates with
the joint cavity and is considered a prolongation of the synovial
capsule. The subcoracoid bursa is considered by most observers to
communicate as well.
The preferred technique of dye injection is by the posterior ap-

76
Figure 62. Cuff tear. The upper left diagram indicates the usual site of the tear, either
partial or complete.The center posterior view of the patient abducting the arm indicates
normal or even adequate scapulohumeral movement with a large but incomplete tear.
The right view shows the complete tear. The lower diagrams show (right) the com-
munication between the shoulder joint in a complete tear, and (left) the lack of com-
munication in a partial tear or degenerated tendon.

proach. The posterior approach does not confuse the test if there is
leakage, whereas in the anterior approach leakage can mar the final
picture (Fig. 63). The site of insertion is a point 1 inch below and 1
inch medial to the angle of the spine of the scapula. A 21-gauge needle
attached to a 20 cc syringe is used, filled with Diodrast dye. After 3 or
4 cc of dye is injected, the site of injection is fluoroscopically viewed.
If it is considered to be in the joint, an additional 10 to 15 cc is
42
injected. 41 -

In an intact joint space, having no communication with the subdel-

toid bursa, a reflux action occurs. The procaine injected backs into the
syringe as the plunger pressure is released. No reflux occurs in the
presence of a cuff tear because no intracapsular pressure is built up.
Approximately 20 cc of dye solution is used, and x-rays are taken with
the shoulder in internal and external rotation, as well as an axial view.
The dye disappears within several hours with no untoward effects.
The normal arthrogram is depicted in Figure 64. The dye balloons

77
 CLAVICLE ACROMION

CAPSULE

TUBEROSITIES

FIGURE 63. Injection technique for intra-articular arthrogram and brisement treatment.
The injection site is a point just inferior and lateral to the coracoid process in the vector
lines (X-X).

out the capsule, filling the subscapular bursa and the biceps pouch.
No dye should appear above the superior border of the humeral head
or above and around the greater tuberosity. Appearance of dye into the
subdeltoid bursa indicates a pathologic connection. Dye in the bursa
appears as a clearly defined "cap" above the humeral head. More fluid
is also permitted during the injection (as much as 40 to 50 cc).

An incomplete tear will not form a well-defined "cap" superiorly

but may form an abnormal irregularity in the otherwise smooth surface
of the normal arthrogram at the site of the greater tuberosity.
"Frozen shoulders" will cause abnormal arthrograms, but not dye
invasion into the subdeltoid bursa. Rather the dye will reveal a gen-
erally constricted, deformed joint space with poor or no filling of the
subscapular bursa or the biceps tendon pouch. Adhesive capsulitis is
not usually associated with cuff tears unless the tear is caused by
"therapeutic manipulations."

TREATMENT
Incomplete Tears

Two schools of thought regarding the nonsurgical treatment of in-

complete cuff tears are diametrically opposed. One concept advocates
placing the arm in a position that approximates the torn fibers and

78
Figure 64. Arthrogram. The shaded area on the schematic shoulder joint depicts the
normal arthrogram. IN is the anterior site of injection into the glenohumeral joint. 1.
The subscapular bursa that normally communicates directly with the shoulder joint and
thus fills in a normal gram. 2. As the dye injection distends the capsule, it hangs as a
dependent pouch under the joint. 3. The superior medial surface of the humerus. 4. In
the arthrogram is a line of lesser density caused by the underlying glenoid labrum. 5.
The synovial lining that is the pouch accompanying the biceps tendon sheath in the
intertubercular groove a distance ofsome 2 inches. A rotator cuff tear will permit the
dye extend into the subacromial bursa, superior to the smooth line above the humeral
to
head, above and "around the corner" of the greater tuberosity (B).

eliminating any movement

that can elongate the cuff for a period of 8
w eeks . The arm
placed in abduction, forward flexion, and external
is

rotation and so held by a plaster spica (Fig. 65).

The rival school of thought advocates immediate active motion as
soon as pain permits. Exercise is supplemented by frequent injections
of Novocain. If abduction from the dependent position is significantly

79
Figure 65. Proper spica cast for the torn cuff treatment. The body spica must hold the
arm (humerus) abducted, flexed forward, and externally rotated. This is the position of
least tension upon the rotator cuff and therefore that of maximum opposition of the torn
ends of the cuff.

weak, an abduction splint is applied, and active abduction exercises

are started from that level of abduction. The use of the splint, as an
assistive device for the exercise, is usually needed for 3 weeks, and
the total exercise program results in a pain-free shoulder action within
8 weeks. This active exercise concept, with no immobilization, is
especially advocated in the older age group in which immobilization
of even brief duration can lead to a "frozen shoulder."
There are advocates of surgical repair of the incomplete cuff tear
with brief immobilization then exercise following the repair. 43

Complete Tears

Surgical repair is indicated immediately upon diagnosing a com-

plete tear.The surgical techniques are beyond the scope of this text but
are well documented in the literature. 2 9,35 Postoperative care fre-
'

quently determines the efficacy of the surgery regardless of the opera-

tion chosen. Here, as in the treatment of incomplete tears, the treatment
varies from complete immobilization in a plaster spica to suspending
the arm in a splint immediately after surgery and beginning gentle
passive movement on the following day. Gradually, passive motion,
then active assisted motion begun, with forward flexion preceding
is

abduction. By the fourth week, the arm is gradually lowered but is

returned to the splint at night. The arm is held in the splint between

80
 WH1TE
?CORD
-
x^-GREY )

FACET
INTERVERTEBRAL
FORAMEN

- -
VERTEBRAL ARTERY FORAMEN
Q) --J
VERTEBRAL
BODY

VENTRAL ROOT
MIXED SPINAL NERVE

Figure 69. Component fibers of a cervical nerve. The relationship of the spinal cord
and cervical spinal nerve to the vertebral body, the intervertebral disk, and facet.

cervical disk, flexion of the neck usually causes or aggravates the pain
and paresthesia. In the presence of cervical spondylosis (so-called
degenerative arthritis), 38 extension of the neck will narrow the inter-
vertebral foramen and impinge the hypertrophied joints of Luschka
against the entrapped nerve root (Fig. 70D).
Compression of the C 6 root causes pain and stiffness of the neck,
pain and numbness into the thumb and first finger, weakness of the
biceps muscle, and depression of the biceps reflex. The referred pain
to the shoulder is vague. "Shoulder pain" is more a dull ache in the
lateral deltoid region and in the upper interscapular region (Fig. 72).
Compression of the C 7 root causes the numbness and pain to refer to
the middle and index fingers with weakness of the triceps muscle and
a depressed triceps jerk. The "shoulder" area of referral is also the
posterior lateral aspect of the deltoid and the superior medial aspect of
the scapula. The C 8 root shoulder area referral is more in the lower
trapezius area and over the scapular area (Fig. 72). 57
Differential diagnosis of the primary shoulder musculoskeletal pain
from cervical referred pain should be considered, but once consid-
ered, it presents no differential problem. The "shoulder pain" is
vague and is reproducible by neck motion, usually forced extension
and rotation to the side of complaint. Paresthesia of the hand and
fingers is claimed, and neurologic deficit of motor weakness and reflex
changes are usual. Movement of the shoulder is free and does not

91
 @-9^§
A B C D

Figure 70. Foraminal opening variations. A. Normal open intervertebral foramen with
neck in neutral position, no rotation and no lateral flexion. B. Extension by backward
gliding of the upper upon the lower vertebra normally narrows the foramen but does not
compress the nerve root. C. Compression of the nerve root by herniation of the inter-
vertebral disk. D. Distortion of the foramen by osteophytic changes of the joints of
Luschka and disk degeneration.

reduplicate the symptoms. The "shrugging" of the pericapsulitis and

the scalene spasm of the cervical diskogenic syndrome, however, may
tax the acumen of the examiner.
Diagnosis of cervical diskogenic disease is made principally on the
basis of history and physical examination. X-rays of the cervical spine
are not diagnostic per se, and even myelography is not conclusive.

92
 LATERAL BENDING FORWARD HEAD TURN

Figure 71. Foraminal closure in head rotation and lateral flexion. The intervertebral
foramina close on the side toward which the head rotates or bends laterally, and they
open on the opposite side.

Response to treatment consisting of traction, collar immobilization,

neck exercises, and posture training may be a conclusive factor.

SPINAL CORD TUMOR

Tumors within the spinal canal of the cervical spine may mimic a
cervical disk herniation in the early stages, but ultimately there is

progression of symptoms and findings. Single nerve root involvement

leads to multiple and bilateral roots being involved. Inevitably there
is compression of the spinal cord, causing upper motor neuron signs

93
Figure 72. Regions of shoulder pain referral from cervical radiculitis. The areas de-
picted by hatching are the areas of vague "shoulder area" referrals frequently com-
plained of by patients. These are not the cervical root dermatomes which are more
specific in C6 C
7 and C H and are referred to the hand, forearm, and fingers. The areas
, ,

shown diagram may be derived from posterior primary rami, or sclerotomes, or

in this
they may be areas of myalgic tenderness.

with weakness and incoordination of the legs and bowel-bladder

dysfunction.
Diagnosis is suggested by the progressive story and findings, multi-
ple segmental levels, and upper motor neuron involvement. Lumbar
puncture revealing abnormal manometries and elevated protein de-
terminations suggest pantopaque myelography and surgical explora-
tion.

BRACHIAL PLEXUS INVOLVEMENT

The brachial plexus may be
the origin of pain felt in the shoulder
region; the etiology conveniently classified into (1) traumatic and
is

(2) mechanical, nontraumatic irritation.

94
 Trauma to the brachial plexus may be caused by penetrating
wounds, fracture-dislocation of adjacent bone structures, or traction
injuries. Injuries to the brachial plexus from shoulder dislocation and
clavicle fracture-dislocation have been discussed under these sub-
jects. Stretch injury to the brachial plexus from distraction between
the neck and arm may present a diagnostic problem, since the
symptom of severe pain may present minimal objective findings. In
this condition the history of traction can be elicited. There is tender-
ness by deep pressure over the neurovascular bundle and the scalene
muscles in the supraclavicular fossa, and pain can be reproduced by
placing stretch on the plexus from distraction of the neck and arm.
Objective findings will implicate sensory and motor involvement of
many roots — —
5 to Ti and many require electromyography for verifi-
cation.
Mechanical nontraumatic brachial plexus compression includes the
clinical conditions encompassed in the cervical dorsal outlet syn-
drome, which includes the cervical rib syndrome, the anterior scalene
syndrome, the pectoralis minor syndrome, the costoclavicular syn-
drome, and the first thoracic rib syndrome. All the symptoms attri-
buted to this syndrome imply compression of the brachial plexus or
the subclavian artery, or both, by bony, ligamentous, or muscular ob-
stacles somewhere between the cervical spine and the lower border of
the axilla. The most common site is the supraclavicular region in the
crowded area containing the first rib, the clavicle, and lower cervical
spine with all the tissues contained therein (Fig. 73).
Many of the symptoms originally attributed to the neurovascular
compression syndrome, at the thoracic inlet, have recently been attri-
buted to compression irritation of the cervical root at the foraminal
level from disk disease, or compression of the median nerve at the
wrist. The latter compression results from volar carpal ligament pres-
sure causing "carpal tunnel syndrome" symptoms of numbness, tin-
gling, and weakness, similar to more proximal plexus compression.

SCAPULOCOSTAL SYNDROME
A frequent cause of shoulder pain with localized tenderness and
arm and hand is the scapulocostal
radiation into distal portions of the
syndrome. It is claimed that this syndrome constitutes 90 percent of
allcases of cervicobrachial pain. 58
This syndrome is also called postural fatigue and affects patients
during their periods of rest. Gravity upon the scapular components is
considered the cause of this syndrome.
As this syndrome also causes symptoms of neurovascular compres-
sion in the supraclavicular fossa it is associated with symptoms attri-

95
Figure 73. Cervical dorsal outlet. Schematic depiction of the course of the brachial
plexus subclavian bundle from the cervical spine over the first rib, and under the
clavicle (CL) with the relationship to the anterior scalene muscle (ASM). (A = Subcla-
vian artery; N = brachial plexus; V = subclavian vein.)

buted to cervical rib, anterior scalene syndrome, claviculocostal syn-

drome, and the pectoralis minor syndrome. Each may be a specific
disease entity, but all are related to the single entity of scapulocostal
postural fatigue. Certainly the kinesiomechanics of this syndrome
prevails in all the associated syndromes, and the treatment is similar
in all.

