The Shoulder Girdle:
Kinesiology Review
Pamela K Levangie, PT, DSC, and Ellen Cook Humphrey, PT, MAPT,
OCS, ATC
Objectives
After reading this continuing education (CE) article and
reviewing shoulder girdle anatomy, you should be able to
meet the following objectives:
• Describe the intra-articular and capsuloligamentous
structure of the sternoclavicular, acromioclavicular, and
glenohumeral joints and the osteokinematic and
arthrokinematic movements that take place at each
joint.
• Describe the interrelationship among the
scapulothoracic, sternoclavicular, and acromioclavicular
joints, including the roles of the coracoclavicular and
costoclavicular ligaments and the muscles that act on
these joints.
• Explain the structural components and synergy of
muscles necessary to stabilize and complete a full range
of active elevation of the arm at the glenohumeral joint.
• Identify factors that may place a shoulder at increased
risk for an impingement problem.
• Explain how a given capsuloligamentous or muscular
restriction to motion of the clavicle, scapula, or
humerus can affect normal movement of the arm.
• Identify factors that may increase the risk of shoulder
girdle hypomobility in a patient who had a mastectomy
with adjuvant radiation.
Pamela K Levangie, PT, DSc, is associate professor,
Physical Therapy Program, Sacred Heart University,
Fairfield, Connecticut. Ellen Cook, PT, MAPT, OCS, ATC,
was instructor, Department of Physical Therapy and
Human Movement Sciences, Northwestern University
Medical School, Chicago, Illinois.
Introduction
In the May 2000 issue of PT, Davies and Durall discussed
rotator cuff impingement, focusing on recognizing atypical
symptoms. This month’s continuing education offering
focuses on shoulder girdle kinesiology in a case involving a
patient who has shoulder dysfunction secondary to a
bilateral mastectomy, high-dose chemotherapy, and breast
implant surgery.
Management of patients with any type of shoulder
dysfunction poses a particular challenge to clinicians,
because they must recall and apply their knowledge of
shoulder girdle kinesiology. Given the complex mobility
and stability components that support shoulder function,
knowledge of anatomy alone is insufficient to understand
the potential sources of pain and dysfunction in the
interdependent joints of the shoulder girdle, cervical spine,
and rib cage.
Through this case example, we will review the bio-
mechanics of the joints of the shoulder girdle that may be
implicated when a patient has shoulder pain and
hypomobility. We will first discuss the history and systems
review that provide a “snapshot” of the case; then, we will
review the kinesiologic considerations that contribute to
the subsequent selection of tests and measures. The initial
examination and the evaluation of examination data
follow. For the purpose of this case, the interdependent
issues of joint integrity and muscle performance for the
shoulder girdle are emphasized in the examination.
Because the primary objective of this case is to review
shoulder girdle kinesiology, we will review prognosis and
intervention only briefly. Knowledge of muscle anatomy
(attachments, innervation, and basic functions) and of joint
configurations (osteology and arthrology) is assumed.
Readers who want to review these elements are
encouraged to refer to a basic anatomy text, such as Gray’s
Anatomy1 or Clinically Oriented Anatomy.2
Examination
History
JD is a 50-year-old woman who has been referred to a
physical therapist by her primary care physician for
management of right shoulder pain. She is a high school
science teacher. Married with two adult children, she lives
in and cares for her own two-story home, commutes to
work 1 hour by car, and walks 2 miles each day.
JD reports intermittent right antero-superior shoulder pain
that began 5 months ago, apparently in connection with
breast implant reconstruction. Symptoms were exacerbated
recently (with no identifiable precipitating factor), leading
her to seek medical attention.
JD describes her pain as dull and aching, with an
occasional sharp twinge aggravated by lifting and reaching
above shoulder level (7/10 on a verbal pain scale [VPS]).
She is independent in activities of daily living (ADL), but
she reports fatigue and pain (5/10 on a VPS) with blow-
drying her hair, household cleaning, or spending any
amount of time at the blackboard at school, and she
reports an inability to fasten her bra behind her back.
Symptoms are relieved to 2/10 on a VPS with rest,
ibuprofen, and ice. JD reports that she is unable to sleep
on her right side because of pain. She is right-hand
dominant.
Prior to the fall of 1997, JD indicated that she was active
and in good health, with only occasional bouts of low back
pain. In the fall of 1997, she had a stage III malignancy
removed from her right breast. Two weeks later, she
underwent a bilateral mastectomy, with prophylactic
removal of the left breast. She opted for implant
reconstruction at the time of her surgery. The left tissue
expander was put into place, but the right tissue expander
was withheld because the lymph nodes were positive for
cancer, indicating a need for adjuvant radiation.
JD received 4 months of high-dose chemotherapy, which
was completed in March 1998. Treatment concluded in
June 1998 after 6 weeks of routine radiation to the right
chest wall and axilla. In October, JD had a tissue expander
inserted for stage I reconstruction of the right breast
mound.
Despite slow tissue expansion over 6 months, the
postradiation fibrotic tissue changes resulted in the
extrusion of the expander through the healed incision. The
expander was removed, and a saline implant was inserted.
After 3 weeks, the sutures were removed, and the incision
reopened 12 hours later. The implant was removed.
Incision healing from the last surgery was compromised,
and complete wound closure took 3 months, with one
wound infection that was treated successfully.
JD reports that a recent set of bone and computed
tomography scans was negative for metastatic disease. She
is currently taking tamoxifen.
Systems Review
The physical therapist performs a systems review as part of
the examination process before determining the complete
battery of tests and measures that will be used to examine
JD.
Cardiovascular/pulmonary system. No impairments
were noted in the cardio-vascular/pulmonary system.
Integumentary system. The physical therapist notes that
the right anterior chest wall incision is 3 inches long,
puckered, and extends diagonally into the axilla. There is a
pronounced anterior axillary fold. The skin over and
around the surgical scar appears to adhere to the
underlying tissue and bone, and the ribs beneath the scar
appear to be depressed relative to the surrounding ribs.
The scar and surrounding tissue are completely immobile
2
and appear to adhere to the thorax. Limited skin mobility
extends into the axilla. The left chest wall shows a well-
healed 4-inch horizontal scar over the implanted breast
mound.
