Median Neuropathy at the Wrist

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17 Median Neuropathy at the Wrist

Median nerve entrapment at the wrist is the most common of all entrapment neuropathies and, consequently, is one of the most frequent reasons for referral for an electrodiagnostic (EDX) study. In nearly all patients, the usual site of compression occurs in the carpal tunnel and results in a constellation of symptoms and signs known as the carpal tunnel syndrome (CTS). Lesions of the C6–C7 nerve roots or, less often, the brachial plexus and the proximal median nerve may be confused clinically with median neuropathy at the wrist, especially in early or mild cases.

For an electromyographer, familiarity with the various nerve conduction and electromyographic patterns associated with CTS is essential. It has long been recognized that in any individual patient with CTS, there may be little correlation between the degree or frequency of clinical symptoms or signs and the abnormalities seen on nerve conduction studies. For example, an occasional patient will have only mild or trivial clinical symptoms yet will have clear signs on physical examination (e.g., dense numbness, wasting of thenar muscles) and evidence of severe axonal loss on nerve conduction and needle electromyography (EMG) studies. On the other hand, there are patients whose clinical history clearly indicates CTS but who show few or no abnormalities on neurologic examination or on routine median motor and sensory nerve conduction studies. It is in these latter patients with early or electrically mild CTS that additional more sensitive nerve conduction studies must be performed in order to demonstrate median nerve slowing at the wrist. By appropriately applying the various electrophysiologic techniques available to study the median nerve, a definite diagnosis can usually be reached, and lesions of the nerve roots, proximal median nerve, or brachial plexus can be excluded.


Understanding the anatomy of the median nerve is the first step toward being able to differentiate entrapment of the median nerve at the wrist from lesions of the proximal median nerve, brachial plexus, and cervical nerve roots, on both clinical and electrophysiologic grounds. The median nerve is formed by a combination of the lateral and medial cords of the brachial plexus (Table 17–1, Figure 17–1). The lateral cord is made up of C6–C7 fibers and supplies median sensory fibers to the thenar eminence, thumb, index, and middle fingers, and motor fibers to the proximal median forearm muscles. The medial cord, composed of C8–T1 fibers, supplies motor fibers to the median muscles of the distal forearm and hand, as well as sensory fibers to the lateral half of the ring finger.

The median nerve descends in the upper arm, giving off no muscular branches. In the antecubital fossa, the nerve lies adjacent to the brachial artery. As it passes into the forearm, the median nerve runs between the two heads of the pronator teres (PT) before giving off muscular branches to the PT, flexor carpi radialis (FCR), flexor digitorum sublimis (FDS), and, in some individuals, the palmaris longus muscles. The anterior interosseous nerve is given off next in the proximal forearm, innervating the flexor pollicis longus (FPL), the medial head of the flexor digitorum profundus (FDP) to the index and middle fingers, and the pronator quadratus (PQ) muscles. The anterior interosseous nerve is considered a pure motor nerve clinically because it carries no cutaneous sensory fibers. However, deep sensory fibers are carried in the anterior interosseous nerve, supplying the wrist joint and interosseous membrane.

Just proximal to the wrist and carpal tunnel, the palmar cutaneous sensory branch arises next, running subcutaneously to supply sensation over the thenar eminence. The median nerve then enters the wrist through the carpal tunnel. Carpal bones make up the floor and sides of the carpal tunnel, and the thick transverse carpal ligament forms the roof (Figure 17–2). In addition to the median nerve, nine flexor tendons traverse the carpal tunnel as well (FDP: four tendons; FDS: four tendons; FPL: one tendon). In the palm, the median nerve divides into motor and sensory divisions. The motor division travels distally into the palm, supplying the first and second lumbricals (1L, 2L). In addition, the recurrent thenar motor branch is given off. This branch turns around (hence, recurrent) to supply muscular branches to most of the thenar eminence, including the opponens pollicis (OP), abductor pollicis brevis (APB), and superficial head of the flexor pollicis brevis (FPB). The sensory fibers of the median nerve that course though the carpal tunnel supply the medial thumb, index finger, middle finger, and lateral half of the ring finger. The index and middle fingers are each supplied by two digital branches (one lateral and one medial); the thumb and ring fingers receive only one branch each (Figure 17–3).