The symptoms occur in the patient while at rest in the upright

position (sitting or standing). The syndrome is a
principal aspect of the
downward rotation of the scapulocostalmotion of the scapula which
rotates the superior-medial aspect of the scapula upward and laterally.

96
 With the downward sagging of the scapula traction upon the levator
scapulae muscle occurs, causing this muscle to become irritated and
ischemic, and thus go into "spasm." The irritated muscle and the local
"trigger" area that develops in the muscle become the clinical
symptom and physical finding that are characteristic of the syndrome
(Fig. 74).
The following additional symptoms may develop:

1. Hemicranial pain (unilateral headache).

2. Pain in the posterolateral aspect of the neck.
3. Radicular symptoms down the ipsilateral upper extremity that
are either vascular or neurologic, or both. The paresthesia may
be unilateral or bilateral, and usually is in the ulner nerve dis-
tribution.

Many of the symptoms, albeit postural, are related to tension upon

the pre- and postvertebral fascia that cause symptoms of myofascilitis
with local and referred symptoms. Moreover, due to the anatomic
proximity of nerves (brachial plexus) and blood vessels (subclavium),
symptoms referable to the neurovascular bundle are explainable.

Anatomy of the Fascia

The prevertebral fascia is a firm membrane lying anteriorly to the

prevertebral muscles (longus cervicis, longus capitis, anterior middle
and posterior scalenes, and the rectus capitis muscles). It is attached to
the base of the skull just anterior to the capitis muscles and descends
downward and blend with the fascia of the
laterally to ultimately
trapezius muscle. In course it covers the scalene muscles and also
its

binds down the subclavian artery and the three trunks of the brachial
plexus (Fig. 75).
The prevertebral fascia crosses (medially) to the transverse proc-
esses of the cervical vertebrae and covers all the cervical nerve roots.
The fascia does not ensheath the subclavian or axillary veins and
therefore does not cause venous congestion. The fascia is firmly ad-
herent to the anterior aspects of the cervical vertebrae and to the
clavicle.
In the posture causing the scapulocostal syndrome symptoms the
depressed scapula places strain upon the fascia as well as the scapular
musculature. This fascial tension, by causing pressure or traction upon
the greater occipital nerve (via the deep cervical fascia), may well
account for the associated hemicranial pain.
Traction upon the muscles of the scapula, the trapezius, and the

97
 LEVATOR SCAPULAE

TRIGGER' SPOT

Figure 74. Levator scapulae "trigger" zone in postural fatigue syndrome. With lateral
downward rotation of the scapula (curved arrows) the superior medial angle of the
scapula moves the insertion of the levator scapulae muscle (V-S, to V-S 2 The muscle
).

under this traction becomes ischemic, inflamed, and thus tender and painful at the
"trigger" site.

levator scapulae causes pain in these muscles. Deep tenderness and

possibly nodules in these muscles are responsible for the symptoms of
myofasciitis in this region. 58
Obliteration of the radial pulse, as noted in the Adson maneuver
(see below), can be attributed to tension of the cervical fascia on rota-
tion of the head and neck. Traction upon the lower trunk of the bra-
chial plexus may well cause the pain and numbness in the ulnar dis-
tribution of the hand which is so common in this syndrome.
Fibromyositis has generally become recognized as a specific pa-
thology that persists after trauma, manifested clinically by painful
muscles, nodules, spasm, and stiffness of joint motion, both actively
and passively. 59,60 This condition has been designated as fibrositis,

98
 MUSCLES

RECTUS CAPITIS

STELLATE
GANGLIA
CERVICIS

LEVATOR SCAPULAE

FASCIA-^ SCALENES

SCAPULA

RIB 1

SUBCLAVIAN
B.V.

Figure 75. Anterior view of prevertebral and muscles. The fascia is a firm mem-
fascia
brane in front of the prevertebral neck muscles. binds these muscles to the subclavian
It

artery and three trunks of the brachial plexus. All the cervical nerve roots are beneath
the fascia. The fascia is attached to the anterior margin of the cervical vertebral bodies
and to the clavicle. The cervical sympathetic trunk lies in front of the fascia.

myofasciitis, myofibrositis, interstitial myofasciitis, and psychogenic

rheumatism, among many
other descriptions.
The actual existence of fibromyositis has been questioned as there
are no confirmatory laboratory findings. Patients do not have fever,
leukocytosis, increased sedimentation rate, or alteration of serum en-
zyme levels. 61 Electromyographic abnormalities have been claimed,
but none are consistently and universally accepted. 62 On the assump-
tion that nodules are inflammatory ("trigger points"), steroids have
also been injected as well as anesthetic agents. The inflammatory
nature of the nodules has been questioned, as many beneficial results

99
have been achieved by the injection of sterile saline or merely dry
needling of the painful site. 63
The symptoms of hemicranial pain (headache) are attributed to one
or more of the following:

1. Pressure upon the greater occipital nerve exerted by the deep

cervical fascia (in the posterior triangle of the neck).
2. Tension upon the periosteum of the cranium at the attachment of
the trapezium or the levator scapulae muscles (traction).
3. Referred pain of cervical origin from increased lordosis causing
nerve root entrapment at the intervertebral foramen. 64

Due to thoracic kyphosis of the "fatigue posture" the fourth and fifth
thoracic nerves can be irritated, causing referred pain at the inferior
angle of the scapula.
The clinical diagnosis is made by:

1. Observation of the posture: dorsal "round back" kyphosis, with

increased compensatory cervical lordosis and a forward head
posture. The presence of sagging shoulders. Histories obtained
of the causative factor(s) contributing to this posture also confirm
in making the diagnosis and in outlining the proper treatment.
2. Elicitation of the "trigger areas" in the scapular antigravity mus-
cles. This may require a careful, meticulous search for the "trig-
ger point" or the referred zone with digital pressure.
3. Elicitation of the neurovascular symptoms and findings by
means of the tests described in subsequent sections of this
chapter, including the Adson sign, the pectoralis minor test,
scalene signs, and claviculocostal signs. 65-67

Treatment

Treatment is basically correction of the faulty posture with amelio-

ration or correction of the causative factors, including depression,
work habits, sitting or standing posture, and self-image.
Improvement of the hypotonic shoulder girdle muscles is also indi-
cated (Figs. 76 and 77). Moist heat application to the neck and shoul-
ders for a period of 20 to 30 minutes. Massage of the deep, painful,
indurated muscles is valuable.
Injection of an anesthetic agent into the "trigger" tender area with
or without a steroid affords relief. Ethyl chloride or vasocoolant spray
to the painful tender muscle, followed by stretching of that specific
muscle, also has been advocated. 68-70 Cervical traction and sleeping
with a cervical pillow complements the therapeutic regime.

100
Figure 76. Standing scapular elevation exer-
cises. With proper posture (tilted pelvis and
flattened cervical lordosis) both arms are rhyth-
mically elevated, held, and slowly lowered. In-
creasing weights are used. Elbows must be fully
extended.

CERVICAL RIB
In the human, only the thoracic spine has fully developed ribs, but
occasionally in the cervical spine the transverse process may be over-
developed or have a supernumerary rib. This is usually bilateral, pre-
dominantly in women, and occurs in less than 1 percent of the popu-
lation. It seldom gives rise to symptoms.
Symptoms attributable to cervical ribs are vascular or neurologic, or
both. The vascular signs are rarely severe and mainfest themselves by
numbness and tingling of the fingertips. Neurologic symptoms in-
clude pain, hypesthesia, hyperesthesia, or paresthesia. Weakness may
be present. The neurologic symptoms seen result predominantly from
involvement of the eighth cervical and first thoracic nerves, with pain
and numbness of the ulnar border of the hand and the last two
phalanges of the ring and little fingers, and weakness of the small
muscles of the hand. It is difficult to visualize compression of the firm
nerve trunk without simultaneous compression of the blood vessels.

101
 ciQ <2^>
Figure 77. Posture-scapular elevation exercises. Patient is seated with back to wall,
hishead and neck pressed against the wall, which decreases the cervical lordosis. With
arms full extended and dependent, weights are lifted in a shrugging motion. Weights
vary from 5 to 30 pounds.

Therefore, without vascular changes, a diagnosis of cervical rib com-

pression should be made cautiously. 71
Treatment should be an intensive, prolonged, conservative regimen
of exercises to (1) improve posture, and (2) improve muscle tone of the
shoulder girdle. Even a mechanical brace assist to shoulder elevation
may be necessary. Surgery, either to resect a cervical rib or to section
the scalene muscle, should be the last resort, unless organic impair-
ment of the subclavician artery is suspected. A "bruit" associated with
pallor, coldness, wasting, and weakness should be studied by retro-
grade arteriography. 72

102
 ANTERIOR SCALENE SYNDROME
The chief symptoms of the anterior scalene syndrome are numbness
and tingling of the arm, hands, and fingers. These sensations of the
hand's "going to sleep" and of "pins and needles" are most prevalent
during the early morning hours and frequently awaken the patient.
Weakness in the fingers may be claimed, and when pain is present, it
is described as deep, dull, and "aching."

Physical findings are minimal or absent. The findings are essen-

tially subjective, and the examination consists of reproducing the
symptoms by specific motions and positions. The scalene anticus test,
also described as the "Adson test" (Fig. 78), consists of turning the
head to the side of the symptoms, extending the head backward,
abducting the arm, and taking a deep breath. By obliterating the radial
pulse in that arm and reduplicating the symptoms complained of by
the patient, the test is considered "positive."
The mechanism by which these maneuvers are considered to re-
produce the symptoms is as follows: the rotated and extended position
of the neck places the scalene muscle under tension, thus narrowing
the angle between it and the first rib to which it attaches. Deep inspi-
ration utilizes the scalenes as accessory inspiratory muscle and el-
rib. The effects
evates the of these actions place traction and compres-
sionupon the neurovascular bundle.
Spasm of the scalene muscle implicated here may be caused from
unusual exertion, posture, occupational stress, or prolonged emotional
tension. More probably, scalene muscle spasm is secondary to cervical
radiculitis due to spondylosis, diskogenic disease, or nerve root sleeve
fibrosis. 73

CLAVICULOCOSTAL SYNDROME
The neurovascular bundle may be compressed between the first rib
and the clavicle at a point where the brachial plexus joins the subcla-
vian artery and courses over the first rib (Fig. 79). The symptoms are
similar to those of the anterior scalene syndrome, and the findings are
minimal. Symptoms in this syndrome are reproduced by obliterating
the radial pulse and by bringing the shoulders back and down. This
postural maneuver is done, first, actively by the patient, then pas-
sively with downward pressure by the examiner. 74 A bruit, which can
be heard when the vessels are compressed and disappears when they
are released, is a good diagnostic confirmation.
The etiologic factors are posture, fatigue, trauma, and stress; thus
the treatment is postural improvement and increase of muscle tone
and endurance.

103
 ^m
i >?

^^ RIB
KIB tLtVAHUr
ELEVATION

Figure 78. Scalene anticus syndrome. A. Relationship of the neurovascular bundle.

The subclavian artery (a) passes behind the anterior scalene muscle, loops over the first
rib, and is joined by the brachial plexus (n). The artery is separated from the subclavian
vein (v) by the anterior scalene muscle. The median scalene muscle (not shown) lies
behind the nerve (n). B. The triangle formed by the scalenes and the first rib. C.
Distortion from turning the head toward the symptomatic side. Compression of the
—
neurovascular bundle the brachial plexus, the subclavian artery, and occasionally the
—
subclavian vein can be pictured from the test maneuver of the anticus scalene syn-
drome.

PECTORALIS MINOR SYNDROME

This syndrome is termed also the hyperabduction syndrome. The

pectoralis minor muscle originates from the third, fourth, and fifth ribs
anteriorly and inserts into the coracoid process of the scapula. The
cords of the brachial plexus together with the axillary artery and vein
descend over the first rib under cover of the pectoralis muscle (see
Fig. 79).
The symptoms of numbness and tingling of the hand are caused by
compression of the neurovascular bundle between the pectoralis
minor muscle and the first rib and may be reduplicated by bringing
the patient's arms overhead, abducted, and slightly backward. This
position stretches the pectoralis minor muscle and narrows the space
through which the neurovascular bundle traverses. The etiologic fac-
tors are similar to the scalene anticus and the claviculocostal syn-
dromes; therefore, the treatment is similar.

104
Figure 79. Claviculocostal and pectoralis minor syndromes. A. Claviculocostal syn-
drome. The neurovascular bundle is compressed between the clavicle and the first rib
by retraction and depression of the shoulder girdles. B. Pectoralis minor syndrome. The
neurovascular bundle may be compressed between the pectoralis minor and the rib
cage by elevating the arms in a position of abduction and moving the arms behind the
head.

