The kinetic chain concept describes the coordinated motion that transmits energy in a synchronized fashion from the lower extremity, through the trunk, to the shoulder, and finally to the ball as it is released[23-25]. Key elements of the kinetic chain are leg strength, body rotation, core strength, scapular position and motion, and shoulder rotation. Inflexibility, weakness, and imbalance of any point in the kinetic chain can create a situation where the arm lags behind the legs and trunk, placing the throwing shoulder in a vulnerable position, increasing stresses about the shoulder and leading to injury.

This concept is vital to the throwing motion and has been broken down in to six distinct phases which comprise the throwing cycle. The first three phases consist of the wind-up, early cocking, and late cocking phases. These phases account for the bulk of the total time spent in the throwing motion (approximately 1.5 s), and they allow proper positioning of the lower extremities, core, and arms in preparation for release of the ball[15,26,27]. In the late cocking phase, the shoulder is placed in abduction (90-100 degrees) and maximal external rotation (170-180 degrees), the position commonly associated with internal impingement[7]. The fourth phase, the acceleration phase, is the phase in which the greatest angular velocity change is seen across the shoulder joint as the ball is propelled forward. This motion occurs at a rotational velocity of over 7250 degrees per second and is the fastest human motion to ever be recorded[24,28-30]. It follows that this phase results in the most injuries, despite being the shortest phase (0.05 s). As the ball is released, the deceleration phase and follow through phase are completed which result in a distraction force across the joint as the arm is slowed (0.35 s).

The “thrower’s paradox” refers to the delicate balance between mobility and stability which allows pitchers to achieve a high level of function[24,31]. To generate rational velocities upwards of 7000°/s, the arc of motion must be expanded to allow maximal external rotation of the shoulder. The normal arc of rotation of a healthy shoulder from maximal internal rotation to maximal external rotation is 180°[31]. The arc of motion in a high-level throwing athlete is shifted posteriorly to allow for increased external rotation at the cost of decreased internal rotation by allowing increased clearance of the greater tuberosity over the glenoid during rotation[2-4,21,23,25]. Increased external rotation is achieved by a number of shoulder adaptations that develop over time including increased retroversion of the humeral head and glenoid, and increased anterior capsular laxity[1,2,4,5,17,32].

Andrews et al[33] and Bigliani et al[34] have suggested that glenohumeral joint laxity is a common finding among throwing athletes. Jobe et al[12,32,35] originally described “subtle instability”, or microinstability, to define the acquired laxity and anterior translation of the humeral head that occurs with the arm in a maximally abducted and externally rotated position. At what point this laxity becomes pathologic is another matter of debate. Subtle instability is postulated to result from repetitive shear stresses during the cocking and acceleration phases and contributes to the development of labral tears and articular-sided rotator cuff tears. Paley et al[17] stated anterior instability is actually the most significant factor in the development of internal impingement.

Alternatively, some authors have posited that microinstability of the shoulder actually protects against internal impingement[3,7,21]. Cadaveric, magnetic resonance imaging (MRI), and arthroscopic studies have consistently shown that contact of the rotator cuff on the posterosuperior labrum is a normal, physiologic occurrence[3,21,23,28]. This theory postulates that the abnormal laxity of the humerus relative to the glenoid actually prevents impingement between the greater tuberosity and superior glenoid.

The anatomic changes allowing for increased external rotation can also result in remodeling of the posterior soft tissues, leading to contracture of the posterior capsule and posterior band of the inferior glenohumeral ligament[21]. This increased external rotation creates increased torsional and shear stress upon the biceps anchor and undersurface of the rotator cuff[1,7,28,32,35,36].

