In this review, we delineate clinical, electrodiagnostic, and radiographic features of ulnar mononeuropathies. Ulnar neuropathy at the elbow (UNE) is most commonly due to lesions at the level of the retroepicondylar groove (RTC), with approximately 25% at the humeroulnar arcade (HUA). The term ‘cubital tunnel syndrome’ should be reserved for the latter. The diagnostic accuracy of nerve conduction studies is limited by biological (e.g. low elbow temperature) and technical factors. Across-elbow distance measurements greater than 10 cm improve diagnostic specificity at the expense of decreased sensitivity. Short-segment incremental studies can differentiate lesions at the HUA from those at the RTC.
Key points
- •
The most common locations for ulnar mononeuropathy are at the retroepicondylar (RTC) groove and the humeroulnar arcade.
- •
Precise localization of the ulnar nerve below and above the elbow with submaximal stimulations improves accuracy of the distance measurement.
- •
The factors that can lead to spuriously low nerve conduction velocity (NCV) across the elbow include a cold elbow and falsely low distance measurements.
- •
Multiple internally consistent abnormalities should be present to ensure accurate diagnosis of ulnar neuropathy at the elbow.
- •
In the setting of ulnar mononeuropathies, when routine electrodiagnostic studies fail to demonstrate focal slowing of NCV across the elbow, short-segment techniques should be done.
- •
The electromyographer should ascertain the specific point of abnormality (ie, the RTC groove, humeroulnar arcade, or other location) prior to surgical referrals.
Introduction
The ulnar nerve may be compressed at several sites. Ulnar neuropathy at the elbow (UNE) is the second most frequent upper extremity compression neuropathy. There are 4 different sites of potential compression in the region of the elbow. The nerve may also sustain focal injury in the wrist and hand and even less frequently in the axilla, upper arm, or forearm. Distinguishing between these different compression sites is not always straightforward. In most cases, the earliest electrodiagnostic findings are demyelinating. Early diagnosis and management can prevent secondary axonal damage and permanent disability.
Introduction
The ulnar nerve may be compressed at several sites. Ulnar neuropathy at the elbow (UNE) is the second most frequent upper extremity compression neuropathy. There are 4 different sites of potential compression in the region of the elbow. The nerve may also sustain focal injury in the wrist and hand and even less frequently in the axilla, upper arm, or forearm. Distinguishing between these different compression sites is not always straightforward. In most cases, the earliest electrodiagnostic findings are demyelinating. Early diagnosis and management can prevent secondary axonal damage and permanent disability.
Relevant anatomy
Anatomic details are important in understanding focal ulnar mononeuropathies. The ulnar nerve branches from the medial cord of the brachial plexus and courses in the forearm just medial to the brachial artery. It passes between the medial intermuscular septum (MIS) and the medial head of the triceps prior to reaching the medial epicondyle. The existence of the arcade of Struthers between the MIS and medial head of the triceps is debatable. The nerve then passes just dorsal to the ME, and into the ulnar groove, ventral to the olecranon process (OP). It subsequently passes beneath the humeroulnar aponeurotic arcade (HUA), a dense aponeurosis between the tendinous attachments of the flexor carpi ulnaris (FCU) muscle typically 1.0 cm to 2.5 cm distal to the ME. The nerve then runs through the belly of the FCU and exits from the muscle through the deep flexor pronator aponeurosis.
In elbow extension, the medial epicondyle and OP are juxtaposed, with the HUA slack and the nerve lying loosely in the groove. With elbow flexion, the OP moves forward and away from the ME. The humeral head of the FCU, attached to the ME, and the ulnar head, attached to the OP, are pulled apart, progressively tightening the HUA across the nerve, resulting in pressure increases up 19 mm Hg in the ulnar groove. In addition, with elbow flexion, the ulnar collateral ligament bulges into the floor of the groove and the medial head of the triceps may be pulled into the groove from behind. In extension, the ulnar groove is smooth, round, and capacious, but in flexion the nerve finds itself in inhospitable surroundings, in a flattened, tortuous, and narrow canal with the HUA pulled tightly across it. In full flexion, the nerve partially or completely subluxes out of its groove in many normal individuals.
