The process of differential diagnosis should give consideration to all conditions which could potentially cause a dysfunction of the median nerve, or its contributories in brachial plexus, C 5 to 8 nerve roots and central nervous system. These combined effects of sensory deprivation and weakness may result in a complaint of clumsiness and loss of grip and pinch strength or dropping things, Differential Diagnosis The final symptoms are weakness and atrophy of muscles of the thenar eminence.

Many patients will report an improvement of symptoms following shaking or flicking of their hand.Īs the disorder progresses, the feeling of tingling or numbness may become constant and patients may complain of burning pain. Patients may notice aggravation of symptoms with static gripping of objects such as a phone or steering wheel but also at night or early in the morning.

The histological changes were thought to be suggestive of dynamic factors as repetitive strain.Ĭlinical Presentation ĬTS onset is generally gradual with tingling or numbness in the median nerve distribution of the affected hand.

Idiopathic CTS is correlated with hypertrophy of the synovial membrane of the flexor tendons caused by degeneration of the connective tissue, with vascular sclerosis, edema and collagen fragmentation.The bilateral characteristic increases in frequency with the duration of symptoms.Idiopathic CTS occurs more frequently in females (65–80%), between the ages of 40 and 60 years 50–60% of the cases are bilateral.In addition, any of the nine flexor tendons traveling through the carpal tunnel can become inflamed and compress the median nerve Repetitive traction and wrist motion exacerbates the negative environment, further injuring the nerve.Nerve dysfunction becomes compromised, and the structural integrity of the nerve itself further propagates the dysfunctional environment- the myelin sheath and axon develop lesions, and the surrounding connective tissues become inflamed and lose normal physiologic protective and supportive function. The compressive element of the pathophysiology includes a detrimental cycle of increased pressure, obstruction of overall venous outflow, increasing local edema, and compromise to the median nerve's intraneural microcirculation.In general, the pathophysiology of CTS results from a combination of compression and traction mechanisms. Synovial hypertrophy in rheumatoid arthritis.Deposition of foreign material, e.g. amyloid.Masses, For example, ganglion cysts, primary nerve sheath tumours.Disease states leading to augmentation of carpal tunnel contents:.Mechanical overuse (considered the most common association).A decrease in the size of the carpal tunnel caused by such conditions as:.There is a wide spectrum of causative pathologies, converging on two mechanisms of disease, both of which lead to entrapment:

Ĭlinical Biomechanics of Carpal Tunnel Syndrome

Carpal tunnel syndrome usually occurs between ages 36 and 60 and is more common in women, with a female-to-male ratio of 2-5:1.

The prevalence of carpal tunnel syndrome is estimated to be 2.7-5.8% of the general adult population, with a lifetime incidence of 10-15%, depending on occupational risk 4.

The most common causes of carpal tunnel syndrome include genetic predisposition, history of repetitive wrist movements such as typing, or machine work as well as obesity, autoimmune disorders such as rheumatoid arthritis, and pregnancy. Ĭarpal tunnel syndrome results from increased pressure in the carpal tunnel and subsequent compression of the median nerve.

One tendon from the flexor pollicis longus.

Four tendons from the flexor digitorum superficialis.

Four tendons from the flexor digitorum profundus.

The carpal tunnel includes the median nerve and nine flexor tendons. The transverse carpal ligament (flexor retinaculum) makes up the superior boundary, and the carpal bones form the inferior border. The carpal tunnel (CT) is formed by a non-extendable osteofibrous wall that forms a tunnel protecting the median nerve and flexor tendons.