SUPERIOR PULMONARY SULCUS TUMORS

Carcinoma of the lung or the Pancoast apical pulmonary tumor may
firstmanifest itself by involvement of the brachial plexus. The pain is
generally severe and diffusely located in the shoulder and arm. In
addition to nerve root involvement, it is common for the tumor to
involve the thoracic ganglion sympathetic chain and give rise to
Horner's syndrome. There are usually associated general systemic
signs and symptoms, positive chest x-ray films, and positive node
biopsies. The specific treatment of the primary condition and for con-
trol of pain is surgery or irradiation. Follow-up treatment by physical
medicine and rehabilitation consists of exercises and the use of indi-
cated modalities.

105
 SUPRASCAPULAR NERVE ENTRAPMENT
Pain in the shoulder can occur as a result of entrapment of the
suprascapular nerve in its passage through the suprascapular fora-
men. 75 The course of the nerve is shown in Figure 49. It originates
from C 5 and C 6 passes behind the brachial plexus to the upper border
,

of the scapula, and passes through the suprascapular notch, where it is

bridged over by the transverse scapular ligament. It then enters the
supraspinatus fossa to supply the branches to the shoulder joint cap-
sule, the acromioclavicular joint, and the supraspinatus and infra-
spinatus muscles. It is essentially a motor nerve; pain felt in its dis-
tribution is attributed to retrograde "myotome" sensory distribution,
and is vague, deep, and poorly described. The posterior lateral aspect
of the shoulder is described as the general area of painful sensation.
Atrophy and weakness of the spinati muscles are frequent observa-
tions.
The nerve becomes fully stretched when the arm is held across the
chest in adduction. Further adduction places stress upon the
scapulothoracic joint and causes traction upon the nerve. Trauma is
the usual mechanism, especially when there is an acromioclavicular
separation allowing further scapular motion forward and medially. 76
Diagnosis is made by eliciting the movement that initiated the pain,
reproduction of the pain by forceful scapular movement forward and
across the chest wall, failure to implicate another etiology or mecha-
nism (negative evidence), and relief by a suprascapular nerve block.
Treatment is to treat any other associated problem, such as acromio-
clavicular separation, immobilization of scapula in position of no
nerve tension, and repeated nerve blocks.

DORSAL SCAPULAR NERVE ENTRAPMENT

The dorsal scapular nerve innervates the rhomboids. It originates
from the C 5 root and shortly after its origin perforates the medius
scalene muscle. It is irritated by any condition that causes mechanical
strain upon, or spasm of, the scalene musculature. The pain felt is dull,
deep, and vague, along the medial edge of the scapula, because the
nerve is principally a motor nerve. When the associated scalene con-
ditions are favorably treated and all but the pain of the dorsal scapular
nerve is relieved, surgical neurolysis is indicated. 76

ARTERIOSCLEROTIC OCCLUSION
Arteriosclerotic occlusion produces a decreased blood flow and a
reduced radial pulse. This conditions causes claudication pain when

106
the patient exercises excessively, and it is relieved by rest. Systolic
bruits are frequently heard. Innominate or subclavian aneurysm, with
or without cervical rib compression, may mimic arteriosclerotic
claudication. Arteriogram or venogram will confirm the clinical diag-
nosis.

107
CHAPTER 6

Sympathetic Referred Pain

Causalgia, reflex sympathetic dystrophy, and the shoulder-hand-

finger syndrome have been grouped into a characteristic medical con-
dition that may cause severe, intractable pain and progressive func-
tional impairment and disability. The pain and ultimate disability is
based on dysfunction of the sympathetic nervous system and thus the
vascular system of the extremities.
The circulation of the upper extremity can be roughly divided into
arterial and venous components.

1. The arterial circulation refers to cardiac pumping action, vascu-

lar tone, and gravitational forces, proceeding from the proximal
to the distal portion of the extremity.
2. The venous return and lymphatic system carry back the circula-
tion proximallyby means of "pumps." The muscles of the hand
and arm force the fluid in a centripetal direction through numer-
ous valves in the venous system and through the lymphatic
channels. Repeated elevation of the arm above the cardiac level
allows gravity to aid this venous blood and lymphatic return.

The major pumps are located in the axilla and the hand (Fig. 80).
These pumps require repeated movement of the shoulder girdle
through adequate range of motion and repeated clenching and re-
leasing of the fingers and wrist. Elevation of the arm above the shoul-
der level facilitates this centripetal flow.
The largest portion of the arterial supply is in the volar aspect of the
hand, whereas most of the venous and lymphatic drainage is in the
dorsal tissues of the hand.
Failure of these pumps to function adequately may lead to a painful
and disabling condition termed shoulder-hand-finger syndrome. This

108
 RTERIAL

uoo
Figure 80. Venous lymphatic pumps of the upper extremity.

syndrome may be initiated at either of the pumping centers (the

shoulder or the hand).
Reflex sympathetic dystrophies have been arbitrarily divided into
major and minor classifications in which causalgia, phantom limb
pain, and the central pains of the thalamus or thalamocortical tracts
constitute the major dystrophies. All other causalgias related to
trauma or disease are considered minor dystrophies. The shoulder-
hand-finger syndrome is in this latter category.
Causalgia is essentially a symptom complex that has gradually be-
come a distinct disease entity. The causalgic aspect of the complex is
appreciation of a persistent "burning pain," usually following trauma.

109
Pain, if it appears, usually arises shortly after injury but may actually
occur after the initial injury has healed or subsided. This causalgic
pain is vague, diffuse, and poorly delineated. It corresponds to no
peripheral radicular or dermatome pattern.
"Burning" pain is associated with vasospastic or vasodilatory
phenomena and is usually described by the patient as severe to excru-
ciating. The initial incident or injury may be minor, but once initiated
it may progress to impairment with irreversible tissue changes.

A voluminous literature has evolved regarding causalgia, with the

introduction of terms such as reflex sympathetic dystrophy, Sudeck's
atrophy, traumatic vasospasm, postinfarction sclerodactylia, post-
traumatic osteoporosis, chronic traumatic edema, and shoulder-
hand-finger syndrome. In this syndrome there is a resultant immo-
bilizing of the involved part, resulting in chronic edema, fibrosis, joint
contracture, and muscle and bone atrophy 77 (Fig. 81).
The inciting traumata that provoke the reflex sympathetic dystrophy
are varied and frequently nonapparent. They include cardiovascular
disease such as hemiplegia or coronary ischemia, cervical disk dis-
ease, mechanical trauma, prolonged bed rest, or even an incident as
innocuous as an intramuscular injection. The inciting factor may be a
subacute peritendinitis of the shoulder, a calcific tendinitis, subluxa-
tion, "frozen shoulder," or a bicipital tendinitis. No overt cause may
have been discovered. A pain must have existed. Immobilization of
the part must have followed. Sympathetic vasomotor reaction must
have been invoked.

PATHOPHYSIOLOGIC MECHANISMS
The pathologic changes discernible in the extremity are frequently
insufficient to account for the severity of the symptoms. The
peripheral and central pathways of pain in this causalgic state are not
well understood neurophysiologically. The sympathetic nervous sys-
tem is universally implicated, and many pathways are described; but
all theories are based on the unproven presence of afferent pain fibers

in the sympathetic nervous system.

The accepted pathways of sensation are shown in Figure 82A. The
segmental nerve arises from various tissues: cutaneous, subcutaneous,
tendons, joints, periosteum, and skeletal muscle. Impulses proceed
proximally through the anterior and posterior primary divisions of the
segmental nerve through the posterior root ganglion and enter the
cord to take various pathways depending on the type of sensation
transmitted. The pain and thermal fibers, immediately upon entering
the cord, synapse at the same segmental level and ascend in the poste-
rior lateral tract to a level several segments higher. Some of the pain

110
 Figure 81. Sequences leading to "frozen" shoulder-hand-finger syndrome.

and temperature fibers decussate and ascend the cord in the lateral
spinothalamic tract. The ipsilateral posterior column transmits posi-
tion sensation, and the anterior spinothalamic columns, tactile sensa-
tion.
Pain sensation entering the cord from the sensory ganglion excites
the internuncial pool in the gray matter of the cord. A reverberating
cycle is initiated that excites the anterior horn cells and causes a motor
response in the peripheral musculature. A simultaneous excitation of
the lateral horn cells occurs, which causes a sympathetic vasomotor
and sudomotor response. This cycle at the segmental level involves

111
Figure 82. Neuron pathways of pain. A. The course of sensory fibers in a segmental
nerve with its ganglion in the dorsal root (G). Upon entrance into the cord, the fibers
ascend on the same side in the posterior lateral tract (PLT) and decussate to cross into
the lateral spinothalamic tract; 2 indicates secondary neurons. The posterior column
(PC) transmits position sense; AST conveys tactile sensation. B. 1 = first-stage neurons
to the cord; 2 = second-stage neurons through the midbrain (MB) into the thalamus (T);
3 = third-stage neurons, the thalamocortical pathways to the cerebral cortex (CC).

112
first-order neurons.The internuncial pool and the pathways from it to
the thalamus constitute the neurons of the second order. The third-
order neuron connects the thalamus to the cerebral cortex through the
corticothalamic cycle.
This three-neuron cycle does not fully explain the observable clini-
cal aspect of vasodilatation in the causalgic state. The "cycle" theory
which would cause excitation of the lateral cells with sympathetic
release would cause vasoconstriction, not dilatation, and dilatation
occurs peripherally. 78 This theory also does not explain fully the relief
of pain from sympathectomy, unless the presence of afferent fibers
(antidromic) in the sympathetic ganglia and trunks is accepted. Figure
83A shows the accepted flow of sympathetic nerve impulses. Figure
83B depicts the antidromic flow of sympathetic impulses coupled
with the cycle of internuncial pool stimuli, which now has acceptable
recognition.
Confirmation of afferent fibers in the sympathetic nerve ganglia and
trunks has been advanced. Retrograde degeneration following section
of the rami communic antes indicates the presence of afferent fibers. 79
In laboratory experiments extensive bilateral dorsal rhizotomies
(eliminating sensory nerve roots) and unilateral sympathectomies al-
lowed the animals to perceive pain on the side where the sympathetic
fibers remained. It was concluded that afferent fibers exist capable of
transmitting pain sensations through the sympathetic trunks along
the segmental nerves to the spinal cord. 80
Treatment of the causalgic state depends upon the duration of the
painful stimulus, the duration of the reverberating internuncial cycle,
and the order (first, second, or third) of neurons involved.

DIAGNOSIS
The shoulder is involved first as a rule, but the painful hand may
precede a specific aspect of the causalgic state. In 1897, Osier de-
scribed shoulder disability in patients suffering from angina pectoris,
and in 1948 the complex of shoulder and hand abnormalities on a
neurovascular basis was formulated. 81 Regardless of the site or source
of the pain sensation, the syndrome follows a specific pattern.
The syndrome occurs with equal frequency in either or both shoul-
ders and, except when caused by coronary occlusion, is most frequent
inwomen. The shoulder is generally involved first, but the painful
hand may precede the shoulder. Three stages of the complex are rec-
ognized.
The shoulder becomes limited in its range of motion, and
"stiff,"
may proceed to a "frozen shoulder." Even in cases following a myo-
cardial infarction, the shoulder initially resembles the pericapsulitis

113
Figure 83. A. The accepted direction of the sympathetic fibers in a segmental
peripheral nerve. The preganglionic myelinated white (W) nerve (Pr), the postgan-
glionic (Po) unmyelinated nerve that leave as gray (G) fibers through the gray ramus of
the ganglion, and proceed distally within the common peripheral nerve. B. The afferent
pathways along the sympathetic nerve. The cycle of the sensory nerve root (S) excites
the intranuncial pool (INP), which in turn excites afferent sympathetic nerves (SY) and
afferent motor impulses (M). LH indicates lateral horn cells; AH, anterior horn.

from other causes. Tenderness about the shoulder is diffuse and not
localized to a specific tendon or bursal area. The duration of the initial

114
shoulder stage, before the hand component begins, is extremely vari-
able. The shoulder may be "stiff" for several months before the hand
becomes involved, or both may occur simultaneously.
The hand and fingers become diffusely swollen. At first the edema
is pitting and may be relieved by prolonged elevation of the arm. This

edema is predominantly noted on the dorsum of the hand and usually

is noted over the metacarpophalangeal and proximal interphalangeal

joints (Fig. 84). The skin over the knuckles becomes puffy and loses
the normal creases. The hand becomes boggy and painful. As the
edema forms under the extensor tendons flexion becomes increas-
ingly more limited. The collateral ligaments, which must elongate to
permit flexion of the metacarpophalangeal joints, become shortened
and thus prevent or limit full flexion (Fig. 85).
Less pumping action is permitted, and with the limited shoulder
action allowing no ability to elevate the arm above shoulder level,
both pumps are restricted.
The skin gradually becomes shiny and atrophic. The edema-con-
taining protein converts into a diffuse, cobweb-like tissue that adheres
to the tendons and joint capsules and prevents further movement.
The joints undergo disuse atrophy of the cartilage, and the capsule
thickens. The bones undergo diffuse osteoporosis. The ultimate hand
posture resembles the intrinsic minus hand (Fig. 86) due to stiffening
of the metacarpophalangeal joint in extension with the tenodesis
flexor action flexing the phalanges.
The evolution of the shoulder-hand-finger syndrome can be item-
ized in the following sequence (see Fig. 81):

1. Impairment of the hand-arm-shoulder venous and lymphatic cir-

culation.
2. Shoulder limitation from numerous causes leading to ultimate
contracture ("frozen shoulder").
3. Metacarpophalangeal limitation due to edema and restricting,
contracted collateral ligaments.
4. Wrist in a restricted, flexed position.
5. Sympathetic nervous system involvement.

