Carpal Tunnel Syndrome 

Updated: Feb 27, 2018

Author: Nigel L Ashworth, MBChB, MSc, FRCPC; Chief Editor: Milton J Klein, DO, MBA 

Overview
Practice Essentials
Carpal tunnel syndrome (CTS) is a collection of characteristic symptoms and signs that
occurs following compression 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.[1, 2] See image below.

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.

Workup

Electrophysiologic studies,[3, 4, 5] including electromyography (EMG) and nerve

conductions studies (NCS), are the first-line investigations in suggested carpal tunnel
syndrome (CTS).[6] Abnormalities on electrophysiologic testing, in association with specific
symptoms and signs, are considered the criterion standard for CTS diagnosis. In addition,
other neurologic diagnoses can be excluded with these test results.

Electrophysiologic testing also can provide an accurate assessment of how severe the damage
to the nerve is, thereby directing management and providing objective criteria for the
determination of prognosis.
Many clinical neurophysiology laboratories are now using ultrasonography as an adjunct to
electrodiagnostic studies. Ultrasonography potentially can identify space-occupying lesions
in and around the median nerve, confirm abnormalities in the median nerve (eg, increased
cross-sectional area) that can be diagnostic of CTS, and help to guide steroid injections into
the carpal tunnel.[7, 8, 9]

Magnetic resonance imaging (MRI) of the carpal tunnel is particularly useful preoperatively
if a space-occupying lesion in the carpal tunnel is suggested.

Management

Given that CTS is associated with low aerobic fitness and increased body mass index (BMI),
it makes some inherent sense to provide the patient with an aerobic fitness and weight-loss
program. Stationary biking, cycling, or any other exercise that puts strain on the wrists
probably should be avoided. The use of modalities (in particular therapeutic ultrasound) may
provide short-term relief in some patients.[10, 11, 12]

Most individuals with mild to moderate CTS (according to electrophysiologic data) respond
to conservative management, usually consisting of splinting the wrist at nighttime for a
minimum of 3 weeks.[10, 13, 14]

Steroid injection into the carpal tunnel has been shown to be of long-term benefit and can be
tried if more conservative treatments have failed.[15]

Patients whose condition does not improve following conservative treatment and patients
who initially are in the severe CTS category should be considered for surgery.[16] Surgical
release of the transverse ligament provides high initial success rates (greater than 90%), with
low rates of complication; however, it has been suggested that the long-term success rate may
be much lower than previously thought (approximately 60% at 5 y). Success rates also are
considerably lower for individuals with normal electrophysiologic studies.[17, 18, 19]

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.[20] 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.