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INTRODUCTION  —  Carpal tunnel syndrome (CTS) refers to the complex of symptoms and signs brought on by compression of the median nerve as it travels through the carpal tunnel. Patients commonly experience pain and paresthesia, and less commonly weakness, in the median nerve distribution. CTS is the most frequent compressive focal mononeuropathy seen in clinical practice.

This topic will review the clinical manifestations and diagnosis of CTS. Other aspects of CTS are discussed separately.

● (See "Carpal tunnel syndrome: Pathophysiology and risk factors" .)

● (See "Carpal tunnel syndrome: Treatment and prognosis" .)

● (See "Surgery for carpal tunnel syndrome" .)

Other disorders involving nerves of the upper extremity are discussed separately. (See "Overview of upper extremity peripheral nerve syndromes" .)

EPIDEMIOLOGY  —  CTS is a common disorder. The estimated prevalence of CTS in the general population is between 1 and 5 percent. CTS is more frequent in females, with a female-to-male ratio of approximately 3 to 1. The epidemiology of CTS is discussed in additional detail separately. (See "Carpal tunnel syndrome: Pathophysiology and risk factors", section on 'Epidemiology' .)

CLINICAL FEATURES  —  The hallmark of classic CTS is pain or paresthesia (numbness and tingling) in a distribution that includes the median nerve territory, with involvement of the first three digits and the lateral half of the fourth digit ( figure 1 ).

● Signs and symptoms – Although the sensory symptoms of CTS are usually limited to the median-innervated fingers, there can be significant variability. The pain and paresthesia may be localized to the wrist or it may involve the entire hand. It is not uncommon for sensory symptoms to radiate proximally into the forearm and, less frequently, to radiate above the elbow to the shoulder, but the neck is not affected [ 1 ].

In more severe cases of CTS, motor involvement leads to complaints of weakness or clumsiness when using the hands, such as difficulty holding objects, turning keys or doorknobs, buttoning clothing, or opening jar lids [ 1 ]. Clinical signs may include weakness of thumb abduction and opposition and atrophy of the thenar eminence.

Bilateral CTS is common, reported as affecting up to 65 percent of patients [ 2 ], though clinical experience suggests that a unilateral initial presentation of CTS is encountered more frequently. In some cases, involvement is subclinical on one side and symptomatic on the other.

● Physical maneuvers – CTS symptoms are often provoked by activities that involve sustained flexing or extending the wrist or raising the arms, such as driving, reading, typing, and holding a telephone [ 1,3 ].

Some patients report temporary improvement in symptoms by shaking or wringing their hands or by placing them under warm running water [ 1 ].

● Clinical course – The symptoms of CTS may be noted initially at night and the pain or paresthesias may awaken patients from sleep. As they progress, symptoms may also be noted during waking hours, especially during activities that require sustained arm positions or repetitive movements. In some cases, there is progression from intermittent to persistent sensory complaints and from paresthesias to sensory loss in the hand. Fixed sensory loss is usually a late finding characterized by a distinctive clinical pattern that involves the median-innervated fingers and spares the thenar eminence. This pattern occurs because the palmar sensory cutaneous nerve arises proximal to the wrist and passes over, rather than through, the carpal tunnel. (See "Carpal tunnel syndrome: Pathophysiology and risk factors", section on 'Anatomy' .)

Motor symptoms, including weakness, typically develop late and in patients with a more severe course. However, some patients with acute CTS, such as those with symptoms due to a bone fracture or other trauma, may report early weakness due to axonal injury.

For patients with mild symptoms, the clinical course of CTS may follow an alternating pattern with periods of remission and exacerbation [ 4 ]. (See "Carpal tunnel syndrome: Treatment and prognosis", section on 'Prognosis' .)

DIAGNOSIS AND EVALUATION  —  CTS should be suspected in patients with symptoms such as pain or paresthesia in the hand or examination findings of sensory loss or weakness in the distribution of the median nerve ( figure 1 ) [ 3 ]. (See 'Clinical features' above.)

The diagnosis of CTS is clinical for patients with characteristic symptoms and signs. Electrodiagnostic and other diagnostic testing can be helpful to confirm or exclude CTS when the clinical diagnosis is uncertain [ 5 ]. Diagnostic testing is also useful for patients with moderate or severe symptoms ( table 1 ) to gauge the severity of nerve compression and to aid in decisions regarding surgical intervention ( algorithm 1 ). Stable patients with symptoms that are mild and classic for CTS may be followed clinically because up to two-thirds improve with nonsurgical treatment [ 6 ]. (See 'Electrodiagnostic testing' below and "Carpal tunnel syndrome: Treatment and prognosis", section on 'Initial nonsurgical treatment for most patients' .)

The combination of characteristic symptoms and signs and confirmatory electrodiagnostic testing appears to be most accurate for the diagnosis of CTS [ 7,8 ].

Clinical diagnosis  —  The likelihood of an accurate clinical diagnosis of CTS corresponds with the number of characteristic symptoms and provocative or mitigating factors listed as criteria for the diagnosis of CTS [ 3 ]. These include:

● Characteristic symptoms

• Dull, aching discomfort in the hand, forearm, or upper arm

• Paresthesia in the hand

• Weakness or clumsiness of the hand

• Occurrence of any of these symptoms in the median distribution

● Provocative factors

• Sustained hand or arm positions

• Repetitive actions of the hand or wrist

● Mitigating factors

• Changes in hand posture

• Shaking the hand

For patients with additional features suggestive of an alternative diagnosis and those with moderate to severe symptoms including sensory loss or weakness, we obtain additional diagnostic testing. (See 'Differential diagnosis' below and 'Diagnostic testing for patients with moderate to severe or atypical symptoms' below.)

Examination  —  Objective sensory and motor deficits corresponding to the median nerve–innervated regions of the hand may be present, but their absence does not rule out the diagnosis of CTS.

● Sensation should be tested in all regions of both hands, forearms, and upper arms ( figure 2 ). Objective sensory deficits on testing usually occur late in the course of CTS; they involve the median-innervated fingers but spare the thenar eminence [ 3 ]. This is a critical finding, as sensory loss over the thenar eminence suggests a median nerve lesion proximal to the carpal tunnel. (See "Carpal tunnel syndrome: Pathophysiology and risk factors", section on 'Anatomy' .)

● Objective weakness can occur in severe or advanced CTS and is typically limited to muscles of the thenar eminence [ 3 ]. This manifests principally as weakness of thumb abduction and thumb opposition. Atrophy of the thenar eminence may be present. Weakness in other hand muscles may suggest a median or other nerve lesion proximal to the carpal tunnel.

Provocative maneuvers  —  Bedside tests performed as part of a clinical examination to elicit symptoms of CTS may improve the diagnostic yield of a clinical evaluation. Provocative maneuvers include the Phalen, Tinel, manual carpal compression, and hand elevation tests. These can be helpful when interpreted in the proper clinical context. However, the sensitivity and specificity of these provocative tests in isolation is moderate at best [ 9,10 ].

