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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 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. In addition, neuromuscular ultrasound is an especially useful adjunct to nerve conduction studies in the diagnosis of CTS and will be discussed later in the chapter.
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 20.1 , Fig. 20.1 ). 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.
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The median nerve descends in the upper arm, giving off no muscular branches. In the antecubital fossa, the nerve lies just medial 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 lateral 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 ( Fig. 20.2 ). 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 ( Fig. 20.3 ).
Patients with CTS may present with a variety of symptoms and signs ( Table 20.2 ). 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.
Highly Suggestive of Carpal Tunnel Syndrome | Possible Carpal Tunnel Syndrome | Inconsistent With Carpal Tunnel Syndrome |
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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 the 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 are often 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 ( Fig. 20.4 ). 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 ( Fig. 20.5 ). The Phalen’s maneuver , whereby the wrist is held passively flexed, may also provoke symptoms ( Fig. 20.6 , 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 patients with CTS; 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 ( Fig. 20.7 ). Isolating the actions of the APB and OP (median-innervated muscles distal to the carpal tunnel) may be difficult because thumb abduction is also subserved 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 20.1 ). 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 20.1 . Although the etiology of idiopathic cases was long considered to be tenosynovitis under 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.
Idiopathic disorders
Repetitive stress
Occupational
Endocrine disorders
Hypothyroidism
Acromegaly
Diabetes
Connective tissue disease
Rheumatoid arthritis
Tumors
Ganglia
Lipoma
Fibrolipoma
Schwannoma
Neurofibroma
Hemangioma
Congenital disorders
Persistent median artery
Congenital small carpal tunnel
Anomalous muscles (palmaris longus, flexor digitorum sublimis)
Infectious/inflammatory
Sarcoid
Histoplasmosis
Septic arthritis
Lyme
Tuberculosis
Tenosynovitis
Trauma
Fractures (especially Colles’ fracture)
Hemorrhage (including anticoagulation)
Other
Spasticity (persistent wrist flexion)
Hemodialysis
Amyloidosis (familial and acquired)
Pregnancy
Any condition that increases edema or total body fluid
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 20.1 , 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 nondominant 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 nondominant hand should raise a red flag to look for a specific underlying cause other than idiopathic CTS. This is one of the situations where neuromuscular ultrasound should be undertaken.
There are several peripheral as well as central nervous system (CNS) lesions that may result in symptoms similar to CTS. The peripheral lesions in 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. 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.
The electrophysiologic evaluation of a patient suspected of having CTS is directed toward the following:
Demonstrating focal slowing or conduction block of median nerve fibers across the carpal tunnel
Excluding median neuropathy in the region of the elbow
Excluding brachial plexopathy predominantly affecting the median nerve fibers
Excluding cervical radiculopathy, especially C6 and C7
If a coexistent polyneuropathy is present, ensuring that any median slowing at the wrist is out of proportion to slowing expected from the polyneuropathy alone
The nerve conduction strategy for evaluating possible CTS is outlined in Box 20.2 . 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.
Routine studies:
Median motor study recording the abductor pollicis brevis, stimulating the wrist and antecubital fossa
Ulnar motor study recording abductor digiti minimi, stimulating the wrist, below groove, and above groove
Median and ulnar F responses
Median sensory response, recording digit 2 or 3, stimulating the wrist
Ulnar sensory response, recording digit 5, stimulating the wrist
Radial sensory response, recording snuffbox, stimulating over the lateral radius
The study is highly suggestive of isolated carpal tunnel syndrome if
The median studies are abnormal, showing marked slowing across the wrist (prolonged distal motor and sensory latencies) and prolonged minimum F-wave latencies. The median compound muscle action potential and sensory nerve action potential amplitudes may be diminished if there is secondary axonal loss or if demyelination has led to conduction block at the wrist. and The ulnar motor, sensory, and F-wave studies are normal and the radial sensory response is normal (making a brachial plexopathy or polyneuropathy unlikely)
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:
Comparison of the median and ulnar mixed palm-to-wrist peak latencies, stimulating the median and ulnar palm one at a time 8 cm from the recording electrodes over the median and ulnar wrist, respectively
Comparison of the median lumbrical and ulnar interossei distal motor latencies, stimulating the median and ulnar wrist one at a time at identical distances (8–10 cm), recording with the same electrode over the 2L/interossei
Comparison of the median and ulnar digit 4 sensory latencies, stimulating the median and ulnar wrist one at a time at identical distances (11–13 cm) and recording digit 4
Median-versus-radial comparison study:
Comparison of the median and radial digit 1 sensory latencies, stimulating the median nerve at the wrist and the superficial radial sensory nerve at the forearm one at a time at identical distances (10–12 cm) and recording digit 1
Median segmental sensory study:
While recording digit 3, stimulate the median nerve at the wrist and in the palm (with the palm-to-digit distance being one-half of the wrist-to-digit distance). Then calculate the wrist-to-palm conduction velocity and compare it to the palm-to-digit conduction velocity.
