Ashley J. Bassett, MD and Steven B. Cohen, MD
ANATOMY AND BIOMECHANICS
The glenohumeral joint is a highly specialized, multiaxial ball-and-socket articulation that yields the greatest joint range of motion in the human body at the expense of skeletal stability. The humeral head is a spherical structure roughly 3 times larger than the glenoid cavity of the scapula. Only 25% to 30% of the head articulates with the shallow glenoid fossa at any given time.1 The scarcity of bony constraint and minimal articular surface contact allow for sizable arcs of shoulder motion but also predisposes to instability. Glenohumeral stability is instead provided by a combination of static soft tissue structures and dynamic restraints.
Static stability is conferred by the glenohumeral geometry, adhesion-cohesion forces mediated by the synovial fluid, glenohumeral capsule, coracoacromial arch, glenoid labrum, and the glenohumeral ligaments. The glenoid fossa has on average approximately 7 degrees of retroversion and 5 degrees of superior tilt relative to the scapular spine, contributing inferior stability to the articulation.2 Synovial fluid stabilizes the glenohumeral joint through the process of adhesion cohesion, where molecular attraction of the synovial fluid to itself, termed cohesion, and to the joint surfaces, termed adhesion, holds the 2 joint surfaces together. An intact glenohumeral capsuloligamentous complex fully seals the joint space, containing the synovial fluid and maintaining negative intra-articular pressure to further add to overall joint stability.
The coracoacromial arch confers anterosuperior stability and is formed by the coracoid, coracoacromial ligament, acromioclavicular joint and clavicle. The glenoid labrum is a fibrocartilaginous structure circumferentially attached to the glenoid rim that is integral to glenohumeral stability. The labrum increases the anteroposterior dimension of the glenoid and deepens the glenoid cavity approximately 50%, expanding the articular surface contact area for the humeral head.2 It also creates a vacuum seal around the glenohumeral articulation and is essential for the concavity compression mechanism of stability generated by the rotator cuff musculature.3 Additionally, the glenoid labrum provides a mechanical bumper to humeral head translation and serves as an attachment point for the glenohumeral ligaments.
Once thought to be mere capsular thickening, the glenohumeral ligaments have been increasingly recognized as vital to the static stability of the shoulder joint. The superior glenohumeral ligament (SGHL) originates on the anterosuperior labrum and inserts just superior to the lesser tuberosity. The coracohumeral ligament (CHL) is closely associated with the SGHL and spans from the lateral surface of the coracoid to the greater and lesser tuberosities, crossing the bicipital groove. The SGHL and CHL are both found within the rotator interval, a triangular-shaped area demarcated superiorly by the anterior edge of the supraspinatus, inferiorly by the superior border of the subscapularis and laterally by the coracoid base. The 2 ligaments work in concert to limit inferior translation and external rotation of the adducted shoulder. The anatomy of the middle glenohumeral ligament (MGHL) is quite variable and may be absent in up to 30% of shoulders.4 Most commonly it originates on the anterior labrum near the SGHL and inserts onto the lesser tuberosity. The MGHL restrains anterior translation of the humeral head with the shoulder in 45 to 60 degrees of shoulder abduction. The inferior glenohumeral ligament (IGHL) arises from the anteroinferior labrum and inserts just inferior to the MGHL. The IGHL is the strongest of the glenohumeral ligaments and is composed of an anterior band, a posterior band, and the axillary pouch. The anterior IGHL (AIGHL) restrains anterior and inferior translation of the humeral head with the shoulder in 90 degrees of abduction and external rotation. The posterior IGHL (PIGHL) limits posterior and inferior translation of the humeral head with the shoulder in 90 degrees of abduction and internal rotation. With the shoulder in neutral rotation and 90 degrees of abduction, the axillary band restrains inferior translation of the humeral head.5
The dynamic stabilizers of the glenohumeral joint include the rotator cuff complex, deltoid, long head of biceps, and the scapular stabilizing muscles. Stability is achieved through a combination of joint concavity-compression, coordinated muscle contraction with balancing of coupled forces, and glenohumeral ligament dynamization through direct attachment to the rotator cuff.6 The rotator cuff complex provides a medially directed force, centering and compressing the humeral head against the glenoid and maintaining the humeral head in a depressed position. During shoulder motion, the synergistic action of the rotator cuff and deltoid muscles maintain balanced force couples in both the coronal and axial planes. Coordinated contraction of the supraspinatus balances the superiorly directed force generated by the deltoid. The posterior rotator cuff, the infraspinatus, and teres minor, are balanced in the transverse plane by the subscapularis anteriorly. The long head of biceps tendon is thought to depress the humeral head during shoulder abduction, providing further superior stability.7