● The Phalen maneuver is performed by having the patient bring the dorsal surfaces of the hands against each other to provide hyperflexion of the wrist while the elbows remain flexed ( picture 1 ). Alternatively, the patient fully may flex the hands at the wrist with the elbow in full extension to provide traction on the median nerve. The flexed position is held for one minute. A positive Phalen sign is defined as pain and/or paresthesia in the median-innervated fingers. Meta-analyses have shown an average sensitivity of 68 percent and specificity of 73 percent for a positive Phalen test [ 10 ]. One prospective study found that Phalen test correlated with CTS severity [ 11 ].

● The Tinel test ( picture 2 ) involves firm percussion performed over the course of the median nerve just proximal to or on top of the carpal tunnel. A positive Tinel test is defined as pain and/or paresthesia of the median-innervated fingers that occurs with percussion over the median nerve. A positive Tinel sign may be less sensitive (50 percent) than the Phalen sign but has similar specificity (77 percent) [ 10 ].

● The manual carpal compression, or Durkan test is performed by applying pressure over the transverse carpal ligament for 30 seconds ( picture 3 ). Pain or paresthesia indicates a positive result. The average sensitivity and specificity of the manual carpal compression test are 64 and 83 percent, respectively [ 10 ].

● The hand elevation test involves having the patient raise the hands above the head for one minute [ 12 ]. The test is positive if it reproduces the symptoms of CTS. The sensitivity and specificity may be similar to or slightly better than those reported for Tinel test and Phalen maneuvers, but few reports have compared these tests directly [ 12,13 ].

● The upper limb neurodynamic test assesses for peripheral nerve mobility and can be used to identify patients with CTS [ 14,15 ]. Patients are instructed to abduct and externally rotate the shoulder, and flex the elbow, each at 90 degrees. Next, the patient supinates the forearm, extends the wrist and fingers, and abducts the thumb. A positive upper limb neurodynamic test suggests restriction of nerve mobility when CTS symptoms occur or worsen with elbow extension.

In a 2022 meta-analysis of 37 observational studies that assessed the diagnostic accuracy of provocative tests that included more than 2600 wrists of patients with CTS, the diagnostic performance of the hand elevation test was better than other provocative tests [ 16 ]. The diagnostic accuracies were:

● Hand elevation test – odds ratio (OR) 128.6, 95% CI 40.6-407.1

● Manual carpal compression – OR 15.8, 95% CI 3.8-66.4

● Phalen test – OR 7.2, 95% CI 4.1-12.9

● Tinel test – OR 5.3, 95% CI 3.5-8.1

● Upper limb neurodynamic test – OR 1.8, 95% CI 0.6-5.2

However, the certainty of these findings is limited by the observational nature of the data, variable protocols used for individual tests, and the small number of studies assessing the upper limb neurodynamic test.

Diagnostic testing for patients with moderate to severe or atypical symptoms  —  We perform electrodiagnostic testing for CTS for all patients with atypical symptoms to confirm the diagnosis and for patients with symptoms that are moderate to severe ( table 1 ) or that progress despite conservative treatment to aid in decisions regarding surgical intervention ( algorithm 1 ).

Imaging of the median nerve with ultrasound or magnetic resonance imaging (MRI) is typically performed for patients with suspected mass lesions or those with atypical symptoms not explained by electrodiagnostic testing.

Electrodiagnostic testing  —  Electrodiagnostic testing with nerve conduction studies (NCS), often supplemented with needle electromyography (EMG), has a high sensitivity and specificity for confirming the diagnosis of CTS and for excluding other conditions in the differential diagnosis [ 5,17 ]. Electrodiagnostic testing is also useful for gauging the severity of median nerve injury because the extent of clinical symptoms may not always correlate with the severity of the injury to the median nerve.

The diagnosis of CTS may be confirmed by results from the NCS. Needle EMG is also performed to identify the integrity of motor units to help select patients for surgical treatment whenever symptoms or NCS findings are moderate to severe ( table 1 ) [ 18-25 ]. As examples, EMG can provide objective evidence of persisting neuronal integrity in some severe cases when sensory and motor responses are absent on NCS; similarly, in some cases where NCS abnormalities are modest, EMG can show evidence of more severe active denervation.

In addition, EMG is warranted in patients with atypical symptoms to exclude other conditions such as polyneuropathy, plexopathy, and radiculopathy [ 18 ]. (See 'Differential diagnosis' below.)

Nerve conduction studies  —  The electrodiagnosis of CTS is made by the demonstration of impaired median nerve conduction across the carpal tunnel in the context of normal conduction elsewhere [ 1,26 ].

The NCS evaluation for CTS involves measurement of conduction velocity across the carpal tunnel as well as determination of the amplitude of sensory and motor responses to determine the severity of injury to the median nerve.

● Impaired nerve conduction – Nerve compression results in damage to the myelin sheath and manifests as delayed distal latencies and slowed conduction velocities. Mild CTS may not produce any nerve conduction abnormalities. With increased compression of the median nerve, focal demyelination can occur. This may result in local conduction block and/or slowing of motor and sensory conduction across the wrist.

● Axon loss – With sustained or more severe compression, axon loss may also occur, resulting in a reduction of the median nerve compound motor or sensory nerve action potential amplitude. Sensory fibers seem to be more sensitive to compression than motor fibers. As a result, sensory fibers typically demonstrate changes on NCS earlier than do motor fibers.

Specific components of NCS to evaluate CTS include:

● Sensory conduction studies involve stimulating branches of the median nerve at the wrist and recording sensory response from digit two or three, depending on clinical symptoms. Results are compared with sensory responses of other nerves including the ulnar (stimulating the wrist and recording at digit five) and radial (stimulating at the lateral radius and recording at the snuffbox) [ 1 ].

● Motor conduction studies most often record from the abductor pollicis brevis muscle, although other muscles can also provide diagnostic information. Results obtained are compared with age-dependent normal values as well as with other nerves of the same hand or the contralateral hand. Comparative motor testing typically includes the ulnar nerve (recording from the abductor digiti minimi while stimulating at the wrist and at the elbow above and below the ulnar groove) [ 1 ].

● Additional comparison studies should be used for patients who have normal routine NCS in the setting of clinical findings suggestive of CTS [ 1 ]. These may include testing the second lumbrical (median) versus interossei (ulnar) distal motor latencies, evaluating sensory latencies at digit four by stimulating the median and ulnar nerves at the wrist individually at identical distances, and comparing palm-to-wrist peak latencies of median and ulnar nerves, each recorded 8 cm from the stimulating electrodes.

In a 2002 systematic review of prospective studies, the sensitivity of various NCS for CTS ranged from 56 to 85 percent, and the specificity ranged from 94 to 99 percent [ 5,17 ]. In a later study of 99 patients without confounding neurologic disorders who met clinical criteria for CTS, NCS (including median and ulnar palmar mixed-nerve studies) were normal in 25 percent [ 27 ].

