Carpal tunnel syndrome

Section 1: Epidemiology and aetiology

Carpal tunnel syndrome (CTS) is the most common nerve entrapment disorder, with a prevalence of 3 per cent in the UK general population.

Women are three times more likely to be affected than men, particularly in middle age.1

CTS is caused by pressure on the median nerve as it crosses the carpal tunnel into the hand. The carpal tunnel essentially consists of the carpal bones on the dorsal surface and the transverse carpal ligament anteriorly. Nine tendons and the median nerve pass through the tunnel, and any swelling of these structures will lead to entrapment of the median nerve.

The most common cause for CTS is non-specific flexor tenosynovitis, often due to repetitive strain, leading to an increase in carpal tunnel pressure. Although there are multiple factors (see box) that may predispose a patient to CTS, a cause is often not found.2 CTS symptoms are also frequently reported in certain occupational activities, although there is debate as to whether CTS may be directly caused by work.

There are good reasons to look for an underlying cause before treating CTS, since in some the symptoms may recur if the underlying cause remains untreated, and in others the prognosis may be better than the initial presentation would suggest.

The prevalence of CTS in pregnancy has been reported as over 50 per cent, particularly in the third trimester.3 However, for the majority, CTS usually resolves spontaneously after delivery.

Rarely, there are cases of median nerve entrapment at both the level of the carpal tunnel as well as proximal to it (for example the neck) referred to as the double crush syndrome.4 In this syndrome, the median nerve that has suffered entrapment, usually at the cervical roots, is more susceptible to entrapment in the carpal tunnel as well.

Common risk factors for carpal tunnel syndrome

  • Repetitive stress to the hand.
  • Vibrating power tools.
  • Assembly line work.
  • Percussion instruments, guitar playing.
  • Pregnancy.
  • Obesity.
  • Hypothyroidism.
  • Diabetes mellitus.
  • Rheumatoid arthritis.
  • Trauma.

Section 2: Diagnosis


The classic and earliest presenting symptom of CTS is nocturnal paraesthesia, numbness or pain in the lateral three (thumb, index and middle) fingers.

Patients often report having to wake up in the night to relieve the symptoms by shaking their hands (the flick sign). While sleeping, the wrist is often in a bent position, which compresses the median nerve.

Patients may also complain of similar symptoms with activities where the wrist is bent (for example driving and cycling) during the daytime. It is therefore important to establish when and which activities induce symptoms.

As CTS progresses, patients may complain of continuous paraesthesia or numbness. In this situation, it is important to ask the patient if symptoms were mainly nocturnal initially.

In many cases, patients may complain of numbness and paraesthesia in the entire hand, rather than just within the median nerve sensory dermatome.

As CTS progresses, these symptoms may radiate up the forearm to the shoulder as well.

The essential part of the history that will point to the diagnosis is again the initial nocturnal nature of the symptoms starting in the hand.

In severe cases, patients may report weakness in hand grip, dropping items or loss of hand dexterity. These symptoms will require an urgent referral.

A thorough neurological examination of the upper limb is essential. On inspection, there may be signs of muscular atrophy in the thenar eminence with accompanying weakness in thumb abduction and opposition. Sensation is usually intact in patients with intermittent sensory symptoms.

In these patients, the classically described Tinel's sign (tapping the median nerve just proximal to the distal wrist crease with a patella hammer) and Phalen's sign (holding the wrist in maximum flexion for 60 seconds) may be positive when a sensation of electric shocks travelling into the hand or paraesthesia in a median nerve distribution is elicited respectively.

Both these signs are dependent on technique, and their sensitivity and specificity for CTS varies widely between studies,5 so they are only useful in supporting the clinical history in making or rejecting a diagnosis.

Apart from trying to elicit a history and clinical examination consistent with CTS, GPs should look for potential secondary causes as well as work-related and recreational activities that could exacerbate symptoms.

Neurological signs in both upper limbs and/or proximal to the wrists should alert the clinician that the pathology may be proximal to the carpal tunnel (for example pronator teres syndrome).

Electromyography (EMG) allows measurement of sensory nerve conduction velocity across the carpal tunnel. It also allows assessment of the severity of motor involvement and identifies the presence of the double crush syndrome, although if this is suspected, it should be specified in an EMG request to be looked for. However, it has a sensitivity of 85 per cent in detecting CTS and may be normal in clinically symptomatic patients.6

High-resolution ultrasound has become an inexpensive investigative modality for CTS. It may demonstrate median nerve swelling, and its sensitivity and specificity may be comparable to EMG. It can be useful in detecting space-occupying lesions (for example ganglion) in the carpal tunnel. However, it is operator dependent and the sensitivity and specificity will vary depending on experience and proficiency.

MRI is even more sensitive at detecting CTS compared with ultrasound and is used when the clinical picture or results of other investigations are inconclusive. However, there are cost implications compared with the other less expensive methods and it is not so readily available.

The gold standard investigation is still EMG, despite the moderate sensitivity and specificity, and imaging studies are only considered if there is uncertainty with the diagnosis or suspicion of a carpal tunnel mass.

Section 3: Management
An underlying cause should be looked for and treated in the first instance. CTS may not settle with treating just the secondary cause either and it often needs to be treated specifically as well.