The only motor branches in the forearm are those to the FCU and flexor digitorum profundus (FDP). The palmar ulnar cutaneous branch (PUC) separates from the main trunk in the mid to distal forearm, and enters the hand superficial to the Guyon canal, supplying sensation to the skin of the hypothenar region. The dorsal ulnar cutaneous (DUC) branch leaves the main trunk 5 cm to 10 cm proximal to the wrist, arcs around the ulna, and innervates the dorsal skin of the medial hand and fingers. The ulnar nerve then enters the hand through the Guyon canal.
The transverse carpal ligament, which arches over and forms the roof of the carpal tunnel, dips downward to form the floor of the Guyon canal. The roof, lateral, and medial boundaries of the canal are formed by the volar carpal ligament and the thin palmaris brevis muscle, hook of the hamate, and the pisiform bone, respectively. Just beyond the transverse carpal ligament, the pisohamate ligament runs from the pisiform bone to the hook of the hamate and forms the distal part of the floor of the canal. The nerve exits the Guyon canal by passing beneath the pisohamate ligament.
In the hand, the nerve bifurcates into the superficial terminal division and the deep palmar division. The superficial terminal portion supplies sensation to the small finger and ulnar half of the ring finger. The deep palmar branch subserves no cutaneous sensation but innervates all of the hypothenar muscles, the third and fourth lumbricals, all of the palmar and dorsal interossei, the adductor pollicis, the deep head of the flexor pollicis brevis, and the first dorsal interosseous (FDI). There are frequent anatomic variations.
Anatomic factors account for much of the susceptibility of the ulnar nerve to injury at the elbow. The lack of protective covering over the nerve in its course through the ulnar groove accounts for its susceptibility to external pressure. Repetitive elbow flexion and extension may predispose to UNE because of the dynamic changes in the nerve’s passageway with motion. With elbow joint derangement due to trauma or arthritic changes, the nerve’s vulnerability increases even further. Valgus deformities increase the stretch on the nerve with elbow flexion, and osteophytic overgrowth further narrows an often already narrow passageway. Most ulnar neuropathies occur at the level of the RTC groove. The nerve may also be entrapped at the HUA or at the point of exit from the FCU.
The internal architecture of the ulnar nerve, particularly the fascicular arrangement, has an important impact on the clinical and electrodiagnostic findings. The fibers destined for the FCU, the PUC, and DUC lie in individual fascicles at the elbow and in a deep dorsolateral position, rendering them less susceptible to damage with UNE. This can create difficulty differentiating UNE from ulnar neuropathy at the wrist (UNW).
Clinical features
In the majority of patients with UNE, the initial symptoms are typically intermittent numbness and tingling in the ulnar nerve distribution, often associated with elbow flexion, particularly at night. These intermittent symptoms may occur over months or years, although in patients with more severe entrapment, permanent symptoms may develop more rapidly. The amount of pain and paresthesia varies, and for some patients the sensory loss is not bothersome. In contrast to carpal tunnel syndrome, where pain is usually a prominent feature, UNE tends to cause numbness and paresthesias and pain is less prominent, often absent. Vanderpool and colleagues state that subjective motor loss may not be noted for months or years, depending on the degree of compression. In contrast, pain and dysesthesias are more frequent components with acute injury to the elbow, pain and dysesthesias are more frequent components. Elbow pain is rare except in acute focal injury.
The sensory abnormalities in ulnar neuropathies do not always conform to the expected distribution due to anatomic variations. Splitting sensory symptoms of the ring finger is highly specific for ulnar neuropathy. C8 radiculopathy and brachial plexopathy are more likely to affect the entire ring finger or spare it completely. In UNE, parasthesias typically involve the digits to a greater extent than the dorsal and palmar aspects of the medial hand, due to relative sparing of the DUC and PUC. The cutaneous field of the ulnar nerve does not extend more than a few centimeters proximal to the wrist crease. Sensory abnormalities in the forearm should raise the suspicion for plexus or nerve root lesions.