If two or more of the previous 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 nerve conduction studies).
Other important considerations:
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.
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.
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.
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-to-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 patients with CTS). 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.
The common median-versus-ulnar comparison tests are (1) median-versus-ulnar palm-to-wrist mixed nerve latencies, (2) median-versus-ulnar wrist–to–digit 4 sensory latencies, and (3) median (second lumbrical)-versus-ulnar (interossei [INT]) distal motor latencies. In each of the comparison studies, identical distances between the stimulator and recording electrodes are used for the median and ulnar nerves. These techniques create an ideal internal control in which several variables that are known to affect conduction time are held constant, including distance, temperature, age, and nerve size. Ideally, the only factor that varies in these paired median-versus-ulnar comparison studies is that the median nerve traverses the carpal tunnel, whereas the ulnar nerve does not. Thus, any preferential slowing of the median nerve compared with the ulnar nerve can be attributed to conduction slowing through the carpal tunnel. The diagnostic yield increases from approximately 75% using routine motor and sensory studies to approximately 95% using these more sensitive techniques.
These sensitive median-versus-ulnar comparison studies are considered abnormal if very small differences between the median and ulnar latencies are found (typically 0.4–0.5 ms). Therefore, meticulous attention must be paid to all technical factors, especially distance measurement, stimulus artifact, supramaximal stimulation, and electrode placement, to obtain reliable and reproducible data . Furthermore, it is essential to avoid overstimulation, which can cause unintentional stimulus spread to an adjacent nerve. In the three studies outlined in the following section, overstimulation with unintentional spread of current to the adjacent nerve may yield a waveform that appears perfectly normal yet obscures the true latency difference between the median and ulnar potentials.
This technique takes advantage of measuring the mixed nerve potential. Mixed nerve potentials consist of both motor and sensory fibers. The sensory fibers in the mixed nerve potential carry both cutaneous sensory fibers, which are measured in routine sensory studies, as well as muscle sensory fibers, which are not measured in routine sensory studies. This is important because the muscle sensory fibers include the Ia afferents from muscle spindles, which are the largest and fastest-conducting fibers and hence have the greatest quantity of myelin sheath. These fibers are very susceptible to demyelination, the primary pathology in CTS. The mixed nerve study also takes advantage of conducting over a very short distance of 8 cm. Because such a short distance is used, most of the conduction time is computed over the area of pathology. Only a short length of normal nerve is included that potentially could dilute any slowing present across the carpal tunnel.
The technique is performed by stimulating the median nerve in the palm, recording the median nerve at the wrist, and comparing it with the ulnar nerve stimulated in the palm and recorded over the ulnar nerve at the wrist ( Fig. 20.8 ). Each nerve is stimulated supramaximally in the palm at a distance of 8 cm from its respective recording electrodes. The median nerve is stimulated in the palm on a line connecting the median nerve in the middle of the wrist to the web space between the index and middle fingers. The ulnar nerve is stimulated in the palm on a line connecting the ulnar nerve at the medial wrist (lateral to the flexor carpi ulnaris tendon) to the web space between the ring and little fingers. Supramaximal responses are obtained for each nerve, and the difference between the onset or peak latencies is calculated.