Sympathetic nervous system involvement may be totally absent,

initially absent, ormay be primary in the causation of the shoulder-
hand-finger syndrome. Some deny the necessity of this component, 82
based on the fact that the syndrome is rarely seen in people who are
less than 40 years old, which is when sympathetic nervous system
abnormalities are most prevalent. Causes considered necessary for
sympathetic nervous system involvement are frequently not present.
When present, the resultant clinical entity is termed reflex sympa-

115
Figure 84. Finger changes in the hand-shoulder syndrome. 1. Normal extension of the
metacarpophalangeal joint with relaxed collateral ligament. 2. Normal flexion of the
metacarpophalangeal joint with the collaterals becoming taut. 3. Edema on the dorsum
of the hand elevates the extensor tendons and prevents flexion. The collateral ligaments
are never fully elongated and develop contracture. This further limits the "pump ac-
tion" of the flexion of the hand.

thetic dystrophy syndrome or causalgia.

Reflex sympathetic dystrophy syndrome has the following classic
signs and symptoms:

1. Pain and swelling in an extremity

2. Trophic skin changes of that extremity which include:
a. Skin atrophy

b. Skin pigmentary changes

c. Hyperhidrosis

d. Hypertrichosis

116
Figure 85. Normal flexion-extension of the metacarpophalangeal joints. Due to the
elliptical shape of the head of the metacarpals, the collateral ligaments are slack with
finger extension and taut when the fingers are flexed.

e. Nail changes
3. Signs and symptoms of vasomotor instability
4. Pain and limited range of motion of the ipsilateral shoulder
5. Precipitating events such as stroke, trauma, and myocardial in-
farction

Most reflex sympathetic dystrophy syndromes are unilateral, but 20 to

35 percent are bilateral. Studies of reflex dystrophy by oscillography,
plethysmography, skin temperature, and venous gas determinations
reveal increased blood flow and increased venous oxygen. In reflex
sympathetic dystrophy syndrome, there are no characteristic
pathologic tissue changes. Ultimately there is radiologic evidence of
periarticular soft tissue swelling and patchy osteoporosis, but these
changes are similar to changes noted in prolonged immobilization. 83
The shoulder-hand-finger syndrome, which is a variant of the reflex
sympathetic dystrophy syndrome, has been considered to evolve into
three stages. These stages need not be in the same sequence, but the
third is usually the residual stage. The stages are not necessarily as
specific or as clearly delineated as stated:

117
Figure 86. Hand patterns. A depicts the hand that resembles the "intrinsic minus
hand." The proximal phalanx remains extended with tenodesis action flexing the distal
phalanges. B resembles the "intrinsic minus hand," with all phalanges extended but
with the metacarpophalangeal joint flexed.

1. Limited shoulder range of motion with or without pain. The

hand has swelling limited initially to the dorsum of the fingers,
knuckles, and wrist. Edema is not usually of the pitting variety
but is firm. The skin loses its normal wrinkles and becomes
shiny. Full flexion of the fingers and all their joints becomes
limited. The wrist tends to assume a flexed posture. The skin of
the hand may be pale and cool or assume a pink hue. The skin is
usually moist with small bubbles of perspiration. In certain
cases, the skinis excessively hypersensitive to touch, pressure,

movement, or temperature variations. The elbow usually shows

no limitation or pain. The wrist is usually exquisitely painful
when extended and also has dorsal edema and tenderness.

118
 2. Shoulder pain subsides and shoulder range may increase. Re-
sidual restriction of movement in both the active and passive
ranges may persist, but this limitation is usually less painful.
Edema of the hand subsides, but the fingers become stiffer. The
skin assumes a pale, atrophic appearance. Hair appears coarser,
as do the nails. Sensitivity decreases. Osteoporosis can now be
visualized on x-ray.
3. There is progressive atrophy of the bones, skin, and muscles.
Limitation of hands, wrists, and fingers increases, leaving the
hand painless but in a useless, atrophied, clawed position.

ETIOLOGY
Initial causalgic pain is mediated through the large delta fibers
which transmit brief, sharp, pricking, localized pain which, when elic-
ited, promptly causes withdrawal. The secondary pain is delayed and
mediated through the small-diameter fibers that are slow-conducting.
This is the pain that is persistent and of a burning quality. In causal-
gia, the macroscopic and microscopic appearance of the involved
nerve lesions is not different from lesions which do not cause burning
pain.
Electrical stimulation of the distal end of the divided nerves in a
peripheral nerve injury with causalgia releases neurokinin, a sub-
stance that is a vasodilator. Neurokinin, which can be retrieved from
the tissues, will cause a burning pain when injected into normal tis-
sues. In causalgia, it is probable that neurokinin is liberated, but this
has not been verified.

TREATMENT
Early vigorous treatment of the shoulder-hand syndrome offers the
only promise of recovery.
The stiff shoulder should be treated, utilizing all medications and
modalities to improve range of motion. Disuse must be avoided, since
it is the predominant instigator of the shoulder phases. Where and

when possible, the underlying cause must be treated as in diaphrag-

matic irritation, myocardial infarction, and gallbladder disease. Re-
gardless of the underlying source of pain, the shoulder and hand must
receive early active treatment.
During the phase of pain relief from the stellate block, gentle, cau-
tious,but positive active physical therapy must be started. Massage,
hot packs, whirlpool, and even ice packs are usually poorly tolerated.
Cool packs about 70° F are usually most soothing. Local irritation may
stimulate more sympathetic fibers.

119
 Active exercises of the shoulder and hand must be instituted as soon
and as energetically as the medical condition permits. Stasis must be
prevented and active circulation stimulated, even though sympathetic
vasospasm exists. Movement of the hand and shoulder "pumps" the
venous blood from the fingers toward the axilla, which, coupled with
an elevated overhead arm position, decreases distal edema. The major
"pumping" action occurs at the metacarpophalangeal joints and the
axilla; therefore edema of the dorsum of the hand impairs the meta-
carpophalangeal pumping action.
The hand and fingers must be kept adequate for their pumping role.
The wrist must be kept flexible so that flexion-extension motion of the
fingers is maintained. In a wrist that is permitted to remain flexed, the
finger flexor tendons are restricted; therefore flexion at the meta-
carpophalangeal and phalangeal joints is impaired. The "pumping
action" of the hand, which occurs predominantly at the metacarpo-
phalangeal joints, is lost. The metacarpal and collateral ligaments are
placed under tension when the hand is flexed, and these must be kept
fully extendible.
In the early dystrophic phase of the hand, sympathetic procaine
block must be instituted immediately. Done early, these blocks are
both diagnostic and therapeutic. An effective block may wear off in 24
hours and have to be repeated. One block may clear the condition
completely, or a second block may need to be performed 5 to 7 days
later. The controversy as to whether repeated blocks should be done
upon cessation of pain is an individual decision. Regardless of cessa-
tion of pain, repeated blocks should be considered when there is
continuation of vasomotor and sudomotor changes (Fig. 87).
An effective stellate block is so judged if there is (1) pain relief; (2)
Horner's syndrome (miosis, enophthalmos, and ptosis; anhidriosis,
injected conjunctiva, slightly flushed face, and blocked nostrils are
also consistent); or (3) a marked rise in the skin temperature. The
technique of performing a stellate block is well documented in the
literature. 84
More permanent benefit from sympathetic intervention can be
prognosticated as:

1. Good
a. one block gives total relief;
if
b. one block reduces pain to a tolerable level;
if
c. if the first block is effective with each subsequent block

being "better."
2. Poor
a. if the first block is effective but each subsequent block is less

effective;

120
 GANGLION
/if^fc CAROTID SHEAl

OQ-BR ACHIAL plexus

'CscalID

Figure 87. Technique of stellate ganglion or brachial plexus block. For a stellate
ganglion nerve block, the trachea is moved to one side and the needle enters between it
and the carotid artery to the vertebral body. The needle then is moved slightly lateral to
the body, and 3 to 5 cc of the anesthetic agent is administered. Aspiration must always
precede infiltration of the anesthetic agent.

b. if the block is only effective during the duration of the

anesthetic agent but there is no residual benefit after the
agent wears off.

If the decision is made, by the physician or at the request of the

patient, not to administer a stellatechemical block, oral or intramus-
cular steroids can be effectively substituted. A usual dose of triam-
cinolone, 100 mg daily, or cortisone, 200 mg daily, for 14 to 16 days
may be of great benefit. The precautions of administering steroids
must obviously be observed.
In addition to oral, intramuscular medication or stellate chemical
blocks, other physical therapeutic modalities must be instituted, in-
cluding all the exercise methods of treatment advocated for the pain-
ful and limited shoulder. For the hand and fingers, vasoconstrictive
techniques to reduce the edema must be instituted. Elastic bandag-
ing, wrapping the fingers with twine (Fig. 88), or use of a Jobst vaso-
pneumatic compressive device can be of value.
Elevation of the arm above shoulder level, achievable range of mo-
tion permitting, is generally attempted. This may be accomplished by

121
 START

Figure 88.Removal of finger edema. Each finger is firmly wrapped with a heavy
twine, beginningat the tip and moving toward the webbing. This procedure should be

performed several times daily and can frequently be done by the patient, using his
uninvolved upper extremity.

placing the arm and hand on a pillow or by suspending it from over-

head equipment (Fig. 89).

PSYCHIATRIC ASPECTS
The full psychiatric implications of reflex sympathetic dystrophy
arebeyond the scope of this text, but the subject cannot be dismissed
altogether from this discussion.
The designation of periarthritic personality is used repeatedly
throughout the literature 31 and varies in meaning from a primary in-
citing cause to the personality resulting from persistent, unrelenting
pain. 1,84 The question has been raised whether the causalgic state is a
purely "psychogenic phenomenon complicated by compensation-
induced voluntary immobilization and aggravated by conversion
hysteria or pathologic malingering. 85
The sensation of pain and the patient's reaction to pain are associ-

122
FIGURE 89. Antigravity treatment of the edematous extremity. The hand and arm are
wrapped, distal to proximal, with an elastic bandage. The hand held by the webrill is
then suspended overhead. This position drains the edema and maintains shoulder
range of motion with the elbow extended.

ated with a state of anguish, displeasure, and fear. In the early phase of
the shoulder or the hand component of minor reflex dystrophy,
movement is avoided because of pain. Interest, judicious sympathy,
and encouragement are necessary to initiate and maintain the active
movement so important in the recovery process. Early interruption of
the "cycle" by stellate blocks prevents the internuncial reverberation
and progression to the second and third neuronal levels where treat-
ment by any means becomes increasingly ineffectual and, in fact, ul-
timately useless.
Continuous sensory input reaching the hypothalamus increases its
reactivity, and stimuli of lesser and lesser intensity respond with ex-
aggerated sympathetic outbursts. 86 It behooves the treating physician
to interrupt the pain cycle early and forcefully. Arresting the patho-
physiologic manifestations early and preventing progression of

123
 PAIN
<z>
IMMOBILIZATION
<3>
Disuse atrophy
<?
CONTRACTURE
<^
OSTEOPOROSIS

DISABILITY DEPRESSION DRUGS DEPENDENCE

Figure 90. The "five Ds" resulting from pain.

symptoms minimize the psychologic factors. 18,87Whether the psycho-

logic factors are primary or secondary is of incidental importance when
the concern is to prevent permanent functional disability (Fig. 90).
Pain perception is subjective and results from the way the sensory
impulses reaching the cortical level are processed and interpreted.
Pain can be influenced by drugs with an analgesic or a hypnotic ac-
tion, but it has been shown to be influenced also by the patient's
attitude and suggestibility. 44
The treatment of pain and its effect, therefore, are multifaceted: (1)
interrupt, eliminate, or minimize the sensory-pain impulse by all

means; prevent secondary manifestations that may become in-

(2)
itiators of pain as well as complicate the primary factors; (3) elevate
the pain tolerance by suggestion, sympathy, and encouragement; (4)
alter the interpretation of pain by drugs or psychotherapy; and (5)
remove the patient's motivation to be disabled, whether it is a mone-
tary compensation or a psychogenic, hysterical manifestation.