Musculoskeletal system. The physical therapist observes
that the right scapula is protracted and tipped forward and
that the right arm is slightly medially rotated. There is a
moderate increase in the cervico-thoracic kyphosis, and the
cervical spine is in mild lateral flexion to the right and
rotation on the left. There is a mildly increased lumbar
lordosis.
JD has pain and hypomobility of the right shoulder girdle.
She reports discomfort (4/10 on a VPS) with active
shoulder abduction. Horizontal adduction do not increase
discomfort; however, JD reports a “pulling” sensation at
the anterior chest wall. JD does not perceive
hyperextension as painful, but it exacerbates the pulling
sensation. JD is able to just reach the back of her head on
the right (2/10 on a VPS) and is able to put her right hand
in the small of her back, but she cannot lift her hand off
her back in that position without pain. Range of motion
(ROM) on the left appears to be adequate for JD’s usual
activities.
With JD in a standing position as she performs the
motions, the physical therapist uses visual observation to
estimate active ROM for the shoulder girdle as 135 degrees
of flexion, 70 degrees of abduction, and 30 degrees of
extension. At JD’s maximal active shoulder abduction,
horizontal adduction is estimated to be 110 degrees, and
horizontal abduction is estimated to be 10 degrees from
the frontal plane.
Neuromuscular system. No impairments were noted in
the neuromuscular system.
With this picture of JD in mind, we will now review the
joint structures of the shoulder girdle that may be
associated with JD’s pain and limited ROM.
Kinesiology: The Shoulder Girdle
The function of the shoulder girdle is to move the long
lever of the upper extremity though a large frame of space
for the placement of the hand. Concomitantly, the
shoulder girdle must provide a stable base from which
hand function can be performed. The structurally
contradictory mobility and stability demands on the
shoulder are met by distributing motion through a set of
open- and closed-chain linkages that contribute in different
ways to the dynamic stability requirements. Interference
with the active or passive components of any one of the
bony interfaces can, and commonly does, change the
dynamic at one or more of the other interfaces. Closer
examination of the functional demands of the linkages is
necessary to understand the possible sources of pain and
hypomobility experienced by JD.
Scapulothoracic joint. Clinicians must know the
components that contribute to scapulothoracic (ST)
position and motion in order to understand how the
glenoid fossa moves to receive the rotating humeral head
and how the scapula adjusts to maintain the proper length
tension in the muscles that move the humerus. The ST
joint is a “functional” joint and does not have the fibrous,
cartilaginous, or capsular connections that characterize
anatomic joints. The scapula is attached to the thorax
anatomically by the articulation between the acromion of
the scapula and the lateral end of the clavicle and by the
articulation between the clavicle and the manubrium of the
sternum. Consequently, the functional ST joint forms a
closed chain with the acromioclavicular (AC) and
sternoclavicular joints (SC), and the motion of the scapula
on the thorax depends on the other two articulations.
The scapula normally sits on the thorax between the
second and seventh ribs, with the medial border
approximately 2 inches from the midline.3 Given the
curvature of the thorax, the scapula typically does not lie in
the frontal plane but rests 30 to 40 degrees anterior to the
frontal plane (medially rotated or winged) and tipped 8 to
20 degrees anteriorly from vertical.4 The ST joint is
capable of the interdependent motions of superior
translation (elevation), inferior translation (depression),
protraction and retraction, and upward and downward
rotation. These motions cannot occur, however, unless
there is adequate integrity of the AC and SC joints.
Together, the ST, AC, and SC joints normally contribute
60 degrees to the elevation of the arm. For our purposes,
elevation is defined as movement of the upper extremity
from the side anywhere between the frontal and sagittal
planes. The ST joint contributes to elevation by upwardly
rotating the glenoid fossa (upward rotation of the scapula).
There is a consensus that the trapezius and serratus
anterior muscles each make important contributions to
producing the upward rotation of the scapula that is
required for elevation (both flexion and abduction) of the
arm; however, there is some disagreement about relative
contributions and sequencing.4-7 These muscles are
particularly important because there are no other muscles
capable of upwardly rotating the scapula and, therefore, no
possibilities for substitution.
Acromioclavicular joint. The acromion of the scapula is
joined to the lateral clavicle at the AC joint. The AC joint
is essentially a plane joint, with variablity among
individuals as to which surface is concave and which is
convex.1 The angle of inclination of the articulating
surfaces also varies considerably from person to person.8
3
The angle of inclination of the articulating surfaces varies
considerably from person to person.8 There also may be a
fibrocartilaginous disk, depending on the individual’s age
and the degree of degeneration in the joint.9 The joint is
supported by a relatively weak capsule and stronger
superior and inferior ligaments that are reinforced
superiorly by aponeurotic fibers of the trapezius and
deltoid muscles.9,10 The coracoclavicular ligament is
composed of two bands (the conoid and trapezoid) that
firmly join the coracoid process of the scapula to the
clavicle, thus maintaining a relatively fixed relationship
between the scapula and the clavicle and enhancing the
stability of the AC joint. The coracoclavicular ligament
plays a critical role in the interdependence of the ST, AC,
and SC joints.
The AC joint would appear to allow 3 degrees of freedom
for the scapula. The first 2 degrees of freedom are not
often appreciated as part of normal function but are key to
keeping the scapula against the rib cage as the scapula
moves around the medial-lateral and superior-inferior
convexity of the thorax.10,11 Terminology for these
motions is used inconsistently in the literature. For the
purposes of this article, the first degree of freedom is
described as medial/lateral rotation of the scapula (motion
of the glenoid fossa around a vertical axis through the AC
joint). Medial rotation at the AC joint allows the scapula to
round the substantial medial-lateral curvature of the rib
cage during scapular protraction. As a result of the medial
rotation of the scapula, the glenoid fossa faces anteriorly
rather than laterally during flexion of the arm and remains
behind the flexed humeral head.
The second degree of freedom at the AC joint is the
anterior and posterior tipping of the superior scapula
(motion around a side-to-side axis through the AC joint).
