Carpal tunnel syndrome

Why should I read this article?

Carpal tunnel syndrome (CTS) is the commonest peripheral nerve problem in the United Kingdom and has considerable employment and healthcare costs. If recognised early it is readily treatable. No established UK guidelines exist for diagnosis and management, but the American Academy of Neurology issued guidelines in 1993, which remain current as no major recent advances have occurred.1

What causes carpal tunnel syndrome?

Carpal tunnel syndrome results from compromise of median nerve function at the wrist caused by increased pressure in the carpal tunnel, an anatomical compartment bounded by the bones of the carpus and the transverse carpal ligament. Although the ends of the tunnel are in free communication with the surrounding tissues, tissue pressure in the tunnel is much higher in patients with CTS (32-110 mm Hg, depending on wrist position) than in patients with normal wrists (2-31 mm Hg.2 Pressures are raised by wrist flexion and extension, and finger flexion.

Intermittent or sustained high tissue pressure in the tunnel impairs microvascular circulation in the median nerve and leads to spurious generation of action potentials, local demyelination, and ultimately axonal loss. It may also stimulate the proliferation of subsynovial connective tissue in the tunnel, according to pathological studies of CTS.3 Anything that reduces the dimensions of the tunnel or increases the volume of its contents will predispose to CTS, and many medical associations have been reported, but most cases are idiopathic.

A study of 4488 individuals recruited from the St Thomas' UK adult twin registry found genetic predisposition to be the single strongest factor in predicting the development of the syndrome.4 Obesity is a risk factor in younger patients.5 The role of occupational and recreational hand use in causation remains controversial. If overuse of the hands does contribute, it may be a relatively minor factor, though most patients report that heavy use of the hands aggravates the symptoms. A Scandinavian survey found population prevalences of 14.4% for median nerve distribution paraesthesias, 3.8% for CTS diagnosed on clinical grounds, 4.9% for neurophysiological focal impairment of the median nerve at the wrist, and 2.7% for neurophysiologically confirmed clinical CTS.6

Incidence peaks in the late 50s, particularly in women, and the late 70s, when the sex ratio is more equal.7 It is also common, transiently, in late pregnancy. Elderly people tend to present with more severe CTS for the same length of history, with 59% of patients aged over 65 having thenar atrophy at presentation compared with 18% of younger patients.8 CTS in older patients is easily confused with other, less treatable, disorders.

When should I suspect CTS?

Although the syndrome encompasses a range of severity (from transient subjective sensory symptoms to irreversible thenar wasting and sensory loss) it should be recognised before permanent deficits develop. Patients woken by paraesthesias or pain—the distribution of which includes median nerve territory (the thumb and first two and a half fingers)—have CTS until proved otherwise. Some patients will also complain of sensory disturbance in the whole hand or pain radiating up the arm to the shoulder. Patients whose paraesthesias are limited to the ulnar side of the hand are unlikely to have CTS.9 About 55%-65% of cases are bilateral at first presentation and most patients present first with the dominant hand.7

Daytime symptoms may be noticed with particular activities, particularly those that involve holding the arms raised. Patients may complain of a perception of swelling of the hand or fingers, but visible swelling is rare and should prompt consideration of other conditions with secondary CTS. Sensory loss in median nerve territory and weakness and wasting of the median innervated thenar muscles are reliable but late indicators of CTS.

The American Academy of Neurology's guidelines state that the likelihood of a diagnosis increases with the number of standard symptoms and provocative factors present (box 1). The most widely used provocative physical tests are Phalen's sign (the provocation of median paraesthesias by flexion of the wrist to 90 degrees for 60 seconds) and Tinel's sign (the provocation of paraesthesias by tapping over the carpal tunnel). These signs have been compared with nerve conduction studies as a diagnostic gold standard in many studies. In such studies, Phalen's sign has sensitivity ranging from 10% to 73% and specificity from 55% to 86%. Tinel's sign has sensitivity ranging from 8% to 100% and specificity from 55% to 87%, the wide ranges probably reflecting the difficulty in standardising the test methods. Both signs are less reliable in advanced CTS.10

On general examination of the patient, be alert for signs of endocrine disease and connective tissue disorders, which can predispose to CTS, and other hand problems such as Raynaud's phenomenon, vibration white finger, trigger finger, and Dupuytren's contracture, which can all coexist with CTS. Many conditions have been mistaken for CTS; box 2 lists some important differential diagnoses.

