Carpal tunnel syndrome (CTS) is the most common focal peripheral neuropathy. CTS is caused by entrapment of the median nerve at the wrist as it traverses through the carpal tunnel.
Acute CTS is a rare compartment syndrome of the carpal tunnel that occurs after major trauma, typically distal radius fracture. Diagnosis is based on clinical history and examination and does not require electrophysiological testing to proceed with surgery as soon as possible to relieve the pressure on the median nerve.[1, 2, 3]
Chronic CTS is a much more common condition and of more gradual onset, with intermittent symptoms initially and slow progression. The condition is often bilateral and almost always more prominent in the dominant hand. The syndrome is characterized by pain, paresthesia, and weakness in the median nerve distribution of the hand that are typically provoked by sleep or activities involving repetitive hand use. Electrodiagnostic studies are helpful to confirm the diagnosis. Treatment in mild cases may be nonsurgical and includes wrist splinting, but many patients require either open or endoscopic carpal tunnel release surgery with usually excellent outcome.
Modifying occupation or ergonomic conditions (eg, tools) may be beneficial. For excellent patient education resources, see Carpal Tunnel Syndrome.
The median nerve is formed by C5-C7 fibers from the lateral cord and C8-T1 fibers from the medial cord of the brachial plexus. Muscular branches of the median nerve innervate most of the forearm flexor muscles and include the anterior interosseus nerve. The palmar cutaneous branch of the median nerve leaves the main trunk proximal to the wrist crease and provides sensation over the thenar eminence. See the image below.
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Anatomy of the median nerve and the carpal tunnel.
Within the hand, the median nerve carries C8-T1 motor fibers to the abductor pollicis brevis, opponens pollicis, and superficial head of the flexor pollicis brevis muscles (thenar or recurrent motor branch) and the first and second lumbrical muscles. It supplies sensory innervation to the palmar surface of the thumb, and digits 2, 3, and the lateral half of digit 4 (via the common palmar digits nerves 1–3).
The median nerve crosses from the distal forearm to the hand through the carpal tunnel. The carpal tunnel is located at the base of the palm, just distal to the distal wrist crease. The floor of the carpal tunnel is formed by the carpal bones that create an arch. The fibrous flexor retinaculum, or transverse carpal ligament (TCL), is the roof of the carpal tunnel on the palmar side. The carpal tunnel is the narrowest at the level of the distal carpal row, at the level of the hook of the hamate bone. Within the carpal tunnel, the median nerve is physiologically flattened in configuration, and this flattening is maximal about 2–2.5 cm distal to the proximal edge of TCL. Along with the median nerve, 9 flexor digitorum tendons (8 tendons of the superficial and deep finger flexors and 1 of the flexor pollicis longus) pass through the carpal tunnel. The TCL is under tension, helps to maintain the carpal arch, and provides a retinacular pulley to the flexor tendons. See the image below.
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Anatomy of the carpal tunnel.
CTS is caused by increased pressure in the carpal tunnel and on the median nerve. Compression of a peripheral nerve induces marked changes in intraneural microcirculation and nerve fiber structure, impairment of axonal transport, and alterations in vascular permeability, with edema formation and deterioration of nerve function.[4] Ischemia is a more significant factor of nerve fiber damage in acute median nerve compression, whereas in chronic entrapment, mechanical distortion plays a greater role. The pathology of idiopathic CTS is a noninflammatory fibrosis of the subsynovial connective tissue surrounding the flexor tendons. Biochemical studies of surgical specimens suggest that a variety of regulatory molecules may be inducing fibrous and vascular proliferation and that this may be a response to mechanical stresses.[5]
In a study of patients with CTS, when the wrist was in neutral position, the mean pressure in the carpal canal was 32 mm Hg versus 2.5 mm Hg in healthy patients.[6] The pressure increased to 94 mm Hg during wrist flexion (healthy patients 32 mm Hg) and 110 mm Hg during wrist extension (healthy patients 30 mm Hg). Carpal tunnel release brought about an immediate and sustained reduction in pressure.
In animal experiments, acute and severe compression caused persistent impairment of intraneural microcirculation due to mechanical injury to blood vessels.[7] In rabbits undergoing a graded compression of the tibial nerve, interference with venular flow was observed at a pressure of 20–30 mm Hg, while arteriolar and intrafascicular capillary flow was impaired at about 40–50 mm Hg. At 60–80 mm Hg, no blood flow ceased completely.[7]
In early or mild CTS, the median nerve has no morphological changes, and neurologic symptoms are intermittent. Prolonged increased pressure on the nerve results in segmental demyelination. The focal demyelination causes short segment conduction delay or conduction block across the site of entrapment. In more severe cases, wallerian degeneration and denervation of the thenar muscles develops.
The peripheral nerves of patients with underlying generalized neuropathies are more susceptible to compression injury, and the condition is associated in up to one third of cases with systemic medical conditions. Most cases of CTS are considered idiopathic. Some patients have an inherited increased susceptibility of the nerve to pressure, and on rare occasions CTS may be familial.