The third degree of freedom for the AC joint is the
traditionally described scapular motion of upward and
downward rotation, which appears to occur around an
anteroposterior axis at the AC joint. Under normal
conditions, however, little if any upward rotation actually
occurs at the AC joint. True upward rotation at the AC
joint requires that the coracoid process of the scapula
move inferiorly and away from the clavicle. The separation
of the coracoid process and clavicle is prevented by the
coracoclavicular ligament that binds these two bony
segments together. The ligament maintains a relatively
constant angle between the clavicle and the superior
border of the scapula (the scapuloclavicular angle). As long
as the coracoclavicular ligament is intact, the scapula
cannot upwardly rotate around an anteroposterior axis at
the AC joint (Fig. 1). Upward rotatory forces applied to
the scapula by the trapezius and serratus anterior muscles,
therefore, produce the motion not at the AC joint but at
the next available linkage in the chain—that is, at the SC
joint.
Given that upward rotation of the scapula relative to the
clavicle cannot occur at the AC joint, it appears that the
primary role of the AC joint is to allow the scapula to
adjust to the changing contour of the thorax through
medial/lateral rotation and anterior/posterior tipping.
Injury to or degenerative changes in the AC joint are
common and increase with age. Pathology of the AC joint
may, in the acute stages, result in pain and hypomobility
secondary to that pain. However, persistent subluxation
and dislocation (hypermobility) or fixation and fusion
(hypomobility) does not appear to result in long-term
functional limitations.12-14
Sternoclavicular joint. The SC joint is an incongruent,
saddle-shaped joint with three degrees of freedom. Its
congruence and stability are substantially enhanced by a
fibrocartilaginous joint disk that diagonally transects the
joint space (from the superior clavicular facet to the
inferior manubrial facet). The joint is further supported by
a strong capsuloligamentous structure. Elevation and
depression of the clavicle at the SC joint requires the large
medial end of the clavicle (convex vertically)1 to glide in a
direction opposite to the motion of the lateral end of the
clavicle. Protraction and retraction require the shallow
antero-posterior concavity of the medial clavicle1 to glide
in the same direction as the movement of the end of the
clavicle.
When active elevation of the arm is initiated, activity in the
upper trapezius muscle will pull the acromion and lateral
end of the clavicle up while the other segments of the
trapezius and the serratus anterior muscles exert an
upward rotatory force on the scapula. The scapula cannot
upwardly rotate at the AC joint, as already noted, because
the coracoclavicular ligament maintains a fixed
scapuloclavicular angle. Rather, the upward rotatory forces
of the trapezius and serratus anterior on the scapula are
dissipated at the next available joint: the SC joint. The
trapezius and serratus anterior muscles produce upward
rotation of the scapula not by rotating the AC joint but by
elevating the clavicle at the SC joint. As the clavicle
elevates, the superior border of the scapula tilts upwardly,
as does the glenoid fossa (Fig. 2a). Clavicular elevation
created by the trapezius and serratus anterior muscles
produces the first 30 degrees of upward rotation of the
scapula and its glenoid fossa. When the costoclavicular
ligament becomes taut, elevation at the SC joint is
complete. There still remains, however, an additional 30
degrees of upward rotation of the scapula that must be
provided to complete a full range of elevation of the arm.
The final 30 degrees of scapular upward rotation that are
needed to complete the ST joint’s contribution to elevation
of the upper extremity is provided through rotation of the
clavicle around its longitudinal axis. As the trapezius and
serratus anterior muscles continue to exert an upward
rotatory force on the scapula, the coracoclavicular ligament
4
still prevents upward rotation at the AC joint. The upward
rotatory force on the scapula can no longer be dissipated
through SC joint elevation, however. As the active muscles
attempt to pull the coracoid process away from the
clavicle, tension in the coracoclavicular ligament (especially
the conoid portion15) builds to the point at which the
posteroinferior attachment of the ligament on the clavicle
is drawn toward the coracoid process. As the inferiorly
located ligament is drawn toward the coracoid process, the
inferior surface of the clavicle is drawn anteriorly, rotating
the clavicle around its longitudinal axis into what might be
termed posterior rotation.
Given the crank or “S” shape of the clavicle, the rotation
of the clavicle causes the acromial end of the clavicle to
flip up (Fig. 2, inset). When the lateral end of the clavicle
flips up, it carries the attached scapula with it, further
tilting the glenoid fossa upwardly through another 30
degrees (Fig. 2b). Longitudinal rotation of the clavicle
presumably requires mobility at both the AC and the SC
joints. However, fixation of the AC joint does not appear
to result in long-term restrictions to clavicular motion.12-14
We can conclude that mobility at the SC joint is mandatory
for full scapular ROM as long as the coracoclavicular
ligament is intact. The need for AC mobility is less clear,
but restriction at either the AC or the SC joint, regardless
of the reason, typically will result in hypermobility of the
other joint as long as that joint is not otherwise restricted.15
In summary, the following four factors are necessary to
achieve the normal 60 degrees of ST contribution to
elevation of the arm:
• SC joint mobility to allow the clavicular elevation
and rotation necessary to swing the glenoid fossa of
the scapula upwardly.
• AC joint mobility to allow anterior and posterior
tipping and medial and lateral rotation of the scapula
to maintain appropriate contact of the scapula with
the thorax.
• Trapezius and serratus anterior muscle activity to
drive the scapula into upward rotation.
• Extensibility of other scapular and clavicular
muscles to allow normal ST motion as well as
clavicular elevation and rotation.
Glenohumeral joint. The articulation of the large humeral
head with the smaller glenoid fossa and differences in the
radii of curvature of the two surfaces make the
glenohumeral (GH) joint incongruent. The glenoid labrum
(a fibrous structure with a fibrocartilaginous transition
zone at its attachment to the periphery of the glenoid
fossa16) increases the depth of the glenoid fossa.17 The
joint capsule is large and loose and is reinforced by several
ligaments, including the superior, middle, and inferior GH
ligaments as well as the coracohumeral ligament.
