ANATOMY, PATHOPHYSIOLOGY, AND

BIOMECHANICS OF SHOULDER INSTABILITY

LTC WILLIAM C. DOUKAS, MD, and KEVIN P. SPEER, MD

Instability in the athlete presents a unique challenge to the orthopaedic surgeon. A spectrum of both static and
dynamic pathophysiology, as well as gross and microscopic histopathology, contribute to this complex clinical
continuum. Biomechanical studies of the shoulder and ligament cutting studies in recent years have generated a
more precise understanding of the individual contributions of the various ligaments and capsular regions to shoulder
instability. An understanding of the underlying pathology and accurate assessment of degree and direction of the
instability by clinical examination and history are essential to developing appropriate treatment algorithms.
KEY WORDS: pathomechanics, pathoanatomy, instability

Because of its tremendous degree of mobility, the gleno-
humeral joint is inherently prone to instability. Muscle
forces are essential for stability in the mid-ranges of
motion, and result in ball-in-socket kinematics. Clinical
instability manifests itself at end-range of motion, and
reflects increased glenohumeral translation involving a
spectrum from microinstability to frank dislocation. Laxity,
which varies considerably between individuals 1,2and occa-
sionally even between shoulders of the same individual,
without symptoms does not constitute instability. Laxity is
required for normal, unrestricted glenohumeral motion,
and can be influenced by age, gender, or chronic repetitive
activities that place the shoulder at risk. There is some
body of evidence that laxity itself renders the shoulder
susceptible to the development of clinical instability. 3
However, laxity can play an adaptive role, especially in the
overhand athlete. 4 Therefore, symptoms must be present
and correlate with objective findings to suggest instability
that warrants further investigation. Functional stability,
which can be defined as maintenance of the humeral head
centered within the glenoid fossa during shoulder motion,
is achieved through synchronous coordination of static
and dynamic components. These include negative intraar-
ticular pressure, glenohumeral bony geometry, the capsulo-
labral complex, and synergistic muscle balance.
BASIC SCIENCE
Negative intraarticular pressure appears to have only a
minimal contribution in maintaining stability, and is most
notably absent in rotator cuff disease or rotator interval
pathology as a result of capsular venting. The role of
negative intraarticular pressure is most important while
the arm is simply at the side in a neutral passive position,
From the Sports Medicine and Shoulder Section, Division of Orthopae-
dic Surgery, Duke University Medical Center, Durham, NC.
Ac~dress reprint requests to LTC William C. Doukas, MD, Department of
Orthopaedics and Rehabilitation, Walter Reed Army Medical Center,
Washington, DC 20307.
Copyright © 2000 by W.B. Saunders Company
1060-1872/00/0803-0001510.00/0
doi:10.1053/otsm.2000.9801
but theoretically can be no more than 20 to 30 lb at t
atmosphere of pressure (14.7 psi × glenoid surface area) (Speer
and Urmey, unpublished data, May 1992). This component is
most likely subclinical except in the acute setting after disloca-
tion, rotator cuff tear, or any other injury resul~ng in capsular
venting, and is important only in the early to midrange of
motion when the capsuloligamentous structures are lax.
Limited joint volume, on the other hand, probably plays a
greater concurrent role in affecting stability because the
result of distraction and translational forces are propor-
tional to the degree of capsular laxity 5 (Fig 1).
Another dynamic factor in glenohumeral stability re-
volves around the concept of concavity-compression. 6 This
results from dynamic compression of the humeral head
into the glenolabral socket by the surrounding rotator cuff
musculature and, perhaps to a lesser degree, the long head
of the biceps, although its role is less clearly- understood. 7-1°
The rotator cuff muscles serve to center the humeral head
in the glenoid thereby countering the translational forces
that are generated oblique to the face of the glenoid by the
primary movers of the shoulder. This mechanism is most
important in the midranges of motion when the capsuloliga-
mentous structures are lax. The efficiency of this mecha-
nism is reduced by as much as 20% if the labrum is entirely
excised. 11 Warner et al I2 have recently shown that the
concavity-compression mechanism can provide greater
glenohumeral stability in the inferior direction than nega-
tive intraarticular pressure or ligament tension in all
degrees of abduction and rotation. This reemphasizes the
role of the "force couple" of the rotator cuff in maintaining
the humerus centered in the glenoid socket.