The concept of double crush syndrome was introduced in 1973 by Upton and McComas.[8] They proposed that focal compression of the nerve proximally predisposes it to injury at a more distal site along its course through impaired axoplasmic flow. The hypothesis remains of uncertain validity; there is no clear association between the frequency and severity of CTS and level of cervical radiculopathy.[9]
Most cases of carptal tunnel syndrome (CTS) are idiopathic. In up to 50% of cases, an underlying condition may be identified that causes a locally reduced space in the carpal tunnel or increased susceptibility to nerve damage. Many metabolic or endocrine conditions are associated with increased risk of CTS, and several risk factors may coexist. Some cases may be attributed to excessive or repetitive hand movements.
Local causes with reduced space in the carpal tunnel include:
Congenital - Congenital small carpal tunnel, anomalous muscles and tendons, vascular anomalies including persistent median artery
Trauma, acute or chronic manifestation due to associated degenerative changes - Distal radius fracture (Colles fracture), dislocation or fracture of one of the carpal bones
Exostosis, osteophytes
Hematoma
Local infection - Septic arthritis, histoplasmosis
One study indicated that in patients who suffer a distal radius fracture, CTS is more likely to develop, within a 9-month postfracture period, in those who undergo open reduction and internal fixation (ORIF). The investigators also reported that the presence of diabetes mellitus was significantly associated with the development of CTS within 9 months following distal radius fracture (adjusted hazard ratio 2.76).[10]
Regional or systemic conditions with reduced space include:
Osteoarthritis
Rheumatoid arthritis
Mucopolysaccharidoses and mucolipidoses
Amyloidosis
Gout
Spasticity with persistent wrist flexion
Systemic conditions with increased susceptibility of nerves to pressure include:
Hereditary neuropathy with liability to pressure palsies (HNPP)
Diabetes mellitus
Other polyneuropathies
Other associated systemic conditions include:
Obesity
Hypothyroidism, hyperthyroidism
Alcoholism
Pregnancy (third trimester, usually bilateral), lactation
Work/activity-related risk is greater for highly repetitive wrist and finger use than forceful hand use. The combination of finger flexion with repetitive wrist motion is probably the most provocative stressor. The classic concept of repetitive motion-induced chronic tenosynovitis resulting in CTS has been questioned. Keyboard data entry has not been established as a cause of CTS.
Familial carpal tunnel syndrome has X-linked dominant (females), autosomal dominant, and recessive (childhood) forms. There is a bilateral presentation and anatomical abnormalities include a narrow carpal tunnel and thick transverse carpal ligaments.
Carpal tunnel syndrome (CTS) is the most common focal peripheral neuropathy. The reported incidence varies by location and methodology used. Prevalence rates for CTS are reported as 1–5% in the general population and 5–15% in industrial settings. An increasing temporal trend has been reported in several studies.[11, 12] A cross-sectional survey reported in 2001 calculated the lowest possible prevalence of symptomatic CTS in the general US population as 3.72%.[13]
Among residents of Olmsted County, Minnesota, the adjusted annual rates of medically diagnosed CTS increased from 258/100,000 in 1981–1985 to 424/100,000 in 2000–2005.[11] For this last period included in the study, the incidence in women was 542/100,000 and in men was 303/100,000. Generally, the most marked increases in CTS incidence were seen in younger age groups of both sexes in the first part of the study period and among older age groups in the final decades of the study. The cause of the increase is unclear, but it corresponds to an epidemic of CTS cases resulting in lost work days that began in the mid-1980s and lasted through the mid-1990s. The elderly present with more severe disease and are more likely to have carpal tunnel surgery.[11]
International
In the general population for a Dutch community, the prevalence rate of undetected CTS was 5.8% in adult women, and an additional 3.4% already carried the diagnosis of CTS. The overall prevalence rate for men was 0.6%.[14]
A primary care study in the United Kingdom from 2000 reported an annual incidence of CTS of 88/100,000 in men, and 193/100,000 in women. New presentations were most frequent in women aged 45–54 years.[15] In this study, CTS was as common as all other entrapment neuropathies combined.
A study in Italy reported a mean standardized annual incidence of 329/100,000 in the Siena area (Tuscany) from 1991–998, with 139 for men and 506 for women. The age-specific incidence for women increased gradually with age, reaching a peak from 50–59 years. In men, there was a bimodal distribution with peaks from 50–59 years and 70–79 years.[12]
A French study of CTS from 2002–2004 in patients aged 20–59 years reported a mean incidence rate per 1000 person-years that was higher in employed than unemployed persons (1.7 vs 0.8 in women and 0.6 vs 0.3 in men). Higher values were blue-collar workers and lower-grade services, sales, and clerical white-collar workers.[16]
Mortality/Morbidity
CTS is associated with high costs to the healthcare system and society. According to 1988 data from the United States, every year an estimated 1 million adults require medical treatment for CTS.[17] About 400,000–500,000 CTS surgeries annually were reported in 1995 with an economic cost of more than 2 billion dollars.[18]
In 1999, CTS cases were associated with a median number of 27 days lost from work, the highest number of any major disabling illness or injury.[19]
Demographics
Findings of the 1988 National Health Interview Survey indicate that CTS is 1.8 times more prevalent in Whites than nonWhites.
