Carpal tunnel syndrome (CTS) refers to the complex of symptoms and signs brought on by compression of the median nerve as it travels through the carpal tunnel. Patients commonly experience pain, paresthesias, and less commonly, weakness in the median nerve distribution. CTS is the most common compressive focal mononeuropathy seen in clinical practice.
This topic review will discuss treatment of CTS. We will also briefly review the etiology, clinical features, and diagnosis of CTS, which are discussed in greater detail separately. (See "Etiology of carpal tunnel syndrome" and "Clinical manifestations and diagnosis of carpal tunnel syndrome".)
The carpal tunnel is formed by the transverse carpal ligament superiorly with the carpal bones inferiorly (figure 1) . It is through this anatomic tunnel that the median nerve travels, accompanied by the nine flexor tendons of the forearm musculature (figure 2) [1-3].
When compression of the nerve occurs, ischemia and mechanical disruption of nerve function may result. Compression induces dysfunctional axonal transport and epidural blood flow due to increased carpal tunnel pressure (CTP) . Pathologic analysis shows edema and thickening of vessel walls within the endoneurium and perineurium, fibrosis, myelin thinning, and nerve fiber degeneration and regeneration [2,4,5].
Upper extremity posture influences CTS by altering CTP. The lowest CTP is seen in a neutral or slightly flexed position, and it increases proportionately with deviation from this posture [2,6-9]. The incidence of CTS is increased in individuals with underlying nerve dysfunction (eg, hereditary neuropathies), diabetes, hypothyroidism, connective tissue diseases, obesity, and pregnancy. (See "Etiology of carpal tunnel syndrome".)