Anomalous innervations may result in atypical findings during electrodiagnostic testing. One of the most frequently encountered variations during evaluation of CTS is a median-to-ulnar anastomosis. The Martin–Gruber anastomosis describes a subgroup of motor fibers that split from the median nerve in the forearm and join the ulnar nerve to innervate the intrinsic muscles of the hand. The Riche–Cannieu anastomosis describes a connection between the recurrent branch of the median nerve in the hand and the deep branch of the ulnar nerve and results in ulnar innervation of the thenar hand muscles. (See "Carpal tunnel syndrome: Pathophysiology and risk factors", section on 'Anatomy' .)

With median nerve studies in patients with CTS and median-to-ulnar anastomoses, the amplitude of the compound muscle action potential is higher with stimulation at the proximal elbow site than with stimulation at the wrist [ 28 ]. Median nerve conduction velocities may be surprisingly fast in the forearm and typically slow across the wrist [ 28,29 ].

Electromyography  —  EMG is a useful component of electrodiagnostic testing in CTS to exclude other conditions, such as polyneuropathy, plexopathy, and radiculopathy, and to assess severity of CTS if surgical decompression is being considered [ 1 ]. EMG is not necessary for patients who have classic signs and symptoms of CTS and confirmatory findings on NCS when there is no suspicion for other etiologies and surgery is not contemplated.

EMG assesses for evidence of pathologic changes in the muscles innervated by the median nerve. When secondary axonal loss is present, EMG may reveal either active denervation (eg, spontaneous activity such as fibrillation potentials, positive sharp waves, and fasciculation potentials) or chronic changes that indicate denervation with subsequent reinnervation (eg, changes in motor unit action potential amplitudes, durations, and recruitment). Such findings are supportive of the diagnosis of CTS in the context of normal findings in both nonmedian-innervated muscles and proximal median nerve-innervated muscles.

Specific components of EMG to evaluate CTS include [ 1 ]:

● Abductor pollicis brevis

● Two or more C6–C7 innervated muscles (eg, pronator teres, triceps brachii, extensor digitorum communis) to look for evidence of cervical radiculopathy

● Additional muscles are typically evaluated if the abductor pollicis brevis is abnormal [ 1 ]. This includes median-innervated muscles proximal to the carpal tunnel (eg, flexor carpi radialis, pronator teres, flexor pollicis longus) to exclude a proximal median neuropathy and nonmedian-innervated muscles (eg, first dorsal interosseous, extensor indicis proprius) to rule out brachial plexopathy, polyneuropathy, and C8 to T1 radiculopathy.

Imaging  —  Imaging of the median nerve with ultrasound or MRI is typically performed for patients with a suspected structural abnormality at the carpal tunnel or those with atypical symptoms not explained by electrodiagnostic testing [ 30-32 ]. Imaging may help to identify anatomic variants associated with CTS such as a tumor, ganglion cyst, bifid median nerve, persistent median artery, or bone or joint disease and can also show median nerve abnormalities such as edema or alterations in blood flow [ 33 ].

● Neuromuscular ultrasound ( image 1 ) may approach the diagnostic sensitivity of electrodiagnostic testing for CTS when performed by a skilled practitioner [ 34 ]. Ultrasound is typically a quicker test to perform and more comfortable for patients. Ultrasound may show imaging evidence suggestive of CTS such as increased median nerve cross-sectional area compared with controls [ 35-39 ]. However, optimal cross-sectional area cut-off for the diagnosis as well as the sensitivity and specificity of this technique have varied in these reports [ 40,41 ]. In a systematic review of the literature, the four highest-quality studies used cut-offs of 8.5 to 10 mm 2 for the diagnosis [ 41 ]. The sensitivities ranged from 65 to 97 percent and the specificities ranged from 73 to 98 percent. Caution is warranted when interpreting ultrasound in older adults, as the sensitivity appears to be significantly lower in patients 80 years and older compared with those younger than 65 years [ 42,43 ]. In addition, ultrasound does not provide presurgical physiologic information about the severity of nerve dysfunction at the median nerve or assess for alternative causes of clinical symptoms (eg, radiculopathy).

Ultrasound may be performed to guide treatment with glucocorticoid injections or minimally invasive surgical release. (See "Carpal tunnel syndrome: Treatment and prognosis", section on 'Glucocorticoid injection' and "Surgery for carpal tunnel syndrome", section on 'Ultrasound-guided techniques' .)

Instructional videos demonstrating proper performance of the ultrasound examination of the wrist and related pathology can be found at the website of the American Medical Society for Sports Medicine. Registration must be completed to access these videos, but no fee is required.

● MRI can detect abnormalities of the median nerve, flexor tendons, vascular structures, and transverse carpal ligament in the region of the carpal tunnel [ 44,45 ]. MRI can identify soft tissue abnormalities and may be useful for unusual cases to rule out a mass lesion. However, the diagnostic utility of MRI for other cases of CTS remains uncertain.

DIFFERENTIAL DIAGNOSIS  —  The differential diagnosis of CTS includes neurologic, musculoskeletal, and vascular conditions that can present with pain, paresthesia, sensory loss, or weakness involving the arm or hand [ 1,30,46,47 ].

Conditions that may present with symptoms isolated to or predominating in the median nerve include cervical spine disorders, brachial plexopathy, proximal lesions of the median nerve, and various types of polyneuropathy.

● Cervical radiculopathy – The most common disorder than can mimic CTS is cervical radiculopathy, particularly with C6 or C7 nerve root involvement [ 1 ]. The symptoms may include arm pain and paresthesia that resemble those of CTS. Features that favor cervical radiculopathy include [ 1,30 ]:

• The presence of neck pain that radiates into the shoulder and arm

• Exacerbation of symptoms with neck movement

• Reduced reflexes (ie, biceps, brachioradialis, and triceps)

• Weakness of proximal arm muscles involving elbow flexion, extension, and arm pronation

• Sensory loss in the forearm or medial palm

C8 and T1 root lesions may also mimic the symptoms or signs of CTS, predominantly involving motor dysfunction.

Although clinical sensory loss may be present in cervical radiculopathy, the sensory nerve action potentials remain unaffected in root lesions due to the more distal location of the sensory nerve cell body. This is an important distinguishing feature from peripheral nerve lesions. (See "Overview of nerve conduction studies", section on 'Sensory nerve conduction' and "Clinical features and diagnosis of cervical radiculopathy", section on 'Electrodiagnostic studies' .)

● Median neuropathy in the forearm – Median neuropathy proximal to the carpal tunnel may occur in the forearm where the nerve passes through the pronator teres muscle. Patients may present with forearm pain and sensory loss involving the entire lateral palm. Features that favor a forearm localization include the findings of sensory loss over the thenar eminence (typically spared in CTS) and weakness of more proximal median-innervated muscles (thumb flexion, wrist flexion, and arm pronation) [ 1 ]. However, electrodiagnostic studies are often required to localize the site of compression appropriately.

