Loss of Scapulohumeral Motion (Frozen Shoulder)

Duplay (1896) was the first investigator to recognize pathologic disorders of extra-articular tissues as possible factors responsible for stiff and painful shoulders. It was his belief that an inflammatory process of the subacromial bursa was the causative agent producing this syndrome. He designated the entity “scapulohumeral periarthritis.” Soon this term came to include a host of heterogeneous cases which presented similar clinical features, namely, all had pain and stiffness in the shoulder region. Since the original work of Duplay many workers have succeeded in extracting from the all-inclusive term “scapulo-periarthritis” many unequivocal entities. Notably among these observers were Painter, Baer, King and Holmes, Mumford and Martin, Codman, Meyer, Pasteur, Gilcreest, and more recently Lippmann, Abbott, Saunders and Hitchcock and Bechtol. Meyer [11] was the first observer to focus our attention on the tendon of the long head of the biceps brachii muscle as a possible source of disorders about the shoulder. He noted in anatomical specimens advanced degenerative abnormalities comprising fraying, shredding, fasciculations and tearing of the fibers of the biceps tendon. Some specimens exhibited partial or complete dislocation of the tendon out of the bicipital groove and several specimens revealed absence of the intrascapular portion of the tendon while the extracapsular portion had attained a bony attachment on the shaft of the humerus in the region of the lesser tuberosity. It was Meyer’s belief that the aforementioned changes were the products of several causes: (1) contact of the tendon with a supratubercular ridge when present, (2) irregularities and excrescences in the floor of the intertubercular groove, and (3) contact of the tendon with raised cartilagenous margins of the head of the humerus or with the lesser tuberosity. He further believed that these alterations were the result of using the upper extremity in a position of abduction and external rotation. His observations were made on the shoulder joints of cadavers in whom no clinical data were available prior to death; therefore it was impossible to evaluate the clinical significance of these alterations. Meyer’s observations were confirmed by the author together with J. B. White and G. Callery in an investigation conducted on shoulder joints which were obtained postmortem from individuals on whom clinical data were available prior to death. It was interesting to note that many of the degenerative and attritional changes described by Meyer were compatible with good, painless function of the shoulder joint. In 1932 Pasteur [13] described a new clinical syndrome “tenobursite” which he believed was responsible for frozen shoulder. He was the first to correlate bicipital tenosynovitis with frozen shoulder. This was followed by the work of Schrager who, for the first time in American literature, described tenosynovitis as an unequivocal entity. Many other workers soon began to recognize the significant role that the tendon of the long head of the biceps brachii muscle played in stiff and painful shoulders. Lippmann [9] in 1943 described adhesive tenosynovitis as the causative agent of frozen shoulder, a concept with which the author is not in total agreement. On the other hand, Codman [3], one of the greatest authorities on lesions of the shoulder joint, wrote “Personally, I believe that the sheath of the biceps tendon is less apt to be involved than are other structures. I have never proved its involvement in a single case. I think that the substance of the tendon of the supraspinatus is the most often involved.” Codman was of the opinion that tendinitis of the rotator tendons was the underlying pathologic disorder responsible for frozen shoulder. In the following study an attempt will be made to show that frozen shoulder is a diffuse inflammatory process implicating all the soft tissue components of the scapulohumeral joint including the biceps tendon and not any one component or an isolated region of the joint; also, that bicipital tenosynovitis is a concomitant finding in all frozen shoulder, that it may be primary or secondary in origin, and that it is responsible for the pain factor which is the most distressing feature of this syndrome. Furthermore, it will be pointed out that once the pain element in frozen shoulders is eliminated, restoration of function can begin and continues until optimum function is regained and all tissues are returned to normal. The observations herein recorded were made on a clinical study of 38 cases, of which 32 were investigated surgically. Correlation of these pathologic findings with those recorded in a previously reported investigation on degenerative lesions of the shoulder joint allows one to reach some logical conclusions concerning the causes and pathogenesis of frozen shoulders.