The superior capsule, superior GH ligament, and
coracohumeral ligament appear to be interconnected.18,19
Harryman et al19 found that the interconnected ligaments
bridged the gap between the supraspinatus and
subscapularis tendons and also had fibrous connections to
those tendons and to the sheath surrounding the long head
of the biceps tendon. This complex of interconnected
tendons and ligaments is referred to as the rotator interval
capsule.19-21 The passive components of the rotator
interval capsule provide the necessary support for
preventing inferior subluxation of the humeral head on the
shallow glenoid fossa in the neutral or dependent position
(0 degrees). When the arm is in the dependent position
with no load or a moderate load, the passive structures
alone can support the humeral head against the downward
pull of gravity without active contributions from
surrounding muscles.22,23 As the upper extremity is
elevated, the superior structures at the GH joint become
slack as GH end-range is approached, and the inferior GH
ligament complex (with its anterior band, posterior band,
and axillary pouch24) becomes more important in limiting
inferior translation of the humeral head.17,21,24
In the middle of the glenohumeral ROM, the
capsuloligamentous complex is largely slack,21 allowing as
much as a 2- to 3-mm distraction of the joint.1
Concomitant medial or lateral rotation of the humerus
affects the relative contributions of these passive structures
as well. The close-packed position of a joint is the point in
the joint ROM where the capsuloligamentous structures
are maximally taut and the joint surfaces are drawn
together. The close-packed position of the GH joint is
considered to be full abduction and lateral rotation.1
Controversy surrounds what are considered to be the
available ranges for elevation at the GH joint. These
ranges apparently vary from person to person, which is not
surprising, given what appear to be substantial individual
and side-to-side differences in articular surfaces and in
capsuloligamentous contributions. The GH joint is most
commonly considered to have 120 degrees of abduction
(frontal plane); however, reports of normal ranges as small
as 90 degrees are not uncommon.3,25,26 Glenohumeral
flexion and elevation in the plane of the scapula (so-called
“scaption”27) are more consistently estimated at 120
degrees, but smaller ranges also have been reported for
this plane of movement.28,29 Full GH abduction requires
simultaneous lateral rotation of the humerus, which is
necessary to prevent the greater tubercle from making
contact with the coracoacromial arch. If sufficient lateral
rotation cannot be provided, the greater tubercle will
impinge on the coracoacromial arch by 60 degrees of GH
motion.9,25 Although scaption presumably allows elevation
to proceed without the necessity of clearing the greater
tubercle, 35 to 40 degrees of lateral rotation has been
found to typically accompany a full range of scaption.30
5
The articulation of the large humeral head with the smaller
glenoid fossa requires the humeral head to glide in a
direction opposite to the motion of the distal humerus in
order for full GH ranges to be completed. These accessory
motions are required to keep the large humeral head
centered in the glenoid fossa. The accessory motions
include translatory glides and rotation of the bone around
its long axis. This rotation around the long axis is referred
to as conjunct rotation1,23 rather than medial and lateral
rotation, because the motion does not add an additional
degree of freedom to the humerus; rather, the motion
serves to minimize migration of the humeral head on the
fossa. Although some of the accessory glides and conjunct
rotations may vary with individual differences in articular
and periarticular influences, it is necessary to center the
humeral head as much as possible during abduction and
scaption because unopposed upward rolling of the
humeral head on the fossa could result in an impingement
of the humeral head into the overhanging coracoacromial
arch.
The potential for upward migration of the humeral head is
accentuated by the direction of pull of the three
components of the deltoid muscle that serve as primary
movers for abduction and scaption. When abduction or
scaption is initiated, the deltoid generates a nearly vertical
upward pull on the humerus that, if unopposed, would
superiorly translate the humeral head into the
coracoacromial arch. Although flexion also tends to
translate the humeral head superiorly on the fossa, the
coracoacromial arch is not in the way, and the primary
movers for flexion (anterior deltoid, coracobrachialis, and
clavicular pectoralis major muscles) produce a more
oblique and, therefore, smaller superiorly directed force.
The muscles of the rotator cuff provide the active forces
needed to offset upward rolling of the humeral head, to
offset the upward translatory pull of the deltoid, and to
center the humeral head on the glenoid fossa. Checks to
superior translation cannot be provided by the passive
structures because the rotator interval capsule is slack
when the arm is elevated and because the inferior GH
ligament complex can restrain inferior but not superior
translations. The capsular structures (along with muscles)
do seem to contribute to the conjunct rotations that
accompany GH motion and to minimize translatory
motions within the joint.17,19,31
Rotator cuff muscles. The supraspinatus, infraspinatus,
teres minor, and subscapularis muscles form the rotator
cuff and are credited with providing dynamic stability to
the GH joint. The combined line of pull of the
supraspinatus, infraspinatus, teres minor, and subscapularis
muscles is nearly perpendicular to the humerus and
directed into the glenoid fossa, making these muscles
strong and effective compressors and stabilizers of the GH
joint.32 The stabilizing function is enhanced by the fibrous
connections of the cuff tendons to the GH capsule.10
Furthermore, the infraspinatus, teres minor, and
subscapularis muscles have a line of pull that is slightly
downward (caudal), allowing the muscles to produce
downward gliding of the humeral head on the fossa.33 The
role of the supraspinatus muscle differs somewhat from
that of the infraspinatus, teres minor, and subscapularis
muscles, because its line of pull would effect gliding of the
humeral head superiorly (cephalad) rather than inferiorly.34
The supraspinatus muscle also is capable of abducting the
GH joint independently of the deltoid muscle and makes
an active contribution to resisting inferior translation of
the humeral head when the arm is at the side and has a
heavy load.23
The long head of the biceps brachii muscle passes through
a tunnel formed by the coracohumeral ligament to reach
the supraglenoid tubercle and has connections through its
sheath to the rotator interval capsule as well as to the
glenoid labrum. It is considered by some to be part of the
rotator cuff mechanism.20 The long head of the biceps
muscle, when active, may augment stability of the GH
joint at lower levels of elevation by centering the humeral
head on the glenoid fossa.35 Although the long head of the
biceps does not appear to be able to contribute directly to
downward gliding of the humeral head,35,36 its role as a
secondary stabilizer of the GH joint is supported by
observations of hypertrophy of the long head in the
presence of rotator cuff tears.35,37
The supraspinatus, infraspinatus, teres minor, and
subscapularis muscles work during active flexion, scaption,
and abduction of the GH joint to offset the upward pull of
the deltoid muscle, stabilize the GH joint, and augment the
rotatory force of the deltoid. The supraspinatus muscle
may be called upon to assist with limiting inferior
translation of the humeral head by gravitational forces.