It is also important to note the role of proprioception in
this mechanism. Histologic studies show that neuroaffer-
ent receptors exist within the capsulotendonous junction
that may act through reflex arcs to help give cortical
feedback on shoulder position and translation. This in turn
may signal appropriate muscle response and sequencing to
avoid injury to the capsuloligamentous structures.13 Warner
et a114 have been able to verify this in the clinical setting,
showing decreased proprioception in patients with instabil-
ity that can be restored with surgical stabilization.
Coordinated scapulothoracic rhythm remains difficult to

Operative Techniques in Sports Medicine, Vol 8, No 3 (July), 2000: pp 179-187 1 79


Fig 1. The role of negative intraarticular pressure. Top"
Inferior translation of the arm is resisted by the increased
negative intraarticular pressure or vacuum effect produced
by a closed system. Bottom: Inferior translation is increased
secondary to loss of the vacuum effect that results from a
vented system. These effects are in turn magnified proportion-
ally with increased capsular laxity. (Reprinted with permis-
sion. s)
study both in cadavers and in vivo. Classic studies teach an
overall 2:1 ratio of glenohumeral to scapulothoracic mo-
tion during abduction, although the plane of elevation
studied was out of plane of the scapula. 15 More recent
studies in the scapular plane indicate that the actual overall
ratio is probably much higher, and varies with the degree
of abduction being higher early on with less difference at
the end. 16 Warner et aP 7 used topographical analysis to
demonstrate increased scapulothoracic asymmetry in pa-
tients with underlying instability, although it is difficult to
determine if this is cause or effect. Failure of the scapula to
effectively rotate under the humeral head during glenohu-
meral elevation may place the soft tissues at additional
risk. At present, it is unclear whether glenoid or humeral
head version play a role in instability. Although most
authors agree that superior tilt of the glenoid appears to
contribute to inferior stability, the role of humeral retrover-
sion in providing anteroposterior stability remains contro-
versial.IS-20
There are conflicting reports in the literature regarding
obligate translational moments occurring during shoulder
motion. Howell et a121 have shown an obligate posterior
180
translation (approximately 4 mm) that occurs with maxi-
m u m extension and external rotation. This was not ob-
served in subjects with documented anterior instability,
presumably from incompetent anterior restraints or loss of
requisite dynamic stabilizing forces. It is likely that these
occur at the extremes of motion when forces are high,
although work done by Harryman et a122showed obligate
translations with end-range passive glenohumeral motion.
These investigators introduced the concept of a capsular
constraint mechanism where obligate translations occur in
the direction opposite of the capsule under tension. They
postulate that these translations are not increased by
ligamentous laxity or insufficiency, but when there is
asymmetric tightening of the capsule.
These studies together do suggest a slight departure
from true ball-in-socket kinematics that probably plays a
significant role in the more subtle forms of instability.
However, recent anatomic studies addressing articular
congruity have shown nearly matching curvature of radii
between the humeral head and the glenoid despite what
appears like an obvious mismatch on plain film radio-
graphs. 23This speaks more to a true ball-in-socket relation-
ship where surface area mismatch probably plays a more
central role in instability than articular incongruity. Glenoid
hypoplasia, therefore, or any other factors that may reduce
glenoid surface area such as glenoid wear, may predispose
toward instability.
The glenoid labrum is known to increase the depth of the
glenoid socket by approximately 50% in all directions and
increase surface area as well. 24 This results in increased
humeral head contact area with a theoretical proportional
decrease in point loading. The labrum also functions as a
"chock block" to preventing translational forces, contribut-
ing approximately 20% to glenohumeral stability with the
joint loaded. 11 This has subsequently been shown to be
more true inferior to the equator of the glenoid, below the
loosely attached superior labrum and often present subla-
bral foramenY
The labrum also often serves as the point of attachment
of the capsuloligamentous structures to the glenoid (Fig 2).
Anteriorly, these include the superior glenohumeral liga-
ment (SGHL), the middle glenohumeral ligament (MGHL)
and the inferior glenohumeral ligament (IGHL) which is
more accurately described as a complex (IGHLC). Normal
anatomic variants of attachment sites at the glenoid margin
have been previously described by Moseley and Over-
gaard 26 and more recently by Rothman et a127: insertion of
the capsule directly into the labrum (type I), insertion of
the capsule into the base of the labrum (type II), and
attachment of the capsule directly onto the glenoid neck
(type III) (Fig 3). More recent work has focused on these
capsuloligamentous structures, and will be discussed briefly
below. It is only with a thorough knowledge of the
contributing static capsuloligamentous elements to clinical
glenohumeral instability that thoughtful treatment algo-
rithms toward the correction of the instability can be
contemplated.
