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.
|Pronator teres||(Main median nerve)||Lateral||Upper/middle||C6–C7|
|Flexor carpi radialis||(Main median nerve)||Lateral||Upper/middle||C6–C7|
|Flexor digitorum sublimis||(Main median nerve)||Lateral/medial||Middle/lower||C7–C8|
|Flexor digitorum profundus (2,3)||Anterior interosseous||Lateral/medial||Middle/lower||C7–C8|
|Flexor pollicis longus||Anterior interosseous||Lateral/medial||Middle/lower||C7–C8–T1|
|Pronator quadratus||Anterior interosseous||Lateral/medial||Middle/lower||C7–C8–T1|
|Abductor pollicis brevis||Recurrent thenar||Medial||Lower||C8–T1|
|Opponens pollicis||Recurrent thenar||Medial||Lower||C8–T1|
|Flexor pollicis brevis (superficial head)||Recurrent thenar||Medial||Lower||C8–T1|
|Thenar eminence||Palmar cutaneous||Lateral||Upper||C6|
|Medial thumb||Digital branch||Lateral||Upper||C6|
|Index finger||Digital branches||Lateral||Upper/middle||C6–C7|
|Middle finger||Digital branches||Lateral||Middle||C7|
|Lateral ring finger||Digital branch||Lateral/medial||Middle/lower||C7–C8|
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.
|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.
Connective tissue disease
Persistent median artery
Congenital small carpal tunnel
Anomalous muscles (palmaris longus, flexor digitorum sublimis)
Fractures (especially Colles’ fracture)
Hemorrhage (including anticoagulation)
Spasticity (persistent wrist flexion)
Amyloidosis (familial and acquired)
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 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.
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.
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
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.
Median motor study recording abductor pollicis brevis, stimulating wrist and antecubital fossa
Ulnar motor study recording abductor digiti minimi, stimulating wrist, below groove, and above groove
Median and ulnar F responses
Median sensory response, recording digit 2 or 3, stimulating wrist
Ulnar sensory response, recording digit 5, stimulating 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 (CMAP) and sensory nerve action potential (SNAP) amplitudes may be diminished if there is secondary axonal loss or if demyelination has led to conduction block at the wrist
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 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:
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/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.
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.
Median-versus-Ulnar Comparison Studies
Median-versus-Ulnar Palm-to-Wrist Mixed Nerve Studies
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 ( Figure 17–8 ). 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.
Median-versus-Ulnar Digit 4 Sensory Latencies
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 medial half innervated by the ulnar nerve ( Figure 17–9 ). 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 median and ulnar onset or peak latencies 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.
Median Second Lumbrical-versus-Ulnar Interossei Distal Motor Latencies
The technique of comparing the second lumbrical (2L)-versus-interosseous (INT) 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 ( Figure 17–10 ). 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 then is 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.