The trapezius, latissimus dorsi, serratus anterior, rhomboids, and levator scapulae muscles work to stabilize the scapula during shoulder motion and thereby increase dynamic stability of the glenohumeral joint. Coordinated contraction of the shoulder girdle musculature is essential for synchronous movement between the scapula and the humerus, termed scapulohumeral rhythm. During shoulder elevation, contraction of the trapezius and serratus anterior rotate the scapula upward while counteracting the downward rotational force generated by the deltoid and rotator cuff complex. The serratus anterior also posteriorly tilts the scapula, directly approximating the scapula to the thorax and constructing a more stable base for shoulder motion. The rhomboids and levator scapulae muscles work synergistically to prevent excessive lateral scapular translation by the upper serratus anterior.8 The periscapular muscles work in concert to produce efficient shoulder motion and further stabilize the glenohumeral joint during range of motion.
Biomechanics of Pitching
Overhead athletes, particularly pitchers, experience significant and repetitive torsional, distractive. and compressive forces at the glenohumeral joint. The sequential phases of an overhead baseball pitch have been well defined and are characterized by synchronous activation of select muscle groups within a kinetic chain. Energy is transmitted from the lower extremities, through the pelvis and trunk, to the upper extremity, and ultimately distally to the hand to power ball release, the so-called kinetic chain.9 The 6 phases of the throwing motion are windup, early cocking or stride, late cocking, acceleration, deceleration, and follow through (Figure 24-1).10
The windup phase begins with initial movement of the lead leg and ends when the lead leg reaches maximum knee height, in a position termed the balance point. The center of gravity is over the back leg to allow efficient generation of maximum momentum once forward motion is initiated. Upper extremity muscle activity and risk of injury are both low in this phase compared to the remainder of the pitching motion.11
The early cocking or stride phase spans begins at the point of maximum lead knee height and ends when the lead foot contact with the pitching mound. Proper positioning of the lower extremities, pelvis, and trunk is crucial for efficient transfer of energy from the lower extremities to the upper extremity. The lead foot should be directed toward home plate or slightly “closed” toward third base to optimize pelvic rotation and energy transfer. Excessively closed lead foot placement can limit pelvic and hip rotation, whereas an excessively open lead foot position can cause premature pelvic rotation, both of which result in less energy transferred to the arm and loss of momentum. The upper extremity must subsequently generate more velocity, increasing the stress on the anterior shoulder and medial elbow and predisposing to injury. At the shoulder, serratus anterior, middle trapezius, rhomboids, and levator scapulae muscles position the scapula in upward rotation and retraction to provide a stable glenoid for humeral head rotation. The deltoid is active early in the stride phase to aid in abduction of the shoulder. The supraspinatus, infraspinatus, and teres minor become active later in the phase to initiate shoulder external rotation.11
The late cocking phase begins with lead foot contact and ends at the point of maximum external rotation of the throwing shoulder. The upper torso continues to rotate, building angular and rotational velocity, as the pelvis reaches maximum rotation. The trunk begins a derotational pattern back toward the lead leg. The trapezius, rhomboids, and levator scapulae muscles retract and rotate the scapula upward to ensure sufficient subacromial space to accommodate hyperabduction of the humeral head without impingement. The infraspinatus and teres minor generate significant humeral external rotation. The supraspinatus is the least active of the rotator cuff complex in this phase and is thought to mainly function to provide glenohumeral compression and humeral head depression, thereby resisting the distraction forces at the shoulder caused by the torque of the rapidly rotating upper torso. As the shoulder reaches maximum external rotation, the subscapularis, pectoralis major, and latissimus dorsi eccentrically contract to terminate external rotation and stabilize the anterior shoulder.
