eMedicine Specialties > Emergency Medicine > Trauma & Orthopedics

Carpal Tunnel Syndrome

Author: Jeffrey G Norvell, MD, Clinical Assistant Professor of Emergency Medicine, University of Kansas School of Medicine
Coauthor(s): Mark Steele, MD, Associate Dean for Truman Medical Center Programs, Professor, Department of Emergency Medicine, University of Missouri-Kansas City
Contributor Information and Disclosures

Updated: Jul 15, 2008

Introduction

Background

Carpal tunnel syndrome (CTS) is a compressive neuropathy of the median nerve at the wrist. The carpal tunnel is located at the base of the palm and is bounded on 3 sides by carpal bones and anteriorly by the transverse carpal ligament. Inside run the median nerve, flexor tendons, and their synovial sheaths.

Pathophysiology

CTS is caused predominantly by compression of the median nerve at the wrist because of hypertrophy or edema of the flexor synovium. Pain is thought to be secondary to nerve ischemia rather than direct physical damage of the nerve.

Frequency

United States

CTS is the most frequently encountered peripheral compressive neuropathy. The estimated lifetime risk of acquiring CTS is 10%, the annual incidence is 0.1% among adults, and overall prevalence of CTS is 2.7%.

Mortality/Morbidity

Early in the course of CTS, the neurologic findings are reversible. If untreated, CTS can result in thenar atrophy, chronic hand weakness, and numbness in the median nerve distribution of the hand.

Sex

CTS is more prevalent in females than in males.

Age

CTS is most common in middle-aged persons.

Clinical

History

Patients typically complain of an intermittent "pins-and-needles" paresthesia in the median nerve distribution of the hand. Pain is generally worse at night than during the day. Patients may awaken with a burning pain or tingling that may be relieved with shaking their hands. Classic CTS is associated with symptoms that affect at least 2 of the first through third digits; symptoms affecting the fourth and fifth digits, wrist pain, and radiation of pain proximal to the wrist may also occur, but classic CTS is not associated with symptoms on the palm or dorsum of the hand.

Symptoms of probable CTS are the same as classic CTS except palmar symptoms may be present, unless confined solely to the ulnar aspect. Possible CTS involves symptoms in at least one of the first 3 digits. The sensitivity of classic or probable CTS symptoms for diagnosing CTS is 80%. CTS is unlikely if no symptoms are present in any of the first 3 digits.

  • Symptoms are most often bilateral, insidious in onset, and progressive in nature.
  • With advanced nerve compression, an aching sensation is persistent and static and may radiate to the forearm and elbow.
  • Inquire with regard to repetitive strain risk, eg, waitperson, assembly packing, computer keyboard work, playing a musical instrument, craftwork.
  • Determine if there has been any significant trauma.
  • Inquire with regard presence of any other predisposing factors listed below under causes.

Physical

  • Weakness of resisted thumb abduction (ie, movement of the thumb at right angles to the palm) is helpful in establishing the electrodiagnosis of CTS.
  • Sensory hypalgesia as demonstrated by diminished ability to perceive painful stimuli applied along the palmar aspect of the index finger when compared with the ipsilateral little finger also is associated with the electrodiagnosis of CTS.
  • Hyperflexion of the wrist for 60 seconds may elicit paresthesia in the median nerve distribution (ie, Phalen sign). A recent review showed the average sensitivity and specificity of the Phalen sign to be 68% and 73%, respectively.
  • Tapping the volar wrist over the median nerve (ie, Tinel sign) may produce paresthesia in the median distribution of the hand. Pooled data show the sensitivity and specificity of the Tinel sign to be 50% and 77%, respectively.
  • Shaking or flicking one's hands for relief during maximal symptoms (ie, Flick sign) has been shown to have a sensitivity of 47% and specificity of 62%.
  • The loss of 2-point discrimination in the median nerve distribution or abductor pollicis brevis atrophy has a high specificity (>90%) but low sensitivity (<25%).

Causes

  • Inflammation of the flexor tendon sheath caused by activities involving repetitive wrist flexion (eg, assembly packing, computer keyboard work, playing a musical instrument, craftwork)
  • Edema from trauma of any type (eg, fractures), which can compress the median nerve
  • Compression of the median nerve from pregnancy or oral contraceptive-related edema
  • Strong association between being overweight or obese and the presence of CTS
  • Acromegaly
  • Rheumatoid arthritis
  • Gout or pseudogout
  • Tuberculosis
  • Renal failure and hemodialysis
  • Hypothyroidism
  • Amyloidosis
  • Has been associated with diabetes mellitus

More on Carpal Tunnel Syndrome

Overview: Carpal Tunnel Syndrome
Differential Diagnoses & Workup: Carpal Tunnel Syndrome
Treatment & Medication: Carpal Tunnel Syndrome
Follow-up: Carpal Tunnel Syndrome
References
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References

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Further Reading

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Keywords

CTS, median nerve compression at the wrist, carpal tunnel syndrome, compressive neuropathy, median nerve, peripheral compressive neuropathy, hand weakness, numbness in the hand, thenar atrophy, hand pain, wrist pain

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Contributor Information and Disclosures

Author

Jeffrey G Norvell, MD, Clinical Assistant Professor of Emergency Medicine, University of Kansas School of Medicine
Jeffrey G Norvell, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Coauthor(s)

Mark Steele, MD, Associate Dean for Truman Medical Center Programs, Professor, Department of Emergency Medicine, University of Missouri-Kansas City
Mark Steele, MD is a member of the following medical societies: American Academy of Emergency Medicine and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Medical Editor

David FM Brown, MD, Assistant Professor, Department of Medicine, Division of Emergency Medicine, Harvard Medical School; Associate-Chief, Attending Physician, Department of Emergency Medicine, Massachusetts General Hospital
David FM Brown, MD is a member of the following medical societies: American College of Emergency Physicians and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

Managing Editor

Eric Legome, MD, Chair, Department of Emergency Medicine, St Vincent's Hospital, Manhattan
Eric Legome, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, Council of Emergency Medicine Residency Directors, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

CME Editor

John D Halamka, MD, MS, Associate Professor of Medicine, Harvard Medical School, Beth Israel Deaconess Medical Center; Chief Information Officer, CareGroup Healthcare System and Harvard Medical School; Attending Physician, Division of Emergency Medicine, Beth Israel Deaconess Medical Center
John D Halamka, MD, MS is a member of the following medical societies: American College of Emergency Physicians, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: Nothing to disclose.

Chief Editor

Rick Kulkarni, MD, Medical Director, Assistant Professor of Surgery, Section of Emergency Medicine, Yale-New Haven Hospital
Rick Kulkarni, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Emergency Physicians, American Medical Association, American Medical Informatics Association, Phi Beta Kappa, and Society for Academic Emergency Medicine
Disclosure: WebMD Salary Employment

 
 
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