Internal impingement is a normal physiological phenom- enon in which the greater tuberosity comes into contact with the posterosuperior glenoid rim in positions of abduction and external rotation. Although its mechanistic function is to prevent excessive external rotation, repeated bouts of abduction, and external rotation, as which occurs with repetitive throwing activities, can lead to symptomatic internal impingement in which both the posterosuperior labrum and posterosuperior rotator cuff become “pinched” between the greater tuberosity and the glenoid rim. This interposition can result in articular-sided posterosuperior cuff tears along with posterior or posterorsuperior labral tears that result in posterior shoulder pain in the abducted and externally rotated shoulder.
The precise biomechanics involved with the development of symptomatic internal impingement have been widely debated over the past 2 decades. Some researchers have concluded that acquired anterior instability is causative, whereas others have refuted this notion, citing more recent studies that have found no correlation between symptomatic internal impingement and anterior glenohumeral translation. Current thinking suggests that symptomatic internal impingement is most likely multi- factorial, involving a combination of physiological remodeling of the shoulder, posterior capsular contracture, and scapular dyskinesis (SICK scapula) that can all lead to a glenohumeral internal rotation deficit (GIRD), humeral hyperangulation, and resulting pathologic findings such as posterosuperior glenoid impingement lesions and superior labral anterior to posterior (SLAP) tears.