The acceleration phase begins at the point of maximum shoulder external rotation and ends at ball release. The trunk continues to rotate toward the lead leg and tilt forward, generating angular momentum that is transmitted to the upper extremity. The serratus anterior protracts the scapula to maintain a stable base as the anterior deltoid and pectoralis major horizontally adduct the humerus to bring the throwing arm anterior to the torso. The anterior shoulder musculature—the subscapularis, pectoralis major, and latissimus dorsi—shift from eccentric contraction to maximum concentric contraction, resulting in high-velocity internal rotation of the humerus. The posterior shoulder muscles—the infraspinatus, teres minor, and posterior deltoid—shift from concentric contraction to eccentric contraction to counteract the enormous force generated as the arm is adducted and internally rotated during this phase.
The deceleration phase begins at ball release and ends at the point of maximum humeral internal rotation, horizontal adduction to 35 degrees, and maximum elbow extension.12 This is the most violent phase of the throwing cycle, characterized by excessive glenohumeral distraction with large posterior and inferior shear forces and extreme eccentric loading of the rotator cuff to resist joint distraction and anterior humeral head translation. The trapezius, serratus anterior, and rhomboid muscles work to decelerate the shoulder girdle and stabilize the scapula. Eccentric contraction of the biceps and brachialis muscles decelerates the rapidly extending elbow and pronates the forearm. The follow-through phase proceeds until forward motion ceases and the pitcher returns to the fielding position. There is minimal muscle activity and joint forces during this phase, lessening the risk of injury.
Maximum torque forces at the glenohumeral joint occur during the late cocking, early acceleration, and deceleration stages. Repetitive excessive torque stress can ultimately result in adaptive structural changes of the glenohumeral joint, as well as the development of true glenohumeral pathology including labral tears, rotator cuff injury, and capsular trauma.
Adaptive Changes of the Glenohumeral Joint
Adaptive anatomic and nonpathologic changes of the glenohumeral joint are often seen in throwing athletes as a result of the repetitive stresses associated with the overhead throwing cycle. It is crucial to recognize these osseous and soft tissue irregularities and differentiate them from true pathology that may warrant intervention. Common osseous adaptations seen in throwing athletes include increased proximal humerus retroversion, increased glenoid retroversion, cystic changes in the posterolateral humeral head, and sclerosis of the posterosuperior glenoid rim. Soft tissue changes include attenuation of the AIGHL and anterior capsule, thickening of the PIGHL and posterior capsule, and alteration in scapular position and motion and overall upper extremity kinematics.13 Bony and soft tissue adaptations both have been postulated to contribute to the altered arc of shoulder motion seen in throwing athletes.