Patients with CTS may present with a variety of symptoms and signs (Table 17–2). Women are affected more often than men. Although CTS usually is bilateral both clinically and electrically, the dominant hand usually is more severely affected, especially in idiopathic cases. Patients complain of wrist and arm pain associated with paresthesias in the hand. The pain may be localized to the wrist or may radiate to the forearm, arm, or, rarely, the shoulder; the neck is not affected. Some patients may describe a diffuse, poorly localized ache involving the entire arm. Paresthesias are frequently present in the median nerve distribution (medial thumb, index, middle, and lateral ring fingers). Although many patients report that the entire hand falls asleep, if asked directly about little finger involvement, most will subsequently note that the little finger is spared.

Table 17–2 Clinical Symptoms and Signs

Highly Suggestive of Carpal Tunnel Syndrome Possible Carpal Tunnel Syndrome Inconsistent with Carpal Tunnel Syndrome
Nocturnal paresthesias awakening patient from sleep Hand, wrist, forearm, arm, and/or shoulder pain Neck pain
Shaking or ringing the hands    
Pain/paresthesias associated with driving or holding a phone, book, or newspaper Perception of paresthesias involving all five digits Paresthesias radiating from neck and shoulder down the arm
Sensory disturbance of digits 1,2, 3, and 4, splitting the fourth digit No fixed sensory disturbance, or sensory disturbance of digits 1, 2, 3, and/or 4 Unequivocal numbness over the thenar eminence
Weakness/wasting of thenar eminence Decreased hand dexterity Weakness/wasting of hypothenar muscles, thumb flexion (interphalangeal joint), arm pronation, and/or elbow flexion/extension
Phalen’s maneuver reproduces symptoms Tinel’s sign over the median nerve at the wrist Reduced biceps or triceps reflexes

Symptoms often are provoked when either a flexed or extended wrist posture is assumed. Most commonly, this occurs during ordinary activities, such as driving a car or holding a phone, book, or newspaper. Nocturnal paresthesias are particularly common. During sleep, persistent wrist flexion or extension leads to increased carpal tunnel pressure, nerve ischemia, and subsequent paresthesias. Patients frequently will awaken from sleep and shake or wring their hands out or hold them under warm running water.

Sensory fibers are involved early in the majority of patients. Pain and paresthesias usually bring patients to medical attention. Motor fibers may become involved in more advanced cases. Weakness of thumb abduction and opposition may develop, followed by frank atrophy of the thenar eminence. Some patients describe difficulty buttoning shirts, opening jars, or turning doorknobs. However, development of significant functional impairment from loss of median motor function in the hand is unusual.

The sensory examination may disclose hypesthesia in the median distribution. Comparing sensation over the lateral ring finger (median innervated) to that over the medial ring finger (ulnar innervated) is often helpful. Sensation over the thenar area is spared because this area is innervated by the palmar cutaneous sensory branch, which arises proximal to the carpal tunnel (Figure 17–4). The Tinel’s sign is often present when tapping over the median nerve at the wrist, which results in paresthesias in the median-innervated fingers (Figure 17–5). The Phalen’s maneuver, whereby the wrist is held passively flexed, may also provoke symptoms (Figure 17–6, top). A wide range of sensitivities and specificities for the Tinel’s sign and Phalen’s maneuver have been reported in the literature. A Tinel’s sign is present in more than half of CTS cases; however, false-positive Tinel’s signs are common in the general population. A Phalen’s maneuver usually produces paresthesias within 30 seconds to 2 minutes in CTS; it is more sensitive than the Tinel’s sign and has fewer false-positive results. Most commonly, the Phalen’s maneuver will produce paresthesias in the middle or index fingers. It should be noted, however, that because the Phalen’s maneuver often is performed with the elbow flexed as well (a provocative maneuver for ulnar neuropathy at the cubital tunnel), this position occasionally may produce ulnar paresthesias in patients with ulnar neuropathy.

The motor examination involves inspection of the hand, looking for wasting of the thenar eminence (severe cases), and testing the strength of thumb abduction and opposition (Figure 17–7). Isolating the actions of the APB and OP (median-innervated muscles distal to the carpal tunnel) may be difficult because thumb abduction is also served by the abductor pollicis longus (radial nerve) and thumb opposition by a combination of the deep head of the FPB (innervated by the ulnar nerve) and the FPL (innervated by the anterior interosseous nerve).