The reported female-to-male ratio ranges from 3:1 to about 10:1. Phalen's original series in 1970 included 280 women and 96 men (female-to-male ratio 3:1).[20] According to data from the 1980s, the prevalence of electrophysiologically confirmed symptomatic CTS is about 3% among women and 2% among men.[21]
Of the patients in Phalen's series, 58% were adults aged 40–60 years.[20]
Carpal tunnel syndrome (CTS) is not fatal, but it can lead to complete, irreversible median nerve damage, with consequent severe loss of hand function, if left untreated. For mild cases, conservative treatment is usually adequate. Surgical decompression usually produces good results. Patients with advanced thenar muscle atrophy usually do not recover fully after surgical decompression. CTS that is caused by or aggravated by an underlying disease (eg, diabetes) has a worse prognosis.
Patients with carpal tunnel syndrome (CTS) typically complain of pain, tingling, and numbness in the dominant hand and affecting digits 1–3 in particular, and awakening them from sleep.
In early CTS, paresthesias are intermittent, and the hand is reported as falling asleep, with pins and needles sensation.
Most often, the symptoms are in the thumb, index, and middle finger. Classic CTS includes symptoms affecting at least 2 of the first 3 digits, but not the palm of dorsum of the hand.
Many patients report that the entire hand falls asleep. Detailed questioning sometimes reveals that digit 5 is not affected. Others, if asked to observe whether the little finger is involved, often note subsequently that it is spared.
A diagram of symptoms in the hand can help patients to localize symptoms. In a clinic-based sample, a diagram of symptoms (Katz hand diagram of classic or probable CTS) had a sensitivity of 61% and a specificity of 71% for the diagnosis of CTS.[22, 23]
Patients with CTS may describe rather diffuse, poorly localized aching that involves the entire hand and radiates to the forearm and elbow and even the shoulder region, but not to the neck.
Patients may report coldness, swelling, dry skin, and/or color changes in the hand. Raynaud phenomenom is more common in patients with CTS.
Nocturnal pain and paresthesias may awaken the patient from sleep when prolonged wrist flexion or extension leads to increased pressure in the carpal tunnel. In a study of patients with brachialgia paraesthetica nocturna, about 40% were diagnosed with CTS.[14] A history of nocturnal symptoms has moderate sensitivity (51–77%) and specificity (27–68%).[23]
Motor involvement may be reported as clumsiness, difficulty buttoning the shirt or opening jars, dropping objects, and weakness.
Provocative factors: Symptoms are worsened by excessive use of the hand, including repetitive wrist motion and during a flexed or extended wrist posture. Discomfort may be provoked by driving or by holding the phone, a book, or a newspaper.
Alleviating factors: Patients often report that they shake the hand to lessen the symptoms, the so-called flick sign, with sensitivity and specificity reported as high (> 90% for both)[24] to moderate (50% and 77%, respectively).[25]
CTS is unlikely if no symptoms are present in any of the first three digits, and in particular if the complaint is wrist pain without pain or paresthesias in the fingers.
Inquire about a trauma to the hand or wrist, occupational or habitual hazards involving repetitive wrist movements, excessive hand use or exposure to vibratory forces, and associated medical conditions (see Causes).
Although patients with carpal tunnel syndrome (CTS) often have difficulty isolating the sensory complaints to the median-innervated digits, sensory findings on examination are typically limited to the distribution of the median nerve. Motor examination often reveals slight weakness of thumb abduction. Thenar muscle atrophy indicates axonal nerve injury in more advanced CTS. The classic motor and sensory signs of CTS including the provocative bedside tests, but do not reliably distinguish among patients with suggestive CTS symptoms between focal median nerve neuropathy as confirmed by electrophysiological testing and other conditions with similar complaints and negative electrophysiological results.
Inspection
See the list below:
Atrophy of the thenar muscle group is a late sign (see Motor examination below).
Trophic changes: Dry skin may be noted over digits 1–3. Many patients report subjective hand swelling,[26] but usually no edema is noted on examination. Raynaud's phenomenon and blanching of the hands may be present.
Square-shaped wrist: A correlation of wrist dimensions with CTS was first reported in 1983.[27] Measured at the distal wrist crease, a ratio of greater than 0.7 for the anterior-posterior dimension divided by the mediolateral dimension had a sensitivity of 69% for electrophysiologically confirmed CTS.[28] An increasing wrist ratio correlates with prolongation of the median nerve sensory latencies and distal motor latencies.[27, 29]
Scars may be noted related to prior injuries or surgeries including prior carpal tunnel release surgery. See the image below.
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Scars from carpal tunnel release surgery.
Sensory findings
See the list below:
In early CTS, the examination may be normal or limited to abnormal sensation to light touch or pinprick over the fingertips of digits 2 and/or 3.
Sensory deficits are noted within the median-innervated hand area that includes the palmar aspects of the medial thumb, the index and middle fingers, and the lateral ring finger.
The sensation over the thenar eminence is spared, as it is innervated by the palmar cutaneous branch of the median nerve that arises proximal to the carpal tunnel.
Rubbing the patient's fingertips with the examiner's own and comparing the sensation in the first 3 digits to the digit 5 is the easiest way to determine sensory loss. Patients may report tingling, pins and needles, a feeling like sandpaper, or as if their fingertips are covered by a thin glove.