The motor disability from ulnar nerve palsy is related to 4 components : strength of pinch between the thumb and adjacent digits, coordination of thumb and digits in tasks requiring precision, synchrony of digital flexion during grasp, and strength of power grasp. Wrist flexion weakness is rarely significant due to normal function of the flexor carpi radialis.
Froment sign is due to weakness of the adductor policus and FDI, with compensation provided by the flexor pollicis longus. The lumbricals flex the metacarpophalangeal joints and extend the interphalangeal joints. In ulnar lesions, unopposed extensor tone at the fourth and fifth metacarpophalangeal joints and unopposed flexor tone at the interphalangeal joints produces the ulnar griffe or claw deformity. Clawing varies, depending on the amount of muscle weakness. A distal ulnar lesion that spares the FDP induces more clawing than more proximal lesions due to greater flexion of the interphalangeal joints of the fourth and fifth digits. The palmaris brevis (PB) sign is a wrinkling of the skin over the hypothenar eminence during 5th digit abduction. This is due to contraction of the PB which is spared with UNW. The elbow flexion test is analogous to the carpal compression test and the Phalen test seeking to elicit ulnar paresthesias on forcefully flexing the elbow and applying pressure over the ulnar groove. Tinel sign is sometimes useful. But some patients have generally mechanosensitive nerves, and only a disproportionately active Tinel sign over the suspect ulnar nerve has any significance. Both have a high incidence of false positives.
The forearm muscles, FCU and FDP, are frequently spared in UNE, so the lack of clinical or electromyographic abnormality in these muscles in no way excludes a lesion at the elbow. Abnormalities of these muscles are more common in lesions in the ulnar groove than compression at the HUA. Sparing seems related to either the redundant innervation via several branchlets from the main ulnar trunk or relative differences in fascicular vulnerabililty. Branches to the FCU do not arise from the ulnar nerve proximal to the elbow.
One of the earliest signs of UNE is weakness of the third palmar interosseous, sometimes manifested by an abducted posture of the small finger (Wartenberg sign). The FDI is easily observed, and the bulk can be palpated and compared with the opposite side. It is particularly useful to test small hand muscles against the strength of an examiner’s like muscles, after the methods described by Wolf. Demonstrating weakness in muscles outside the ulnar nerve distribution is vital for recognizing lower brachial plexopathies, C8 radiculopathies, and motor neuron diseases.
Ulnar nerve lesions in the wrist and hand can cause a confusing array of clinical findings, ranging from a pure sensory deficit to pure motor syndromes with weakness, which may or may not involve the hypothenar muscles. Of the different lesions of the ulnar nerve near the wrist, the most common and extensively reported is a compression of the deep palmar branch. In their now classic article, Shea and McClain classified ulnar compression syndromes of the wrist and hand into 3 types. In type I, the lesion is proximal to or within Guyon canal, involves both the superficial and deep branches, and causes a mixed motor and sensory deficit, with weakness involving all the ulnar hand muscles. In type II, the lesion is within Guyon canal or at the pisohamate hiatus, involves the deep branch, and causes a pure motor deficit with a variable pattern of weakness depending on the precise site of compression. A type III lesion is in Guyon canal or in the palmaris brevis, involves the superficial branch only and causes a purely sensory deficit. In the type I and III lesions, sensory loss should spare the dorsum of the hand, innervated by the DUC branch, and should also largely spare the hypothenar eminence because its innervation is via the palmar cutaneous branch, which arises proximal to the wrist. Other proposed UNW classification schemes add nominal value.