It is important to emphasize that CTS is a clinical diagnosis. It represents a constellation of clinical symptoms and signs caused by compression and slowing of the median nerve at the wrist. However, there are patients who have median nerve slowing at the wrist on nerve conductions but who have no clinical signs or symptoms. Such patients do not have CTS per se and do not need directed therapy. This situation is encountered most often in patients with an underlying polyneuropathy in whom preferential slowing at common sites of compression is not unusual. Often, patients with an underlying polyneuropathy may be found to have incidental slowing at several entrapment sites, including the median nerve at the wrist, ulnar nerve at the elbow, and peroneal nerve at the fibular neck. For example, a patient with numbness and tingling of both feet from a mild alcohol-induced or diabetic polyneuropathy may have relative slowing of the median nerve across the wrist on nerve conduction studies yet may have no complaints of pain, paresthesias, or weakness in the hands. According to the EDX studies, such a patient has a median neuropathy at the wrist superimposed on an underlying polyneuropathy, but the patient does not have CTS. This distinction is important, because in this case treatment with splinting, injection, or surgery is not appropriate. The point is again underscored that nerve conduction and EMG studies can be properly performed and interpreted only with knowledge of the clinical history and physical examination.


The reported causes of CTS are numerous (Box 17–1). Despite this exhaustive list, most cases are idiopathic. Indeed, idiopathic cases present with the same signs and symptoms as CTS caused by the other conditions listed in Box 17–1. Although the etiology of idiopathic cases was long considered to be tenosynovitis of the transverse carpal ligament, pathologic evaluation typically shows little evidence of inflammation. In most cases, edema, vascular sclerosis, and fibrosis are seen, findings consistent with repeated stress to connective tissue. Compression results in symptoms by way of ischemia and demyelination and, if it is severe enough, wallerian degeneration and axonal loss.

Occupations or activities that involve repetitive hand use clearly increase the risk of CTS (e.g., typists, data entry workers, mechanics, and carpenters). From the exhaustive list given in Box 17–1, the conditions most often associated with CTS, other than idiopathic, are diabetes, hypothyroidism, rheumatoid arthritis, amyloidosis, and pregnancy. One important clue to an underlying cause, other than idiopathic, is the presence of CTS in the non-dominant hand. In idiopathic cases, the dominant hand is nearly always the affected hand; if symptoms are bilateral, then the dominant hand is more affected than the contralateral hand. CTS that is significantly worse in the non-dominant hand should raise a red flag to a specific underlying cause other than idiopathic CTS.

Differential Diagnosis

There are several peripheral as well as central nervous system (CNS) lesions that may result in symptoms similar to CTS. The peripheral lesions that enter into the differential diagnosis include median neuropathy in the region of the elbow, brachial plexopathy, and cervical radiculopathy. The most common among the disorders that may be confused with CTS is cervical radiculopathy, especially lesions of the C6 or C7 root, which may cause both pain in the arm and paresthesias similar to those that characterize CTS. The important clinical clues that suggest radiculopathy rather than CTS are pain in the neck, radiation from the neck to the shoulder and arm, and exacerbation of symptoms by neck motion. Key points in the physical examination that suggest radiculopathy are abnormalities of the C6–C7 reflexes (biceps, brachioradialis, triceps), diminished power in proximal muscles (especially elbow flexion, elbow extension, arm pronation), and sensory abnormalities in the palm or forearm, which are beyond the distribution of sensory loss found in CTS.

Median neuropathy at the elbow and brachial plexopathy are very uncommon, especially in comparison to the incidence of CTS. If present, however, they may easily lead to clinical confusion. Important clues on physical examination that suggest a more proximal lesion of the median nerve are sensory disturbance over the thenar eminence and weakness of median innervated muscles proximal to the carpal tunnel, especially distal thumb flexion (FPL), arm pronation (PT and PQ), and wrist flexion (FCR). In brachial plexus lesions, the neurologic examination may reveal abnormalities similar to those noted in cervical radiculopathy, although the distribution of reflex abnormalities, weakness, and sensory loss may be more widespread, beyond the distribution of one spinal segment.