The proximal humerus originates as a retroverted structure in utero and progressively derotates through childhood and adolescence until approximately age 16 years.14 The proximal humeral physis is most resistant to tensile forces and least resistant to torsional forces.15 In the skeletally immature overhead throwing athlete, repetitive rotatory forces at the proximal humeral growth plate can limit the natural physiologic derotation and lead to increased proximal humerus retroversion at skeletal maturity. Whereas the average adult has less than a 5-degree difference in mean retroversion between the dominant and nondominant arm, throwing athletes demonstrate a significant greater difference in mean retroversion between the dominant throwing arm and nondominant arm.16,17 Collegiate and professional throwers demonstrate greater than 10 degrees of increased retroversion in the dominant shoulder compared to the nondominant arm, as well as increased glenoid retroversion. These osseous changes are associated with a greater arc of shoulder external rotation and greater total arc of shoulder motion, thought to enhance performance and potentially decrease risk of shoulder injury. By positioning the glenohumeral joint in greater baseline external rotation, humeral and glenoid retroversion is thought to decrease the strain on the anterior capsuloligamentous structures and maximize the rotational torque generated during the throwing cycle.18,19
Structural changes of the joint capsule and glenohumeral ligaments are also seen in throwing athletes and contribute to alteration in glenohumeral motion. The posterior capsule of the dominant shoulder demonstrates increased thickness and decreased tissue elasticity compared to the nondominant shoulder in overhead-throwing athletes.20,21 This soft tissue adaptation develops in response to excessive and repetitive tensile stresses experienced by the posterior capsuloligamentous complex. In the deceleration phase of the throwing cycle, the posterior rotator cuff and posterior glenohumeral capsule counteract the extreme joint distraction forces generated during the acceleration phase. Recurrent tensile forces and microtrauma concentrated at the posteroinferior capsule and PIGHL may ultimately trigger a fibroblastic healing response with increased collagen production, capsular hypertrophy, and loss of tissue compliance.22 Tightening of the posterior capsule is thought to protect the shoulder by better mitigating the distractive forces at the glenohumeral joint during deceleration. Posterior capsule tightness also shifts the humeral head center of rotation posteriorly and superiorly, which can lead to anterior pseudolaxity by detensioning the anteroinferior capsuloligamentous structures.13 Anterior pseudolaxity without subluxation should not be mistaken for be true pathologic anteroinferior capsular attenuation with resultant anterior laxity.
Many of the structural adaptations of the glenohumeral joint observed in the throwing athlete are nonpathologic and may in fact serve to increase shoulder range of motion and enhance athletic performance. Increased shoulder motion has been correlated with greater arm cocking and ball velocity in elite pitchers.23 However, as with any adaptive response, too much compensation along the spectrum of structural change can disrupt the delicate balance of the glenohumeral joint mechanics and progress to shoulder injury.
Glenohumeral instability comprises a spectrum of pathology ranging from subtle subluxation episodes to frank dislocation. Instability may arise from an acute traumatic event, repetitive microtrauma to the shoulder, or generalized ligamentous laxity. Shoulder instability may be further categorized as unidirectional, including anterior or posterior instability, or multidirectional. Instability in the overhead throwing athlete is a unique entity and has been described as subtle instability or pathologic acquired laxity resulting from repetitive microtrauma to the glenohumeral joint and capsuloligamentous complex.24,25
In overhead-throwing sports, the shoulder is very susceptible to injury due to substantial forces concentrated at the glenohumeral joint during the pitching cycle. With continued high-intensity throwing, the repetitive stress eventually exceeds the tensile strength and repair capabilities of the static joint restraints and progressive damage occurs. The capsule and glenohumeral ligaments are progressively attenuated, allowing for subtle subluxation of the glenohumeral joint. The dynamic joint stabilizers initially compensate for this microinstability by increasing muscle activity during shoulder motion; however, in the setting of continued activity, the dynamic stabilizers eventually fatigue. As the compensatory mechanisms wane, glenohumeral instability worsens and subluxation events become more frequent. Recurrent humeral head subluxation results in damage to the labrum, glenoid rim, and humeral head, as well as impingement of the rotator cuff. Ultimately, a combination of capsular laxity, labral detachment, osseous defects of the humeral head or glenoid, and rotator cuff pathology contribute to progressive shoulder pain and dysfunction.