The technique of comparing median-versus-ulnar digit 4 sensory latencies takes advantage of the fact that, in most individuals, the sensory innervation to the fourth digit (ring finger) is split, with the lateral half innervated by the median nerve and the medial half innervated by the ulnar nerve ( Fig. 20.9 ). Thus, if identical distances are used, the latencies stimulating each nerve can be directly compared. The antidromic technique is performed by stimulating the median and ulnar nerves at the wrist, one at a time, with recording ring electrodes placed over digit 4 (G1 over the metacarpophalangeal joint and G2 over the distal interphalangeal joint). Identical distances must be used for both (range 11–13 cm). Supramaximal responses are obtained, and the difference between the median and ulnar onset or peak latencies is recorded. The study also can be done orthodromically, stimulating with the ring electrodes over digit 4 as just described and recording the median and ulnar nerves at the wrist at identical distances. We do not recommend the latter method because, with orthodromic stimulation at digit 4, co-stimulation of the median and ulnar nerves cannot be avoided, and spread of the potential from the adjacent nerve may contaminate the recorded SNAP at the wrist.
The technique of comparing the second lumbrical (2L)-versus-interosseous distal motor latencies takes advantage of two facts: (1) motor fibers are easy to record and more resistant to compression than sensory fibers, and (2) the median 2L muscle lies just above the ulnar INT. In some cases of generalized polyneuropathy with superimposed CTS, the SNAPs and mixed nerve potentials may be absent. In severe cases, the routine median CMAP recording the APB may also be absent, whereas the motor fibers to the second lumbrical and ulnar INT are still recordable.
CMAPs from both the median-innervated 2L and the ulnar-innervated INT can easily be recorded by placing an active electrode (G1) slightly lateral and distal to the midpoint of the third metacarpal, with the reference electrode over the proximal interphalangeal joint of the second digit, and stimulating the median and ulnar nerves at the wrist, respectively ( Fig. 20.10 ). The motor point to the 2L is identified when the active recording electrode has been placed such that stimulation of the median nerve at the wrist elicits a waveform with the fastest rise time and an initial negative deflection. Because the 2L cannot be seen or palpated, moving the active electrode slightly may be necessary to ensure the electrode is optimally placed. In some individuals, if the sensitivity is increased, a small mixed nerve potential will be seen slightly before the onset of the 2L CMAP. This is a normal finding, especially in younger patients. If this small mixed nerve potential is present, the latency should be measured from the onset of the 2L CMAP, not from the onset of the mixed nerve potential. The ulnar nerve is then stimulated supramaximally at the wrist, at the same distance, leaving the recording electrodes in place . A CMAP from the underlying ulnar INT muscles will be easily elicited. The ulnar CMAP is generally larger than the median CMAP. Identical distances (range 8–10 cm) must be used to compare the difference between the distal latencies.
The normal values for the three median-versus-ulnar comparison studies are given in Table 20.3 . In our laboratory, the palmar mixed nerve peak latency difference is the most sensitive study, followed closely by the digit 4 sensory and 2L-INT motor studies. However, there is a very high degree of correlation among the results of the three studies. In one comparison study, two of the three studies yielded abnormal results in 97% of all patients with mild CTS. In a patient in whom only one of the median-versus-ulnar comparison studies is abnormal, one should be hesitant to make a definite electrodiagnosis of CTS (see Chapter 9 ).
Study | Nerve | Stimulate | Record | Distance (cm) | Significant Difference (ms) |
---|---|---|---|---|---|
Palmar mixed | Median | Median palm | Median nerve at wrist | 8 | ≥0.4 |
Ulnar | Ulnar palm | Ulnar nerve at wrist | 8 | ||
Digit 4 sensory | Median | Median nerve at wrist | Digit 4 | 11–13 a | ≥0.5 |
Ulnar | Ulnar nerve at wrist | Digit 4 | 11–13 | ||
Lumbrical-interossei | Median | Median nerve at wrist | Lateral to the mid-third metacarpal (over the second lumbrical and interossei) | 8–10 a | ≥0.5 |
Ulnar | Ulnar nerve at wrist | Lateral to the mid-third metacarpal (over the second lumbrical and interossei) | 8–10 |
a Must use the identical distance for median and ulnar nerve stimulation.