Terminology
Careless use of terms, such as tardy ulnar palsy and cubital tunnel syndrome, has resulted in a nosologic quagmire. In 1878, Panas first described UNE developing long after an elbow injury, and the term, tardy ulnar palsy , was later applied to UNE after remote elbow trauma, generally after an old fracture or dislocation. The term soon degenerated into a nonspecific, generic term for any UNE, on the weak presumption that trauma must have occurred but patients simply could not recall it. The HUA as a site of ulnar compression was first described in 1916 by the British neurologist Dr F. Buzzard and his surgical colleague, Mr P. Sargent. The observation was lost until the 1950s when Osborne, Fiendel, and Stratford rediscovered it. Osborne referred to the condition as spontaneous ulnar paresis. The HUA is sometimes referred to as Osborne band.
Feindel and Stratford introduced the term, cubital tunnel syndrome , to refer to patients with compression of the nerve by the HUA. They were attempting to define a subgroup of patients who suffered from a focal entrapment at the origin of the FCU and who could be spared a transposition procedure and managed with simple release of the aponeurotic arcade. The title of their article is illuminating, The Role of the Cubital Tunnel in Tardy Ulnar Palsy . As with tardy ulnar palsy, the term, cubital tunnel syndrome, soon degenerated into a useless, nonspecific, generic label for any UNE. Most physicians believed cubital tunnel refers to the nerve’s subcutaneous passage through the ulnar groove and that cubital tunnel syndrome is synonymous with UNE, a serious misperception of the original intent. The authors restrict the use of the term to cases due to constriction by the HUA.
Etiology
There are 4 locations in the region of the elbow where the ulnar nerve may suffer compression: at the MIS, in the RTC groove, at the HUA, and at the point of exit from the FCU. Lesions in the RTC groove account for the vast majority of cases, but HUA compression is also common. In the 2 studies that have convincingly addressed the issue, there is remarkable concordance in the incidence of RTC abnormalities (69% and 62%) and HUA abnormalities (ie, cubital tunnel syndrome [23% and 28%]) and changes in both the RTC and HUA (8% and 10%). Other investigators disagree. Kline and colleagues reported 460 cases of ulnar entrapment at the elbow localized with intraoperative NAP inching. Conduction abnormalities always lay just proximal to and through the ulnar groove; there were only 8 cases of HUA entrapment. The exit compression syndrome is infrequent but turns up regularly if examiners are sensitive to its existence. The nerve can rarely be compressed by the MIS or arcade of Struthers proximal to the elbow.
Lesions occur in the RTC groove for several reasons, including acute or chronic external pressure, bony or scar impingement, anomalous muscles or bands, chronic stretch, particularly in the presence of a valgus deformity, and, rarely, mass lesions. In 30% to 50% of cases, no specific cause is discovered in spite of careful investigation, including surgical exposure.
Causes of UNW include extrinsic compressive neuropathy, fractures of the wrist, thrombosis of the ulnar artery secondary to trauma, and masses within Guyon canal, such as a ganglion.
Recurrent subluxation of the ulnar nerve
Subluxation is often listed as a cause of UNE, but its role is far from clear. Childress examined 1000 normal, asymptomatic people and found an incidence of ulnar nerve subluxation of 16%. All these patients were asymptomatic, and the majority had the condition bilaterally. The incidence of subluxation in patients with UNE and how it compares with that in the general population is unknown. It is not clear by any means that subluxation predisposes to UNE and could help prevent UNE by allowing the nerve to escape from a narrow groove during flexion. If subluxation does predispose to UNE, it could be a result of the repetitive rubbing of the nerve across the epicondyle causing a RTC neuropathy (friction neuritis). Just as plausibly, subluxation could cause angulation of the nerve under the HUA during elbow flexion and result in HUA compression.