● Cervical spondylotic myelopathy and cervical polyradiculopathy – Cervical spine myelopathy or polyradiculopathy may present with symptoms similar to CTS but usually involves bilateral sensory loss and motor dysfunction in the hands and may also include dysfunction in nonmedian nerve territories [ 47 ]. (See "Cervical spondylotic myelopathy", section on 'Clinical presentation' .)

● Brachial plexopathy – Patients with brachial plexopathies may sometimes manifest with predominant symptoms suggestive of dysfunction to an individual nerve, such as the axillary, long thoracic, anterior interosseous, radial, median, or a cutaneous nerve. However, the examination findings more commonly reveal weakness, sensory loss, or diminished reflexes outside the distribution of the median nerve and usually involve more than one spinal segment. (See "Brachial plexus syndromes" .)

Other conditions characterized by multifocal or diffuse symptoms may sometimes be included in the differential diagnosis of CTS when presenting early with prominent median nerve symptoms. This includes central nervous system lesions, motor neuron disease, compartment syndrome involving the forearm or hand, fibromyalgia, osteoarthritis and inflammatory arthropathy involving the small joints of the hand, Raynaud phenomenon, and ligamentous injury, which can present in ways similar to CTS, although for the most part these entities are easily distinguished.

● Ischemic stroke – Small ischemic strokes restricted to the cortical region of the primary motor cortex responsible for movement of the contralateral hand may mimic the weakness seen in CTS [ 48,49 ]. However, patients with stroke in this "hand knob" region typically report sudden onset of symptoms, lack pain, and have weakness of muscles innervated by median and radial and/or ulnar nerves on examination. (See "Clinical diagnosis of stroke subtypes" .)

● Motor neuron disease – Amyotrophic lateral sclerosis (ALS) or other forms of motor neuron disease can present with asymmetric hand involvement that may predominantly involve the thenar hand intrinsic muscles. The absence of pain argues against CTS. More importantly, ALS essentially never presents with weakness of a single muscle. (See "Clinical features of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Initial presentation' .)

● Forearm or hand compartment syndrome – Patients with compartment syndrome can present as pain with passive stretch and a firm compartment palpated over the forearm or hand; it may be confused with CTS or other peripheral nerve injury if pain and sensory deficits involve the median nerve territory. However, the distribution of pain may be more widespread with progression of compartment syndrome when the ulnar and dorsal sensory radial nerves are also compromised [ 46 ]. In addition, acute compartment syndrome typically occurs in the setting of trauma, which helps differentiate it from CTS. (See "Acute compartment syndrome of the extremities", section on 'Clinical features' .)

● Fibromyalgia – Symptoms in fibromyalgia frequently include numbness and tingling radiating down the arm. However, the sensory symptoms may not be restricted to the median nerve and the chronic widespread musculoskeletal pain and fatigue that is typical of fibromyalgia is unusual in patients with CTS. (See "Clinical manifestations and diagnosis of fibromyalgia in adults" and "Differential diagnosis of fibromyalgia" .)

● Arthritis – Patients with osteoarthritis and rheumatoid arthritis or other inflammatory arthropathies may present with wrist pain that radiates to or involves the hand. Features suggestive of arthritis over CTS include bilateral involvement, involvement of joints other than the wrist, and joint swelling. (See "Clinical manifestations and diagnosis of osteoarthritis", section on 'Hand' and "Clinical manifestations of rheumatoid arthritis", section on 'Hands' .)

Osteoarthritis and rheumatoid arthritis are also risk factors for CTS. Inflammatory changes from these conditions may cause localized symptoms as well as CTS due to anatomic compression at the carpal tunnel. (See "Carpal tunnel syndrome: Pathophysiology and risk factors", section on 'Arthritis' .)

● Raynaud phenomenon – The vasoconstriction that occurs with the Raynaud phenomenon (RP) may produce digital pain and paresthesia. However, RP symptoms occur typically as episodes provoked by cold temperatures or stress and are accompanied by skin pallor or cyanosis. (See "Clinical manifestations and diagnosis of Raynaud phenomenon", section on 'Signs and symptoms of Raynaud phenomenon' .)

● Pain from a ligamentous disruption – The pain that accompanies ligamentous injury of the wrist may be similar to pain in CTS but is typically more localized and does not involve the volar surface of the wrist or thenar region seen in CTS. (See "Evaluation of the adult with subacute or chronic wrist pain", section on 'Differential diagnosis by regions of the wrist' .)

SOCIETY GUIDELINE LINKS  —  Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Carpal tunnel syndrome" .)

INFORMATION FOR PATIENTS  —  UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5 th to 6 th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10 th to 12 th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or email these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

● Basics topics (see "Patient education: Carpal tunnel syndrome (The Basics)" and "Patient education: Hand pain (The Basics)" )

● Clinical features – The hallmark of classic carpal tunnel syndrome (CTS) is pain or paresthesia (numbness and tingling) in a distribution that includes the median nerve territory, with involvement of the first three digits and the radial half of the fourth digit ( figure 1 ). (See 'Clinical features' above.)

• Diurnal character – The symptoms are typically worse at night and characteristically awaken affected patients from sleep.

• Location of pain – The pain and paresthesia may be localized to the wrist, involve the entire hand, or radiate proximally to as high as the shoulder ( figure 2 ).

• Provoking features – CTS symptoms are often provoked by activities that involve flexing or extending the wrist or raising the arms.

• Severe manifestations – Fixed sensory loss is usually a late finding characterized by a distinctive clinical pattern that involves the median-innervated fingers and spares the thenar eminence. In severe CTS, motor involvement leads to complaints of weakness or clumsiness when using the hands. Clinical signs may include weakness of thumb abduction and opposition and atrophy of the thenar eminence.

● Clinical diagnosis – The clinical diagnosis of CTS is made in patients with pain or paresthesia in the hand or examination findings of sensory loss or weakness in the distribution of the median nerve ( figure 1 ). (See 'Diagnosis and evaluation' above.)

Provocative maneuvers for CTS include the Phalen, Tinel, manual carpal compression, hand elevation, and upper limb neurodynamic tests. These can be helpful when interpreted in the proper clinical context. However, the sensitivity and specificity of these tests are moderate at best. (See 'Provocative maneuvers' above.)

● Electrodiagnostic confirmation and evaluation – Electrodiagnostic testing is warranted for all patients who have atypical symptoms to confirm the diagnosis and for patients with symptoms that are moderate to severe ( table 1 ) or that progress despite conservative treatment to aid in decisions regarding surgical intervention ( algorithm 1 ). (See 'Diagnostic testing for patients with moderate to severe or atypical symptoms' above.)

The electrodiagnosis of CTS is made by the demonstration of impaired median nerve conduction across the carpal tunnel in the context of normal conduction elsewhere. Electromyography is used along with nerve conduction studies to exclude other conditions, such as polyneuropathy, plexopathy, and radiculopathy, and to assess severity CTS if surgical decompression is being considered. (See 'Electrodiagnostic testing' above.)