124
CHAPTER 7

Traumatic Pain

Shoulder dislocations at the glenohumeral joint occur anteriorly in

90 percent of shoulder dislocations. The remaining 10 percent dislo-
cate posteriorly. The prevalence of anterior dislocations is attributed
to the anatomic weakness of the anterior aspect of the joint.
Brief review of the anatomy of the glenohumeral joint, described in
Chapter 1, reveals the capsule to be thin and loose. The capsule is
reinforced anteriorly by folds called the glenohumeral ligaments.
These ligaments attach from the humerus and fan out to attach to the
superior anterior aspect of the glenoid fossa, partly to the glenoid
lab rum, and partly bone of the scapula. An opening
to a portion of the
in the capsule frequently exists between the superior and middle
glenohumeral ligaments, termed the foramen of Weitbrecht. This may
be a frank perforation or may be covered by a thin layer of capsule.
The articular cavity connects with the subscapular fossa through this
opening. The humeral head dislocates through this opening, and dis-
locations may recur due to fraying or actual destruction of the middle
glenohumeral ligament (Fig. 91).
In dislocations the glenoid labrum may be partially or completely
detached with the tear occurring in the anteroinferior aspect. 88 If the
concept is accepted that the glenoid labrum contains no fibrocartilage
but is merely a redundant fibrous fold of the anterior capsule that
disappears when the humerus is externally rotated, this "pouch" in-
vites dislocation. The humeral head can protrude into this pouch,
especially if an anatomic variant of the middle humeral ligament exists.
There are four types of dislocation, the most common being the
subcoracoid. The subclavicular and subglenoid types are less frequent
and may be a progression of the subcoracoid type. All anterior types
can change into any other of the anterior types. The type of dislocation
is so termed depending upon the site of the humeral head in relation

125
BICEPS TENDON
LONG HEAD

FORAMEN OF
WEITBRECHT

Figure 91. Anterior capsule, glenohumeral ligaments, and avenue of anterior shoulder
dislocation. A. The three folds of the anterior capsule forming the glenohumeral liga-
ments humerus to the glenoid fossa. B. A tear is
that attach from the anterior ridge of the
shown between the superior and middle ligament (foramen of Weitbrecht),
in the area
which may be covered by a thin capsule or may be a direct opening. C. As the head of
the humerus moves forward and downward, it emerges through the opening.

to the glenoid seat when the diagnosis is made. The fourth type —the
posterior or subspinous — is rare (Fig. 92).
Primary anterior dislocations occur with equal frequency regardless
of age, but recurrence of dislocation is highest in the young (teens and
twenties) and decreases after age 45. There is less recurrence in those
cases in which the primary dislocation was severe as a result of the
greater hemorrhage and therefore the greater scar formation in heal-
ing.

MECHANISM OF DISLOCATION
Anterior dislocations result from abduction-external rotation inju-
ries.Trauma usually "catches" the muscles that protect the joint un-
prepared, or is of sufficient force to overwhelm the muscles. In
younger people the anterior glenohumeral ligaments "give," whereas
in older people the posterior supports, the greater tuberosity, or the
supraspinatus and infraspinatus tendons tear, permitting the head of
the humerus to "roll" over the anterior rim. The capsule and gleno-
humeral ligaments remain intact (Fig. 93).
A frequent explanation offered for anterior dislocation is depicted in
Figure 94. As stated by Codman, "the capacity for rotation will be less
1

as the arm ascends until, in complete elevation, tuberosities and proc-

esses will be locked in a fixed position." To elevate the arm fully in

126
 SUBCLAVICULAR

SUBSPINOUS
(POSTERIOR)

SUBCORACOID

SUBGLENOID

Figure 92. Four types of shoulder dislocation. The subcoracoid dislocation is the most
frequent and the subspinous (posterior), the least common. All three anterior disloca-
tions —
the subcoracoid, the subglenoid, and the —
subclavicular may alternate. The type
designated depends upon the position of the humeral head in relation to the glenoid
seat at the time of diagnosis.

the coronal plane, the arm must be externally rotated. In the sagittal
plane internal rotation of the arm is necessary to achieve full eleva-
tion. If either rotational adjustments are violated and force is applied
to accomplish elevation, a fulcrum is created whereby the distal force
causes downward and anterior displacement of the proximal head.
The mechanism of primary dislocations and recurrent dislocations
was considered to differ in past literature, but present concepts imply
a similar mechanism with recurrence being easier as a result of the
primary dislocation having been incorrectly treated. 89
The method of dislocation is most often caused by a fall on the
outstretched arm (Fig. 94, parts 1^). The trauma drives the head
forward against the anterior capsule. 9
A less frequent cause of redislocation is the occurrence of bony
lesions at the time of primary dislocation in which there is fragmenta-
tion of the anterior bony ridge or a posterior lateral defect, the so-
called compression notch of Hermodsson. 90 91 Special x-ray techniques
'

are required to see this defect. 92 The mechanism is alleged to be a

pivoting motion around a strong coracohumeral ligament that causes
compression of the posterolateral portion of the humeral head against

127
FIGURE 93. Relationship of age of patient to mechanism of anterior dislocation. Y
shows the normal relationship, in the young, of the head of the humerus (H) to the
glenoid fossa (Gl) with intact posterior tissues (pt) consisting of the supra- and infra-
spinatus tendons attached to the greater tuberosity. The capsule (c) is intact, albeit thin
and loose. The mechanism of dislocation in the young causes tear through the anterior
capsule [X arrows). O. In older people, the posterior tissues tear [X arrow), or the
greater tuberosity avulses. In this latter mechanism the head of the humerus "rolls"
over the anterior rim of the glenoid but does not tear the anterior capsule.

the sharp posterior rim of the glenoid, so that a compression defect

results (Fig. 95).
Posterior dislocation, though rare, must be recognized early; oth-
erwise, reduction becomes difficult, and postreduction complications
may result. The
posterior dislocation finds the head behind the
scapula, usually caused by trauma to the flexed, abducted arm. The
trauma is usually a blow to the front of the shoulder, causing forceful
backward movement of the head. Posterior dislocation may occur
during convulsion.

DIAGNOSIS OF DISLOCATION
In anterior dislocation, since the humeral head does not occupy its
usual position, the round appearance of the shoulder is lost. The
acromion appears to be unusually prominent because of the hollow
space beneath, caused by the absence of the humerus. All movements
are limited and painful. Because the head is "locked" in a medial

128
DISLOCATION BY
HYPERABDUCTION

$/? *k TU

Figure 94. Mechanism of dislocation: "hyperextension theory." Abduction with the

humerus in internal rotation or forward flexion with the arm in external rotation be-
comes limited by the acromial arch. Forceful elevation when this point of impingement
has been reached uses the arch as a fulcrum and dislocates the proximal head by causing
it to descend and move forward.

position, the lower end of the humerus "sticks out," and the elbow
will not reach the trunk. If the dislocation proceeds to a subglenoid
position, the arm may be locked in full abducted position (luxatio
erecta ).
arm fixed in internal rotation, and any
Posterior dislocations find the
motion attempting external rotation is impossible. Regaining the neu-
tral position may be prevented. The coracoid is prominent, and fre-
quently the humerus can be palpated posteriorly under the scapular
spine. ,

X-rays of anterior dislocation are diagnostic, but routine views in

cases of posterior dislocation may reveal little or no abnormality.
Routine anteroposterior views in posterior dislocation may be
suggestive, but auxiliary and tangential views are necessary to confirm
the diagnosis.
Persistent pain following a shoulder dislocation may mean an asso-

129
 B

Figure 95. Infra-articular fracture in recurrent shoulder dislocation ("notch lesion of

Hermodsson"). A strong coracohumeral ligament acts as a pivot point that causes the
humerus to compress against the posterior rim of the glenoid and cause a compression
fracture (indenture) in the posterolateral aspect of the humerus.

ciated cuff tear, a glenoid labrum tear, or an avulsion fracture of the

may be needed for absolute diagnosis
greater tuberosity. Exploration
of cuff or glenoid labrum tears, whereas x-ray usually reveals the
tuberosity fracture.

TREATMENT
Closed reductions of uncomplicated anterior dislocations are
usually possible. Gentle traction and anesthesia may be necessary
with the patient lying prone on a table and the arm dangling. Reduc-
tion usually can be accomplished. The original Hippocratic method is
still practiced. Traction is applied to the arm along the side of the body

while the surgeon's stocking foot placed in the axilla as counter-

is

pressure. While traction is arm is brought in toward the

applied, the
body; thus the head is levered outward around the fulcrum created by
the manipulator's foot.
No discussion of closed reduction of an anterior dislocation would
be complete without mentioning Kocher's method, 93 depicted in Fig-
ure 96 and discussed in the legend. A certain skill and definite gentle-
ness are necessary in this maneuver. Frequently, reduction may be
accomplished and not realized by the surgeon. A "click," usually con-
sidered reduction, may merely be a change from one form of disloca-
tion to another, not a complete reduction. The external rotation phase

130
 \

ALL MOVEMENT /
PAINFUL

SUBCORACOID TRACTION IN EXTERNAL ROTATION 80°

DISLOCATION SLIGHT ABDUCTION --TRACTION MAINTAINED

ELBOW BROUGHT TO INTERNAL ROTATION SPLINT AND SLING

FRONT OF CHEST HAND TO OPPOSITE 3WEEKS TO PREVENT
EXTERNAL ROTATION SHOULDER EXTERNAL ROTATION
MAINTAINED

Figure 96. Kocher manipulation for closed treatment of dislocation. All movements
should be done smoothly and gently. Traction should be maintained constantly. Once
reduced, the arm is splinted for 3 weeks to prevent external rotation.

of the maneuver may tear the subscapularis or even cause a spiral

fracture of the humerus.
arm is bound to the chest wall in a sling support
After reduction, the
to prevent external rotation. During this 3-week splinting, the wrist
and fingers should he actively and frequently exercised. After 3 weeks
the splint is removed, and active exercises to strengthen adduction,
internal rotation, and abduction in the internally rotated position of
the humerus should be started, supervised, and encouraged. No active
assisted exercises and no passive stretching exercises should be done.
Isometric active exercises are very valuable here.
If an avulsion of the supraspinatus tendon or an avulsion fracture of
the greater tuberosity of the humerus exists, the arm must be splinted
to hold the humerus in an abducted, externally rotated, and forward
flexed position horizontally. This position is maintained in an airplane
splint.
Reduction of a posterior dislocation is usually done under general
anesthesia. Gentle traction, in the line of the humerus, with simul-
taneous pressure exerted from behind the head, will bring the head
into the cradle of the glenoid. External rotation of the humerus may be
necessary to reduce the dislocation. Once reduction of the arm is
accomplished, the arm is splinted in a plaster cast in external rotation

131
and a slight abduction, with the humerus (elbow) slightly behind the
midline of the trunk. In 3 weeks, active exercises are begun, with
avoidance of any passive stretching, and stress is placed on external
abduction exercises. Full range is usually achieved in 6 weeks.
Dislocations of long duration in which there are glenoid changes,
old unrecognized dislocations, cuff tears, or unreduced avulsion frac-
tures may require open reduction. The surgical techniques are be-
yond the scope of this text.
In older people who suffer an anterior dislocation (see Fig. 93), the
tear of the posterior structures prolongs the convalescence, and a de-
gree of stiffness, pain and disability is the rule. The treatment of older
patients, therefore, differs from that of younger people in that, with
redislocation being rare but stiffness and pain being frequent, pro-
longed immobilization must be avoided, so usually within 10 days
pendular exercises are begun. Surgical intervention for recurrent an-
terior dislocation attempts any procedure that will buttress the ante-
rior capsule of the joint or will prevent external rotation. In posterior
dislocation transplant of the subscapularis may be necessary.
Open reduction of avulsion fractures of the greater tuberosity is
indicated when closed reduction has left a fragment displacement of 1
cm or more. Screw fixation of the fragment is necessary. A lesser
displacement with intact periosteum will heal after approximation by
closed reduction.
The complications of dislocation, other than tear, of the supra-
spinatus tendon and avulsion fracture of the greater tuberosity include
nerve and blood vessel injury. Nerve injuries to the brachial plexus
usually involve the posterior cord (radial, axillary, subscapular, and
thoracodorsal nerves); thus, since the muscles innervated are the del-
toid (axillary nerve), triceps (radial nerve), latissimus dorsi
(thoracodorsal nerve), and the teres major (subscapular nerve), there
is weakness of the extensors and elevators, and internal rotation of the

arm (Fig. 97). Whereas nerve lesions are rare in fractures of the upper
end of the humerus, they are frequent in dislocation. The axillary
nerve can be damaged as it circles around the surgical neck of the
humerus and thus cause paresis or paralysis of the deltoid muscle. 40
The axillary blood vessels may be injured, with the hand becoming
— —
blue, then cold and pale a pulse deficit and swelling being noted
in the axilla. Early recognition and emergency surgical intervention
are mandatory. 94

ACROMIOCLAVICULAR LESIONS
The acromioclavicular joint as the site of pain in the shoulder is
frequently overlooked. This joint is subject to the various arthritides

132
 A.illory N.

'Circumflex K

cs c6

N. median

Figure 97. Schematic brachial plexus. Emphasis (shaded area) is placed on the poste-
riorcord forming the radial, axillary, and subscapular nerves, this being the cord most
often involved in shoulder separation.