As for CNS disorders, transient paresthesias may be seen in patients with focal seizures, migraine, and transient ischemic attacks and occasionally are misinterpreted as symptoms of CTS. In exceptional cases, patients referred to the EMG laboratory for suspicion of CTS will be found to have a small lacunar infarct involving the lateral thalamus and internal capsule, causing hand clumsiness and sensory disturbance predominantly affecting the median-innervated digits. In addition to the presence of other evidence of CNS dysfunction, such as limb spasticity and brisk reflexes, the major differentiating factor is the lack of pain. One should always question the diagnosis of CTS in the absence of pain.

Electrophysiologic Evaluation

The electrophysiologic evaluation of a patient suspected of having CTS is directed toward the following:

Nerve Conduction Studies

The nerve conduction strategy for evaluating possible CTS is outlined in Box 17–2. The pathophysiology of CTS typically is demyelination, which, depending on the severity, may be associated with secondary axonal loss. In moderate to advanced cases, the electrodiagnosis usually is straightforward. On routine median studies, a demyelinating lesion at the carpal tunnel results in slowing of the distal motor and sensory latencies. If there is either demyelination with conduction block or axonal loss, the distal compound muscle action potential (CMAP) and sensory nerve action potential (SNAP) amplitudes, stimulating the median nerve at the wrist, will be decreased as well.

Box 17–2

Recommended Nerve Conduction Study Protocol for Carpal Tunnel Syndrome

Routine studies

The study is highly suggestive of isolated carpal tunnel syndrome if


No further nerve conductions are necessary, proceed to electromyography (EMG).

If the median studies are completely normal or equivocal, proceed with the median-versus-ulnar comparison tests, the median-versus-radial comparison test, or the median segmental sensory study.

Median-versus-ulnar comparison studies

Median-versus-radial comparison study

Median segmental sensory study

If two or more of the above studies are abnormal, there is a high likelihood of carpal tunnel syndrome. Proceed to EMG. If these studies are normal, consider alternative diagnoses, especially cervical radiculopathy (note: a small number of patients with CTS can have normal NCSs).

Other important considerations:

1. If there is a co-existent polyneuropathy, the case will be more challenging. The question will be: is the median nerve slowing out of proportion to the slowing associated with the polyneuropathy. It is possible that all the motor and sensory latencies may be prolonged from the polyneuropathy itself. In addition, it would not be uncommon that the sensory and mixed studies may be absent, in which case the palmar mixed, digit 4, and digit 1 comparison studies cannot be used. In this situation, the lumbrical – interosseous comparison is often the most useful internal comparison study, as these motor responses usually remain present in a polyneuropathy.

2. In the unusual situation wherein there is a co-existent ulnar neuropathy at the wrist, all of the median versus ulnar internal comparison studies may be unhelpful, as both the median and ulnar latencies may be prolonged. In this situation, the median versus radial internal comparison study or the median segmental sensory study would be most useful.

3. If there is a co-existent ulnar neuropathy at the elbow (which would not be uncommon), the ulnar mixed and sensory responses may be absent, in which case the palmar mixed and digit 4 studies cannot be used. In this situation, the median versus radial internal comparison study, the median segmental sensory study, or the lumbrical – interosseous comparison would be most useful.

4. If the distal median motor or median sensory amplitudes are low, this may denote either axonal loss or distal conduction block. The only way to differentiate between these two is to stimulate the median nerve in the palm and compare the amplitudes with wrist stimulation. Any palm/wrist ratio >1.6 for sensory and >1.2 for motor amplitudes denotes some conduction block.

In patients with typical CTS, the median distal motor and sensory latencies, and minimum F wave latencies, are moderately to markedly prolonged. However, there are a group of patients with clinical symptoms and signs of CTS in whom these routine studies are normal (approximately 10–25% of CTS patients). In such patients, the electrodiagnosis of CTS will be missed unless further testing is performed using more sensitive nerve conduction studies. Those studies usually involve a comparison of the median nerve to another nerve in the same hand. The ulnar nerve is the nerve most commonly used for comparison; less often the radial nerve is used.

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