Anterior Glenohumeral Instability
In the late cocking and early acceleration phases of the throwing cycle, the glenohumeral joint is subject to a tremendous external rotational torque with significant shear forces applied to the anteroinferior capsuloligamentous complex. Over time, the repetitive insult leads to gradual tensile failure and attenuation of the anterior capsule with a subtle increase in glenohumeral translation.26 Increased activity of the posterior deltoid and rotator cuff complex compensates for the mild glenohumeral instability, but with continued overhead throwing the dynamic stabilizers gradually fatigue. Without the support of the surrounding musculature, the anteroinferior capsular tissue experiences increased loads and eventually fails. Although progressive stretching and redundancy of the anterior capsule is most often the mechanism of anterior instability, isolated tears of the anterior capsule and humeral avulsion of the glenohumeral ligament have also been reported in professional baseball players with anterior microinstability.27,28
Excessive anterior translation of the humeral head during the late cocking and early acceleration phases results in tearing of the anterior and anteroinferior labrum (Bankart lesion) with further loss of glenohumeral stability. As the humeral head subluxates anteriorly, it contacts the coracoacromial arch and can lead to subacromial impingement and rotator cuff tendinitis. The undersurface of the posterior rotator cuff complex may also impinge on the posterosuperior border of the glenoid rim during excessive anterior humeral head translation with development of partial articular-sided rotator cuff tears (internal impingement).
Posterior Glenohumeral Instability
Osseous morphology of the glenoid and proximal humerus contributes to the static stability of the glenohumeral joint, and altered anatomy has been linked to the development of posterior instability.29 Humeral head and glenoid retroversion, glenoid hypoplasia, posterior glenoid bone loss—acutely traumatic or attritional—and reverse Hill Sachs lesions of the proximal humerus are all associated with recurrent posterior glenohumeral instability. Increased retroversion of the humeral head and glenoid is a bony adaptation seen in overhead throwers and facilitates the supraphysiologic range of shoulder motion in these athletes. It is also thought to predispose throwers to posterior instability by generating an easier vector of posterior subluxation of the humeral head on the glenoid.30
The soft tissue stabilizers, the posterior capsuloligamentous complex and glenoid labrum, are particularly at risk for injury in 2 specific phases of the throwing cycle: late cocking and deceleration. During the late cocking phase, the arm is held in hyperabduction and maximum external rotation. Hyperangulation of the humerus in this position can result in internal impingement of the rotator cuff against the posterior glenoid and labrum. With repetitive throwing, degeneration and tearing of the posterior labrum may occur and contribute to loss of static glenohumeral stability. In the deceleration phase, the posterior rotator cuff and capsuloligamentous complex is subject to extreme tensile forces as the humerus continues to violently adduct, flex, and internally rotate following ball release. Repetitive eccentric stress can ultimately precipitate tensile failure of the posterior supraspinatus or anterior infraspinatus along the bursal surface of the rotator cuff. Diminished rotator cuff function in this phase leads to even greater tensile forces being transmitted to the posterior capsule and PIGHL. Recurrent microtrauma to the posterior capsuloligamentous complex may result in gradual attenuation and capsular laxity.31
Glenohumeral Internal Rotation Deficit
Repetitive tensile strain applied to the posterior capsule and ligamentous structures may conversely trigger a fibrotic healing response and capsular hypertrophy with loss of soft tissue compliance and limitation of shoulder motion. Glenohumeral internal rotation deficit (GIRD) is a change in rotational motion of the shoulder joint characterized by increased external rotation with a corresponding loss of interval rotation of greater than 25 degrees compared to the nonthrowing shoulder.32 Development of posteroinferior capsular contracture is thought to be the predominant underlying etiology of GIRD. Takenaga et al used ultrasound to measure the thickness and elasticity of the posterior capsule in 45 collegiate pitchers with the diagnosis of GIRD. The mean stiffness and thickness of the posteroinferior capsule was significantly greater in the throwing shoulder compared to the nonthrowing shoulder.21 Osseous anatomy may also contribute to the development of GIRD.33 A study by Noonan and colleagues demonstrated that pitchers with GIRD had a mean side-to-side difference in humeral retroversion of 19.5 degrees compared with the nondominant shoulder, whereas those without GIRD had only a 12.3-degree side-to-side difference in retroversion.34
The pathologic alteration of shoulder motion seen in throwers with GIRD results from stretching of the anterior soft tissues that resist external rotation—the coracohumeral ligament, rotator interval, and anterior capsuloligamentous complex—and contracture of the posterior soft tissues—the PIGHL, posterior capsule, pectoralis minor, and short head of the biceps—with subsequent posterior shift of the glenohumeral center of rotation.35 Excessive external rotation strains the biceps anchor, which can ultimately “peel back” under tension, culminating in injury to the superior and posterior labrum. Owing to the posterior shift of the humeral head center of rotation, impingement of the rotator cuff between the greater tuberosity of the humerus and the posterosuperior glenoid can occur, resulting in articular-sided partial rotator cuff tears (internal impingement).
