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Other Causes of Impingement

In addition to outlet impingement, recent clinical and lab investigations have led to other mechanisms of impingement. These include functional overload, intrinsic tendonopathy, and internal anatomic impingement.

Functional overload results from excessive strain within the tendon from repetitive overuse or a one-time overload. The subsequent inflammation and tendonitis can lead to a continuous cycle, which leads to further impingement symptoms.

Eventually, partial thickness cuff tears may result. These tears can occur within the tendon, or at the tendon-bone interface. The worst case of functional overload is a traumatic complete rotator cuff tear.

Intrinsic tendonopathy or tendonosis is a degenerative process that occurs over time. As such, it is seen more commonly in the elderly. Histological studies have shown that with aging, tendon collagen fibers increase in diameter and become less organized. Biochemical changes include an increase in collagen, a decrease in mucopolysaccharides and a decrease in water content.

A lower level of vascularity is also observed in the aged tendon. This combination of loss of cellular integrity and decreased vascularity predisposes the older tendon to an increased incidence of injury.

It should be noted that the term internal or secondary impingement refers to a different condition. Due to arthroscopy, it has only recently been described as a source of pain and dysfunction. Internal impingement occurs in the overhead position with abduction and maximal external rotation (throwing position). In this position the supraspinatus and infraspinatous tendons impinge on the posterior superior aspect of the glenoid labrum.

In overhead athletes, repetitive internal impingement can lead to labral injury and rotator cuff tears. The cuff tears created by this mechanism are typically partial thickness articular sided tears.

At arthroscopy, kissing lesions can often be identified between the superior labrum and undersurface cuff when the arm is placed in abduction and external rotation. Anterior capsular laxity as well as posterior capsular contracture often coexist and can exacerbate the symptoms.

When conservative measures fail to improve symptoms, surgical intervention should be considered. Arthroscopic debridement alone has had a success rate of approximately 70 to 80% .

Capsular imbrication, either open or arthroscopic, has also been recommended as a treatment to address the anterior capsular laxity. Success for this operation has ranged from 68% to 97%. In addition, a tight posterior band of the inferior glenohumeral ligament complex (PIGHL) has recently been identified as contributing to the pathology. Arthroscopic release of this thickened structure has been shown to be effective in the 10% of patients who do not respond to posterior capsular stretching.

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