● Differential diagnosis – The differential diagnosis of CTS includes neurologic, musculoskeletal, and vascular conditions that can present with pain, paresthesia, sensory loss, or weakness involving the arm or hand. The most common disorder than can mimic CTS is cervical radiculopathy, particularly with C6 or C7 nerve root involvement. (See 'Differential diagnosis' above.)

ACKNOWLEDGMENT  —  The UpToDate editorial staff acknowledges Kevin Scott, MD, who contributed to earlier versions of this topic review.

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Diagnosis and Clinical Presentation of Carpal Tunnel Syndrome

• First Online: 28 March 2020

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• John R. Fowler 3  

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Carpal tunnel syndrome typically presents with paresthesias in the thumb, index, middle, and radial half of ring finger. These symptoms are typically worse at night and may be exacerbated by activities that include wrist flexion. The diagnosis can be confirmed using clinical examination and/or a number of diagnostic tests including electrodiagnostic testing, CTS-6, ultrasound, and other validated diagnostic tools. The sensitivity and specificity of these diagnostic tests vary widely in the literature and are highly susceptible to the population being chosen and the cut-offs used for diagnosis. Electrodiagnostic testing has been traditionally considered the reference standard for diagnosis. However, recent data has found relatively high rates of false positives in asymptomatic individuals. Most studies show little benefit to additional testing in patients with “classic” carpal tunnel syndrome. However, additional testing may be indicated to rule out a more proximal site of nerve compression, systemic disease such as polyneuropathy, or in patients with atypical symptoms. Clinical diagnostic tools may offer cost-savings as screening tools when used in place of electrodiagnostic testing.

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Fowler, J.R. (2020). Diagnosis and Clinical Presentation of Carpal Tunnel Syndrome. In: Sotereanos, D., Papatheodorou, L. (eds) Compressive Neuropathies of the Upper Extremity. Springer, Cham. https://doi.org/10.1007/978-3-030-37289-7_3

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• Published: 06 March 2023

Vasculitis presenting as carpal tunnel syndrome: a case report

• Mohammad Rahbar 1 &
• Neda Dolatkhah   ORCID: orcid.org/0000-0003-1358-1003 1  

Journal of Medical Case Reports volume  17 , Article number:  84 ( 2023 ) Cite this article

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Carpal tunnel syndrome is the most common focal mononeuropathy which presents with pain in the wrist and hand, paresthesia, loss of sensation in the distribution of the median nerve, and in more severe cases, weakness and atrophy of the thenar muscles. Meanwhile, carpal tunnel syndrome can present as an initial manifestation of underlying systemic vasculitis disorder and result in severe physical disabilities.

Case presentation

A 27-year-old Iranian man was referred to our electrodiagnosis center with a clinical diagnosis of carpal tunnel syndrome in April 2020. Surgical intervention had been taken into account for him because of unsuccessful conservative therapies. On admission, thenar eminence was reduced. Electrodiagnostic findings were not compatible with median nerve entrapment at the wrist. All sensory modalities in the distribution of the right median nerve were decreased. Additionally, a mild increase in erythrocyte sedimentation rate was noted in laboratory tests. Because of the high vasculitis suspicion, we recommended the nerve biopsy and/or starting a high-dose corticosteroid. However, the surgery release was performed. After 6 months, the patient was referred for progressive weakness and numbness in the upper and lower limbs. After documentation of vasculitis neuropathy by biopsy, a diagnosis of non-systemic vasculitic neuropathy was confirmed. A rehabilitation program started immediately. Rehabilitation led to gradual improvement and recovery of function and muscle strength, and no complications remained, except mild leg paralysis.

Conclusions

Physicians should be suspicious of the median nerve vasculitis mononeuropathy in a patient with carpal tunnel syndrome-like symptoms. Median nerve vasculitis mononeuropathy as an initial presenting feature of vasculitis neuropathy can further result in severe physical impairments and disabilities.

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Introduction

Carpal tunnel syndrome (CTS) is the entrapment and traction of the median nerve at the level of the wrist transverse carpal ligament and is the most prevalent upper extremity neuropathy, with a higher prevalence in the female population [ 1 , 2 ]. The prevalence of CTS symptoms is 7.8 percent in the working population [ 3 ]. The characteristic presentation of CTS includes numbness, with or without “pins-and-needles” pain in the median nerve distribution area, including the palmar side of the first, second, and third fingers, and the radial half of the fourth finger, which often worsens at night or in the early morning [ 4 ]. Sometimes, patients’ description of symptoms is not completely consistent with median nerve involvement, such as symptoms perceived in all the fingers, the whole hand, forearm, arm, and shoulder, which also do not associate with the disease severity [ 5 ].

Conventionally, the diagnosis of CTS is clinically based. However, the diagnostic worth of several clinical examinations is controversial in the medical literature [ 6 , 7 , 8 ]. Furthermore, some patients with clinically diagnosed CTS have underlying rheumatologic, neurological, or musculoskeletal disorders such as peripheral polyneuropathy, cervical radiculopathy, plexopathy, proximal median mono-neuropathy, and misleading indicators in trauma that may describe their symptoms [ 9 ].

Vasculitis consists of a group of disorders, defined as the blood vessel wall destruction as a result of the infiltration of inflammatory cells [ 10 ]. Involvement of the peripheral nervous system is a usual complication of systemic vasculitis [ 11 ]. Although the typical form of peripheral nervous system involvement is mononeuritis multiplex (35–65%), it can present as focal axonal mononeuritis [ 10 , 12 ]. Because of the step-by-step, progressive form of involvement, it is not unlikely to see mononeuritis at the initial stage of the disorder. The median nerve, in the area just proximal to the elbow, is one of the most involved nerves in this situation. This is important because the patient may be primarily supposed to have acute CTS [ 11 ].

As a result of these diagnostic problems, including uncharacteristic clinical features, suspicion of several diagnoses, ruling out a particular diagnosis, or establishing a clinical suspicion, a patient with probable CTS is referred for electrodiagnostic evaluation (EDX) [ 13 , 14 ]. EDX may also be applied to assess the severity and prognosis, pre- and postoperative assessment and preparation of other management approaches, medico-legal and compensation matters, and baseline and screening destinations [ 15 , 16 ].

EDX has become common in the CTS diagnosis since the 1950s, with a sensitivity of 78–95% and specificity of 80–95% [ 17 , 18 , 19 ]. The test measures showed median nerve physiological delays through reduced electrical conduction speed caused by compression, demonstrating the inflammation and axon loss degree [ 20 ]. This is valuable when the clinical findings are unclear [ 21 , 22 ].

The application of EDX has some inadequacies. It is an invasive method with a long examination time and a high cost. Even for EDX-confirmed median neuropathy cases, different presentation is possible because of underlying probable systemic disease [ 23 ]. EDX abnormal findings do not predict the CTS severity. However, in many cases, when EDX is used together with clinical history and physical examination, the diagnosis can be done with a reasonable level of confidence [ 24 ].