Asynchrony of scapulothoracic motion and alterations both in static and dynamic scapular positioning has been associated with glenohumeral instability.36 Scapular dyskinesis arises from dysfunction of the periscapular muscles due to fatigue, trauma, or nerve injury. The resulting muscular imbalance can alter the normal scapulohumeral rhythm during the overhead-throwing motion. Specifically, patients with shoulder instability have exhibited excessive protraction and delayed retraction with shoulder elevation, linked to decreased activity in the lower trapezius and serratus anterior muscles.37 During the normal overhead-throwing motion, the scapula must retract in the cocking phases to keep the glenoid centered under the humerus. Failure of the scapula to retract appropriately results in hyperangulation of the humerus to achieve maximum external rotation with increased stress transmitted to the anterior capsuloligamentous complex.38 Loss of normal scapulohumeral motion also results in altered throwing mechanics and inefficient transfer of energy from the trunk to the arm with loss of ball velocity. Athletes may subsequently increase the work of the shoulder to compensate for lost velocity, which further increases strain on the glenohumeral stabilizers.
A thorough history and physical examination is critical when evaluating a throwing athlete for glenohumeral instability. Very few throwing athletes will report overt symptoms of instability; rather, diminished performance and shoulder pain are often the primary complaints.39 Concerns related to performance include loss of pitching velocity, loss of command of the pitch, and change in pitching mechanics. The onset, timing, and location of shoulder pain, as well as exacerbating and relieving factors, should be carefully determined. Most throwing athletes with instability cannot recall a particular inciting event or acute trauma to the shoulder. They often detail a gradual onset of intermittent deep shoulder pain that is reproduced by certain arm positions or in specific phases of the throwing cycle. Anterior shoulder pain in the late cocking phase, with the arm in an abducted and externally rotated position, can be indicative of anterior capsuloligamentous pathology. Posterior shoulder pain in the deceleration and follow-through phases, with the arm in an adducted, flexed, and internally rotated position, is more suggestive of injury of the posterior capsule and labrum. It is common for these athletes to report more than one location of pain that occurs in different phases of the throwing cycle, related to concomitant pathology such as subacromial impingement or rotator cuff/biceps tendinitis. Rotator cuff pathology is common in throwing athletes and is often characterized by night pain. Patients should be questioned about mechanical symptoms, such as grinding, clicking, or catching because these are associated with labral tears. Though less common, instability-related symptoms can be described as a feeling of the arm going dead or a frank sensation of the shoulder slipping out. Lastly, details about past treatment should be obtained, including prior shoulder immobilization, physical therapy and modalities, injections to the shoulder girdle, or surgical intervention.