Another extremely sensitive internal comparison study includes the wrist-to-palm versus palm-to-digit sensory conduction velocity (segmental sensory conduction studies across the wrist). This test is more technically challenging than the others listed previously but is extremely sensitive in detecting CTS. This technique compares the sensory conduction velocity along the median nerve at two segments of identical distance: the wrist-to-palm segment and the palm-to-digit segment. Digit 3 is the preferred finger to record from due to its longer length. The recording electrodes (G1, G2) are placed at the proximal and the distal interphalangeal joints, respectively. Placing G1 at the proximal interphalangeal instead of the metacarpal-phalangeal joint allows more distance between it and the stimulator (and less stimulus artifact). The median nerve is then stimulated at the wrist at a fixed distance to G1. The median nerve is next stimulated at the palm, with the recording ring electrodes left in place, at half the wrist-to-digit distance ( Fig. 20.11 ). If the EMG machine is set up to automatically compute the wrist-to-palm and palm-to digit conduction velocities, any distance can be used. Otherwise, making the palm-to-digit distance half that of the wrist-to-digit distance (e.g., 7 cm and 14 cm) greatly simplifies the mathematical equation. In this situation, the wrist-to-palm conduction velocity is then computed by multiplying the palm-to-digit conduction velocity by the wrist-to-digit conduction velocity, and then dividing it by the quantity of the palm-to-digit conduction velocity times two, minus the wrist-to-digit conduction velocity ( Fig. 20.12 ). In normal subjects, the wrist-to-palm segment (i.e., the segment across the carpal tunnel) is equal to or faster than the distal segment (palm-to-digit) because proximal nerve normally conducts faster than distal segments, secondary to larger nerve diameter and warmer temperatures. In CTS, there is a reversal of this normal pattern; the proximal segment (wrist-to-palm) conducts more slowly than the distal palm-to-digit segment. In general, any slowing of more than 10 m/s is considered abnormal.
Another technique useful in demonstrating CTS, first described by Kimura and later by others, involves segmental stimulation (“inching”) of the median nerve across the carpal tunnel ( Fig. 20.13 ). One looks for an abrupt change in latency or increase in amplitude above normal control values, recording either a median CMAP at the APB or a median digital SNAP at the index or middle finger.
Kimura’s method begins at 4 cm proximal to the distal wrist crease and continues to 6 cm distal to the wrist crease, with segmental stimulation at 1-cm increments. For each 1-cm increment, latency usually increases 0.2 to 0.3 ms. Any abrupt change in latency greater than this is highly suggestive of focal demyelination. Although the inching technique has the advantage of showing the exact site of the lesion, its effectiveness often is limited by difficulty stimulating the nerve at the sites just distal to the wrist crease. The technique is particularly difficult to perform recording the median CMAP because stimulation of motor fibers at 1-cm increments following the course of the recurrent thenar branch of the median nerve can be quite difficult. Furthermore, stimulation in the palm often requires rotation of the anode to prevent excessive stimulus artifact ( Fig. 20.14 ).
Rather than measuring a change in latency, comparing the CMAP or SNAP amplitudes stimulating at the wrist and palm can be technically easier and can yield additional information about the underlying pathophysiology ( Fig. 20.15 ). Wrist and palmar stimulation can be performed for either median motor or sensory studies. Only single palm and wrist stimulations are required, whereas inching requires stimulation at multiple 1-cm increments. Several technical factors must be taken into account. First, as noted earlier for motor studies, the anatomy of the recurrent thenar motor branch is such that for stimulating the motor branch in the palm, the stimulator often must be placed beyond the thenar eminence with the anode rotated distally to prevent excessive stimulus artifact ( Fig. 20.14 ). Second, the examiner must be aware of normal values when comparing amplitudes proximal and distal to the carpal tunnel. There is always some drop in amplitude proximally compared with distally due to greater temporal dispersion and phase cancellation with proximal stimulation. The effects of normal temporal dispersion and phase cancellation are always greater for sensory fibers than for motor fibers. In normal median nerves, the ratio of the distal to proximal CMAP amplitude does not exceed 1.2, whereas the ratio of distal to proximal SNAP amplitude does not exceed 1.6. Larger ratios suggest some element of conduction block ( Fig. 20.16 ). This assumption presumes that both stimulations are supramaximal, that there is no co-stimulation of adjacent nerves, and that the baseline is not obscured by shock artifact or noise that precludes an accurate amplitude measurement.