Therefore, matching and comparing the EDX findings and CTS symptoms is very critical for physicians in clinical practice. In this way, suspicion should be focused on another existing pathology in the disparity between symptoms and EDX findings. In this article, we report a vasculitic neuropathy case in a 27-year-old man, and the symptoms of unilateral median nerve neuropathy in the initial stages of the disorder.

A 27-year-old man from Iran was referred to the physical medicine and rehabilitation outpatient clinic at Tabriz University of Medical Sciences on 23 April 2020. He had no significant medical, family, or psychosocial history. First, he noticed pain and weakness in his right hand when he woke up on the morning of 20 March 2020 (1 month previous). Then, thenar atrophy gradually developed. Thenar atrophy and numbness of the hand did not improve with conservative treatments such as nonsteroidal anti-inflammatory drugs, physical methods (such as ultrasound therapy (US), low-level laser therapy), wrist splinting in the neutral position, and home exercises. He was diagnosed with CTS according to the clinical history and physical examination. Therefore, surgical intervention was considered for him. He was referred to our EDX center for redocumentation before surgical release.

He had no history of any injection at this region, and no evidence of systemic disease. On physical examination, he had right-hand thenar atrophy and numbness. About 2 weeks after the onset of the symptoms, a nerve conduction study (NCS) showed unobtainable sensory nerve action potential (SNAP) in median innervated fingers, and poorly evoked compound muscle action potential (CMAP) in abductor pollicis brevis (APB) muscle. NCS in other nerves of the right upper and left limb was normal. Needle electromyography (EMG) study of right thenar muscles revealed a reduced recruitment pattern with severe acute neurogenic changes.

On admission, an impaired function of the thumb (lack of ability to abduct and oppose the thumb, and decreased grip strength decrease of the affected hand) and lateral thenar muscle atrophy was evident. But the point to consider was that all sensory modalities had been reduced in the median nerve distribution and thenar eminence. Given that the thenar eminence is supplied by the median nerve palmar cutaneous branch, which branches off proximal to the carpal tunnel, the decreased sensation over the thenar eminence is not a common finding in CTS. So, we suspected a median nerve lesion proximal to the carpal tunnel and performed further NCS, and searched for other EDX explanations.

We noticed that the SNAP of the right palmar cutaneous branch of the median nerve was unobtainable. Additionally, the median nerve compound nerve action potential (CNAP) study in the forearm, while stimulating this nerve at the wrist and recording at the antecubital fossa, was unobtainable. By moving the nerve stimulation point toward the proximal, CNAP was still unobtainable up the junction of the distal one-third and proximal two-thirds at the forearm. Proximal to this junction, the nerve stimulation showed normal CNAP. The median nerve CNAP on the other side was normal. Needle examinations of median innervated right forearm muscles were normal.

These findings made us suspect “pseudo-CTS” (median nerve neuropathy at the lower forearm). This disorder is due to nerve entrapment or injury at locations other than the carpal tunnel, usually, the lower forearm, but shows similar signs and symptoms. By localizing the possible site of the median neuropathy by EDX, some potential causes of the median neuropathy at this region were compressive or sharp trauma to the forearm, a mass or ganglion cyst compressing the nerve, and vasculitis. The clinical exam was unremarkable for any penetrating injury or mass. Considering no history of any injection, and no evidence of systemic disease, we requested laboratory studies.

Surveys showed a mild increase in erythrocyte sedimentation rate (ESR) to 35 mm/h. The full blood count and other serologic markers, including antineutrophil cytoplasmic antibodies (ANCA), antinuclear antibodies, paraneoplastic antibodies, and anti-Ro/La antibodies, the immunologic markers for syphilis, hepatitis B and C, human immunodeficiency virus (HIV), and serum and urine protein electrophoresis were unremarkable. Routine urine analysis was normal.

Accordingly, we diagnosed median nerve vasculitic neuropathy and recommended neuropathy site exploration and/or starting a high dose of prednisolone therapy. Unfortunately, the attending physician and the patient did not accept these impressions and recommendations, and surgical intervention was performed.

After 6 months of surgery, the patient was referred to our center again. Now, he had “progressive weakness and numbness” in his upper and lower limbs and was not able to walk independently. He used an axillary crutch. The matter was that, over the 6 months after surgery, the patient had seen several attending physicians and finally had been hospitalized for diagnostic workups and treatment. The nerve biopsy sample had exhibited a reasonably severe injury of myelinated nerve fibers, in addition to the epineural arteriolar walls surrounding endoneurial microvessels and perineurium inflammatory infiltrations.

After the surveys, “nonsystemic vasculitis neuropathy (NSVN)” was diagnosed for the patient. The patient was referred after intravenous steroid pulse therapy and relative improvement of weakness and pain, for managing the remaining disabilities and impairments.

In the examinations, the skin and cranial nerves were normal. We failed to detect any evidence of systemic lesion. The deep tendon reflexes (DTRs) were absent, and all sensory modalities had decreased. Muscle atrophy was evident in the lower limbs, and to a lesser extent in the upper limbs. Motor clinical assessment revealed asymmetrically diminished motor strength (measured by British Medical Research Council muscle strength grading [ 25 ]) in the four limbs (3–5/5 in upper limbs, and 2–3/5 in lower limbs). NCS data revealed asymmetric axonal peripheral polyneuropathy, compatible with mononeuritis multiplex.

A rehabilitation program, which involved daily 1-h physiotherapy (PT) sessions for 3 days a week, started immediately.

Rehabilitation led to gradual improvement and recovery of function and muscle strength, and after 18 weeks of treatment, no complications remained except mild leg paralysis.

Here, we reported a 27-year-old man with unilateral hand thenar atrophy and numbness, later diagnosed as NSVN. The diagnosis of the patient was delayed due to the suspicion of CTS, which was followed by progressive motor weakness and paresthesia in his upper and lower limbs. This reminds us that occasionally uncommon neurological symptoms may show the onset of NSVN. On the other hand, a fraction of clinically suspicious patients with CTS may have other neurological diagnoses.

This case underscores the need for the EDX physician to be keenly aware of the various presentations of neurological and musculoskeletal disorders, and to perform a comprehensive neurological, musculoskeletal, and physical examination when necessary. Inquiries into work and recreational activities in addition to the laboratory tests may be useful. Patient management and referring physician satisfaction are optimized by these additional evaluations. Meanwhile, various other electrophysiologic, neurologic, and vascular disorders are also diagnosed.

NSVN is usually considered in the differential diagnosis of localized neuropathy, limited to the small arterioles of peripheral nerves, and probably muscles, without systemic involvement [ 26 ]. It is an uncommon disorder with necrotizing inflammation, causing peripheral nerve ischemic injuries. However, except for mild-to-moderate ESR elevation, the other indices of systemic inflammation are commonly absent. The EDX feature is a predominantly axonal nerve damage pattern. NSVN classification criteria are not consistent, and diagnostic criteria for vasculitic neuropathy are not partially identical because of different pathologic definitions of vasculitic neuropathy [ 27 ]. Patients present with stepwise progressive painful asymmetric multifocal distal predominant neuropathy, with acute or subacute onset. Sometimes early diagnosis might be challenging since the NSVN sequence is slow and can manifest with mononeuropathy, mononeuropathy multiplex, or symmetric polyneuropathy [ 28 ].