Despite the need for increased laxity, adequate stability must be maintained to prevent symptomatic humeral head subluxation, often achieved through further posterior capsular contracture. When present, these alterations can contribute to internal impingement and lead to rotator cuff tears, labral tears, capsular injuries, chondral injuries, and biceps tendon pathology. These findings were confirmed in a cadaveric model by Grossman et al[26], who reported on a simulated posterior capsular contraction model which led to GIRD and posterosuperior translation of the humeral head during the late cocking, ultimately resulting in SLAP injuries. Each of these processes can lead to pain, decreased velocity, loss of control, and diminished endurance in the throwing athlete.

Clinically, loss of 15 degrees or more of internal rotation in the throwing shoulder compared to the non-dominant arm is commonly seen. The potential for injury increases once this threshold has been reached. Burkhart et al[21,37], have reported that shoulders with an internal rotation deficit > 25 degrees are at increased risk for development of SLAP lesions as a result of increased posterosuperior peel back on the labrum. In addition, Dines et al[38] have shown that throwers with ulnar collateral ligament insufficiency at the elbow demonstrated a significant amount of GIRD as compared to players without a history of elbow injury.

Kibler[39] has defined scapular dyskinesis as an alteration in the normal resting position of the scapula or an alteration in the normal dynamic scapular motion. The scapula serves as an important link in the kinetic chain. When the scapula is unable to effectively transmit energy from the trunk to the pitching arm or stabilize the shoulder properly, pitching mechanics become inefficient and pitching velocity can suffer. Pitchers will then compensate by recruiting other surrounding musculature and increasing stress across the shoulder joint[39].

Scapular motion has been found to be more intricate than once thought. Instead of the proposed 2:1 ratio of humeral to scapular motion during forward elevation, recent studies have shown the scapula to have a more complex role in shoulder motion. Scapular motion is now defined in three planes: Internal/external rotation around a vertical axis, upward/downward rotation around a horizontal axis, and anterior/posterior tilt around a horizontal axis[39]. The intricate scapular positioning is controlled dynamically by force couples generated by the trapezius, serratus anterior, latissimus dorsi, and rhomboid musculature. These muscular couples contract before rotator cuff activation, allowing the cuff to contract against a stable scapular base[40].

Myers et al[41] have previously reported that throwers normally develop upward rotation, internal rotation, and retraction of the scapula during forward elevation of the humerus. Scapular dyskinesis may result from inflexibility or imbalances in periscapular muscles secondary to fatigue, direct trauma, or nerve injury[25]. In pitchers with poor scapulothoracic rhythm, there is a trend toward scapular internal rotation and protraction around the rib cage resulting from inflexibility or imbalances in the periscapular musculature[41]. When the scapula is ineffective in stabilizing the shoulder, the rotator cuff is forced to over-compensate to stabilize the glenohumeral joint. These loads are then transmitted to the superior glenoid and the articular surface of the rotator cuff tendons and can lead to injury. This alteration in function is thought to be an independent factor in the development of internal impingement. It follows that scapular dyskinesis has been reported in up to 100% of patients with internal impingement[40,42].

Once a diagnosis of internal impingement is made, non-operative management should be recommended as the first line treatment. The proper non-operative treatment can be tailored based on stages set forth by Jobe discussed earlier[35]. Patients in Stage I (those with complaints of stiffness and difficulty warming up but without localized posterior shoulder pain) should be prescribed a course of nonsteroidal anti-inflammatories and rest. Patients in Stage II (those with isolated posterior shoulder pain) usually require four to six weeks of rest and can also benefit from physical therapy[1]. Physical therapy has been shown to be both therapeutic and protective against further injury in several studies[21,22,31].

Given the pathophysiologic mechanism of internal impingement, therapy is focused on correction of aberrant shoulder range of motion and scapular dyskinesis. To that end, special attention should be paid to correction of GIRD through the “sleeper stretch” which allows posterior capsular stretching. In a study of high-level tennis players performing daily “sleeper stretch” exercises, patients were found to have significant increases in both internal rotation and total rotation, as well as a 38% decrease in the prevalence of shoulder problems[21] (Figure 4). In addition, scapular stabilization exercises should be recommended. As the throwing motion involves the entire body through the kinetic chain, core strengthening and lower body strengthening must also be stressed simultaneously. Lastly, proper throwing mechanics should be enforced, especially for younger athletes.

