bio mechanics of shoulder instability

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 glenohumeral 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 1,2 and 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 intraarticular pressure, glenohumeral bony geometry, the capsulolabral 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 dislocation, 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 proportional 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 capsuloligamentous structures are lax. The efficiency of this mechanism 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 negative 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 instability 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 7 9

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 permission. s )

study both in cadavers and in vivo. Classic studies teach an overall 2:1 ratio of glenohumeral to scapulothoracic motion 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 patients 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 glenohumeral 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 retroversion 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

translation (approximately 4 mm) that occurs with maximum extension and external rotation. This was not observed 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 a122 showed 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. 23 This speaks more to a true ball-in-socket relationship 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, contributing 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 ligament (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 algorithms toward the correction of the instability can be contemplated.

T R A U M A T I C I N S T A B I L I T Y

The athlete is subject to numerous repetitive loads during participation in sports that often can lead to symptoms of

1 8 0 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 dislocation 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 pathophysiology. 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-

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.

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Fig 2. Sagittal representation of the glenohumeral capsuloligamentous anatomy. A, anterior; P, posterior; B, biceps; SGHL, superior glenohumeral ligament; MGHL, middle glenohumeral ligament; IGHLC, inferior glenohumeral ligament complex (AB = anterior band, AP = axillary pouch, PB = posterior band); PC, posterior capsule. (Reprinted with permission. 34)

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 instability. 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, 34,35 using arthroscopy and histologi- cal analysis, have further delineated the IGHLC into anterior and posterior bands with an interposed axillary pouch. This has been compared with a hammock providing reciprocating restraint to translation in the 90 ° abducted 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

SHOULDER INSTABILITY 1 81

A . b d .

Fig 4. Reciprocating action of the IGHLC. Top left: In increasing 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. 38 This 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 considered 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 capsuloligamentous 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 mm 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 creation of the anterior lesion. Clinically, the injury complex

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. 42 This 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 multidirectional 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 way 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 Biem 46 have recently reported a case involving both a Bankart and HAGL lesion. Therefore, tissue failure can be seen anywhere along the bone-capsuloligamentous-bone complex of the IGHLC. Single lesions alone do not appear to be solely responsible for the clinical manifestation of instability where the underlying cause is more likely multifactorial in nature.

To this end, Bigliani e ta] 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 properties 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, unpublished 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.

1 82 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 recurrent 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 concurrent 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 components, especially superiorly above the equator. Although O'Brien et a134,35 have 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 translation 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 glenohumeral 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. 36,37,53 Harryman 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 translation by 50% and inferior translations by 100%, suggesting resultant overlap in magnitude and direction of the various capsular regions to the overall instability pattern.

Inferior Translation: Static Stabilizers

Warner et a136 have shown that an increase in the acromiohumeral 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 a154 also showed the importance of this anterior superior region of the shot~Jder capsule in inferior translation. Incising this rotator :interval capsule increased the subsequent inferior translation by more than 100%. Of note, imbricating this rotator interval capsule decreased inferior translation to a

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 translation. 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 multidirectional 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 magnitude of the inferior component of this complex can indicate the overall pathoanatomy of instability (Fig 5).

MICROTRAUMATIC 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 mechanics, 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 ( +extension), generates tremendous humeral angular velocities and rotational torques that, over time, can weaken the anterior static restraints and lead to trauma on the undersurface 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 stabilizers. 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-

SHOULDER INSTABILITY 183

Fig 5. The magnitude of an associated sulcus sign with documented anterior instability can indicate the overall pathoanatomy 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 abduction, a defect or insufficiency in the SGHL or rotator interval capsule should be considered. (Reprinted with permission. 74)

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 impingement; typically, symptoms include pain posteriorly without 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 a164 that 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 rotation, 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 a166 have 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-

terior and superoinferior directions. Anterior translation increased by approximately 6 mm with a slight increase in inferior translation as well. These persisted despite application 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.

A T R A U M A T I C I N S T A B I L I T Y

Atraumatic instability is most likely a misnomer since epidemiology studies have failed to prove a causal relationship between instability and congenital laxity. An embryological 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 contralateral 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 structures. Redundancy of the rotator cuff interval is also often present and probably contributes to increased laxity, especially in the posterior and inferior directions, s4 Osseous abnormalities are not generally present. Muscle imbalance,

184 DOUKAS AND SPEER

especially weakness of the rotator cuff, can lead to depen- dency on the capsule as the p r imary restraint to translational forces, which m a y ul t imately result in fatigue failure beyond the viscoelastic material propert ies of the capsule. This ul t imately results in capsular stretching that may progress to symptoms of instability.

Clinically, these patients may have many of the stigmata associated wi th generalized joint laxity, including genu recurvatum, hyperextensibi l i ty of the elbows and metacar- pophalangeal joints, as well as the ability to passively abduct the thumb to forearm. Therefore, it is impor tant to pe r fo rm a thorough examinat ion of the shoulder to determine the direction and magni tude of the instability pat tern so that the appropria te t reatment is provided.

CLINICAL EXAMINATION

After a thorough history that includes onset, circumstances, direction, frequency, and magni tude, the clinical examinat ion is the essential first step in determining the pat tern and degree of the instability. Several interrelated factors come to bear including patient relaxation and cooperat ion as well as fundamenta l principles of proper physical examinat ion techniques. Scapular stabilization is a critical prerequisi te for accurate assessment of glenohumeral pathology. The clinical examinat ion is based on the initial concentric reduct ion of the humera l head within the glenolabral socket. This is done by posit ioning the shoulder in the scapular plane, initially maintaining neutral rotation. Manual force is placed at the elbow to concentri- cally reduce the humera l head. Anterior and posterior forces are then applied to the proximal humerus in varying degrees of rotation and elevation, and the amount of translation is graded (Fig 6). Altcheck et a172 have devel- oped a grading system in which translation is grade 1+ (the examiner can translate the humera l head fur ther in the anterior or poster ior direction than the contralateral shoulder, bu t not jump the humera l head over the labral rim), 2 + (the examiner can subluxate the humera l head over the

Fig 6. Examination under anesthesia demonstrating 3+ anterior translation. (Reprinted with permission. 7s)

glenoid rim, but the humera l head spontaneously returns to the neutral posit ion when 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 examinat ion may be considered pathologic. For posterior instability, only a 3 + examination is considered truly pathologic in athletes since many normal shoulders can be subluxated up to 50% posteriorly. Comparison with the opposite, nonaffected shoulder is essential.

Inferior translation is measured by the sulcus sign. The shoulder is first held in 0 ° of abduction, neutral rotation, and neutral f lexion/extension. The acromiohumeral interval is then palpated and graded: 1+ (acromiohumeral interval up to 1 cm), 2+ (acromiohumeral interval mea- sures be tween i to 2 cm), or 3 + (acromiohumeral interval greater than 2 cm). The interpretat ion of the sulcus sign as pathologic should be reserved for examination grades of 2+ or greater. A pathologic sulcus (--2 +) at 0 ° of abduct ion that persists in external rotation is highly suggestive of a rotator cuff interval lesion. This is commonly associated with bidirectional or multidirectional instability, and must be considered in the overall assessment of the instability pattern.

Examination under anesthesia, which can be instrumen- tal in delineating subtle instability patterns, should be compared with examination in the clinic and the examination of the opposite shoulder. Unders tanding the anatomy, pathophysiology, and biomechanics of the shoulder, combined with a thorough clinical examination and a clear definition of the pathoanatomy, can then be synthesized to form the basis for the most effective t reatment strategy.

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bio mechanics of shoulder instability

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