The infraspinatus and teres minor (and perhaps, to a lesser
extent, the supraspinatus) muscles make an additional
contribution to GH abduction by providing the lateral
rotation necessary to clear the greater tubercle. As a result
of the multi-dimensional roles of the supraspinatus,
infraspinatus, teres minor, and subscapularis muscles,
chronic overuse results in degenerative changes that
increase with age even if such changes are not
symptomatic.9,10,38 The supraspinatus muscle is particularly
vulnerable because it is either active (in elevation activities)
or passively stretched (with the arm in the dependent
position) during a large portion of a person’s waking
hours. The position of the supraspinatus muscle and
tendon below the coracoacromial arch also contributes to
increased risk for impingement and degenerative changes.
Coracoacromial arch. The coracoacromial arch is an
osteoligamentous vault consisting of the coracoid process,
the coracoacromial ligament, and the acromion process. It
serves the functions of preventing superior dislocation of
the humeral head and protecting the humeral head from
downwardly directed forces at the lateral shoulder.
6
The suprahumeral space between the humeral head and
the arch contains the subacromial bursa, the supraspinatus
muscle and tendon, the superior GH capsule, and part of
the tendon of the long head of the biceps brachii muscle.
When the suprahumeral space is reduced, the potential for
painful impingement and compromise of these structures
exists. Anatomic factors that may narrow the space
include, but are not limited to, the shape and orientation of
the inferior acromion,17 changes in the growth epiphysis of
the acromion, acromial spurs, AC osteophytes, and a large
coracoacromial ligament.20 The space also can be
narrowed dynamically if the superior translatory pull of the
deltoid muscles during attempted elevation of the arm is
not sufficiently offset by the inferior pull of the
infraspinatus, teres minor, and subscapularis muscles.
When the rotator cuff and the deltoid are working in
appropriate synergy, the humeral head remains relatively
centered on the glenoid fossa, and little superior
displacement occurs.30,39 There is still evidence, however,
that the pressures in the subacromial bursa increase with
elevation of the loaded upper extremity. These pressure
increases may be attributable to the increased volume of
the supraspinatus muscle as it contracts during the activity
and occupies more of the suprahumeral space. Cailliet9
notes that subacromial bursitis and supraspinatus tendinitis
often occur simultaneously (primary subacromial bursitis is
rare) because the inferior portion of the subacromial bursa
is the outer sheath of the supraspinatus muscle and
tendon. Inflammation of the supraspinatus tendon can
therefore create secondary subacromial bursitis.
Total scapulohumeral motion. In addition to
considering the individual structures of the shoulder,
physical therapists should consider the coordinated
interaction of the ST and GH joints in producing elevation
of the upper extremity.
Medial rotation and lateral rotation of the arm primarily
are functions of the GH joint. Full scaption and abduction
of the arm require not only 90 to 120 degrees of GH
motion but also 60 degrees of upward rotation of the
scapula that must involve the SC joint and, to a lesser
extent, the AC joint. Flexion of the arm has requirements
similar to those of abduction but includes the additional
requirement of scapular protraction that must accompany
upward rotation.
Various researchers have conducted extensive
investigations of the ratio of GH to ST movements. A
substantial variability in ratios of GH to ST movements
has been found between individuals and under different
load conditions.40,41 The rhythm or timing of GH and ST
movements essentially is irrelevant to clinical examination,
however, because any interference with any component of
the movement at the various linkages will alter the
sequencing and ratio of the movement. Every patient will
use whatever motion is available, regardless of ratios and
proportions. For instance, if only GH motion is available,
the patient still should be able to achieve 90 to 120 degrees
of elevation (subject to the position of the scapula).
Correspondingly, if the GH joint is immobilized by fusion
or adhesive capsulitis, the scapula still can achieve its full
60 degrees of upward rotation and the arm still can move
60 degrees from the side (assuming neutral GH
positioning). Partial contributions from each joint also can
occur if both joints encounter restrictions. On the other
hand, hypermobility of one component may develop in
response to mobility restrictions elsewhere in the complex.
The only mandatory sequence in movement of the
shoulder girdle linkages is at the SC joint. The
costoclavicular ligamentous restriction of clavicular
elevation (contributing the first 30 degrees to scapular
upward rotation) must be reached before tension in the
coracoclavicular ligament will be sufficient to rotate the
clavicle (contributing the final 30 degrees to scapular
upward rotation). Hyperextension of the arm is
accomplished largely through GH mobility (with some
scapular tipping). Motions such as horizontal abduction
and adduction of the arm, however, require both GH
motion and scapular retraction and protraction,
respectively (including mandatory SC contributions).
Tests and Measures
As JD’s examination proceeds, the physical therapist must
choose tests and measures to identify impairments of
normal function in these kinematic and kinetic
components of the shoulder that may contribute to JD’s
clusters of signs, symptoms, and impairments. The
physical therapist will then evaluate the examination
findings and, based on the evaluation, form a diagnosis
and prognosis and select appropriate interventions.
Sensory integrity. Although sensory integrity is examined
commonly in patients with shoulder dysfunction to
determine whether there is cervical nerve involvement,
patients who have had surgery for breast cancer frequently
have sensory changes that need to be identified before
proceeding with other components of the hands-on
examination.
JD is insensitive to light touch and pinprick in a 1- to 2-
inch margin around the scar and in an area extending into
the axilla and posteromedially down the right arm almost
to the elbow (Fig. 3). This distribution is indicative of
deficits of the right intercostobrachial and medial brachial
cutaneous nerves.
Range of motion. To begin differentiating between GH
and ST limitations, the therapist decides to use passive
ROM with overpressure as described by Kaltenborn,42
7
accessory mobility, and goniometric measurements. The
therapist also wants to explore the nature of the limitation
at the involved joints; that is, to explore whether the
dysfunction appears to be consistent with contractile or
passive (inert) structures.43 The goniometric measurement
of total active and passive ROM, as well as ROM with a
manually stabilized scapula (GH ROM), are shown in the
Table.
ROM values and passive end-feels for the joints of the left
shoulder girdle are within normal limits.44 Overpressure
for right passive extension and horizontal adduction have
firm end-feels, with resistance encountered before pain.