Testing with pinprick may document decreased sensation (hypalgesia) in median innervated fingers versus digit 5, and may be particularly useful in comparing the affected lateral aspect of the ring finger from the nonaffected medial (ulnar) aspect. Occasionally, the patients report hyperalgesia instead of numbness.
Decreased 2-point discrimination is less useful due to low sensitivity, but fairly specific. Testing of vibration is of uncertain value.
Motor examination
See the list below:
Inspect the hand for thenar muscle atrophy suggestive of CTS that may be noted only by comparing both hands. Assess the hypothenar and first dorsal interosseus muscles for comparison that should be normal in isolated focal median neuropathy, but may show atrophy in patients with C8 radiculopathy or polyneuropathy.
Test the abductor pollicis brevis (APB) muscle strength:
Isolating the muscle action of abductor pollicis brevis is difficult. Typically, the muscle strength is tested for a movement perpendicular to the palm against the examiner's fingers. The abductor pollicis longus (radial nerve) contributes to thumb abduction function, and the combination of the flexor pollicis brevis, deep head (ulnar nerve) and the flexor pollicis longus (anterior interosseous nerve of the median nerve) contribute to opposition movement.
In many patients with CTS, no clear weakness of the APB or thenar atrophy is present.
The intact function of the long finger flexors of the forearm as tested by the Ok-sign (Flexor pollicis longus, Flexor digitorum profundus innervated by the anterior interosseus branch) differentiates CTS from more proximal lesions affecting the median nerve.
Severe atrophy of the APB muscle is more often noted in elderly patients with long-standing symptoms who present with hand clumsiness and relatively minor pain.
Diagnostic bedside tests
Provocative tests (symptom replication tests) may assist in the clinical diagnosis of CTS by exacerbating or reproducing the symptoms reported by the patient. However, the tests have low validity. In 1 study of patients with CTS symptoms and subsequent neurophysiological testing, the probability of CTS ranged from 35% to 70% for positive test results and from 41% to 62% for negative test results.[30]
Tinel sign: Radiating paresthesias into the hand and the median innervated fingers are provoked by tapping over the palmar wrist region overlying the carpal tunnel. The sensitivity varies greatly and is estimated as 50%; the specificity is estimated at 73%.[25]
Phalen test: Holding the hand in maximally flexed position at the wrist for 60–120 seconds may elicit paresthesia distally within the median nerve distribution. Phalen performed the test by having the patient rest the elbows on a table, hold the forearms vertically, and then allow the hands to drop with complete wrist flexion for 1 minute. The sensitivity is reported as 68% (greater than for the Tinel sign), and the specificity as 73%.[25] Time to onset of symptoms may be documented in the chart with earlier onset, indicating greater CTS severity; advanced CTS is suggested by onset within 20 seconds.
Carpal compression test (median nerve compression test): Pressure is applied by the examiner with both thumbs on the palmar aspect of the patient's wrist.[31] Estimates are 64% for sensitivity and 83% for specificity according to one study,[25] but vary widely.[19]
Reverse Phalen test: Holding the hand in hyperextension position at the wrist may similarly worsen or reproduce the complaints within one minute. This test is less commonly used than the Phalen test.
Tethered median nerve stress test: Tension of the median nerve is produced by simultaneous extension of the supinated wrist and the distal interphalangeal joint of the index finger for 1 minute. Patients with chronic CTS report pain over the volar aspect of the proximal forearm.[32] A sensitivity of 43% was reported compared with 56% with Phalen and 42% with Tinel sign. In spite of his low sensitivity, in some cases this test is the only clinical positive sign.[33]
Tourniquet test: Application of a tourniquet or inflated blood pressure cuff at the upper arm results in paresthesias in median-innervated digits.
Symptom relief test
With the affected hand facing upward, the distal metacarpal heads are gently squeezed. Stretching of digits 3 and 4 may also be used. These maneuvers may diminish the paresthesias in patients with CTS.
Blood tests to screen for underlying rheumatologic or inflammatory disease or other treatable systemic conditions known to be associated with carpal tunnel syndrome (CTS), if suspected:
Fasting blood glucose and hemoglobin A1c
Thyroid function (thyroid stimulating hormone [TSH])
Wrist magnetic resonance imaging (MRI) has the greatest sensitivity and specificity of the available imaging modalities for the diagnosis of carpal tunnel syndrome (CTS) but is usually not necessary.[34] Current MRI research is focusing on the use of diffusion tensor imaging (DTI) and tractography of the median nerve in the diagnosis of carpal tunnel syndrome.[35, 36] Tractography in patients with chronic compression of the median nerve typically shows that mean fractional anisotropy values in the median nerve are significantly lower within the carpal tunnel than in locations proximal to the carpal tunnel. Preliminary results suggest that quantitative evaluation of the median nerve with DTI is precise, and that in patients with unilateral involvement, the healthy contralateral nerve can be used as an internal control.[37]
Computed tomography (CT) scan of the wrist may be helpful in patients with subtle bony trauma.
Wrist ultrasonography may evaluate the soft tissues of the carpal tunnel including the tendons and the median nerve and allow cross-sectional measurement of the carpal tunnel.
Wrist radiograph can be used if a fracture (old or recent) is suspected.
Cervical spine radiograph and/or MRI can be used if cervical radiculopathy is suspected.