In CTS, if wrist stimulation yields a low CMAP or SNAP amplitude, there are two possible explanations: (1) there is conduction block secondary to demyelination across the carpal tunnel with the underlying axon intact, or (2) there has been secondary axonal loss ( Fig. 20.17 ). Comparing the amplitudes obtained with wrist and palmar stimulation can easily sort out these two possibilities. Take the following example:
Case A | Case B | |
---|---|---|
CMAP (stimulate wrist, record APB) | 2 mV | 2 mV |
CMAP (stimulate palm, record APB) | 6 mV | 2 mV |
In both cases, when the median nerve is stimulated at the wrist, the recorded CMAP is low (normal value >4.0 mV). When the palm is stimulated in case A, however, the CMAP amplitude increases by an additional 200%; the distal-to-proximal amplitude ratio is 3.0, signifying conduction block. In contrast, there is no change in amplitude in case B, signifying that the low amplitude is secondary to axonal loss.
Comparison of the median-versus-radial digit 1 sensory latencies takes advantage of the fact that, in most individuals, digit 1 (the thumb) is innervated by both the median and radial nerves ( Fig. 20.18 ). The basic concept is the same as in the median-versus-ulnar digit 4 sensory study: the median and radial nerves are stimulated at the wrist, using identical distances, with recording ring electrodes over digit 1 (G1 over the metacarpophalangeal joint and G2 over the interphalangeal joint). The radial nerve is stimulated at the wrist along the lateral border of the radial bone. Using the same distance, the median nerve is stimulated at the wrist in the usual location. Supramaximal responses are obtained at each stimulation site, and the onset or peak latencies are compared. Although this technique is popular in some laboratories, stimulating the nerves at identical distances may be difficult because the median nerve travels to the thumb at an angle, which can hinder measurement of its true distance. Any difference between the median and radial latencies greater than or equal to 0.5 ms is considered abnormal.
This technique compares the minimum F-wave latency stimulating the median and ulnar nerves at the wrist, recording the APB and abductor digiti minimi muscles, respectively. In normal individuals, the minimum F-wave latency from the median nerve is approximately 1–2 ms shorter than the minimum F-wave latency from the ulnar nerve. A reversal of this pattern is considered abnormal ( Fig. 20.19 ). This test is nonspecific, however, because the F wave measures conduction along the entire length of nerve, from the recording electrode to the spinal cord. Although this study can confirm a problem with the median nerve, it cannot localize the lesion to the wrist. It is generally used only as confirmatory evidence for a diagnosis of CTS, in conjunction with abnormalities noted using more sensitive techniques.
The recommended EMG approach to a patient with CTS is outlined in Box 20.3 . The EMG strategy is designed with the clinical differential diagnosis in mind (i.e., proximal median neuropathy, brachial plexopathy, C6–C7 radiculopathy). The key muscle to check is the APB. In mild or early cases of CTS, the APB often is normal. In later or more severe cases, EMG may reveal secondary axonal loss resulting in denervation and reinnervation. In general, the hand muscles are best approached with a smaller-gauge needle. Because examination of the APB often is painful for patients to tolerate, it is best to begin the study with a different C8–T1-innervated muscle, such as the first dorsal interosseous (FDI). The APB can be examined next. Although some electromyographers may prefer to study the APB toward the end of the examination, there is the potential problem that the patient may quit the study before this key muscle can be studied, especially if the patient is generally intolerant of the EMG examination.
Abductor pollicis brevis (APB)
At least two C6–C7-innervated muscles (e.g., pronator teres, flexor carpi radialis, triceps brachii, extensor digitorum communis) to exclude a cervical radiculopathy
If APB is abnormal, the following additional muscles should be sampled:
At least one proximal median-innervated muscle (e.g., flexor carpi radialis, pronator teres, flexor pollicis longus) to exclude a proximal median neuropathy (note: the pronator teres may be spared in pronator syndrome)
At least two other non-median, lower trunk/C8–T1-innervated muscles (e.g., first dorsal interosseous, extensor indicis proprius) to exclude a lower trunk brachial plexopathy, polyneuropathy, or C8–T1 radiculopathy
Note: If the carpal tunnel syndrome is superimposed on another condition (e.g., polyneuropathy, plexopathy, radiculopathy), a more detailed electromyographic examination will be required.