TRAUMATIC INSTABILITY
The athlete is subject to numerous repetitive loads during
participation in sports that often can lead to symptoms of
DOUKAS AND SPEER
instability. These events range from violent forces that can
frankly dislocate the joint to more subtle forces that lead to
plastic deformation of the static restraints. Pure anterior-
inferior dislocations by far remain the most common of
instability patterns, although overlap in direction and
magnitude have been more recently recognized in defining
instability patterns. 2s The mechanism of anterior disloca-
tion is typically an abrupt abduction/external rotation
(+ extension) force about the shoulder. Appreciation of the
circumstances involving the first episode of instability is
essential to understanding the underlying pathophysiol-
ogy. Recurrence rates in the younger population remain
large in most recent series 29 and may be underestimated
because it often difficult to ascertain or quantify activity
avoidance; furthermore, most of these studies have not
included subluxation as an integral part of the symptom
complex. 3°,31 Although recurrence rates are reported to
deci[ine in older patients, more recent studies have sug-
/ pouch. This has been compared with a hammock provid-
Fig 2. Sagittal representation of the glenohumeral capsulo-
ligamentous anatomy. A, anterior; P, posterior; B, biceps;
SGHL, superior glenohumeral ligament; MGHL, middle gleno-
humeral ligament; IGHLC, inferior glenohumeral ligament
complex (AB = anterior band, AP = axillary pouch, PB =
posterior band); PC, posterior capsule. (Reprinted with per-
mission. 34)
SHOULDER INSTABILITY
Fig 3. Variations in the anterior capsular insertion of the
glenohumeral joint as described by Moseley and Over-
gaard. 26 (Reprinted with permission7 3)
gested higher persistence of symptoms in this subgroup. 32
Associated neurologic and rotator cuff injuries in older
patients are much more frequent and should be considered
in their evaluation to avoid early misinterpretation.
Anterior Translation: Static Stabilizers
Histologic analysis of the shoulder capsule has identified
relatively constant thickenings that comprise individual
ligaments. Selective cutting experiments have helped delin-
eate function of these specific ligaments in varying degrees
of abduction and rotation. Biomechanical studies have
further elucidated the individual contributions of these
various ligaments and capsular regions to shoulder insta-
bility. Earlier work done by Turkel et aP 3 showed that the
anterior band of the IGHLC is the primary restraint to
anterior translation with the arm at 90 ° of abduction, with
less influence with decreasing amounts of abduction. More
recently, O'Brien et al, 34,35using arthroscopy and histologi-
cal analysis, have further delineated the IGHLC into
anterior and posterior bands with an interposed axillary
ing reciprocating restraint to translation in the 90 ° ab-
ducted shoulder varying with the degree of internal and
external rotation (Fig 4). The IGHLC also serves to prevent
inferior translation in increasing amounts of abduction. 36,37
At lower levels of elevation, the MGHL and subscapularis
were found to act as more significant stabilizers with the
SGHL having a minor role in anterior stability at even
lesser degrees of abduction.
The detachment of the IGHLC from the anterior glenoid
1 81
 A . b d .
Fig 4. Reciprocating action of the IGHLC. Top left: In increas-
ing neutral abduction, the IGHLC becomes progressively
taut. With internal rotation (I.R.), increasing tension is gener-
ating in the posterior band as it moves superiorly thus
preventing posterior translation of the humeral head. Con-
versely, with external rotation (E.R.), increasing tension is
generated in the anterior band as it moves superiorly, thus
preventing anterior translation of the humeral head. (Re-
printed with permission. 34)
and labrum is referred to as the Bankart lesion. 38This is not
one specific anatomic defect, but rather a cluster of lesions
all of which render the IGHLC incompetent at the glenoid
margin. Although his name is attached to this anatomic
lesion, Bankart was not the first to describe it or to suggest
its operative repair. Broca and Hartmann 39 in 1890, and
Perthes 4° in 1906, emphasized the importance of anterior
detachment of the capsule from the glenoid in recurring
anterior instability of the shoulder. Because of recent
investigations, the Bankart lesion is now less often consid-
ered the all or none essential lesion, but it is the most
common lesion encountered. Biomechanical studies have
failed to show significant increased translation with a
simulated Bankart lesion alone, suggesting that other
pathomechanics like plastic deformation of the capsuloliga-
mentous structures play a major role in the development of
instability. 41 Creation of this lesion was found to cause a
multidirectional increase in humeral head translation;
however, maximum excursion was very small, measuring
only 3.4 m m in the inferior direction at 45 ° of abduction.