If mononeuropathy is seen in uncommon entrapment or compression region, the initial presentation of vasculitis neuropathy should be suspected. High clinical suspicion and early diagnosis can prevent other neuromuscular disorders and debilities due to peripheral and/or central neuropathy in the case.

EDX helps disclose typical vasculitic neuropathy findings, comprising acute or subacute axonal loss in sensory and motor nerve fibers, usually in an irregular, multifocal feature. However, when slower conduction or block at common entrapment locations is the only finding (such as in wrist median neuropathy), physicians should consider other reasons for possible compression neuropathies, such as diabetes and nonvasculitic rheumatoid arthritis (RA) [ 29 ].

Laboratory study should consist of a complete blood count (CBC), metabolic assessments (electrolytes, blood urea nitrogen (BUN), creatinine (Cr), and fasting blood glucose), ESR, c-reactive protein (CRP), in addition to antinuclear antibody (ANA), rheumatoid factor (RF), antineutrophil cytoplasmic antibodies (ANCA), hepatitis B and C, and cryoglobulins [ 30 ]. Serum complement measurements are requested in suspected mixed cryoglobulinemia or systemic lupus syndromes (SLE). Serum protein electrophoresis, measurement of concentrations of extractable nuclear antigen and angiotensin-converting enzyme (ACE), and HIV infection assessment are also required [ 31 ].

When vasculitis is doubted in such patients, the peripheral nerve biopsy is very valuable. Furthermore, due to the long-term treatment necessity with possible toxic medication, the vasculitis diagnosis generally requires histological confirmation [ 31 ]. In this study, biopsy specimens showed severe myelinated nerve fiber injuries due to inflammatory infiltrations.

NSVN treatment is principally immunosuppressive therapy, started as soon as possible. The standard immunosuppressive therapy is a combination of corticosteroids (prednisone) and cyclophosphamide (CYC), methotrexate (MTX), or azathioprine for 7 to 12 months. In corticosteroid monotherapy, a follow-up is required and when the signs of neuropathy progression are seen, CYC, MTX, or azathioprine must be added. The NSVN prognosis is better than other systemic vasculitides [ 32 ]. Frequently, neurological deficits resolve over time, and the disease is remitted for years without relapsing.

We guess that numerous patients with the clinical suspicion of CTS referred to community-based EDX settings may have other musculoskeletal and neurologic disorders instead. We further hypothesize that patients with EDX findings consistent with CTS have more diverse clinical presentations than patients whose analyses are negative for CTS. Identification of patients with positive and negative clinical presentations may allow the referring medical doctor to select more precisely the patients who would benefit most from EDX studies.

This case emphasizes the importance of suspecting NSVN in acute-onset symptoms identical to severe CTS. Median nerve EDX can help with differential diagnosis in such patients. Additionally, this case showed a suspected rare disorder—when there are atypical or treatment-refractory symptoms, it is very important for physicians in clinical practice to take note of these.

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We are grateful to the personnel of the Physical Medicine and Rehabilitation Research Center of Tabriz University of Medical Sciences who assisted us to conduct this case report.

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Rahbar, M., Dolatkhah, N. Vasculitis presenting as carpal tunnel syndrome: a case report. J Med Case Reports 17 , 84 (2023). https://doi.org/10.1186/s13256-023-03801-8

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• Carpal tunnel syndrome

Carpal tunnel syndrome is one of the most common hand conditions. It is caused by pressure on the median nerve in the carpal tunnel of the wrist. The carpal tunnel is a narrow passageway surrounded by bones and ligaments on the palm side of the hand. When the median nerve is compressed, symptoms can include numbness, tingling and weakness in the thumb and fingers.

Wrist anatomy, health conditions and possibly repetitive hand motions can contribute to carpal tunnel syndrome.

Proper treatment usually relieves the tingling and numbness and restores hand function.

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Symptoms of carpal tunnel syndrome usually start gradually and include:

Tingling and numbness. Tingling and numbness may occur in the fingers or hand. Usually the thumb, index, middle and ring fingers are affected, but not the little finger. You might have a feeling like an electric shock in these fingers. These symptoms often occur while holding a steering wheel, phone or newspaper, or they may wake you from sleep.

The sensation also can travel from the wrist up the arm.

Many people "shake out" their hands to try to relieve their symptoms. The numb feeling may become constant over time.

• Weakness. People with carpal tunnel syndrome may experience weakness in the hand and drop objects. This may be due to numbness or to weakness of the thumb's pinching muscles, which also are controlled by the median nerve.

When to see a doctor

See your healthcare professional if you have symptoms of carpal tunnel syndrome that interfere with your usual activities and sleep patterns. Permanent nerve and muscle damage can occur without treatment.

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Carpal tunnel syndrome is caused by pressure on the median nerve.

The median nerve runs from the forearm through a passageway in the wrist to the hand, known as the carpal tunnel. The median nerve provides sensation to the palm side of the thumb and all of the fingers except the little finger. This nerve also provides signals to move the muscles around the base of the thumb. This movement is known as motor function.

Anything that squeezes or irritates the median nerve in the carpal tunnel space may lead to carpal tunnel syndrome. A wrist fracture can narrow the carpal tunnel and irritate the nerve. This also may occur due to swelling and inflammation caused by rheumatoid arthritis or other diseases.

Many times, there is no single cause of carpal tunnel syndrome. Or the cause may not be known. It may be that a combination of risk factors contributes to the development of the condition.

Risk factors

Several factors have been linked with carpal tunnel syndrome. Although they may not directly cause carpal tunnel syndrome, they may increase the risk of irritation or damage to the median nerve. These include:

Anatomical factors. A wrist fracture or dislocation can alter the space within the carpal tunnel. Arthritis that causes changes to the small bones in the wrist can affect the carpal tunnel. These changes can put pressure on the median nerve.

People who have smaller carpal tunnels may be more likely to have carpal tunnel syndrome.

Sex assigned at birth. Carpal tunnel syndrome is generally more common in women. This may be because the carpal tunnel area is relatively smaller in women than in men. Or it may be due to the effect of hormones on the lining of the tendons in the carpal tunnel.

Women who have carpal tunnel syndrome also may have smaller carpal tunnels than do women who don't have the condition.