A baseline EMG is helpful if the diagnosis is unclear but in most cases of nocturnal paraesthesia with no motor signs, treatment may be initiated without testing. EMG may also be normal in mild cases and a trial of treatment should be considered if the suspicion is high.

If the history and signs are not entirely consistent with CTS, a referral to secondary care (neurology, rheumatology) should be made. However, if the diagnosis of CTS is clear, the following treatment strategies can be used.

In most patients with CTS with mainly nocturnal or intermittent sensory symptoms, conservative measures are appropriate. These include wrist splints to be used overnight or during activities that may exacerbate the symptoms. It is essential to note that wrist splints should only be used for a limited period over the course of the day, to avoid weakening the wrist in the long term.

NSAIDs may also be helpful in treating common causes of CTS, including flexor tenosynovitis, by reducing swelling.

A referral to secondary care for a steroid injection should be made after a trial of wrist splints for one month if there is inadequate response or if symptoms recur.

Local steroid injection
In patients with CTS where splinting has failed or if sensory symptoms are continuous, a steroid injection into the carpal tunnel is very successful, particularly in cases less than one year in duration without motor involvement. However, there is a risk of symptom recurrence after a single injection.7 Generally, if more than two steroid injections have been necessary, surgery should be considered as the next step if symptoms recur.

In patients with CTS with motor weakness or obvious thenar muscle wasting, an urgent referral to secondary care for surgical decompression (such as orthopaedics or plastic surgery) should be made. EMG studies demonstrating motor involvement will be helpful in identifying subtle motor weaknesses.

Surgery is also indicated when steroid injections have failed or in the presence of progressive neurological deterioration. In most patients, day case surgery involving either open or endoscopic release of the transverse carpal ligament is the definitive treatment for CTS.

Section 4: Prognosis
Splinting alone has a success rate of 50 per cent after three months compared with 80 per cent for surgery, but the difference in relief is even greater after one year.8

Local steroid injections in mild cases are superior in symptom relief (90 per cent response) compared with surgery in the first six months, but long-term relief again is better in the surgical group.9 Often, more than one injection will be required in the first year for a good response.

In patients with persistent symptoms/signs after surgical release, it is important to keep in mind that the rate of recovery depends upon the severity of the initial nerve deficit, the adequacy of surgical release and the possibility of double crush syndrome.

The physician should also be aware that some complications of surgery, including scar pain and wrist weakness may be confused with the original CTS symptoms. An EMG study should be requested first to demonstrate objective evidence of median nerve deterioration.

Occupational CTS
There is considerable controversy surrounding the relationship between CTS and work activities, with many patients receiving time off and compensation while others argue that CTS is not a work-related problem.10

The main argument is that CTS is not caused by work, but that occupational activities may exacerbate an already compromised median nerve. However, the literature does suggest that the prevalence of CTS is significantly higher in the industrial setting but not as much in an office environment.

Although frequent computer users often complain of hand paraesthesia, only a proportion of these are proved to be CTS.11

Epidemiological studies have also identified risk factors that predispose patients to CTS at work, including repetitive work with hands.

The most effective way to prevent CTS at the workplace is taking frequent breaks from repetitive actions. Practical ergonomic adaptations to the workplace are often required.

Contributed by Dr Jeffrey Lee, consultant rheumatologist at Barnet Hospital, Hertfordshire.

1. Atroshi I, Gummesson C, Johnsson R et al. Prevalence of carpal tunnel syndrome in a general population. JAMA 1999; 282: 153-8.

2. Sternbach G. The carpal tunnel syndrome. J Emerg Med 1999; 17: 519-23.

3. Pazzaglia C, Caliandro P, Aprile I et al. Multicenter study on carpal tunnel syndrome and pregnancy incidence and natural course. Acta Neurochir Suppl 2005; 92: 35-9.

4. Upton A, McComas A. The double crush in nerve entrapment syndromes. Lancet 1973; 2: 359-62.

5. Kuschner S, Ebramzadeh E, Johnson D, Brien W, Sherman R. Tinel's sign and Phalen's test in carpal tunnel syndrome. Orthopedics 1992; 15: 1,297-1,302.

6. Witt J, Hentz J, Stevens J. Carpal tunnel syndrome with normal nerve conduction studies. Muscle Nerve 2004; 29: 515-22.

7. Kanaan N, Sawaya R. Carpal tunnel syndrome: modern diagnostic and management techniques. Br J Gen Pract 2001; 51: 311-4.

8. Gerritsen A, de Vet H, Scholten R. Splinting vs surgery in the treatment of carpal tunnel syndrome. A randomised controlled trial. JAMA 2002; 288: 1,245-51.

9. Ly-Pen D, Andreu J-L, de Blas G. Surgical decompression vs local steroid injection in carpal tunnel syndrome. A one-year, prospective, randomised, open, controlled clinical trial. Arhritis Rheum 2005; 52: 612-9.

10.Werner R. Evaluation of work-related carpal tunnel syndrome. J Occup Rehabil 2006; 16: 207-22.

11.Atroshi I, Gummesson C, Ornstein E et al. Carpal tunnel syndrome and keyboard use at work: a population-based study. Arthritis Rheum 2007; 56: 3,620-5.

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