Furthermore, anterior translation in neutral rotation was
not increased with complete excision of the labrum.
This study also confirmed increased tension patterns in
the posterior capsule with translational forces after cre-
ation of the anterior lesion. Clinically, the injury complex
1 82
resulting in anterior instability involves not only damage
to the anterior restraints, but also injury to the posterior
structures as well, such as the impression fracture on the
posterolateral aspect of the humeral head. 42This circumfer-
ential injury pattern was first purposed by Perthes in his
original article 4° and later espoused by Warren 43 in his
circle concept of capsuloligamentous instability of the
shoulder. A substantial lesion anywhere in the capsule
affects motion of the humeral head not only on the side of
the lesion but in other directions as well. The multidirec-
tional increase in translation seen with a simulated Bankart
lesion underscores the complex capsular interdependence
of the shoulder joint.
It is now well established that most capsulolabral lesions
are in some w a y associated with instability. Other variants
have also been recently described, such as the anterior
labral periosteal sleeve avulsion (ALPSA),44 which also
renders the IGHLC incompetent at the glenoid, as well as
the humeral avulsion of the glenohumeral ligaments
(HAGL) lesion 45 where the pathology is found laterally at
the capsular insertion on the humerus. Warner and Biem46
have recently reported a case involving both a Bankart and
HAGL lesion. Therefore, tissue failure can be seen any-
where along the bone-capsuloligamentous-bone complex
of the IGHLC. Single lesions alone do not appear to be
solely responsible for the clinical manifestation of instabil-
ity where the underlying cause is more likely multifactorial
in nature.
To this end, Bigliani eta] 47 have performed a cadaveric
study that supports the role of plastic deformation in
addition to insertional detachment of the IGHLC in the
development of anterior instability. In this study, the
inferior glenohumeral ligament was divided into 3 bone-
ligament-bone preparations: the anterior band, the anterior
axillary pouch, and the posterior axillary pouch. The
specimens were loaded in tension to failure. Strain to
failure for all of the bone-ligament-bone preparations
averaged 27%. Three modes of failure were observed: at
the site of the glenoid insertion (40%), in the midsubstance
of the ligament (35%), and at the site of the humeral
insertion (25%). Even when failure occurred at the site of
the glenoid insertion, it occurred only after significant
elongation of the IGHL.
A follow-up study performed by this same group also
looked at the geometric and strain-rate-dependent proper-
ties of the IGHL. 48 At the strain rates tested, bone-to-bone
strain was always greater than midsubstance strain, indicat-
ing that when the IGHL is stretched, tissue near the
insertion sites will experience much greater strain than the
tissue in the midsubstance. Insertion failures were more
likely at the slower strain rates, and midsubstance tears
occurred predominantely at the higher strain rate. The
elastic and plastic behavior of the IGHLC under tensile
load has also been investigated (Lintner and Speer, unpub-
lished data, January 1996). The IGHLC was shown to have
a combination of elastic and plastic properties at all load
levels tested. At the lower anterior displacement levels, the
IGHLC exhibited a relatively greater amount of elasticity
with little plastic deformation. As the loads and anterior
displacement increased, the elastic properties diminished
and the amount of plastic deformation gradually increased
to the point of ligament failure.
DOUKAS AND SPEER
 Several clinical studies have reinforced that capsular
injury can occur concurrently with a Bankart lesion during
an anterior dislocation. Rowe et a149,5°found an abnormal
capsular redundancy in 28% of patients who had recurrent
anterior dislocations and in 26% of those who had recur-
rent subluxations in their series. These investigators also
found that the anterior aspect of the capsule was stretched
or elongated in 86% of operative procedures that failed.
Appreciation of intrasubstance capsular injury with concur-
rent Bankart lesions provides a more accurate anatomic
basis for decision making.
