Carpal tunnel syndrome is a common cause of motor and sensory symptoms in the hand. The complications that result can lead to limitations of activities of daily living and time away from work. This article summarizes the investigation and treatment of this disorder in light of the result from recent clinical trials.
Carpal tunnel syndrome (CTS) is the most common entrapment neuropathy and one of the most important causes of lost days at work. The incidence is 139 per 100,000 person years for men and 506 for women.
The sex ratio varies from 2:1 in the UK to over 20:1 in South Korea. It is often present in both hands. Repetitive wrist movements, high-force hand grip and the use of vibrating tools have been associated with an increased prevalence. In many countries, CTS is recognized as a compensable occupational disease.
Anatomy and Pathophysiology
The medial cord of the brachial plexus from roots C8 and T1 from the motor supply of the median nerve while sensory fibres from the lateral aspect of the hand run in the lateral cord, from roots C5, C6 and C7. The terminal branches of the median nerve supply the thenar muscles (abductor pollicis brevis, flexor pollicis brevis, opponens pollicis) and the lateral two lumbricals. A number of anomalies are found in normal individuals at all levels of the nerve, e.g. the median and musculocutaneous nerve may be fused, the ulnar may supply all the thenar muscles and the median may supply the intrinsic muscles. These variations need to be considered during electrophysiological assessment. The floor and sides of the carpal tunnel are formed by the eight carpal bones. The tranverse carpal ligament forms the roof; it is attached to the hook of hamate and pisiform on the ulnar side and the scaphoid and trapezium on the radial side.
CTS is a sonsequence of compression of the median nerve within the carpal tunnel resulting in mechanical compression and local ischaemia. A rise in intracarpal canal pressure leads to reduced epineural blood flow and intrafascicular oedema. Histological examination of synovial biopsies shows a marked increase in fibroblast density, collagen fibre size and vascular proliferation compared with controls, changes that are similar to those seen after injury to other tissues. With time, changes in the myelin sheath and axonal injury are evident on nerve conduction testing. Over its long course, the median nerve becomes susceptible to compression at sites other than the carpal tunnel. In the pronator syndrome, the nerve is compressed by the pronator teres muscle, causing numbness in the hand and forearm tenderness. A proximal branch of the median nerve, the anterior interosseus nerve, may be compressed, producing weakness confined to the flexor pollicis longus, flexor digitorum profundus and pronator quadratus but without sensory loss.
The clinical features in patients with electrophysiologically confirmed CTS are variable, but numbness over the lateral aspect of the hand is a typical feature of the syndrome, which may be more obvious during sustained grip, such as while reading a newspaper or driving. Initial symptoms may be intermittent but become more sustained as disease progresses. Awakening from sleep or symptoms upon awakening are common complaints. The majority of cases are idiopathic, but CTS is associated with conditions such as diabetes mellitus, renal dialysis, rheumatoid arthritis, thyroid dys-function, pregnancy and use of oral contraception.
Most CTS patients present with these classical symptoms but clinicians should be aware of atypical presenting feature.
A self-administered hand diagram has been devised to classify the level of centainty of the diagnosis into classic, probable, possible and unlikely; however, it was found to be unhelpful in the Asian population. Individuals with a high body mass index (BMI) of >29 are 2.5times more likely to develop CTS thatn those with a BMI <20.
For patients with CTS associated with other medical conditions such as hypothyroidism, treatment of the underlying disorder alone may resolve hand symptoms. Advise on avoiding activities that would exacerbate the disease should be given. Carpal Tunnel decompression is recommended at the outset for patients who have clinical or electrophysiological evidence of severe CTS and in those with symptoms of acute onset (e.g. post-traumatic). Splinting with or without steroid injection would be the first line treatment for patients with mild to moderate CTS, in view of the fact that a minority would respond with first line treatment. Carpal tunnel release can be subsequently offered to those who do not respond to splinting and anti-inflammatory injection and to those who relapse. Failure to respond to carpal tunnel release is unusual; reasons include initial misdiagnosis, incomplete division of the flexor retinaculum, iatrogenic nerve branch injury and perineural fibrosis. Re-examination of the diagnosis and surgical re-exploration should be considered in these cases.