Abstract
Carpal tunnel syndrome (CTS), a common neuropathy of the upper limb, is highly prevalent in diabetic patients. Recent findings indicate that changes in median nerve elasticity and its gliding characteristics may contribute to the development of CTS. Normally, each nerve should be able to adapt to the positional changes by passive movement relative to the surrounding tissues. This ability is provided by a gliding apparatus around the nerve trunk in the surrounding soft tissue. The fascicles of nerve trunks can also glide against each other (interfascicular gliding). Sonoelastography indicates that nerve elasticity is decreased in patients with CTS compared to healthy patients. Moreover, decreased nerve elasticity in diabetes mellitus type II is associated with increased neuropathy, especially in peripheral nerves. Biomechanical factors, oxidative stress, and microvascular defects are also observed in diabetic neuropathy and account for different complications. A reduction in the elasticity of peripheral nerves may be related to decreased interfascicular gliding because of the biomechanical changes that occur in neuropathy. Surgical treatments, including nerve release and reduction of carpal tunnel pressure, improve peripheral gliding but do not resolve disease symptoms completely. According to the evidence, interfascicular gliding dysfunction is the most important factor in the pathogenesis of CTS in diabetic patients. Available evidence suggests that biomechanical variations affect interfascicular gliding more than peripheral gliding in diabetic patients. Decreased nerve elasticity is strongly correlated with decreased interfascicular gliding. It is further hypothesized that the concurrent use of antioxidants and pharmacological treatment (neuroprotection) such as alpha lipoic acid with carpal tunnel release in diabetic patients may alleviate the interfascicular gliding dysfunction and improve median neve elasticity. Decreased nerve elasticity and interfascicular gliding dysfunction play significant roles in the pathogenesis of CTS in diabetic patients.