Chest CT scan, chest radiograph, or brachial plexus MRI can be used in patients with suspected brachial plexopathy or thoracic outlet syndrome.
The clinical bedside examination, including diagnostic provocative tests, have low validity, and patients with CTS symptoms should be referred directly for neurophysiologic examination. Electrodiagnostic studies remain the criterion standard for diagnosis of CTS, but should always be interpreted in combination of the clinical symptoms and signs.
Nerve conduction study (NCS)
NCS measures the sensory and motor nerve conduction velocity (latency) and amplitudes across the wrist. Any focal median nerve conduction delay implies a demyelinative lesion of the median nerve. In mild or early CTS, there is usually conduction delay of sensory fibers only, without prolongation of distal motor latency. In more severe CTS, focal conduction block or secondary axon loss results in decreased median nerve sensory and motor amplitudes. Routine NCS may miss the diagnosis of CTS in up to 25% of cases. The sensitivity is greatly improved by measuring the median nerve latency within a shorter segment across the wrist in comparison to an adjacent nerve for the same distance. The clinical diagnosis of CTS may thus be confirmed with a high degree of sensitivity (>85%) and specificity (>95%).[38]
Electrodiagnostic protocol
Multiple techniques are used to diagnosis CTS. A typical electrodiagnostic protocol is summarized below.
Antidromic sensory NCS are recorded from a median innervated digit, typically by placing ring electrodes on the index finger, with electrical stimulation at the wrist at a distance of 14 cm.
For internal median nerve comparison, the sensory potential from the index finger is also recorded by stimulation in the palm of the hand, at a midpoint between the wrist stimulation site and the recording ring electrode on the index (7 cm to each). The upper normal limit for the peak latency of the distal segment is 1.9 ms. The upper limit for the calculated peak latency difference between the wrist and palm stimulations is 1.6 ms.
Antidromic sensory NCS of the ulnar nerve is recorded with ring electrodes on digit 5 and stimulation at the wrist (on the ulnar aspect). The median motor response is recorded with surface electrodes over the abductor pollicis brevis muscle (APB) and stimulation at the wrist and elbow.
If the above routine median NCS is not diagnostic, the median nerve latency across the transcarpal segment is measured in comparison to an adjacent nerve (ulnar or radial).[39, 40] This strategy may be particularly helpful in mild CTS cases and in patients with underlying polyneuropathy to detect superimposed focal median conduction delay. Sensitivity and specificity of these internal comparison studies depends greatly on the upper normal limit (cutoff) values. In patients with ulnar neuropathy, the comparison should be to the radial nerve or by internal median nerve comparison of the wrist segment versus the finger segment.
Median versus ulnar palmar mixed nerves studies (orthodromic) with stimulation at the palm and recording from the wrist at a distance of 8 cm. A palmdiff of 0.4 ms or greater is abnormal.
Median versus ulnar nerve distal sensory latencies to the ring finger, with stimulation at the wrist, at a distance of 14 cm (antidromic). A ringdiff of 0.5 ms or greater is abnormal.
Median versus radial nerve distal sensory latencies to the thumb with stimulation at the wrist, at a distance of 10 cm (antidromic). A thumbdiff of 0.5-0.7 ms or greater is abnormal.
Needle electromyography (EMG) testing is optional for the diagnosis of CTS. It may be needed to differentiate CTS from cervical radiculopathy. In cases where surgery is being considered, it may document severity of CTS by documenting denervation to the APB muscle.
Robinson et al[39] recommended the use of the combined sensory index (CSI) defined as the sum of the 3 latency differences listed above under 5) with higher sensitivity and reliability than the individual tests. Sensitivity for the tests was palmdiff 69.7%, ringdiff 74.2%, thumbdiff 75.8%, and CSI 83.1%. Specificity was 95.4–96.9%. Requiring 1, 2, or 3 tests to be abnormal yielded sensitivities of 84.8%, 74.2%, or 56.1%, respectively, but specificities of 92.3%, 98.5%, and 100%, respectively.
In a follow-up retrospective report on a larger patient group (300 hands), the same authors determined endpoints for individual tests that confidently predicted the results of the CSI; for ranges between these endpoints, further testing was required. These ranges were palmdiff 0–0.3 ms, ringdiff 0.1–0.4 ms, and thumbdiff 0.2–0.7 ms.[41] A smaller prospective study of the same technique documented the overall superiority of the SCI versus individual tests for diagnostic accuracy, but when individual tests were markedly abnormal, it was not necessary to perform all 3 nerve conduction studies.[42]
Electrodiagnostic studies in carpal tunnel syndrome
A 2022 report of the American Association of Electrodiagnostic Medicine, American Academy of Neurology, and the American Academy of Physical Medicine and Rehabilitation recommended the following electrodiagnostic studies in patients with suspected CTS (see below for sensitivity and specificity of Techniques A–K):[38]
Perform a median sensory NCS across the wrist with a conduction distance of 13-14 cm (Technique G). If the result is abnormal, compare the result of the median sensory NCS to the result of a sensory NCS of 1 other adjacent sensory nerve in the symptomatic limb (Standard).