Overpressure for right medial rotation, lateral rotation, and
horizontal abduction have firm end-feels, again with
resistance encountered before pain. The end-feels for
abduction and flexion are limited by spasms, with pain
reported before onset of resistance. These observations
would appear to be consistent with a GH capsular pattern
that will need to be explored with joint integrity and
mobility testing.43
A comparison of total passive ROM values for right
shoulder flexion and abduction to the values obtained with
the scapula stabilized suggests both GH and ST limitations
of motion. Although GH flexion is close to the normal
range of 120 degrees, combined GH and ST (total) flexion
suggests a primary limitation in the ST contribution to the
motion in flexion. Glenohumeral abduction is substantially
less than the 90 to 120 degrees that the therapist would
expect for that joint alone. When the ST contribution is
added (for total ROM), only an additional 30 degrees of
range is obtained, suggesting both GH and ST limitations.
Medial rotation and lateral rotation, primarily GH motions,
are both limited. The substantial limitation to lateral
rotation can account for much of the restriction in GH
abduction, because an inability to laterally rotate the
humerus will result in early impingement of the greater
tubercle into the coracoacromial arch and is consistent
with the pain experienced by JD with both active and
passive abduction. Glenohumeral flexion does not require
lateral rotation to clear the greater tubercle, and JD shows
little or no restriction of GH flexion. The therapist
hypothesizes that the primary limitation to GH abduction
is related to the lateral rotation limitation.
Both flexion and abduction show a restriction of
approximately 30 degrees of ST motion. The therapist
reasons that, because both motions normally require 60
degrees of upward rotation of the scapula, a restriction of
upward rotation should be considered. An essentially
normal finding for horizontal adduction ROM indicates
that the contributing components of GH adduction and
scapular protraction are within normal limits. Horizontal
abduction, however, is sufficiently limited that both the
GH contribution and ST retraction need to be investigated
further. The therapist proceeds to examine joint integrity
and mobility as a way to narrow down the involved
structures and test these hypotheses.
Joint integrity and mobility. Examination of joint
mobility is based on the conceptual framework that
osteokinematic restrictions may be related to
arthrokinematic restrictions. Evidence of an association
between arthrokinematic and osteokinematic restrictions,
however, is largely empirical, and reliability of judgment of
joint glides has not been demonstrated in the literature.
Although not definitively diagnostic, suspected limitations
of arthrokinematic glides and atypical end-feels have the
potential to contribute to our hypotheses about affected
structures and tissues that need intervention. The therapist
therefore links the arthrokinematic findings to other
examination findings.
Accessory glides of a joint are tested where the GH
capsule is as loose as possible. For JD, accessory glides of
the right GH joint are restricted (estimated to be grade 2
on a scale from 0 to 642), with capsular end-feels and
resistance before pain in the inferior, anterior, and
posterior directions. Accessory glides of the left GH joint
appeared to be within normal limits and reasonably
symmetric (estimated to be grade 3), with capsular end-
feels and resistance before pain.
These observations lead the therapist to hypothesize that
the right GH restrictions observed during the ROM
examination may have had a capsuloligamentous
component in addition to a possible limitation in the
extensibility of muscular and other extracapsular tissues.
Long-axis traction applied to the humerus is limited
(estimated to be grade 2) by spasm. This finding suggests
inflammation of the superior GH structures (rotator
interval capsule and passive supraspinatus muscle).
Imposing an inferior glide on the humerus (as is done with
longitudinal traction) would be expected to place tension
on the superior GH structures (evoking pain if
inflammation is present), whereas during other passive GH
joint motions, these structures would generally become
more slack. Manual glides of the right AC joint (anterior,
posterior, cephalad, and caudal) are slightly limited
(estimated to be grade 2) compared with those of the left
(estimated to be grade 3), all with capsular end-feels and
resistance before pain. Manual glides of the left SC joint
are within normal limits (estimated to be grade 3), with
capsular end-feels and resistance before pain), whereas
those of the right are estimated to be grade 3 for anterior,
grade 2 for caudal and cephalad, and grade 1 for posterior
glides (all with capsular end-feels).
In the saddle-shaped SC joint, a restriction in posterior
glide may be associated with a limitation in clavicular (and
scapular) retraction, because the anteroposterior concavity
8
of the medial end of the clavicle is expected to move in the
same direction as the lateral end of the clavicle.
Restrictions in cephalad and caudal glides may be
associated with limitations in clavicular (and scapular)
depression and elevation, respectively, because the vertical
convexity of the medial end of the clavicle is expected to
glide in a direction opposite to the motion of the lateral
end of the clavicle. The therapist would expect joint glide
(arthrokinematic) restrictions at the SC joint to be
consistent with decreased scapular motion.
Manual movements of the scapula on the thorax on the
left are within normal limits. On the right, with the patient
in a prone position, the scapula is observed to be
protracted and anteriorly tipped, as was found when JD
was in the standing position. Manual movements of the
scapula on the thorax are estimated to be grade 3 for
lateral glide (protraction) and grade 2 for caudal glide and
for downward rotation, each with firm end-feels and
resistance before pain. Manual movements of the scapula
cephalad (elevation), medially (retraction), and into upward
rotation are estimated to be grade 1, with firm end-feels
and resistance before pain. The findings for the scapula are
consistent with those for arthrokinematics of the SC joint,
and they lead the therapist to expect limitations in scapular
elevation, retraction, and upward rotation. Although SC
restrictions may be the primary cause of ST limitations, it
also is possible that some other factor may be limiting
scapular mobility and producing secondary adaptive
shortening of the capsuloligamentous structure of the SC
joint. None of the SC, AC, or ST glides reproduces JD’s
pain. The therapist decides to examine the contractile
elements.
Muscle performance. All shoulder girdle musculature on
the left appear to be within normal limits (5/5), as
estimated by manual muscle testing.45 Right shoulder
extensors are 5/5, and horizontal adductors are 4/5, with
mild discomfort described as a “pulling” sensation. Flexors
and medial rotators are 5/5 within the available range.