(osteo-,rheumatoid, tuberculous, and traumatic), to osteochondritis,

and numerous traumata causing contusion, sprain, and separation. 95
to
This joint is relatively weak and inflexible for the constant burden
and repeated stresses it bears. Heavy laborers who lift objects over-
head or carry weights on their shoulders and participants in competi-
tive contact sports have frequent stress applied to the acromion or the
acromioclavicular joint. Whether the stresses to this joint are direct or
indirect, the mechanism of trauma is identical.
The mechanism of acromioclavicular joint disruption has been well
documented. 96,97 Force applied to the acromion or the glenohumeral
joint from above causes the scapula to rotate around the coracoid,
which becomes a fulcrum. The superior and inferior acromioclavic-
ular ligaments, being intrinsically weak, give way and the joint dis-
locates (Fig. 98). A downward force of greater intensity lowers the
clavicle upon the first rib, and the rib becomes the fulcrum. The
coracoclavicular and the coracoacromial ligaments tear (see Figs. 2
and 30), causing a complete acromioclavicular separation. Sufficient
force can fracture the clavicle.
Incomplete subluxations may tear the intra-articular meniscus (see
Fig. 29) and lead to degenerative, painful arthritis of the acromio-
clavicular joint. Muscular action upon the joint enhances the dislocat-
ing forces that cause acromioclavicular dislocation. The upper
trapezius muscle fibers elevate the clavicle, while the deltoid muscle,
supplementing the gravity effect of the weight of the arm, pulls down
upon the acromion (see Fig. 33).

133
Figure 98. Mechanism of acromioclavicular separation. A. The normal relationship of
the clavicle to the scapula with intact coracoclavicular and coracoacromial ligaments. B.
The rotation of the scapula with the coracoid (c) acting as a fulcrum under the clavicle.
Trauma (T) is from above. Contact of coracoid is at arrows cc. C. Further force
to clavicle
from T causes the clavicle to descend further and impinge upon the first rib at point cr,
causing the ligaments to tear and complete separation of the acromioclavicular joint
(Ac).

Trauma may occur from the opposite direction. A fall upon the
stress upward along the shaft of the humerus and
elbow transmits the
rotates the scapula in the opposite direction, causing elevation of the
acromion at the clavicular end. The ligaments from the coracoid proc-
ess to the clavicle remain intact, but the acromioclavicular ligaments
can tear. The meniscus can also be ruptured by this stress action.

DIAGNOSIS
Degenerative arthritis occurring from trauma to the acromiocla-
vicular joint causes pain over the shoulder region. There is little or
no radiation of pain into the arm. 98 Tenderness over the acromiocla-
vicular jointis usual. Movement of the shoulder is pain-free until the

scapular phase of the scapulohumeral rhythm involves motion of the

scapula. Total elevation of the shoulder girdle such as "shrugging" the
shoulder causes pain. Confirmation of the acromioclavicular joint as
the source of pain may be made by abolishing the pain with a Novo-
cain injection into the joint. X-rays are difficult to interpret when a
frank acromioclavicular separation is not present.
Dislocation of the acromioclavicular joint produces a characteristic
deformity known as a "shoulder pointer." The separation permits the
scapula to fall away from the clavicle, and the acromion lies below and
in front of the clavicle. The outer end of the clavicle can frequently be
palpated in the supraspinatus region. If there is merely subluxation of
the acromioclavicular joint with injury confined to the acromiocla-
vicular ligaments and the coracoclavicular ligaments remain intact, all

134
 It

Figure 99. Immobilization of acromioclavicular separation: strapping. A. The anterior

view in which a circular sling presses down on the clavicle and elevates the arm. A pad
protects the clavicle (cp) and the elbow (ep). The wrist is held by a simple sling around
the neck (si). B. The lateral view shows the direction of pull from the circular strap:
down upon the clavicle (d), and elevation of the arm (u). If there is no sling, the weight
of the arm pulls the acromial fragment down, and the muscles elevate the clavicle, thus
separating the acromioclavicular joint. The pads protect the nerves in the shoulder and
elbow regions.

135
that can be seen or palpated is an unduly prominent clavicle. The
outer edge of the clavicle "steps" down to the acromion. X-rays
suggest subluxation" when the acromial and clavicular edges are in-
congruous in their relationship. X-rays taken of the shoulders with the
patient in the upright position, holding weights in both hands, can
reveal acromioclavicular separation.

TREATMENT
Simple strapping and comfort slings for 10 days usually suffice in a
mild injury. "Simple strapping," however, must be carefully done. 100
The limb is encircled by a strap that elevates the elbow below and
depresses the clavicle above. A pad is placed in the axilla. The hand is
suspended in a sling from the neck. Pads are placed at the elbow and
at the clavicle before strapping to protect against nerve and bony
pressure. Immobilization for 3 weeks is indicated if there is subluxa-
tion, and 6 weeks if there is complete dislocation (Fig. 99). Reduction
and immobilization for the subluxation can be done with a plaster
101
cast.
The treatment of complete dislocation of the clavicle with rupture of
the coracoclavicular ligament remains a controversial matter. The
present concept favors surgical removal of the distal end of the clavi-
cle and resuture of the ruptured coracoclavicular ligament. 102 This
procedure is advocated because most methods of internal fixation of
the two opposing articular surfaces (by wire, tendon, or screw) fail to
secure a sturdy, pain-free, and moveable joint. The advocates of re-
section further support their concepts by considering the clavicle to
be an "unnecessary" bone. 103

136
CHAPTER 8

Biceps Tendinitis and Tear

The kinetics of the biceps was discussed in Chapter 1 and dia-

grammed in Figure 35. The tendon of the long head of the biceps lies
in the bicipital groove of the humerus and at the upper end of the
groove angles inward thus crossing over the head of the hu-
at 90°,
merus upper edge of the glenoid fossa. As shown in
to insert at the
Figure 9, it penetrates the cuff in an opening between the supra-
spinatus tendon and the subscapulars tendons of the cuff. It is invagi-
nated by a downward sleeve of the synovial capsule as it passes under
the transverse humeral ligament (see Fig. 5). This ligament holds it
within the bicipital groove, and as the tendon passes over the humeral
head, it is intra-articular, but extrasynovial.
The relationship of the biceps tendon to the head of the humerus
and to the cuff insertion causes it to undergo degenerative changes in
association with cuff degeneration. It shares all associated inflamma-
tory dysfunctions of the tissues within the suprahumeral joint.
The biceps tendon does not move within the unmoving humerus.
Movement of the tendon is relative to the bicipital groove as the
groove moves under the tendon (Fig. 35). The greatest displacement
of the humerus against the biceps tendon is with the arm internally
rotated and elevated in a forward flexed position. In this motion the
bicipital groove slides along the tendon toward the insertion on the
glenoid; therefore the tendon descends in the groove. When the arm is
abducted and flexed backward, the opposite movement occurs, but
with a lesser amplitude.
The biceps has no vector force to abduct or elevate the humerus
from the dependent position. Only when the arm is externally rotated,
which places the biceps muscle and tendon in a straight line, can its
muscular action have abducting force. This is a "trick" maneuver
learned by patients with paralyzed deltoid muscles and has no effec-
tive force.

137
 PATHOLOGY
The tendon of the long head of the biceps undergoes the same
changes noted in the cuff tendons. Calcification is rarer in
attritional
this tendon than in the cuff tendons. Rupture, however, is as common.
The direct attachment of the short head of the biceps into the coracoid
process makes rupture less frequent. The peculiar angulation and
stress points of the long head make rupture here also more frequent
than tearing of the insertion upon the bicipital tuberosity of the
radius. 104
The biceps tendon may subluxate or dislocate from the bicipital
groove. A cuff tear, capsular tear, and tearing of the transverse bicipital
ligament must occur to permit dislocation of the biceps tendon (Fig.
100).
Tenosynovitis of the biceps tendon occurs but is rare and probably
occurs with concurrent inflammation of the surrounding cuff struc-
tures.

DIAGNOSIS
Pain in the glenohumeral joint region with slight limitation of mo-
tion has usually been noted for months or years, indicating degen-
erative changes in the cuff region. The tendon tears as a painful
"snap," followed by swelling and ecchymosis in the region of the
bicipital groove below the deltoid muscle. This is followed by the
characteristic bulging of the biceps muscle near the antecubital fossa
at the lower half of the humerus. There is also a "hollow" where the
upper belly of the biceps was. Flexion and supination of the forearm,
especially against resistance, increases the bulging at the lower third
of the upper arm. Power of forearm supination is decreased, but elbow
flexion remains strong because of the remaining short head of the
biceps, the brachialis muscle, and the forearm flexors.
If the "snap" is caused by subluxation of the tendon from the bicip-
ital groove rather than tendon tear, there must be an associated cap-

sular tear. In subluxation of the tendon, there is tenderness over the

bicipital groove area; the tendon can be snapped by forward flexing
and abducting the arm, then returning it to the dependent neutral
position. Pain radiates down the biceps belly in both avulsion or sub-
luxation of the biceps tendon.
A clinical Yergason's sign, 105
sign diagnostic of bicipital tendinitis is

in which pain and tenderness over the bicipital groove is felt when the
elbow is flexed and the forearm supinated against resistance or when
the elbow is extended, the arm carried backward, and the forearm

138
Figure 100. Biceps tendon The tendon most frequently tears in its superior por-
tear.
tion within the bicipital groove region. The muscle belly bulges in the lower aspect of
the humerus. The clinical appearance is shown in the right arm as viewed from the front
and the side.

supinated. These signs are of value principally when there is no

rupture causing the characteristic "bulging."

TREATMENT
Surgical repair is important only for cosmetic reasons or when
forceful supination of the forearm is necessary for the patient's occu-

pation. If repairis indicated, suturing the end of the tendon to the

lower portion of the bicipital groove will improve appearance and

supination strength. If merely improvement of strength is needed, the
end of the tendon can be carried to and attached to the coracoid proc-
ess.
Disability from a tear of the biceps tendon is usually minimal. After
surgical repair, total disability exists for approximately 8 weeks.

139
CHAPTER 9

The Shoulder
in Hemiplegia
The patient who becomes afflicted with a hemiplegia ("stroke")
frequently has involvement of the shoulder that causes disability and
frequently causes pain.
Return of function or at least improvement in function of the shoul-
der is important for resumption of hand function, activities of daily
living, safe balance, transfer activities, and effective ambulation. Se-
vere pain in the shoulder may pose a considerable obstacle to suc-
cessful rehabilitation.
There are numerous factors that influence the adequate return of
meaningful function of the upper extremity after a stroke:

1. natural evolutional sequence of recovery;

2. spasticity;
3. development of primitive reflex synergy patterns;
4. apraxia;
5. articular contracture;
6. peripheral sensory deficit;
7. perceptual involvement;
8. intellectual impairment.