If the initial median sensory NCS across the wrist has a conduction distance greater than 8 cm and the result is normal, 1 of the following additional studies is recommended:
Comparison of median sensory or mixed nerve conduction across the wrist over a short (7-8 cm) conduction distance (Technique C) with ulnar sensory nerve conduction across the wrist over the same short (7-8 cm) conduction distance (Technique D) (Standard)
Comparison of median sensory conduction across the wrist with radial or ulnar sensory conduction across the wrist in the same limb (Techniques B and F) (Standard)
Comparison of median sensory or mixed nerve conduction through the carpal tunnel to sensory or mixed NCSs of proximal (forearm) or distal (digit) segments of the median nerve in the same limb (Technique A) (Standard)
Perform a motor conduction study of the median nerve recording from the thenar muscle (Technique H) and of 1 other nerve in the symptomatic limb to include measurement of distal latency (Guideline).
Supplementary NCS: Comparison of the median motor nerve distal latency (second lumbrical) to the ulnar motor nerve distal latency (second interossei) (Technique J), median motor terminal latency index (Technique I), median motor nerve conduction between wrist and palm (Technique E), median motor nerve compound muscle action potential (CMAP) wrist to palm amplitude ratio to detect conduction block, median sensory nerve action potential (SNAP) wrist to palm amplitude ratio to detect conduction block, short segment (1 cm) incremental median sensory nerve conduction across the carpal tunnel (Option).
Perform needle electromyography of a sample of muscles innervated by the C5-T1 spinal roots, including a thenar muscle innervated by the median nerve of the symptomatic limb (Option).
Sensitivity and specificity of electrodiagnostic techniques
For each electrodiagnostic technique to summarize results across studies, sensitivities were pooled from individual studies by calculating a weighted average. In calculating the weighted average, studies enrolling more patients received more weight than studies enrolling fewer patients. Specificities were similarly pooled by calculating the weighted average.[38]
Technique A: Median sensory and mixed nerve conduction (wrist and palm segment vs forearm or digit segment)
Sensitivity: 0.85
Specificity: 0.98
Technique B: Comparison of median and ulnar sensory conduction (wrist and ring finger)
Sensitivity: 0.85
Specificity: 0.97
Technique C: Median sensory and mixed nerve conduction (wrist and palm)
Sensitivity: 0.74
Specificity: 0.97
Technique D: Comparison of median and ulnar mixed nerve conduction (wrist and palm)
Sensitivity: 0.71
Specificity: 0.97
Technique E: Median motor nerve conduction (wrist and palm)
Sensitivity: 0.69
Specificity: 0.98
Technique F: Comparison of median and radial sensory conduction (wrist and thumb)
Sensitivity: 0.65
Specificity: 0.99
Technique G: Median sensory nerve conduction (wrist and digit)
Sensitivity: 0.65
Specificity: 0.98
Technique H: Median motor nerve distal latency
Sensitivity: 0.63
Specificity: 0.98
Technique I: Median motor nerve terminal latency index
Sensitivity: 0.62
Specificity: 0.94
Technique J: Comparison of median motor nerve distal latency (second lumbrical) to ulnar motor nerve distal latency (second interossei)
Conservative treatment is usually recommended for mild-to-moderate carpal tunnel syndrome (CTS), at least initially.
A lightweight plastic/Velcro splint in a neutral position that allows semifree finger movement is recommended. The wrist splint should be worn primarily at night (regularly) and as needed during daytime (during manual activity). Precautions should be taken to prevent a persistently stiff wrist caused by prolonged immobilization.
Patients should modify activity to reduce wrist flexion, extension, rotation, finger flexion, and forceful gripping.
Steroid injections
A local steroid injection[43] may be particularly helpful in patients with mild CTS and intermittent symptoms. Local injection may also have a diagnostic or prognostic role as a predictor of response to surgical release. Corticosteroids (methylprednisolone acetate [DepoMedrol] 10–20 mg or triamcinolone acetonide [Kenolog] 10–20 mg) are injected adjacent (proximal) to the carpal tunnel, after local anesthesia. Care must be taken not to inject the carpal tunnel, any tendon, or the nerve itself. Such an injection may increase the intracarpal tunnel pressure and cause additional nerve injury. The effect of steroid injections may be seen within a few days and often lasts for several weeks or months. The effect is usually only temporary and usually wears off by 1 year. It may be particularly helpful in pregnant patients or those with temporary medical conditions such as hypothyroidism.
