Abstract
textabstractCarpal tunnel syndrome (CTS) is the most common compression neuropathy, yet the cause of the compression is in most cases idiopathic. The most common clinical finding associated with the nerve compression is non-inflammatory fibrosis of the subsynovial connective tissue (SSCT) which surrounds the flexor tendons in the carpal canal. The normal SSCT has a multi-layer gliding mechanism, reminiscent of a series of sleeves around the tendon, with each successive sleeve being connected to its neighbors with fine collagenous fibers. We have conducted a series of experiments which have outlined the pathology, kinematics and material properties of the SSCT in normal individuals and in individuals with CTS, and have identified specific features within the SSCT of individuals with CTS that suggest that injury to the SSCT may play a role in the etiology of CTS. Specifically, we have identified evidence of a shearing injury of the SSCT, with fibrosis, and obliteration o! f the gliding, sleeve-like mechanism, being greatest close to the tendon, and with a tendency of greater degrees of fibrosis being observed in more severe cases of CTS. This fibrosis may be associated with tethering of the SSCT to the underlying tendon, which may increase the work of finger movement in patients with CTS, and impair differential finger movement. Based on these observations, we propose a vicious cycle of SSCT injury and repair as a working hypothesis of the etiology of CTS, and have developed a rabbit model to test this hypothesis in vivo.
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