Carpal Tunnel Syndrome 

  • Author: Nigel L Ashworth, MBChB, MSc, FRCPC; Chief Editor: Robert H Meier III, MD   more...
 
Updated: Nov 3, 2011
 

Background

Carpal tunnel syndrome (CTS) is a collection of characteristic symptoms and signs that occurs following entrapment of the median nerve within the carpal tunnel. Usual symptoms include numbness, paresthesias, and pain in the median nerve distribution. These symptoms may or may not be accompanied by objective changes in sensation and strength of median-innervated structures in the hand. See image below.

The hands of an 80-year-old woman with a several-yThe hands of an 80-year-old woman with a several-year history of numbness and weakness are shown in this photo. Note severe thenar muscle (abductor pollicis brevis, opponens pollicis) wasting of the right hand, with preservation of hypothenar eminence.
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Pathophysiology

Until the advent of electrophysiologic testing in the 1940s, carpal tunnel syndrome (CTS) commonly was thought to be the result of compression of the brachial plexus by cervical ribs and other structures in the anterior neck region. It is now known that the median nerve is damaged within the rigid confines of the carpal tunnel, initially undergoing demyelination followed by axonal degeneration. Sensory fibers often are affected first, followed by motor fibers. Autonomic nerve fibers carried in the median nerve also may be affected.

The cause of the damage is subject to some debate; however, it seems likely that abnormally high carpal tunnel pressures exist in patients with CTS. This pressure causes obstruction to venous outflow, back pressure, edema formation, and ultimately, ischemia in the nerve.

The risk of development of CTS appears to be associated, at least in part, with a number of different epidemiologic factors, including genetic, medical, social, vocational, avocational, and demographic.[1] A complex interaction probably exists between some or all these factors, eventually leading to the development of CTS. Definite causative factors, however, are far from clear.

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Epidemiology

Frequency

United States

The incidence of carpal tunnel syndrome is 1-3 cases per 1000 subjects per year; prevalence is approximately 50 cases per 1000 subjects in the general population. Incidence may rise as high as 150 cases per 1000 subjects per year, with prevalence rates greater than 500 cases per 1000 subjects in certain high-risk groups.

International

A paucity of population-based studies of carpal tunnel syndrome (CTS) exists; however, the incidence and prevalence in developed countries seems similar to the United States (eg, incidence in the Netherlands is approximately 2.5 cases per 1000 subjects per year; prevalence in the United Kingdom is 70-160 cases per 1000 subjects).[2, 3, 4] CTS is almost unheard of in some developing countries (eg, among nonwhite South Africans).

Mortality/Morbidity

Carpal tunnel syndrome is not fatal, but it can lead to complete, irreversible median nerve damage, with consequent severe loss of hand function, if left untreated.

Race

Whites are probably at highest risk of developing carpal tunnel syndrome (CTS). The syndrome appears to be very rare in some racial groups (eg, nonwhite South Africans).[4] In North America, white US Navy personnel have CTS at a rate 2-3 times that of black personnel.[5]

Sex

The female-to-male ratio for carpal tunnel syndrome is 3-10:1.

Age

The peak age range for development of carpal tunnel syndrome (CTS) is 45-60 years. Only 10% of patients with CTS are younger than 31 years.

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Contributor Information and Disclosures
Author

Nigel L Ashworth, MBChB, MSc, FRCPC  Professor and Chief, Division of Physical Medicine and Rehabilitation, Glenrose Rehabilitation Hospital, University of Alberta

Nigel L Ashworth, MBChB, MSc, FRCPC is a member of the following medical societies: American Association of Neuromuscular and Electrodiagnostic Medicine, Australian & New Zealand Association of Neurologists, British Medical Association, Canadian Association of Physical Medicine and Rehabilitation, Canadian Medical Association, Canadian Society of Clinical Neurophysiologists, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

Specialty Editor Board

Benjamin M Sucher, DO, FAAPMR, FAOCPMR  Medical Director, EMG Labs of AARA (Arizona Arthritis & Rheumatology Associates)

Benjamin M Sucher, DO, FAAPMR, FAOCPMR is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, American Osteopathic Association, and American Osteopathic College of Physical Medicine and Rehabilitation

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Patrick M Foye, MD  Associate Professor of Physical Medicine and Rehabilitation, Co-Director of Musculoskeletal Fellowship, Co-Director of Back Pain Clinic, Director of Coccyx Pain Service (Tailbone Pain Service: www.TailboneDoctor.com), University of Medicine and Dentistry of New Jersey, New Jersey Medical School

Patrick M Foye, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation, American Association of Neuromuscular and Electrodiagnostic Medicine, Association of Academic Physiatrists, and International Spine Intervention Society

Disclosure: Nothing to disclose.

Kelly L Allen, MD  Medical Director, Medevals

Disclosure: Nothing to disclose.

Chief Editor

Robert H Meier III, MD  Director, Amputee Services of America; Active Medical Staff, Presbyterian/St Luke's Hospital, Spalding Rehabilitation Hospital, Select Specialty Hospital; Consulting Staff, Kindred Hospital

Robert H Meier III, MD is a member of the following medical societies: American Academy of Physical Medicine and Rehabilitation and Association of Academic Physiatrists

Disclosure: Nothing to disclose.

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The hands of an 80-year-old woman with a several-year history of numbness and weakness are shown in this photo. Note severe thenar muscle (abductor pollicis brevis, opponens pollicis) wasting of the right hand, with preservation of hypothenar eminence.
Sensory nerve conduction studies from the left hand of a patient with a several-year history of numbness and weakness (responses from the median nerve in the right hand were completely absent). Note marked slowing of the conduction velocity (CV) to 29.8 and 25.5 m/s for digits 3 and 1, respectively (normal >50 m/s). The amplitude for both also is reduced markedly (normal >10). These findings are consistent with carpal tunnel syndrome.
Motor nerve conduction studies from the left hand of a patient with a several-year history of numbness and weakness (responses from the median nerve in the right hand were completely absent). Note that the conduction velocity (CV) across the carpal tunnel segment slows severely to 18.3 m/s (normal >50 m/s) and that the distal motor latency is prolonged at 6.3 ms (normal < 4.2 ms). Amplitudes are low for the wrist and elbow stimulus sites at 4.7 mV (normal >5 mV), but amplitudes are 31% higher distal to the carpal tunnel (at the palm). This discrepancy may represent conduction block (neurapraxia) at the level of the carpal tunnel or coactivation of the ulnar branch to adductor pollicis. Needle electromyography is required to determine whether axonal loss is present.
 
 
 
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