Posterior Translation: Static Stabilizers
Unlike the anterior structures, the posterior capsule is
relaf:ively thin with less clearly defined ligamentous com-
ponents, especially superiorly above the equator. Although
O'Brien et a134,35have described a posterior thickening or
band of the IGHLC, other investigators 47 have found its
presence to be inconsistent. This may in part reflect
variation in sampling depending on glenohumeral position-
ing. This region has, however, been shown to be the
primary capsuloligamentous restraint to posterior transla-
tion at higher degrees of elevation and internal rotation. 51
These same authors also reported that if, in isolation, the
posterior capsule was completely incised, the glenohu-
meral joint did not dislocate posteriorly. For dislocation to
occur in the flexed, adducted, and internally rotated
shoulder, in addition to the posterior capsule, the anterior-
superior quadrant of the capsule, or rotator cuff interval,
had to be incised as well. Anatomically, this triangular
space lies between the the anterior aspect of the supraspi-
natt~s tendon and the superior border of the subscapularis
tend on, which help form the roof and floor of the biceps
aperture, respectively. This region also contains the SGHL
as well as the larger, extraarticular coracohumeral ligament
(CHL), which both run parallel in course. There is evidence
that the CHL is more of an infolding of the anterior-
superior capsule and not a true ligament because it lacks
collagenous organization on the microscopic level. 52 The
SGHL and, perhaps to a lesser degree, the CHL serve as
secondary restraints to posterior translation in the flexed,
adducted, and internally rotated shoulder. 36,37,53Harryman
et a154 have also shown the importance of the rotator cuff
intel~cal tissue in posterior and inferior translation. Incision
of the rotator interval capsule increased posterior transla-
tion by 50% and inferior translations by 100%, suggesting
resultant overlap in magnitude and direction of the vari-
ous capsular regions to the overall instability pattern.
Inferior Translation: Static Stabilizers
Warner et a136have shown that an increase in the acromio-
humeral interval, demonstrated by a palpable sulcus sign
at 0 ° of abduction, reflects the status of the superior
structures of the shoulder, specifically the SGHL and CHL,
as well as overall capsular integrity via the negative
intra articular pressure effect. Harryman et a154also showed
the importance of this anterior superior region of the
shot~Jder capsule in inferior translation. Incising this rota-
tor :interval capsule increased the subsequent inferior
translation by more than 100%. Of note, imbricating this
rotator interval capsule decreased inferior translation to a
SHOULDER INSTABILITY
degree less than the intact state with a subsequent loss of
external rotation.
At 0 ° of abduction, the IGHL plays only a minor role in
inferior stability; however, with increasing amounts of
abduction beyond 45 °, the anterior and posterior bands of
the IGHL become the primary stabilizers to inferior transla-
tion. 36 With rotation, the IGHL has an even greater role in
resisting inferior translation. At 90 ° of abduction, the
posterior band of the IGHL becomes the primary restraint
to inferior translation. A sulcus sign at neutral elevation
that persists in external rotation is highly suggestive of a
substantial rotator interval lesion. This results in increased
intracapsular volume that may contribute to multidirec-
tional or bidirectional instability, a concept introduced by
Pollock and Bigliani. as This work has expanded on that
done by Matsen et a155 that emphasized the distinction
between traumatic unidirectional instability (TUBS) and
atraumatic multidirectionals (AMBRI). At present, there is
more recognition of a clinical continuum where the magni-
tude of the inferior component of this complex can indicate
the overall pathoanatomy of instability (Fig 5).
M I C R O T R A U M A T I C INSTABILITY
Overhead athletes involved in events such as throwing,
swimming, and tennis put the shoulder at considerable
risk of injury. Placing the shoulder at the extremes of
motion under rigorous conditions renders it susceptible to
the development of instability through a mechanism of
plastic capsular deformation. Improper throwing mechan-
ics, either primary or adaptive, do not allow safe genera-
tion and dissipation of energy about the shoulder. The
concept of internal impingement has been introduced by
Walch et aP 6 and Jobe et al. 57 Repetitive throwing motion,
specifically forced abduction and external rotation ( +exten-
sion), generates tremendous humeral angular velocities
and rotational torques that, over time, can weaken the
anterior static restraints and lead to trauma on the under-
surface of the rotator cuff against the posterosuperior
glenoid. This has been postulated to result from fatigue of
the rotator cuff and parascapular musculature, which leads
to microtrauma and stretching of the anterior static stabiliz-
ers. Subsequently, there is loss of the obligate posterior
humeral translation that normally accompanies external
rotation, and the humeral head remains in a more anterior
position. This in turn leads to trauma on the undersurface
of the supraspinatus and infraspinatus tendons causing
pain and weakness that further aggravates the instability. 58
Biomechanical studies have shown that the posterior cuff is
capable of decreasing strain in the IGHL in the cocking
phase of throwing. 59 Glousman et aP ° showed, through
dynamic electromyographic analysis, decreased activity of
the internal rotators and serratus anterior during cocking
motion in throwing athletes with underlying anterior
glenohumeral instability, although it is difficult to conclude
whether this is cause or effect. The infraspinatus muscle
pattern was found to be no different from normal controls.
