Thoracic outlet syndrome (TOS) is not a single disorder but a collection of abnormalities in the same anatomic area that elicit similar symptoms. The many causes of TOS are best classified into one of three groups; osseous, traumatic, and nontraumatic. Although patients with traumatic TOS constited 86% of our last 600 patients with TOS who underwent surgical treatment, the precise mechanism underlying the condition remains obscure. To determine if there was microscopic abnormalities, 45 anterior and middle scalene muscles from patients with traumatic TOS were studied by means of histochemical stains applied after freezing of the muscles. The results revealed a consistent abnormal histologic patterns in patients with traumatic TOS: type II fibers were atrophied; there was an increase in the average number of type I fibers (78% versus 53% in muscle from control patients); and there was a significant increase (mean: 36%) in connective tissue (muscle from control control patients average less than 15%). Although type II fiber atrophy and type I fiber predominance are seen in a variety of other conditions, their association with fibrosis is rare. Following neck injuries, the changes in the anterior and middle scalene muscles are compatible with trauma, suggesting that fibrotic scalene muscles are an important cause of symptoms in traumatic TOS.
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