In the overhead athletes, the “dead arm” syndrome has long been recognized as a potentially career-ending condition. Historically, the specific pathology has been poorly understood; only recently has greater insight been achieved into etiology; however, treatment remains controversial.

Athletes often complain of pain during the late cocking and acceleration phase, as the arm moves forward. The arm then “goes dead” and the athlete has loss of velocity and control; this, along with pain, prevents continued throwing and results in compromised performance. Various conditions have been observed, and debate concerning which model of pathology is most accurate is further complicated by the fact that
these conditions may be present in asymptomatic throwing athletes, thus suggesting a spectrum of variation, often with no clear distinction from the adaptive to the pathologic changes.

Internal impingement is a topic that has been controversial and also can be very confusing. Originally described by Walch et al. (4) as naturally occurring impingement between the posterior superior rotator cuff and the glenoid rim with arm in position of abduction and external rotation. Others noted this same occurrence in asymptomatic throwing athletes.

Jobe (5) later popularized the term as a pathologic condition occurring in overhead athletes leading to throwing injury. In this model, anterior capsular insufficiency was the inciting occurrence that subsequently led to further disability and the “dead arm.” Loss of integrity of the capsule is a direct result of hyperangulation of the throwing arm. The symptoms are exacerbated by the loss of the posterior rollback, which leads to anterior translation and results in greater internal impingement posteriorly. If untreated, it may lead to posterior labral tears, Superior Labrum Anterior and Posterior (SLAP) lesion due to peel-back, and partial thickness articular-sided rotator cuff tears. Treatment is focused at correcting the underlying instability and treating any additional pathology. Reports of capsulolabral reconstruction have shown some success in allowing pitchers to return to their previous level of competition (6,7).

The Morgan-Burkhart model (7a, 7b) suggests that the posterior capsular contracture is the inciting occurrence in the cascade of disability and injury. Posterior capsule tightness has long been recognized as a component of the throwing shoulder (8,9,10,11,12); at what point this becomes pathologic has been less well delineated. As the shoulder develops progressively worsening posterior contracture, the glenohumeral contact point is shifted further posterior and superior when the shoulder is in abduction and external rotation. A relative redundancy of the anterior capsule is observed due to the tightening of the posterior capsular structures—this is what has been observed as anterior capsular stretching in the Jobe model. As the thrower attempts to reach his or her set point for throwing, hyperangulation and hyperexternal rotation forces cause tensile overload of the rotator cuff leading to partial tears; additionally, a dynamic peel-back phenomenon generates SLAP lesion of the labrum. Glenohumeral Internal Rotation Deficit (GIRD) is defined as the loss in degrees of internal rotation as compared with the contralateral shoulder, with the arm positioned in 90 degrees of abduction and external rotation. Burkhart et al. (13) believe that symptomatic GIRD is present when the deficit is 25 degrees or greater. Treatment focuses on stretching the posterior capsule with the use of “sleeper stretches.” Although the nonsurgical treatment is usually successful, those who do not respond to relative rest, stretching, and strengthening programs may be candidates for arthroscopy, debridement, and occasional posterior capsulotomy, which is often performed with treatment of other coexistent pathology.

Labral pathology is well recognized as a component of the disabled throwing shoulder. The acromym SLAP describes the location of pathology, Superior Labrum Anterior and Posterior. It was first observed by Andrews (13a) in throwing athletes and was later named by Snyder. Multiple subtypes have been described. Some believe that SLAP lesion is the most common pathologic entity associated with the throwers “dead arm” (9,13,14). If left untreated, athletes typically cannot return to throwing. Debate has existed concerning the mechanism of injury during throwing. Fleisig et al. (15) and Andrews et al. (16) proposed a deceleration mechanism of injury, as the bicep contracts to slow down the arm in follow through. This tensile load acts to pull the biceps and superior
labral complex from the bone. Burkhart et al. (13) support an acceleration mechanism of injury. As the shoulder is positioned in abduction and external rotation coinciding with late cocking and acceleration, the labrum is peeled off the glenoid rim. Kuhn et al. (17) performed experimental comparison of the two mechanisms in a cadaveric model; their results support the acceleration mechanism. Treatment is dictated by the stability of the biceps/labral complex. If complex is unstable, a repair is necessary; if stable, a débridement of damaged tissue may be adequate. Surgical repair has been very successful in allowing return to throwing, some reports approaching 90% (14).