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Clinical Review

Carpal tunnel syndrome

BMJ 2014; 349 doi: https://doi.org/10.1136/bmj.g6437 (Published 06 November 2014) Cite this as: BMJ 2014;349:g6437

Rapid Response:

Mariano E. Menendez, research fellow and David Ring, professor of orthopaedic surgery

Middleton and Anakwe (1) reviewed the epidemiology, diagnosis, and treatment of carpal tunnel syndrome. We would like to offer several points for consideration.

First, it is worth restating that best evidence supports the concept that idiopathic median neuropathy at the carpal tunnel is due to a genetically narrow tunnel, with environmental factors such as hand use exerting a minor, less consistent, and more debatable epigenetic role.(2-11) Given the psychological power and negative implications of speculative causal associations and the large medical and non-medical readership of this journal, this paper represents a missed opportunity to put an end to the strong cultural conception (likely a full fledged myth) that repetitive hand use (e.g. typing) causes carpal tunnel syndrome. Carpal tunnel syndrome is not pain with typing. The primary symptom of a genetically narrow carpal tunnel is intermittent numbness. Numbness that can, at times, be so intense that it is unsettling or painful.

Second, an important point of debate is whether carpal tunnel syndrome is a progressive disease or not. The authors claim that “good evidence suggests that carpal tunnel syndrome is not necessarily progressive and that the simple method of splinting is all that is sometimes required to control symptoms”, but provide no references for this statement. In our impression, the collective evidence to date makes the case that a genetically narrow tunnel occurs bilaterally and progresses to permanent numbness, weakness, and atrophy if left untreated. Problems arise when we confuse symptom relief with modification of pathophysiology.

Third, patients with advanced disease evidenced by thenar atrophy, weakness of palmar abduction, and constant numbness should expect that some or all of these problems will persist after surgery.(12-16)

Fourth, it should be emphasized that surgery to increase the size of the carpal tunnel is the only known disease-modifying treatment.(17-24) None of the commonly used non-operative strategies (e.g. corticosteroid injections, wrist splinting, activity modification or rest) are proved to be disease modifying. Patients and healthcare providers may be safest considering these treatments as palliative at best until proved otherwise. Specifically, if we emphasize relief of symptoms, there is a risk that patients with decreased symptoms will present years later with permanent nerve damage. We don’t treat the symptoms of hypertension or diabetes—we treat the disease in order to limit pathophysiology. Idiopathic median neuropathy at the carpal tunnel syndrome may merit a similar approach.

Fifth, the authors recommend the use of electrophysiological testing in patients who experience no improvement in symptoms after surgery. Yet, it is well established that electrophysiological tests do not always return to normal after surgery, particularly for more advanced pathology.(25-29) Their utility among patients with electrophysiologically severe disease following carpal tunnel release may be limited. It is an error to measure electrophysiology after carpal tunnel release and interpret measurable median nerve pathology as an indication of incomplete release or other pathophysiology. Patients who have carpal tunnel release for advanced median neuropathy with permanent nerve damage may not experience relief of constant numbness, atrophy, or weakness of palmar abduction no matter how many surgeries they have. Patients who have surgery for pain rather than numbness are often unsatisfied with the result of surgery, but this is more likely because the diagnosis was incorrect than that the surgery could have been done better.

A review article in a prominent medical journal is an opportunity to correct common misconceptions that are prevalent among health professionals and laypersons alike. We contend that the most constructive, practical, optimistic, and accurate way to conceive of carpal tunnel syndrome based on current best evidence is that it is idiopathic median neuropathy at the carpal tunnel, due to a genetically narrow tunnel, unrelated to activity, causing intermittent numbness progressing to permanent numbness, which can only be prevented by surgery to increase the size of the carpal tunnel. All things considered, it seems better to treat carpal tunnel syndrome according to these principles until future research refutes them. In our opinion, treating carpal tunnel syndrome as an activity related injury causing wrist pain and modifiable by nonoperative treatments exposes patients to the harm of unnecessary disability, unnecessary surgery, and permanent nerve damage due to under treatment.

References
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Competing interests: No competing interests

08 November 2014
David Ring
Professor of Orthopaedic Surgery
Mariano E. Menendez
Department of Orthopaedic Surgery, Hand and Upper Extremity Service, Massachusetts General Hospital, Harvard Medical School
Boston, Massachusetts, USA