Any or all of these factors may be involved in residual impairment and

pain.
In patients who suffer hemiplegia the upper extremity usually
undergoes various stages in the natural sequence of the involvement.
Initially the extremity becomes flail. This may be momentary or per-
sistent with varying decreases of severity or duration.
During the flail stage subluxation may occur that adds to the re-
sidual disability, contributes to pain, and impairs restoration of func-
tion. There are numerous concepts of the causation of subluxation,

140
Figure 101. Mechanism of glenohumeral subluxation. The diagram at left depicts the
change of glenoid angle X-B when the scapula is rotated. The humerus becomes ab-
ducted (B) and subluxes downward. The right diagram shows "seating" of the head of
the humerus supported by cuffX-Y, when the glenoid angle is physiologic X-A. When
the scapula rotates, the angle becomes vertical X-B, and the cuff no longer "seats" the
head X-Y 2 The humerus subluxes downward.
.

and attempts at prevention or correction are dependent upon the con-

cept accepted.
The glenohumeral joint maintains its stability by:

1. The angulation of the glenoid fossa, which is dependent upon

the position of the scapula on the costal wall.
2. The tone of the supraspinatus muscle within the cuff.
3. The ability of the cuff muscles to contract reflexly upon any
abduction of the humerus.
4. The isometric and intermittent isotonic contraction of the del-
toid.
5. Possibly the integrity of the superior aspect of the glenohumeral
capsule.

If any of the above are impaired, the glenohumeral joint may sublux
(Fig. 101).
The change in the angulation of the scapula that alters the normal
angle of the glenoid fossa can result from temporary or residual paresis
(flaccidity) of the scapular muscles (Fig. 102). Upon cessation of the
flaccid stage the onset of spasticity can cause the scapula to rotate
downward and forward (Fig. 103).

141
 X
'
\

gj
13
»3
p
m
IS
&*

Figure 102. Scapular depression. A. Scapular alignment with a straight spine (X-Y
glenoid angle). B. Paresis with downward rotation of the scapula (A-B glenoid angle). C.
Relative downward rotation of the scapula with functional scoliosis (C-D glenoid
angle).

Figure 103. Spastic medial scapular

muscles. In spasm of the rhomboid mus-
cles that normally rotate the scapula, the
glenoid fossa alignment is lowered and the
angulation made vertical.

142
Figure 104. Shoulder slings. These slings are designed to support the arm and mini-
mize downward subluxation of the glenohumeral joint. They have not been proven to
prevent subluxation and hold the arm in a flexed position.

During the flaccid stage the arm must initially be protected from
excessive capsular and cuff stretch caused by the weight of the de-
pendent arm. This is accomplished by means of a sling. The "ideal"
sling has yet to be designed or universally accepted. Several types
currently used are depicted in Figures 104 through 107.
The corrections required of a splint are:

1. Elevation of the scapula.

2. Seating of the head of the humerus into the glenoid fossa.
3. Elevation support of the humerus.
4. Substitution of the supraspinatus cuff function.

All splints attempt these corrections but fail to do so in part.

The vast majority of "stroke" patients progress into the spastic stage
with or without complete development of the flexor synergy (Fig.
108). In this synergy pattern the shoulder remains depressed but as-
sumes an internally rotated, posteriorly flexed position. The remain-
der of the arm distally has the arm adducted, the elbow flexed, the
forearm pronated, and the wrist and fingers flexed. Any or all of these
pattern components may be present, but any deviation may occur.
The patient now has resistance to any passive motion and markedly
limited active motion in the direction opposed to that of the synergy.
Attempting abduction external rotation and elevation of the shoulder
may be notably unsuccessful. This attempted motion may also be
painful.
Treatment is essentially that of the neurologic sequelae of the
"stroke" by one of numerous techniques (e.g., Bobath, P.N.F., Rood).

143
FIGURE 105. Rood sling. The use of elastic tubing gives kinetic support (A) and stimu-
latesextension of the arm. By proper application, the forearm is supinated (B). The
hand is held in a cone (C) that spreads the fingers and thumb while radially deviating
the wrist. The scapula is elevated and derotated (D).

Figure 106. Proposed design for prevention of subluxation. A. The glenohumeral joint
is elevated to the desired physiologic angulation. B. The head of the humerus is
adducted into the "seated" position. C. The humerus is elevated into the suprahumeral
fossa. D. The cuff is replaced by the splint. £. The sling attaches to the humerus at the
site of deltoid insertion and elevates the humerus into the suprahumeral joint space.

During the flaccid stage techniques to initiate muscular contraction

and return of tonus are indicated. If there is sensory deficit the
problem is accentuated. Sensory stimulation is attempted by icing,
brushing, tapping, rubbing, or even pinching. Any sensory input will
conceivably initiate a reflex motor response that ultimately may be

144
Figure 107. Wheel chair arm sling. A holds the shoulder forward, flexed, and
adducted. B supports the elbow in an extended position. C and D keep the wrist and
fingers extended. E permits movement of the entire arm.

trained to be under voluntary control. Use of gravity also may initiate

motor response. All these techniques must be utilized with full reali-
zation that subluxation must be avoided or minimized. They must be
used with alternating sling support and with proper positioning when
the patient is inactive.
Contracture of the joint(s) is not to be feared during the flaccid stage
but may occur with the onset of spasticity. Daily observation and
examination of the arm will reveal the onset of spasticity early in the
development of the "stroke."
During the phase of flaccidity electrical stimulation of the paretic
muscles has value in maintaining muscle fiber integrity as well as
being a sensory stimulus. Biofeedback is currently being developed
and evaluated in muscle reeducation.
Once spasticity develops the shoulder requires constant position-
ing. This is to minimize the development of the synergy pattern. The
arm must therefore have:

145
 DEPRESSED

^PROTRACTED

DUCTED
INTERNALLY
ROTATED

XED

Figure 108. Flexor synergy of the upper extremity.

1. The humerus elevated into the glenoid fossa.

2. The shoulder placed in slight abduction, forward flexion, and
external rotation.
3. The elbow extended and supinated.
4. The wrist, fingers, and thumb extended, abducted, and supinated.

There are numerous treatment techniques, both in terms of physical

and occupational therapy, that have value in treating the spastic stage
and initiate neuromuscular reeducation. Specific discussion and
evaluation of these numerous techniques are beyond the intent of this
text, but some generalizations are warranted.
Of the many modalities ice has proven to give beneficial support in
reducing spasticity, especially the prolonged use of ice applied to the
spastic muscle. 23 Pattern exercises have been advocated by Knott and
Voss, 106 reflex inhibition by Bobath, 107 and numerous other techniques
have been promoted, all based upon neurophysiologic concepts.
The predominant pattern that defies amelioration is the persistence
of adduction and internal rotation. The opposing patterns of abduction
and external rotation of the arm and shoulder not only have weakness
as well as inability of initiation, but are restricted by the opposing
spasticity of the adductors and internal rotators. Ultimately contrac-
ture of the shoulder develops, and passive range of motion is re-
stricted as well as active motion. Pain results.

146
 Hemiplegic pain can be best treated as pain in the shoulder is
treated. These pain-relieving procedures include suprahumeral in-
jection of steroids and anesthesia, intra-articular injections of
anesthetic agents with or without steroids, suprascapular nerve
blocks, and various oral medications. In the spastic shoulder, how-
ever, nerve blocks to decrease spasticity have value.
Phenol in diluted solutions, injected into the motor nerves of the
spastic muscles or into the motor end plates of the spastic muscles, has
many advocates. 108-111
Depending upon the severity of the spasticity, the use of the tonic
neck reflexes is valuable, as is the use of gravity. These have been
well documented in the literature. 112
The shoulder-hand-finger syndrome occurs occasionally in the
hemiplegic patient and has characteristics identical to those discussed
in Chapter 6.

147
CHAPTER 10

Visceral Referred Pain

Pain in the region of the shoulder can have its site of origin in a
viscus, with the shoulder or scapula as the referred site. To be un-
aware of this and attribute all pain in the shoulder girdle region to a
faulty scapulothoracohumeral mechanism is to miss a potentially seri-
ous medical or surgical diagnosis.
Visceral reflex and referred pain to the shoulder region has been
widely discussed, although the exact neural mechanism remains
speculative. A diseased viscus can refer pain to a remote part of the
body: conditions of the diaphragm can cause pain in the neck and
shoulder; gallbladder disease can radiate to the shoulder "tip" gastric;

disease can refer between the shoulder blades; and angina pectoris or
myocardial infarction can be felt in the shoulder, neck, and arm.
A given spinal segment supplies autonomic nerve fibers to a spe-
cific viscus, and that same nerve supplies a specific skin area (der-
matome). As the viscera become diseased, they set up afferent au-
tonomic impulses to the cord that travel (in the cord) to the thalamic
center. From the thalamic center the sensation travels to (and is felt in)
a somatic (referred) area. 113 These have been described as viscerosen-
sory reflexes. Head 114 mapped out the sensory areas of these cutane-
ous nerves.
The diaphragm the most frequent source of extrinsic disease re-
is

ferring pain to the shoulder region. Pain is referred through the

phrenic nerve, the afferent fibers of which originate usually in the

third and fourth cervical segments (constantly from the C 4 segment
and variably from C 3 and C 5 ). 40 The phrenic nerve has many sites of
possible irritation as descends vertically in front of the anterior
it

scalene muscle through the superior thoracic outlet within the

mediastinum, along the pericardium, to finally innervate the superior
and inferior surfaces of the central diaphragm. Irritation of the dia-

148
 ^7^

Figure 109. Visceral sources of "shoulder" pain. The word "shoulder" is used
vaguely in referred pain from visceral sites. Pain that originates in the shoulder is
localized directly over the glenohumeral area (S). Irritation of the diaphragm (D) causes
referred pain in the trapezius area. Myocardial origin (H and A) refers pain to the axilla
and left pectoral region. Gallbladder irritation (GB) refers pain to the tip of the shoulder
and posteriorly in the scapular region.

phragm refers pain to the supraclavicular region, the trapezius, and

the superior angle of the scapula. 115
Pulmonary infarction, which involves the diaphragmatic surface of
the lung, may cause shoulder pain. 116 Myocardial ischemia via the
cardia plexus through the upper four thoracic spinal segments causes
referred pain in the infraclavicular and ulnar region. This referred
pain usually left-sided. Involvement of the aortic arch refers to the
is

right side of the neck, whereas the transverse and descending aortic
arch refers to the left side of the neck and shoulder.
A perforated abdominal viscus causing pneumoperitoneum will
frequently be revealed only by pain in the shoulder area. Gallbladder
disease and irritation of the hepatic parenchyma frequently elicit

149
scapular and shoulder pain associated with deep epigastric tender-
ness.The referred sites of pain from extrinsic sources are diagrammed
in Figure 109.

150
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109. Mroczek, N., Halpern, D., and McHugh, R.: Electromyographic retraining in
hemiplegia. Arch. Phys. Med. Rehabil. 59(6):258, 1978.
110. Stockmeyer, S.A.: An interpretation of the approach of Rood to the treatment of
neuromuscular dysfunction. Am. J. Phys. Med. 46(1):900, 1967.
111. Khalili, A. A., and Betts, H.B.: Management of Spasticity with Phenol Nerve
Blocks. RD-2529-M. U.S. Department of Health, Education and Welfare, Social
Rehabilitation Service, Washington, D.C., 1970.
112. Cailliet, R.: The Shoulder in Hemiplegia. F.A. Davis, Philadelphia, 1980.
113. Livingston, W.K.: Pain Mechanism. Macmillan, New York, 1943.
114. Head, H.: On disturbances of sensation with especial reference to the pain of
visceral disease. Brain 16: L- 133, 1893.
115. Capps, J. A., and Coleman, G.H.: Experimental and Clinical Study of Pain in
Pleura, Pericardium and Peritoneum. Macmillan, New York, 1932.
116. Lelan, J.L.: Visceral aspects of shoulder pain. Bull. Hosp. Joint Dis. 14:71-73,
1953.