Therefore, microinstability appears to occur as an intrinsic
phenomenon and may be reversible to some degree with
neuromuscular conditioning.
Subtle anteroinferior instability in the younger, competi-
tive athlete is now less often mistaken for outlet impinge-
183

ment. Although true subacromial impingement can occur,
this is more often a finding in the older recreational athlete.
Jobe et a161-63 have categorized overhead athletes with
shoulder pain into 4 subgroups. Group I includes patients
with pure impingement without signs of instability, and
generally are over the age of 35 years. Group II patients
have primary instability with secondary internal impinge-
ment; typically, symptoms include pain posteriorly with-
out overt complaints of instability. These patients have a
positive relocation test (relief of pain with a posteriorly
directed force in the abducted, externally rotated shoulder)
in addition to positive impingement signs. Group III
patients have increased ligamentous laxity with signs and
symptoms of instability. Group IV patients have classic
anterior instability manifest on examination as true appre-
hension that is relieved with the relocation maneuver.
There is some evidence that eccentric loads on the biceps
anchor during the deceleration phase of throwing can lead
to superior labral anterior and posterior (SLAP) lesions as
described by Snyder et a164that may in turn contribute to
instability. 6°,65 By acting to increase joint compression, the
long head of the biceps appears to play both a static and
dynamic role in glenohumeral stability. 1° In internal rota-
tion, it limits anterior translation, and in external rotation,
it limits posterior translation, both of which are more
pronounced at lower levels of elevation. Furthermore,
Rodosky et a166have shown in a cadaveric model that, with
simulated rotator cuff forces, activation of the biceps
decreases the stresses on the IGHL with the arm in an
abducted and externally rotated position. Pagnani et a167
created lesions of the superior portion of the glenoid
labrum, both complete and incomplete (excluding the
biceps anchor), and tested the effects on glenohumeral
translation with and without an application of force to the
biceps. The capsule was vented in each shoulder before
testing to eliminate the effect of negative intraarticular
pressure. Incomplete lesions had no significant effect on
glenohumeral translation; however, complete lesions that
also destabilized the biceps anchor resulted in significant
increases in glenohumeral translation both in the anteropos-
184
Fig 5. The magnitude of
an associated sulcus sign
with documented ante-
rior instability can indi-
cate the overall patho-
anatomy of the instability
pattern. A lesion in the
IGHLC can account for a
small sulcus sign at 0 ° of
abduction. However, with
sulcus signs of 2+ or
greater in neutral abduc-
tion, a defect or insuffi-
ciency in the SGHL or ro-
tator interval capsule
should be considered.
(Reprinted with permis-
sion. 74)
terior and superoinferior directions. Anterior translation
increased by approximately 6 m m with a slight increase in
inferior translation as well. These persisted despite applica-
tion of a force to the biceps. This was most notable in the
lower and midranges of elevation in neutral and internal
rotation where the SGL and MGHL exert the greatest
influence on stability. This evidence supports the clinical
finding that SLAP lesions can present with subtle forms of
shoulder instability.
ATRAUMATIC INSTABILITY
Atraumatic instability is most likely a misnomer since
epidemiology studies have failed to prove a causal relation-
ship between instability and congenital laxity. An embryo-
logical study performed by Uhthoff and Piscopo 68 showed
anterior capsular redundancy of the shoulder suggesting a
congenital etiology. Laxity itself, however, does not appear
to be the sole reason for instability because excessive
bilateral shoulder laxity is quite common in adolescence in
the absence of any symptoms. 69 This inherent capsular
laxity decreases with age. Furthermore, no conclusive
evidence currently exists that suggests an underlying
collagen synthesis disorder that can account for or predict
individuals at risk of the development of instability. 7°
It is difficult to define "atraumatic" because activities of
daily living and improper shoulder mechanics may lead to
tissue damage on the molecular level. It is possible that
atraumatic instability is actually secondary to repetitive
microtrauma because bilateral laxity is often present.