The positions for horizontal abduction and lateral rotation
are modified because of range limitations, with resistance
from horizontal adduction and medial rotation,
respectively. Right horizontal abductors are measured as
5/5, lateral rotators measured as 4/5, and abductors
measured as 3+/5, with both of these resisted motions
reproducing JD’s pain symptoms. The right serratus
anterior muscle is measured as 5/5, and the upper
trapezius and the levator scapula muscles are measured as
5/5 within the available range.
Positional modification for testing of the middle trapezius,
lower trapezius, and rhomboid muscles is required. The
therapist places JD in the prone position, with her right
shoulder brought over the edge of the table. Because her
arm cannot be brought overhead for testing of the lower
trapezius, JD is instructed to actively depress the scapula
against manual resistance. Some weakness (estimated to be
4/5) is evident.
When the patient is placed in the starting position for
testing of the middle trapezius and rhomboids, no further
scapular retraction actively or passively is available. Manual
resistance on the scapula against retraction with downward
rotation at JD’s end-range indicates weakness (estimated to
be 4/5).
Manual muscle testing of the muscles of the GH joint
indicates pain and weakness with both abduction and
lateral rotation. Scapulothoracic muscle testing confirms
limitations of motion, but the identified muscle
weaknesses are minimal and are more likely to be
secondary to positional faults rather than causative.
The impingement sign46 and the supraspinatus test47 yield
positive results. The apprehension, relocation, Speed’s, and
Yergason’s tests47 yield negative results.
Evaluation
JD’s pattern, degree, and location of pain (anterosuperior
shoulder pain) with active, passive, and resisted abduction;
resisted lateral rotation; and passive longitudinal traction
are consistent with a grade II acute supraspinatus tendinitis
and subacromial bursitis.
The pain at 70 degrees of active abduction occurs at the
beginning of the 60- to 120-degree “painful arc” that is
typical of supraspinatus inflammation,9 although JD’s
range limitation precludes a true positive finding. Pain in
this range from supraspinatus inflammation is thought to
occur because the supraspinatus muscle normally shows
peak activity (and, therefore, peak tension) through this
range, whereas the suprahumeral space in which the
tendon lies is simultaneously being reduced as the greater
tubercle approaches the coracoacromial arch.9
Pain with passive longitudinal traction on the humerus is
consistent with supraspinatus inflammation because this
action places stress on the supraspinatus muscle and
tendon. The pain experienced by JD with overpressure on
abduction may indicate additional involvement of the
subacromial bursa just above the supraspinatus muscle.
Results of the special tests for the shoulder appear to
confirm supraspinatus tendinitis and rule out GH
instability. Although supraspinatus tendinitis is considered
multifactorial and can occur without a significant
history,9,20 the physical therapist must determine whether
JD’s other biomechanical limitations are contributing to or
potentially causing the problem.
9
JD does not have passive lateral rotation beyond the
neutral position. Capsuloligamentous restrictions found on
examination might have contributed to restricted lateral
rotation. The comparative mobility of medial rotation and
flexion at the joint, however, would appear to argue against
capsuloligamentous restriction as a sole source of the
restriction in lateral rotation.
The therapist believes that JD’s history might provide
some clues to additional causes. JD had surgery and
radiation involving the anterior chest wall and axilla.
Radiation is known to result in fibrotic changes and
potential vascular compromise to the skin and underlying
tissues.48,49 JD also had a tissue expander inserted under
the pectoralis major muscle, as is typically done in implant
reconstruction. There is evidence that the expansion
process alone (without adjuvant radiation) can result in
muscle fiber degeneration and interstitial fibrosis.50 The
subsequent failure of the skin expansion in JD’s case is
consistent with more severe fibrotic changes than might be
considered typical. The potential for radiation- and
expansion-induced soft tissue changes might have been
further accentuated by the subsequent surgeries when the
right implant extruded.
There is little or no skin mobility in the area of the scar,
and the skin appears to adhere to the underlying thorax.
The sternal portion of the pectoralis major muscle,
however, should lie between the skin and the thorax. On
the right, the therapist could not trace the pectoralis major
muscle inferiorly from the superior margin of the scar.
These findings might indicate that the sternal portion of
the muscle is atrophied and completely adherent to the
skin above and the thorax below. Fibrosis and lack of
extensibility of the sternal pectoralis major muscle could
produce the limitation of lateral rotation in JD. A
limitation of lateral rotation (and possibly of accompanying
conjunct rotation) could lead to supraspinatus tendon
impingement, because the greater tubercle cannot clear the
coracoacromial arch in abduction of the arm.
The pectoralis minor muscle is found deep to the
pectoralis major. Both the pectoralis major and minor
muscles are separately enveloped by the clavipectoral
fascia. The clavipectoral fascia and pectoralis minor muscle
also might be involved in the fibrotic changes resulting
from radiation and surgery and, consequently, contribute
to the findings. JD’s scapular resting position of
protraction and anterior tipping is consistent with
pectoralis minor muscle tightness, as are the active and
passive limitations of scapular retraction, elevation, and
upward rotation. Tightness of the pectoralis minor muscle
and the resulting faulty scapular posture can change the
position of the acromion, narrow the suprahumeral space,
and increase the likelihood of impingement, even in the
absence of the other pathology presented by JD.4,9
The clavipectoral fascia surrounds the pectoralis muscles,
attaches to the lateral clavicle and coracoid process, and
blends with the axillary fascia.1 If it also has been subjected
to fibrotic changes—as might be anticipated, given its
location—lack of extensibility in this fascia could restrict
clavicular motion.
Although the shortening of or fibrotic changes in the
pectoralis minor muscle and clavipectoral fascia alone
theoretically can account for a substantial portion of the
scapular limitation of motion, JD had axillary node
dissection and axillary radiation. Either of these procedures
may create fibrotic changes in the axillary soft tissues and
in the underlying serratus anterior muscle that could
further compromise scapular mobility.49 To explore the
clinical hypothesies of tissue fibrosis, the therapist asks JD
to repeat the active motions of scapular elevation,
depression, and retraction and to report altered sensation.
The patient reports a stretching or pulling sensation in the
axilla or its margins with all test movements. The
stretching or pulling is consistent with, although not
necessarily a definitive indication of, fibrosis in the anterior
chest wall and in the axilla.
