Carpal tunnel syndrome pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1] Associate Editor(s)-in-Chief: Mohammadmain Rezazadehsaatlou [2]
Overview
Carpal tunnel syndrome (CTS) is known as a common pathology in hand. Most common diagnosis of CTS is idiopathic but it is accepted that the median nerve neuropathy could be caused due to the chronic increased pressure within the carpal tunnel. But the exact pathophysiology of this pressure increase is not well known yet. CTS usually occurs due to the mechanical compression and/or local ischemia. CTS is diagnosed based on symptoms such as numbness, tingling and/or burning in the distribution of the median nerve in the hand. However, the symptoms are frequently documented outside the distribution of the median nerve as well. The CTS has a complex pathophysiology and it happens due to the interactions of many mechanisms.
Pathophysiology
Increased carpal tunnel pressure
Normal pressure of carpal tunnel is ranged from 2 to 10 mm Hg. The carpal tunnel is a anatomic space surrounded by the carpal bones on the medial, dorsal, and lateral sides and the the flexor retinaculum located on the palmar side and nine flexor tendons and the median nerve are concealed by the subsynovial connective tissue (SSCT). It is clear that the CTS is a chronic peripheral nerve compression neuropathy, but its pathophysiology are less clear. Various studies have confirmed that the increased canal pressure can be found in patients with CTS; this elevation is correlated with clinical signs in patients. Fro example tenosynovitis or synovial fibrosis, are known as the potential cause of elevation in carpal tunnel pressure. Another proposed mechanism is canal stenosis. Pathological changes of ligaments surrounding nerves such as changes in the connective tissue density and/or its flexibility are believed to be the main cause of this pressure elevation. Experimental studies raveled that there is a relationship between the duration, and amount of carpal tunnel with the median nerve dysfunction. Meanwhile, the higher carpal tunnel pressure leads to the ischemic compression of the median nerve.
Synovial tissue hypertrophy
Hypertrophy of the synovial tissue of the flexor tendons cis another cause of increased carpal tunnel pressure and consequently leading to the CTS occurrence and progresion. Meanwhile, its been reported that the increased expression of prostaglandin E2 and/or VEGF and tenosynovitis are the important risk factors to the development of symptomatic and idiopathic CTS, respectively. Then, the constrictive scar tissue around the median nerve leads to the tethering of the median nerve. Also, the synovial tissue increases the volume of tissue ( the most common area in this regard are: the entrance and exit regions of the canal) by the inflammatory thickening which finally leads to the increased pressure within the carpal tunnel.
Median nerve connective tissue alterations
It’s been found that in neuropathic disorders the nerves at the site of compression are narrowed and they’ve been enlarged at the proximal and distal segments. This compression cause the Demyelination of the nerve which can spread to the whole internodal segment which consequently interrupts the leaving the axonal function. The persisted compression interrupts the bloodflow to the endoneural capillary system changes the blood-nerve barrier, and leads to the endoneural edema. The edema causes the nerve swelling, which affects the movement of the nerve within the anatomical compartment.
Median nerve microcirculation injury
Ischemic vascular injuries are aslo known as the essential factors in CTS. An increase pressure within the tunnel could cause a vasculature breakdown which leads to the inflammatory cells and proteins accumulation. Also, the biochemical disturbances of microvascular structure of the nerve leads to a reduction in the endoneurial blood flow and also the oxygen tension. On the other hand, the local compression could change the intraneural circulatory and leads to the higher permeability of endoneurial vessels which leads to the edema of the endoneurial space; . the edema affects the diffusion distance for oxygen from the capillaries, which leads to hypoxia.