The APB study frequently is painful and difficult for some patients to tolerate. It is best not studied first but also best not left for the end of the electromyographic study in case the patient is unable to tolerate the entire examination.
If the APB is abnormal, proximal median-innervated muscles and at least two other non-median C8–T1/lower trunk-innervated muscles should be sampled. In addition, C6–C7-innervated muscles should be sampled to exclude a cervical radiculopathy. The PT and FCR are very helpful muscles to sample because they can be used both as proximal median and C6–C7-innervated muscles. Some electromyographers have difficulty with the notion that the C6–C7-innervated muscles are important to sample, because the distal median hand muscles are innervated by the C8–T1 roots. One must remember that the distribution of numbness (not the weakness) in CTS may be very similar to the numbness noted in C6–C7 radiculopathies. Of course, because each case is different, the electromyographer must always be willing to modify each study throughout the testing, based on abnormalities noted as the study progresses.
It is not uncommon for a patient who has previously undergone carpal tunnel release surgery to be referred for EDX studies. The patient may either have recently undergone surgery with no clinical improvement or may have developed recurrent symptoms a long period of time after successful carpal tunnel decompression. In some cases, the patient will not have had a preoperative EDX study to confirm the diagnosis of CTS, which further complicates the issue. Thus, every electromyographer should be aware of what happens to nerve conduction study abnormalities after successful carpal tunnel release surgery. In general, the distal latencies and amplitudes improve both for median motor and sensory studies. However, this may take many weeks to months, and in some studies, improvement continues up to a year after surgery. However, some slowing may persist indefinitely. In the authors’ experience:
Median distal motor latencies improve and usually return to the “normal” range. Never do distal latencies remain in the demyelinating range (i.e., >130% the upper limit of normal) after successful carpal tunnel release.
Median sensory latencies improve and usually return to the “normal” range. Never do conduction velocities remain in the demyelinating range (i.e., <75% the lower limit of normal) after successful carpal tunnel release.
Median motor amplitudes improve and return to the normal range.
Median sensory amplitudes may or may not improve. Many remain in a slightly reduced or borderline normal range.
The sensitive internal comparison studies (i.e., palmar mixed studies, digit 4 study, digit 1 study, lumbrical-interosseous study, and segmental sensory study) remain abnormal indefinitely, showing some slowing of median conduction across the carpal tunnel.
Although these findings are seen most often after carpal tunnel release surgery, analogous findings are seen for other entrapments. This begs the question: after successful release surgery, why do the median conductions not completely return to normal? The answer involves knowledge of normal myelination, demyelination, and then remyelination ( Fig. 20.20 ). As noted in Chapter 2 , the process of myelination begins in utero, and full myelination of peripheral nerves does not occur until approximately age 3. Thus, by age 3, all the myelin and all the internodes have been laid down ( Fig. 20.20A ). However, between childhood and adulthood, while the limb grows in length, resulting in longer internodes, the number of internodes does not change ( Fig. 20.20B ). In entrapment neuropathies, such as CTS, demyelination occurs at the site of compression, resulting in interruption of the internodes at the site of compression ( Fig. 20.20C ). When the compression is successfully released, remyelination can then occur. However, the new internodes are short, the same distance apart that they were when originally laid down as a child ( Fig. 20.20D ). Therefore, more nodes are required to remyelinate the original site of compression. When remyelination is completed, nerve impulses can once again travel successfully up and down the nerve. However, remember that the time of conduction (and hence conduction velocity) is completely dependent on the depolarization time at the nodes of Ranvier. The greater the number of nodes of Ranvier, the more depolarizations, and hence, the longer total time of depolarization. Thus, conduction velocity across the remyelinated area of prior compression will be slower than normal because of the increase in the number of nodes. In any situation where there has been demyelination and then remyelination, sensitive techniques will always demonstrate a slightly slower conduction time across the remyelinated segment. Accordingly, one must always be cautious when interpreting any mild “slowing” on nerve conduction studies in patients who have undergone carpal tunnel release.
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