155
 Index

Abduction. See Arm, abduction of. "trick" abduction and, 37

Acromial process, 4-5 Biceps tendon
Acromioclavicular joint, 2 glenohumeral capsule and, 7, 9
capsule of, 29 location of, 137
coracoclavicular ligament and, movement of, 35-37, 137
29-30 tear of
lesions of diagnosis of, 138-139
mechanism of, 133-134 pathology of, 138
susceptibility to, 132-133 treatment of, 139
treatment of, 135, 136 tenosynovitis of, 138
meniscus of, 28-29 transverse humeral ligament and,
Acromiocoracoid arch. See Coracoac- 13-14
romial arch. Brachial plexus
Adhesive capsulitis. See "Frozen Pancoast tumors and, 105
shoulder." schematic view of, 133
Adson test, 103 shoulder pain and, 94-95
Analgesics. See Musculoskeletal pain, Bursa, subdeltoid, 47-48
treatment of. Bursitis
Anterior scalene syndrome, 103, 104 as secondary phenomenon, 47-48
Arm, abduction of formation of, 45-47
active, 21 obliterative. See "Frozen shoul-
glenohumeral movement of, 18, der."
19 treatment of. See Musculoskeletal
integrated movement in, 26-27 pain, treatment of.
passive, 21
planes of, 17, 18 Calcific tendinitis. See Tendinitis,
scapular rotation and, 27-28 calcific.
"trick," 37 Capsule, glenohumeral, 6-9
Arteriosclerotic occlusion, 106-107 Capsulitis, adhesive. See "Frozen
Arthritis, degenerative, 134.See also shoulder."
Acromioclavicular joint, le- "Carpal tunnel syndrome," 95
sions of. Causalgia. See Shoulder-hand-finger
Arthrography, glenohumeral, 76-78, syndrome.
79 Cervical nerve root pressure. See
Radiculitis.
Biceps Cervical rib
mechanism of, 3, 34-37 symptoms of, 101

156
Cervical rib continued subcoracoid, 125
treatment of, 102 treatment of, 130-132
Claudication, arteriosclerotic occlu- types of, 125-126
sion and, 106-107 Dorsal scapular nerve entrapment,
Clavicle 106
rotation of, 31
scapular attachment to, 29-30 Exercises
sternal attachment to, 31 active, 67-68
Claviculocostal syndrome, 103 assistive, 67, 68
Codman (pendular) exercises, 54-56 "chin-up," 59
Compression notch of Hermodsson, classification of, 67
127-128, 130 discomfort and, 68-69
Congruous joints, 4-5 external rotation, 58
Coracoacromial arch, 3, 9-10 knee-bend, 59, 61
Coracoclavicular ligament, 29-30 overhead, 62
rupture of, 136 passive, 67-68
Coracohumeral ligament, 9, 10 pendular, 54-56
Cortisone, anesthetics and, 61, 65 post-manipulation, 72-73
Costoclavicular ligament, 31 "push-up," 58
Costosternal joint, 2 range of motion, 88-89
Costovertebral joint, 2 resistive, 67
Critical zone, 14-15, 16 rhythmic stabilization, 71, 72-73
Cuff muscles scapular mobility, 64
actions of, 10-11, 19-21 table-top, 60, 61
infraspinatus, 12 "wall-climbing," 63
subscapularis, 12-13 "wand," 59
supraspinatus, 11-12
teres minor, 12 FlBROMYOSITIS
Cuff tear diagnosis of, 99-100
arthrographic study of, 76-78, 79 manifestations of, 98
causes of, 74-75 treatment of, 100
complete, 75 Flaccidity, hemiplegic, treatment of,
treatment of, 80-81 143-145
diagnosis of, 74-76 Flexor synergy, 143, 146
incidence of, 74 Foramen of Weitbrecht, 8-9
incomplete, treatment of, 78-80 "Frozen shoulder"
sites of, 74. See also Critical zone. arthro grams of, 78
causes of, 82-84
Deltoid muscle, 15 definition of, 82
abduction action of, 21, 22, 23 diagnosis of, 84-85
function of, 17, 18 mechanism of, 84
paresis of, 76 periarthritic personality and, 69, 82
Depression, sympathetic pain and, treatment of
122-124 drugs in, 87
Diaphragm, referred shoulder pain exercises in, 88-89
and, 148-149 ice packs in, 88
Dislocation manipulation in, 87-88
anatomic aspects of, 125 objectives of, 86
anterior, 126-127 outcome of, 85
diagnosis of, 128-130
hype rextens ion theory of, 129 Gallbladder disease, referred
mechanism of, 126-128 shoulder pain and, 149-150
posterior, 128, 129, 131-132 Gastric disease, referred shoulder
recurrence of, 126, 127 pain and, 148

157
Glenohumeral joint, 1, 3 Muscles
arthrographic study of, 76-78, 79 glenohumeral
capsule of, 6-9 deltoid. See Deltoid muscle,
ligaments of, 8 rotator cuff, 10-15
classification of, 4 scapular, 22-26
dislocations at. See Dislocation, Musculoskeletal pain
female portion of, 5 diagnosis of, 48-53
male portion of, 17 "trigger points" in, 50
movement of, 7, 8 sites of, 39
cuff muscles in, 19-21 treatment of
nature of, 17-18 exercises See Exercises,
in.
requirements of, 18-19 failure of improvement
in, 69-70
musculature of, 10-17 heat packs in, 57-58
stability of, maintenance of, 141 ice packs in, 53, 55
Glenoid fossa, 5, 6 immobilization in, 55
Glenoid labrum, 5 manipulation technique in,
°\
I 68-69, 70-71
Hemiplegia, shoulder function and nonsteroidal anti-inflammatory
factors influencing, 140 drugs in, 59-60
flaccid stage in, 143-145 opiates in, 59
flailstage in, 140-141 postacute phase in, 67
spastic stage in, 145-147 radiotherapy in, 64
subluxation and, 140-141 rhythmic stabilization technique
Hepatic parenchymal irritation, re- in, 71, 72-73

ferred shoulder pain and, steroids in

149-150 injection of, 60-65
Hermodsson, compression notch of, 60
oral,

127-128, 130 Myofibroses. See Fibromyositis.

Humerus, movement of, 17-21
Hyperabduction syndrome. See Pec- Nerve, cervical, component fibers of,
toralis minor syndrome. 90,91
Nerve block
stellate ganglion,120-121
Incongruous joints, 4-5
suprascapular, 57, 64-65
Infraspinatus muscle, 12
Nerve entrapment
dorsal scapular, 106
Joints
suprascapular, 106
congruous, 4-5
Neurokinin, causalgia and, 119
incongruous, 4-5
Neurologic referred pain
shoulder girdle, articulation of, 1-4.
anterior scalene syndrome and, 103
See also specific joint.
arteriosclerotic occlusion and,
106-107
KOCHER method for dislocation, 130, brachial plexus and, 94-95
131 cervical rib and, 101-102
claviculocostal syndrome and, 103
LATISSIMUS dorsi muscle, 26 dorsal scapular nerve entrapment
Levator scapula muscle, 24-25 and, 106
Ligaments fibromyositis and, 98-100
coracoclavicular, 29-30 pectoralis minor syndrome and, 104
coracohumeral, 9, 10 pulmonary sulcus tumors and, 105
costoclavicular, 31 radiculitis and, 90-93
glenohumeral, 8 scapulocostal syndrome and, 95-
transverse humeral, 13-14 100

158
Neurologic referred pain continued also Shoulder-hand-finger
spinal cord tumor and, 93-94 syndrome,
suprascapular nerve entrapment causes of, 110
and, 106 classification of, 109
Notch of Hermodsson, 127-128, 130 psychiatric aspects of, 122-124
Novocain, injectable steroids and, signs and symptoms of, 116-117
61-65 Rheumatism, psychogenic. See Fi-
bromyositis.
OBLITERATIVE bursitis. See "Frozen
Rhomboid major muscle, 25
shoulder."
Rhomboid minor muscle, 25
Occlusion, arteriosclerotic, 106-107 Rhythmic stabilization technique, 71,
72-73
Osteofibrous case, 84
Rood sling, 144
Rotator cuff. See Cuff muscles; Cuff
Pain tear.
causes of, outline of, 40-41
musculoskeletal. See Musculo-
skeletal pain, SCALENE anticus syndrome. See An-
neurologic referred. See Neurologic terior scalenesyndrome.
referred pain, Scalene anticus test. See Adson test.
sympathetic referred. See Sympa- Scapula, 4, 6
thetic referred pain, depression of, 141, 142
traumatic. See Acromioclavicular movement of, 22-26
joint, lesions of; Dislocation,
rotation in, 27-28
visceral referred. See Visceral re-
Scapulocostal joint, 2
ferred pain.
Scapulocostal syndrome
Pancoast apical pulmonary tumor, 105 cause of, 95
Pectoralis major muscle, 25-26 diagnosis of, 100
Pectoralis minor syndrome, 104
fibromyositis and, 98-100
Pendular exercises, 54-56 prevertebral fascia and, 97
Periarthritic personality, 69, 82, 122
symptoms associated with, 95-97
Periarthritis. See "Frozen shoulder."
treatment of, 100
Pericapsulitis. See "Frozen shoul- Scapulohumeral joint. See Gleno-
der." humeral joint.
Postural fatigue. See Scapulocostal
Scapulohumeral rhythm
syndrome. characteristics of, 26-27
Prevertebral fascia, 97 definition of, 1
Procaine, injectable steroids and, of, 27
designation
62-63 humeral phase of. See Glenohu-
Pulmonary infarction, referred shoul- meral joint, movement of.
der pain and, 149 scapular phase of. See Scapula,
Pulmonary sulcus tumors, 105 movement of.
Serratus anterior muscle, 23-24
Radiculitis Short rotators. See Cuff muscles.
characteristics of, 90-91 Shoulder, "frozen." See "Frozen
diagnosis of, 91-93 shoulder."
Referred pain "Shoulder blade." See Scapula.
neurologic. See Neurologic referred Shoulder girdle
pain. component joints of, 1-4. See also
sympathetic. See Sympathetic re- specific joint.
ferred pain. composite movements of, 32-34.
visceral. See Visceral referred pain. See also Scapulohumeral
Reflex sympathetic dystrophy. See rhythm.

159
Shoulder-hand-finger syndrome management of, 119-122
causes of, 108-110 pathophysiologic mechanisms of,
diagnosis of 110-113
initial manifestations in, 113-115 psychiatric aspects of, 122-124
stages in, 117-119 upper extremity circulation and,
sympathetic nervous system in- 108-109
volvement in, 115-116 Synergy, flexor, 143, 146
evolution of, 111, 115 Synovial capsule, glenohumeral, 6-9
pathophysiology of, 110-113
psychiatric aspects of, 122-124 Tendinitis
reflex sympathetic dystrophy and, abduction and, 39, 42
109, 115-117 aging and, 42
treatment of bicipital,137-139
physical therapeutic techniques calcific,43-45
in, 121-122 causes of, 38-39
stellate ganglion block in, 120- diagnosis of, 48-53
121 treatment of. See Musculoskeletal
Shoulder joint. See Glenohumeral pain, treatment of.
joint. Teres minor muscle, 12
Slings, types of, 143, 144, 145 Transverse humeral ligament, 13-14
Spasticity, hemiplegic, treatment of, Trapezius muscle
145-147 lower, 23
Spinal cord tumor, 93-94 upper, 22
Stellate ganglion nerve block, 120- Traumatic pain. See Acromioclavicu-
121 lar joint, lesions of; Disloca-
Sternoclavicular joint, 2, 31-32 tion.
"Stiff shoulder." See "Frozen shoul- "Trigger points"
der." pain diagnosis and, 50
"Stroke," shoulder function and. See postural fatigue and, 97, 98, 99
Hemiplegia, shoulder func- Tumors
tion and. pulmonary sulcus, 105
Subluxation spinal cord, 93-94
hemiplegia and, 140-141
sling to prevent, 144 VISCERAL referred pain
Subscapularis muscle, 12-13 abdominal perforated viscus and,
Superior pulmonary sulcus tumors, 149
105 diaphragm and, 148-149
Suprahumeral joint, 2-3 gallbladder disease and, 149-150
components of, 10 gastric disease and, 148
nature of, 9 hepatic parenchymal irritation and,
Suprascapular nerve block, 57, 64-65 149-150
Suprascapular nerve entrapment, 106 pulmonary infarction and, 149
Supraspinatus muscle, 11-12 sources of, diagram of, 149
function of, 19-20
Sympathetic referred pain WEITBRECHT, foramen of, 8-9
causes of, 108-110 Wheel chair arm sling, 145
diagnostic considerations in, 113-
119 Yergasons sign, 138-139

160
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about this series . . .

Dr. Cailliet's delightful books have been helpful to

doctors all over the world, providing common-sense
guides for diagnosis and treatment of painful or
disabling conditions in various parts of the body.
One of the outstanding features of these books is

the concise and detailed descriptions of the struc-

ture and functional anatomy of each region, with
excellent drawings graphically expanding the
author's lucid text.
These books have been acclaimed by reviewers
everywhere. Some comments:
"would be difficult to recommend too highly."
"delightfully informative."
and understandable."
"practical, readable,
"always a valuable and clear-cut approach" (to
treatment)

the other titles:

FOOT AND ANKLE PAIN
HAND PAIN AND IMPAIRMENT
KNEE PAIN AND DISABILITY
LOW BACK PAIN SYNDROME
NECK AND ARM PAIN
SOFT TISSUE PAIN AND DISABILITY

0-8036-1613-9