Repeated use beyond 2–3 injections is not recommended due to the greater risk of damage to the flexor tendons, including tendon rupture. Other complications include increased median nerve deficit, local infection, and reflex sympathetic dystrophy. A study comparing daily application of lidocaine 2.5% plus prilocaine 2.5% (EMLA) with a single injection of methylprednisolone acetate found that the anesthetic cream was effective and well tolerated.[44]
Despite research indicating the effectiveness of corticosteroid injections in the treatment of CTS, one literature review found such injections to be of very limited benefit. The investigators reported that, compared with placebo or splinting, corticosteroid injections showed a small benefit on the Symptom Severity Scale (SSS) of the Boston Carpal Tunnel Questionnaire (BCTQ) before the first 3 months, but one that was below the minimal clinically important difference. No SSS benefit was found at 6 months. The Functional Status Scale of the BCTQ showed no benefit to steroids at any point in 6-month follow-up.[45]
However, according to one literature review that looked at studies with at least 1-year follow-up, evidence suggests that symptom improvement from corticosteroid injections is sufficient to allow many patients with CTS to delay or avoid further intervention. The investigators found that carpal tunnel release surgery was eventually performed in 41.6% of patients in the study, with the median/mean time between injection and surgery ranging from 128 to 446 days. Reinjection was performed in 29% of patients.[46]
A short course of nonsteroidal anti-inflammatory medication is often recommended, if there is no contraindication, without clear evidence of its effectiveness. Nonsteroidal anti-inflammatory medications (NSAIDs) are frequently prescribed for this condition; caution patients to watch for the usual adverse effects. Short-term diuretic treatment may be helpful in patients with limb swelling. One study in patients with mild-to-moderate CTS found that short-term, low-dose oral steroid treatment (prednisolone, 20 mg qd x 2 wk, then 10 mg qd x 2 wk) was more effective than treatment with a diuretic or an NSAID.[47] A follow-up study found that 2 weeks of prednisolone provided long-term results comparable to those with 4 weeks of treatment.[48]
Acupuncture can be an alternative for patients with mild-to-moderate CTS who cannot tolerate oral steroids or have a contraindication to their use, or for those who do not opt for early surgery. In a randomized, controlled study, short-term acupuncture treatment proved aws effective as short-term low-dose prednisolone.[49]
Other alternative therapies include yoga-based programs for stretching, strengthening, and relaxation and chiropractic therapy.
The decision to proceed to carpal tunnel release (CTR) surgery should be driven by the preference of the patient.[50] Surgery is indicated in most patients with moderate–to-severe carpal tunnel syndrome (CTS).[51]
In a literature review of patients with severe CTS, researchers reported that significant improvements occurred following carpal tunnel release. Across the range of evaluated studies, the investigators found that paresthesia completely resolved in 55–98% of hands; pain, in 64–100% of hands; and weakness, in 60–75% of hands. In addition, numbness resolved in 39–94% of hands, and improvements occurred in power grip, key, tripod, index-thumb pulp pinch, and thumb opposition.[52]
According to a 2008 Cochrane review, surgical treatment of CTS relieved symptoms significantly better than splinting. A significant proportion of people treated medically eventually required surgery, and the risk of reoperation in surgically treated patients was low. Complications were more common in the surgical arm (RR 1.38, 95% CI, 1.08–1.76).[53]
In a 2005 comparison study of open CTR with steroid injection, surgery resulted in better symptomatic and neurophysiologic outcome but not grip strength in patients with idiopathic CTS over 20 weeks.[54]
In a 2009 randomized multicenter study of patients with CTS without denervation, surgical treatment led to modestly better outcome than multimodality, nonsurgical treatment (including hand therapy and ultrasonography).[55]
Regardless of the specific technique used, surgical treatment of carpal tunnel syndrome should involve complete division of the flexor retinaculum.
Indications for surgical decompression include:
Acute CTS due to local trauma (fracture, hematoma, infection) (requires surgical decompression as soon as possible)[56]
Mass lesion (eg, nerve tumor, ganglion cyst)
Failure to respond to conservative therapy (recommended time ranges from 2–7 weeks to 1 year[50] )
Severe CTS on clinical examination
Significant weakness or atrophy of the thenar muscles
Persistent numbness and paresthesias in the median sensory territory
Decreased compound motor action potential on NCS
Denervation in distal median innervated muscles on electromyography
Surgery techniques
Surgery includes complete resection of the transcarpal ligament by open or endoscopic techniques.
Classic open CTR surgery requires a longitudinal incision from the distal wrist crease to the palm, about 5–6 cm in length. Modifications with limited open release surgeries have been described.
Endoscopic surgery is done by either single or dual portal techniques, with overall similar success rate than open surgery.[57]
According to a Cochrane review in 2004, no strong evidence supports open or endoscopic surgery for CTR, and the decision seems to be guided by surgeon and patient preferences.[58]
The overall success rate with endoscopic CTR surgery is reported as 96.5%, with a complication rate of 2.7% and a failure rate of 2.6%.[59]
The endoscopic technique has a slightly higher risk of injury to the median nerve. In some reports, patients with endoscopic surgery experience less pain and have earlier return to work and daily activities.[59]
Complications
Transient paresthesias of the ulnar and median nerves are common after surgery. Tenderness of the surgical scar is greater after open surgery and may persist for up to 1 year. Superficial palmar arch injuries, reflex sympathetic dystrophy, and flexor tendon lacerations can occur.
Causes of incomplete relief from surgery include incomplete section of flexor retinaculum, multifactorial hand symptoms, and an incorrect preoperative diagnosis.
No specific diet is indicated for patients with carpal tunnel syndrome (CTS). A low-salt diet may be indicated if fluid retention is a contributing factor.
The effectiveness of vitamin B-6 supplementation is questionable, but many patients use it on their own as adjunct therapy. Although doses of less than 200 mg daily are unlikely to cause adverse effects, patients should be monitored for vitamin B-6 toxicity, particularly when high doses are taken over long periods.[60]
One European study has reported reduction in symptoms and functional impairment with alpha-lipoic acid, 600 mg, and gamma-linolenic acid, 360 mg, daily for 90 days in 112 patients with moderately severe carpal tunnel syndrome.[61]
Prolonged, repetitive use of the wrist (especially with force) may aggravate carpal tunnel syndrome (CTS). The following ergonomic changes in the workplace can be helpful:
Work should be placed 10–12 inches in front of the eyes.