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Figure 4 Demonstration of the “sleeper stretch”.

Corticosteroid injections directed at the posteroinferior glenoid rim have been described[52]. These injections have mostly been used for diagnostic, rather than therapeutic, purposes. To this point, no compelling data has been published to support injections for internal impingement and should be used judiciously due to the potential risk of permanent tendon damage.

Due to the spectrum of pathology seen in internal impingement, multiple operative treatment options exist. Paley et al[17] published a series demonstrating > 80% incidence of concomitant articular-sided rotator cuff tear in professional overhead athletes with internal impingement. Often, this tear will be associated with an adjacent “kissing lesion” seen as a labral tear. Historically, treatment of these lesions has included debridement or repair and possible acromioplasty, with mixed results. Andrews et al[11] published a series of thirty-six overhead athletes with articular-sided partial tears of the supraspinatus that underwent arthroscopic debridement. They found 85% were able to return to their premorbid level of function, which they attributed to stimulation of tendon healing via debridement. Similarly, Sonnery-Cottet et al[20] performed arthroscopic debridement on twenty-eight tennis players with articular-sided partial tears and glenoid lesions. Seventy-nine percent were able to return to play, but 91% still had some persistent pain.

Historically, most surgeons have felt that lesions involving more than half of the thickness of a rotator cuff tendon should be repaired. Some authors support completion of these partial tears to aid in soft-tissue mobilization, followed by standard double-row repair[53-55]. More recent data suggests that partial tears up to 75% in high-level throwing athletes should be debrided unless they involve the anterior cable of the rotator cuff. The high forces that throwing athletes generate subject the cuff to intense stress and threaten the repair integrity[56]. In cases involving injury to the anterior cable, the anterior cable can be repaired and the partial thickness posterior cuff injury can be debrided. If partial tear completion and repair is indicated, a lateralized double-row repair as described by Dines et al[57], should be considered as it has shown favorable outcomes in professional overhead throwing athletes, allowing restoration of a more anatomic footprint.

Additional pathology seen in internal impingement includes SLAP tears, biceps tenosynovitis, and degenerative changes in the humeral articular surface[7,58]. Meister et al[45] reported their results of twenty-two overhead athletes with internal impingement who underwent debridement of the rotator cuff, biceps, and labrum. A subset of patients also underwent arthroscopic removal of a Bennett lesion. Only 55% of the cohort had returned to their premorbid level at 6 years post-op. Neri et al[59] also evaluated a cohort of high-level overhead athletes who underwent Type II SLAP repairs at a mean of three years follow up and found that only 57% were able to return to their pre-injury level of competition, while an additional 25% returned to sport but were limited by pain. These marginal results may be due to the higher demand elite overhead athletes place on their shoulders and higher expectations amongst the study group. In addition, Neri et al[59] showed that a statistically significant correlation did exist between the presence of partial-thickness rotator cuff tears and the inability to return to pre-injury level of play (Figure 5).

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Figure 5 Type 2B SLAP tear s/p repair.

Andrews et al[60] have suggested that the poor results of debridement alone could be attributed to unaddressed subtle anterior laxity. As a result, they advocated for concomitant open anterior stabilization. They reported a 92% success rate at an average of close to three years postoperatively in a cohort of twenty-five athletes. Other studies have had less-optimistic results[35].

Lastly, some authors have proposed osseous procedures to address the osseous changes which heavily contribute process of internal impingement. Riand et al[61] reported on humeral osteotomies to increase humeral retroversion in twenty patients who had continued pain after arthroscopic debridement. Eleven of the twenty patients were able to resume sports activities at the same level, and five were able to resume sports at a lower level.