O'Driscoll and Evans 3 found a 25% subsequent contralat-
eral involvement after treatment. Atraumatic instability
includes the diagnosis of multidirectional instability (MDI)
as first described by Neer and Foster. 71 In this subset of
patients, the inferior pouch is often found to be patulous
with global attenuation of the capsuloligamentous struc-
tures. Redundancy of the rotator cuff interval is also often
present and probably contributes to increased laxity, espe-
cially in the posterior and inferior directions, s4 Osseous
abnormalities are not generally present. Muscle imbalance,
DOUKAS AND SPEER
especially weakness of the rotator cuff, can lead to depen-
d e n c y on the capsule as the p r i m a r y restraint to transla-
tional forces, which m a y ultimately result in fatigue failure
b e y o n d the viscoelastic material properties of the capsule.
This ultimately results in capsular stretching that m a y
progress to s y m p t o m s of instability.
Clinically, these patients m a y have m a n y of the stigmata
associated with generalized joint laxity, including genu
recurvatum, hyperextensibility of the elbows and metacar-
pophalangeal joints, as well as the ability to passively
abduct the t h u m b to forearm. Therefore, it is i m p o r t a n t to
p e r f o r m a t h o r o u g h examination of the shoulder to deter-
mine the direction and m a g n i t u d e of the instability pattern
so that the appropriate treatment is provided.
CLINICAL EXAMINATION
After a t h o r o u g h history that includes onset, circum-
stances, direction, frequency, and magnitude, the clinical
examination is the essential first step in determining the
pattern and degree of the instability. Several interrelated
factors come to bear including patient relaxation and
cooperation as well as f u n d a m e n t a l principles of p r o p e r
physical examination techniques. Scapular stabilization is
a critical prerequisite for accurate assessment of glenohu-
meral pathology. The clinical examination is based on the
initial concentric reduction of the h u m e r a l h e a d within the
glenolabral socket. This is done b y positioning the shoul-
der in the scapular plane, initially maintaining neutral
rotation. Manual force is placed at the elbow to concentri-
cally reduce the h u m e r a l head. Anterior and posterior
forces are then applied to the proximal h u m e r u s in varying
degrees of rotation and elevation, and the a m o u n t of
translation is g r a d e d (Fig 6). Altcheck et a172 have devel-
o p e d a grading system in which translation is grade 1+
(the examiner can translate the h u m e r a l head further in the
anterior or posterior direction than the contralateral shoul-
der, b u t not j u m p the h u m e r a l h e a d over the labral rim), 2 +
(the examiner can subluxate the h u m e r a l h e a d over the
Fig 6. Examination under anesthesia demonstrating 3+ ante-
rior translation. (Reprinted with permission. 7s)
SHOULDER INSTABILITY
glenoid rim, but the h u m e r a l head spontaneously returns
to the neutral position w h e n the applied force is with-
drawn), or 3+ (the examiner can lock the humeral head
over the glenoid rim). For anterior instability, a 1+ or
greater examination m a y be considered pathologic. For
posterior instability, only a 3 + examination is considered
truly pathologic in athletes since m a n y normal shoulders
can be subluxated u p to 50% posteriorly. Comparison with
the opposite, nonaffected shoulder is essential.
Inferior translation is m e a s u r e d b y the sulcus sign. The
shoulder is first held in 0 ° of abduction, neutral rotation,
and neutral flexion/extension. The acromiohumeral inter-
val is then palpated and graded: 1+ (acromiohumeral
interval u p to 1 cm), 2+ (acromiohumeral interval mea-
sures b e t w e e n i to 2 cm), or 3 + (acromiohumeral interval
greater than 2 cm). The interpretation of the sulcus sign as
pathologic should be reserved for examination grades of
2+ or greater. A pathologic sulcus (--2 +) at 0 ° of abduction
that persists in external rotation is highly suggestive of a
rotator cuff interval lesion. This is c o m m o n l y associated
with bidirectional or multidirectional instability, and must
be considered in the overall assessment of the instability
pattern.
Examination u n d e r anesthesia, which can be instrumen-
tal in delineating subtle instability patterns, should be
c o m p a r e d with examination in the clinic and the examina-
tion of the opposite shoulder. U n d e r s t a n d i n g the anatomy,
pathophysiology, and biomechanics of the shoulder, com-
bined with a t h o r o u g h clinical examination and a clear
definition of the pathoanatomy, can then be synthesized to
form the basis for the most effective treatment strategy.
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