Diagnosis
JD has impaired joint mobility and integrity, impaired
muscle performance, and impaired range of motion—
impairments that are consistent with dynamic subacromial
impingement in the right shoulder,31 an acute stage II
supraspinatus tendinitis,45 and probable subacromial bursal
involvement. JD’s functional limitations include
restrictions in her ability to perform ADL. Based on the
framework used in the Guide to Physical Therapist
Practice (Guide), the physical therapist makes a diagnosis
of “Impaired Joint Mobility, Motor Function, Muscle
Performance, and Range of Motion Associated With
Localized Inflammation.”51
Hypothesized shortening and fibrotic changes in the
glenohumeral capsule, pectoralis major and pectoralis
minor muscles, clavipectoral fascia, and axillary soft tissues
appear to be limiting ST and GH joint mobility. Additional
or secondary limitations to SC and AC joint mobility
appear to be contributing to altered scapulohumeral
mechanics and increasing the risk of impingement.
Prognosis
According to the Guide, it is estimated that 80% of all
patients in the chosen diagnostic pattern will demonstrate
a return to premorbid level of function within 8 to 16
weeks, with physical therapy ranging from 6 to 24 visits.51
The physical therapist expects the prognosis for JD to be
atypical compared with that of other patients in this
diagnostic pattern. Because of the anticipated fibrotic
tissue changes, the potential for vascular compromise of
the affected tissues, and the increased risk of lymphedema
in a patient who has undergone lymph node dissection and
10
axillary radiation, the therapist expects a delay in goal
achievement and limitations in the outcome.
Plan of care. With JD, the therapist identifies the
following main goals to address
pathology/pathophysiology, impairments, functional
limitations, disabilities, risk factor reduction/secondary
prevention, and patient satisfaction:
• Joint integrity and mobility of shoulder are
improved.
• Muscle performance (strength, power, endurance)
in shoulder is increased.
• Lymphedema is prevented.
• Range of motion is increased.
• Risk of secondary impairments (eg, subacromial
impingement) is reduced by improving posture.
• Tolerance of positions and activities is increased.
• Ability to perform movement tasks is increased.
• Pain is decreased.
• Joint and soft-tissue swelling, inflamation, or
restriction related to supraspinatus tendinitis is
reduced.
Intervention
As noted, the emphasis of this CE offering is on the
review of kinesiology of the shoulder girdle in a patient
with pain and hypomobility. However, because the
purpose of any examination and evaluation is to guide
intervention, we will discuss how the findings might
influence the physical therapist’s clinical decisions.
Therapeutic Exercise
As a passive stretching program is initiated, faulty postural
alignment also must be addressed to reduce the risk of
impingement. The patient must be educated to improve
cervical, cervicothoracic, and shoulder girdle alignment. An
adjunct program of strengthening of key muscle groups
can begin during the acute phase with isometric scapular
and GH stabilization in all directions. Submaximal
resistance to painful motions should be used until the
motions are pain free. As acute inflammation subsides, a
home program of resisted GH and ST motions can be
added
Manual Therapy Techniques (Including
Mobilization and Manipulation)
JD’s hypomobility has both extra-articular and capsular
components. The GH, SC, and AC capsular restrictions
indicate a need for joint mobilization. The direction and
degree of force applied during joint mobilization are
suggested by end-feels and by the pain/resistance
sequence.43 The scapula also appears to require
mobilization of the restricted muscles and soft tissues. The
therapist begins with mobilization of the scapula while the
acute inflammation at the GH joint is addressed.
The acute inflammation suggested by the findings might
be managed through anti-inflammatory medications
prescribed by JD’s surgeon, rest/relief positions, accessory
mobilizations for longitudinal distraction, and
physiological mobilizations for abduction.
The shortened and fibrotic extra-articular tissues of the
right anterior chest wall and axilla indicate the need for
scar mobilization and soft tissue mobilization. Scar
mobilization must proceed carefully, given the absence of
pain sensation and the possible compromised vascularity
indicated by the patient history. The target muscles for soft
tissue mobilization should be those showing evidence of
fibrotic changes or those anticipated to be in the radiation
field.52,53 Shortening of these same muscles suggests the
need for passive stretching of the muscles, but this action
should not be initiated until end-ranges no longer produce
acute pain or spasm. When the patient is ready, passive
stretching with an emphasis on flexion, abduction, external
rotation, and horizontal abduction of the arm can be
taught as part of a home program.
Electrotherapeutic Modalities and
Physical Agents and Mechanical
Modalities
The physical therapist may select electrotherapeutic
modalities and supportive taping to help reduce pain and
minimize tension on potentially inflamed structures.
Cautions
Several cautions unrelated to shoulder mechanics and
specific to JD should be noted. Any soft tissue
mobilization techniques or attempts to lengthen the
involved muscles must be performed with consideration of
the hypothesized fibrotic tissues, the potential for vascular
compromise of the tissues, and JD’s sensory deficits.
There is some evidence that sound agents (ultrasound)
may increase tumor growth.54 Furthermore, because of
concerns about increasing blood flow in the vicinity of
tumors, some texts of physical agents caution against the
use of sound and thermal agents in areas where there is or
may be malignancy.55-57 JD has not shown signs of
lymphedema to date. The risk, however, is long-term (up
to decades later) and is compounded by the combination
of axillary node dissection, axillary radiation, and surgery in
the radiated area.58 Lymphedema precautions include
avoiding the following in the involved arm59:
• Tissue trauma that could lead to local swelling or
inflammation (including routine injections or
blood draws).
• Exposure to extreme temperatures.
11
• Circumferential tissue constriction.
• Heavy lifting or vigorous repetitive movements
against resistance.59
The last precaution is particularly important as the physical
therapist formulates an exercise program for the patient.
Finally, consideration should be given to possible
entrapment of components of the brachial plexus in the
fibrotic tissues below the clavicle.60 Each of these
precautions argues for proceeding cautiously with
treatment and for careful and consistent communication
with the patient regarding her perceptions of pain,
stretching, exertion, or neuropathic symptoms.
The case discussed here is complex and certainly not
typical of patients with supraspinatus tendinitis. JD’s
history and findings provide a particular challenge both to
our understanding of shoulder girdle kinesiology and to
the planning of intervention strategies.
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Figure 1.

Figure 2a–2b.

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Figure 3.

Table.

15