• Nerve-damaging conditions. Some chronic illnesses, such as diabetes, increase the risk of nerve damage, including damage to the median nerve.
• Inflammatory conditions. Rheumatoid arthritis, gout and other conditions that cause swelling, known as inflammation, can affect the lining around the tendons in the wrist. This can put pressure on the median nerve.
• Medicines. Some studies have shown a link between carpal tunnel syndrome and anastrozole (Arimidex), a medicine used to treat breast cancer.
• Obesity. Being obese is a risk factor for carpal tunnel syndrome.
• Body fluid changes. Fluid retention may increase the pressure within the carpal tunnel, irritating the median nerve. This is common during pregnancy and menopause. Carpal tunnel syndrome that happens with pregnancy generally gets better on its own after pregnancy.
• Other medical conditions. Certain conditions, such as thyroid disorders, kidney failure and lymphedema, may increase the chances of getting carpal tunnel syndrome.

Workplace factors. Working with vibrating tools or on an assembly line that requires repeated movements that flex the wrist may create pressure on the median nerve. Such work also may worsen existing nerve damage. Pressure on the nerve can be worse if the work is done in a cold environment.

However, the scientific evidence is conflicting and these factors haven't been established as direct causes of carpal tunnel syndrome.

Several studies have evaluated whether there is a link between computer use and carpal tunnel syndrome. Some evidence suggests that mouse use, but not the use of a keyboard, may be related to carpal tunnel syndrome. There has not been enough quality and consistent evidence to support extensive computer use as a risk factor for carpal tunnel syndrome. However, computer use may cause a different form of hand pain.

• Ideal seated workstation posture

Lessen stress on the hands and wrists to help prevent carpal tunnel syndrome. While using a keyboard, do not bend the wrists all the way up or down.

There are no proven strategies to prevent carpal tunnel syndrome, but you can lessen stress on the hands and wrists with these methods:

• Reduce your force and relax your grip. If your work involves a cash register or keyboard, for instance, hit the keys softly.
• Take short, frequent breaks. Gently stretch and bend your hands and wrists periodically. Alternate tasks when possible. This is especially important if you use equipment that vibrates or that requires you to exert a great amount of force. Taking a break for even a few minutes each hour can make a difference.
• Watch your form. Do not bend your wrist all the way up or down when using a keyboard. A relaxed middle position with the wrists parallel to the floor is best. Keep your keyboard at elbow height or slightly lower.
• Improve your posture. The wrong posture can occur when you adjust your body to view a computer screen rather than adjusting the screen height and distance to a correct posture. The wrong posture rolls shoulders forward, shortens the neck and shoulder muscles, and compresses nerves in the neck. This can cause neck pain and also may bother the hands and arms.
• Change your computer mouse. Make sure that your computer mouse is comfortable to use and doesn't strain your wrist.
• Keep your hands warm. You're more likely to develop hand pain and stiffness if you work in a cold environment. If you can't control the temperature at work, put on fingerless gloves that keep the hands and wrists warm.

Carpal tunnel syndrome care at Mayo Clinic

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• Chien HS, et al. Aromatase inhibitors and risk of arthritis and carpal tunnel syndrome among Taiwanese women with breast cancer: A nationwide claims data analysis. Journal of Clinical Medicine. 2020; doi:10.3390/jcm9020566.
• Yung M, et al. Modeling the effect of the 2018 Revised ACGIH Hand Activity Threshold Limit Value (TLV) at reducing risk for carpal tunnel syndrome. Journal of Occupational and Environmental Hygiene. 2019; doi:10.1080/15459624.2019.1640366.
• Amadio PC (expert opinion). Mayo Clinic. Nov. 22, 2023.
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• American Academy of Orthopaedic Surgeons. Management of Carpal Tunnel Syndrome Evidence-Based Clinical Practice Guideline. https://aaos.org/quality/quality-programs/upper-extremity-programs/carpal-tunnel-syndrome/. Accessed Oct. 26, 2021.
• Hunter AA, et al. Surgery for carpal tunnel syndrome. https://www.uptodate.com/contents/search. Accessed Oct. 26, 2021.
• Computer workstations: Positions. Occupational Safety and Health Administration. https://www.osha.gov/etools/computer-workstations/positions. Accessed Nov. 20, 2023.
• Ami TR. Allscripts EPSi. Mayo Clinic. Nov. 14, 2023.
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• Rakel D, et al., eds. Carpal tunnel syndrome. In: Integrative Medicine. 5th ed. Elsevier; 2023. https://www.clinicalkey.com. Accessed Nov. 20, 2023.
• Schrier VJMM, et al. An incision-less ultrasound-guided carpal tunnel release technique. Techniques in Hand and Upper Extremity Surgery. 2020; doi:10.1097/BTH.0000000000000305.
• Forte AJ, et al. A systematic review of peripheral neuropathies in breast cancer-related lymphedema. Hand. 2022; doi:10.1177/1558944720963944.
• Genova A, et al. Carpal tunnel syndrome: A review of literature. Cureus. 2020; doi:10.7759/cureus.7333.
• Chou RC, et al. Ultrasound-guided percutaneous carpal tunnel release: A systematic review. PM&R. 2023; doi:10.1002/pmrj.12801.
• Carpal tunnel exercises: Can they relieve symptoms?
• Carpal tunnel release
• Carpal tunnel symptoms: Role of nonsurgical treatment
• Carpal tunnel syndrome surgery: Immediate and long-term results
• Carpal Tunnel Tune-Up

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Carpal tunnel syndrome

Affiliations.

• 1 Westmead Clinical School, University of Sydney, Sydney, NSW, Australia.
• 2 Northern Beaches Clinical School, Macquarie University, Sydney, NSW, Australia. Electronic address: [email protected].
• PMID: 38697747
• DOI: 10.1016/B978-0-323-90108-6.00005-3

Median neuropathy at the wrist, commonly referred to as carpal tunnel syndrome (CTS), is the most common entrapment neuropathy. It is caused by chronic compression of the median nerve at the wrist within the space-limited carpal tunnel. Risk factors that contribute to the etiology of compression include female gender, obesity, work-related factors, and underlying medical conditions, such as hypothyroidism, pregnancy, and amyloidosis. The diagnosis is made on clinical grounds, although these can be confounded by anatomical variations. Electrodiagnostic studies, which are specific and sensitive in diagnosing CTS, support the diagnosis; however, a subgroup may present with normal results. The advent of imaging techniques, including ultrasound and MRI, further assists the diagnostic process. The management of CTS is divided into the nonsurgical approaches that include hand therapy, splinting and corticosteroid injection, and surgical decompression of the carpal tunnel. Although several surgical techniques have been developed, no one method is more effective than the other. Each of these management approaches are effective at providing symptom relief and are utilized at different severities of the condition. There is, however, a lack of consensus on standardized diagnostic criteria, as well as when and to whom to refer patients for surgery.

Keywords: Carpal tunnel syndrome; Electrodiagnostic testing; Magnetic resonance imaging; Median neuropathy; Neurologic examination; Surgical management; Ultrasound.

Copyright © 2024 Elsevier B.V. All rights are reserved, including those for text and data mining, AI training, and similar technologies.

Publication types

• Carpal Tunnel Syndrome* / diagnosis
• Carpal Tunnel Syndrome* / therapy
• Decompression, Surgical / methods