Examination begins with careful inspection of the bilateral upper extremities and shoulder girdles, taking note of overall posture and symmetry. It is normal for the dominant extremity of a throwing athlete to have greater muscular development than the contralateral nondominant extremity.40 The deltoid, supraspinatus, and infraspinatus muscles are evaluated for atrophy. Atrophy of the supraspinatus and/or infraspinatus musculature suggests chronic rotator cuff dysfunction or suprascapular nerve injury. The static and dynamic positioning of the scapula is assessed for scapular dyskinesis and compared to the contralateral shoulder girdle. Resting scapular drooping or scapular winging with active elevation may be due to periscapular muscle fatigue or intra-articular pathology and should be noted. Shoulder landmarks should be palpated for tenderness, including the acromioclavicular joint, coracoid process, biceps tendon, greater tuberosity, posterior cuff, and capsule. Tenderness to palpation of the anterior joint line is often found in patients with anterior glenohumeral instability but is a nonspecific finding also seen in patients with impingement syndrome. Palpation of the posterior glenohumeral joint elicits tenderness in approximately 60% of patients with posterior instability.41
Shoulder range of motion should be assessed in the sitting position, as well as in the supine position to stabilize the scapula and eliminate scapulothoracic contribution to glenohumeral motion. Forward elevation in the scapular plane, and internal and external rotation at 0 degrees and 90 degrees of shoulder abduction are recorded and compared to the contralateral shoulder. Throwing athletes frequently exhibit increased shoulder external rotation with an associated loss of internal rotation in their dominant shoulder. This alteration in glenohumeral rotation is often due to adaptive nonpathologic changes of the glenohumeral anatomy and is associated with a preserved total arc of shoulder motion that is symmetric to the contralateral shoulder. Loss of the total arc of shoulder rotation, specifically in the setting of internal rotation deficit, is a common finding in the evaluation of an injured throwing athlete. Strength testing should include specific evaluation of the rotator cuff musculature and periscapular stabilizers. The pinch test can be used to assess scapular retraction strength.42 Inability to hold an isometric pinch of the scapula for 15 seconds indicates periscapular weakness.
Shoulder ligamentous stability is tested in the anterior, posterior, and inferior directions using a number of specialized examination maneuvers summarized in Table 24-1. Stability tests are performed on the bilateral shoulders. Increased laxity is expected in the dominant shoulder of a throwing athlete compared to the nondominant shoulder. Therefore, it is important to note whether distinct subluxation of the humeral head can be produced and if these provocative maneuvers reproduce the patient’s symptoms. Anterior shoulder instability is best evaluated with the patient in the supine position. The anterior apprehension, Jobe relocation, and anterior release tests can be used to assess for symptoms related to anterior instability, including a sensation of instability or anterior shoulder pain. Most throwers with subtle anterior instability will endorse anterior shoulder pain but no frank apprehension during these provocative maneuvers. The Jobe relocation test has high sensitivity and specificity if apprehension is the primary symptom; however, the diagnostic accuracy of this exam maneuver is poor if pain alone is evaluated.43 Reproduction of symptoms with the anterior release test is 90% sensitive for the diagnosis of occult anterior glenohumeral instability.44
The anterior drawer, posterior drawer, and load-and-shift tests are all used to measure translation of the humeral head and grade laxity using the modified Hawkins scale. Grade 1+ indicates increased translation to the glenoid rim but no subluxation, grade 2+ indicates subluxation of the humeral head over the glenoid rim, and grade 3+ indicates dislocation of the humeral head over the glenoid rim that does not spontaneously reduce.45 Throwing athletes are expected to have grade 1+ anterior laxity, and grade 2+ posterior laxity is not uncommon. Anterior laxity of grade 2+ or greater is usually suggestive of a pathologic condition. Recurrence of symptoms during these stress maneuvers, including pain and/or apprehension, is also considered a positive finding for anterior or posterior instability.46 Additionally, the jerk test and the Kim test both load the posterior labrum and can be used to assess specifically for posterior labral pathology and posterior instability.47 The jerk test has been shown to be more accurate for direct posterior labral tears, whereas the Kim test is better at identifying posteroinferior labral tears.48