Elbows should be postured at an angle of 85–100°.
Shoulder should be in the vertical position, with abduction no greater than 20°.
Wrist should be in the neutral position, without ulnar or radial deviation, with minimal flexion or extension.
Environmental conditions such as temperature extremes and vibration should be minimized.
In May 2024, the American Academy of Orthopaedic Surgeons (AAOS) released updated evidence-based clinical practice guidelines on the management of CTS. Recommendations based on strong or moderate evidence included the following:[62]
CTS-6 can be used to diagnose carpal tunnel syndrome, in lieu of routine use of imaging (ie, ultrasonography) or nerve conductions velocity (NCV)/electromyography (EMG).
MRI and Upper Limb Neurodynamic Testing should not be used to diagnose CTS.
Corticosteroid injection does not provide long-term improvement of carpal tunnel syndrome however, short-term use for symptom relief is acceptable.
PRP Injection does not provide long-term benefits (leukocyte rich or leukocyte poor PRP) and is not a standard treatment for CTS.
There is no difference in patient reported outcomes between a mini-open carpal tunnel release and an endoscopic carpal tunnel release and both are accepted surgical techniques for the treatment of CTS.
Local anesthesia only may be used for CTS release surgical procedures.
There is insufficient evidence of benefit for routine supervised physical therapy following CTS surgery.
There splinting after carpal tunnel release has not demonstrated functional or outcome benefits and should not be used.
NSAIDs and/or acetaminophen should be used after carpal tunnel release for pain management.
The guidelines give a limited recommendation based on low evidence against the following nonoperative treatments, which overall performed no better than placebo:[62]
Acupressure
Insulin injection
Heat therapy
Magnet therapy
Nutritional supplementation
Oral diuretic, NSAID, anticonvulsant
Phonophoresis
A limited recommendation against the following nonoperative treatments due to the lack of improvement on long-term patient reported outcomes:[62]
Clinical Context:
For relief of mild to moderately severe pain; inhibits inflammatory reactions and pain by decreasing activity of cyclooxygenase, which is responsible for prostaglandin synthesis.
Clinical Context:
For relief of mild to moderately severe pain and inflammation. Small dosages indicated initially in patients with small body size, the elderly, and those with renal or liver disease.
Doses >75 mg do not increase therapeutic effects.
Administer high doses with caution and closely observe patient for response.
Clinical Context:
May inhibit cyclooxygenase, which in turn inhibits prostaglandin biosynthesis. These effects may result in analgesic, antipyretic, and anti-inflammatory activities.
These agents have analgesic and antipyretic activities. Their mechanism of action is not known, but they may inhibit cyclooxygenase activity and prostaglandin synthesis. Other mechanisms may exist as well, such as inhibition of leukotriene synthesis, lysosomal enzyme release, lipoxygenase activity, neutrophil aggregation, and various cell-membrane functions. Various NSAIDs may be used.
Friedhelm Sandbrink, MD, Assistant Professor of Neurology, Georgetown University School of Medicine; Assistant Clinical Professor of Neurology, George Washington University School of Medicine and Health Sciences; Director, EMG Laboratory and Chief, Chronic Pain Clinic, Department of Neurology, Washington Veterans Affairs Medical Center
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Neil A Busis, MD, Chief of Neurology and Director of Neurodiagnostic Laboratory, UPMC Shadyside; Clinical Professor of Neurology and Director of Community Neurology, Department of Neurology, University of Pittsburgh Physicians
Disclosure: Serve(d) as a director, officer, partner, employee, advisor, consultant or trustee for: American Academy of Neurology<br/>Serve(d) as a speaker or a member of a speakers bureau for: American Academy of Neurology<br/>Received income in an amount equal to or greater than $250 from: American Academy of Neurology.
Chief Editor
Nicholas Lorenzo, MD, CPE, MHCM, FAAPL, Co-Founder and Former Chief Publishing Officer, eMedicine and eMedicine Health, Founding Editor-in-Chief, eMedicine Neurology; Founder and Former Chairman and CEO, Pearlsreview; Founder and CEO/CMO, PHLT Consultants; Former Chief Medical Officer, MeMD Inc
Disclosure: Nothing to disclose.
Additional Contributors
Stephen A Berman, MD, PhD, MBA, Professor of Neurology, University of Central Florida College of Medicine
[Guideline] The American Academy of Orthopaedic Surgeons. Evidence-Based Clinical Practice Guideline on: Management of Carpal Tunnel Syndrome. Available at https://www.aaos.org/globalassets/quality-and-practice-resources/carpal-tunnel/carpal-tunnel-2024/cts-cpg.pdf. May 18, 2024; Accessed: September 22, 2024.
Anatomy of the median nerve and the carpal tunnel.
Anatomy of the carpal tunnel.
Scars from carpal tunnel release surgery.
Scars from carpal tunnel release surgery.
Anatomy of the carpal tunnel.
Anatomy of the median nerve and the carpal tunnel.
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