What laboratory investigations are needed?

Plain x ray examination of the hand is not cost effective in idiopathic CTS—an American study concluded that costs were $5869 (£2850; €4250) to $20 115 for each finding of therapeutic significance.11 A check for diabetes, however, is inexpensive and appropriate. Most patients with CTS will be in an age group where undetected hyperglycaemia is common. The value of blood tests to screen for connective tissue disease and thyroid function is uncertain, particularly in the absence of any clinical indication other than CTS.12

Complex investigations are not necessary before starting conservative treatment in clinically obvious cases. However, in cases of diagnostic doubt, and before surgery, nerve conduction studies should be carried out. The American Academy of Neurology's guidelines suggest electrodiagnostic studies and therapeutic trials with non-invasive treatment as the strategies of choice when clinical diagnosis is uncertain. Nerve conduction studies should include sufficient measurements to localise median nerve dysfunction to the carpal tunnel, evaluate its severity, and exclude more widespread neuropathy.13 Neurophysiological severity of CTS can be expressed on the 7 point Canterbury scale (0=no abnormality, 6=no recordable median motor or sensory potentials), which I have shown correlates with surgical prognosis.14

However, nerve conduction studies have a small false negative rate; a precise figure is not available for this because no better test exists for comparison as a gold standard. However, with modern nerve conduction studies, it is probably around 5-10%. In east Kent, 4.3% of 3544 successful carpal tunnel decompressions had normal preoperative nerve conduction studies (unpublished personal data).

Conversely not all patients with a neurophysiologically demonstrated median neuropathy at the wrist necessarily have symptoms related to that. An alternative, or ideally complementary, approach is provided by high resolution ultrasonography of the median nerve. In a blind comparison with nerve conduction studies as a gold standard, ultrasonography achieved 89% sensitivity and 69% specificity.15 However, this study retrospectively optimised the ultrasound measurement cut-off values to achieve the best possible diagnostic performance and is limited in any case by the lack of an absolute diagnostic standard for comparison.

Magnetic resonance imaging can make similar measurements of median nerve dimensions but is more expensive. Ultrasonography is more comfortable than nerve conduction studies for patients but will not detect other nerve problems that may be contributing to the presentation. Ultrasonography may show unsuspected structural abnormalities of relevance, such as bifid median nerves, persistent median arteries, or space occupying lesions in the tunnel, but these are rare and even more rarely do they dictate alternative management.

How is CTS treated?

Many treatments, both conventional and complementary, have been suggested for CTS (box 3). Few are supported by good quality evidence from randomised controlled trials. The available studies have been well summarised in a series of reviews by the Cochrane Collaboration. 16 17 18 19

The recommendations of the American Academy of Neurology for treatment remain reasonable. The academy suggests splinting, activity modification, and non-steroidal anti-inflammatory drugs—and possibly diuretics if there is limb swelling—as conservative treatment, followed by steroid injection and surgery if these fail or in patients with progressive motor deficit. However, activity modification, diuretics, and non-steroidal anti-inflammatory drugs have no positive support from any randomised trials. Meta-analysis of several randomised trials shows that vitamin B-6 supplementation has a negligible therapeutic effect.19

The purpose of treatment is to alleviate the symptoms and, in some people, prevent worsening of the condition. A few, mostly elderly, patients have thenar wasting but no symptoms. Little is to be gained from surgery in such cases. CTS is not necessarily progressive. The condition in some patients may fluctuate slightly for many years—with more symptoms during periods of heavy hand use or variation with the seasons—without progressing to irreversible median nerve damage. The condition may even remit spontaneously. In one study 23% of participants improved over 12-15 months without active intervention though this was not a randomised trial and the researchers were not able to rigorously control factors such as activity modification instituted by the patients.20 The potential benefits of treatment must be viewed against this background. Only three treatments are supported by a substantial body of experimental evidence: splinting, steroids, and surgery.