Electrophysiologic evaluation
Electrodiagnosis can play several roles in the evaluation of ulnar neuropathies. It can document the presence of a mononeuropathy; localize the lesion to any of several locations in the wrist, forearm, or elbow; and distinguish a mononeuropathy from a plexopathy, radiculopathy, polyneuropathy, or motor neuron disease. An abnormality can be confirmed prior to surgery and can be used to quantitate recovery following treatment. There are, however, limited data relating quantitative results of studies with prognosis after surgery. Electrodiagnosis of the ulnar nerve at the elbow is not nearly as straightforward as that of the median nerve at the wrist. The diagnostic yield is less and the interpretations of the data often more difficult. There are many possible techniques to use, and several studies have suggested useful approaches that are not commonly used in EMG laboratories.
Nerve conduction studies
Ulnar Neuropathy at the Elbow
There have been several problem areas in the electrodiagnosis of UNE. These include controversy over the best elbow position, the ideal length of the across-elbow segment, and the value of absolute slowing in the above elbow (AE) to below elbow (BE) segment in contrast to a relative slowing of the AE-BE segment compared with the BE-wrist segment.
Technical errors are a major source of misdiagnosis. Care should be taken to insure supramaximal stimulation, especially at the BE site where the ulnar nerve lies deep in the FCU distal to the HUA. A common error is to stimulate too far posteriorly for the AE site, which can significantly alter the latency. The nerve curves acutely around the elbow and moves quickly toward the biceps, not the triceps. To minimize error, the AE and BE nerve locations can be mapped with submaximal stimulations before carrying out the conduction studies. It is frequently difficult to accurately measure around the curved elbow with a standard flat tape measure. A useful trick is to use a more flexible electrode wire lead to measure, marking the distance from the end of the wire placed at the AE site down to the point of BE stimulation, then laying the wire atop a tape measure to get the distance. The elbow should be in the same position used to obtain the reference values, and no change in position should be permitted between stimulation and measurement.
The difficulties with elbow position relate to the discrepancies between true nerve length and measured skin distance in different elbow positions. In extension, the nerve has redundancy, which progressively plays out with flexion. In extreme flexion, the nerve begins to stretch and slide distally and may partially or completely sublux. In extension, skin distance is falsely short compared with true nerve length, causing spurious and artifactual conduction slowing. In extreme flexion, if subluxation occurs, the skin distance is falsely long, causing spurious quickening.
Checkles and colleagues, in a now classic article, first pointed out the remarkable difference in CV between an extended and a flexed position. Absolute AE-BE NCVs in the range of 35 m/s to 38 m/s and differences in the range of 20 m/s to 30 m/s between the AE-BE segment compared with the BE-wrist segment have been regularly reported in controls studied with the elbow extended. This position-related, artifactual slowing likely explains the high incidence of subclinical UNE reported by some investigators. It is not clear that there is any difference in the relative diagnostic sensitivity of the different elbow positions in detecting abnormalities in patients with clinically defined UNE, as long as appropriate reference values are used. It is clear that consistency is paramount. A standard position must be used for stimulation as well as for the measurement of distance, and this must be the same position used for obtaining the reference values. The American Association of Neuromuscular and Electrodiagnostic Medicine (AANEM) practice parameter on the electrodiagnosis of UNE concluded the most logical elbow position for ulnar conduction studies was moderate flexion, 70° to 90° from horizontal ( Box 1 ).
- 1.
When using moderate-elbow flexion (70°–90° from horizontal), a 10-cm across-elbow distance, and surface stimulation and recording, the following abnormalities suggest a focal lesion involving the ulnar nerve at the elbow:
- a.
Absolute motor NCV from AE to BE of less than 50 m/s
- b.
An AE to BE segment greater than 10 m/s slower than the BE-wrist segment
- c.
A decrease in compound muscle action potential (CMAP) negative peak amplitude from BE to AE greater than 20%
- d.
A significant change in CMAP configuration at the AE site compared with the BE site
- e.
Multiple internally consistent abnormalities
- a.
- 2.
If routine motor studies are inconclusive, the following procedures may be of benefit:
- a.
NCS recorded from the FDI muscle
- b.
An inching study
- a.
- 3.
Needle examination should include the FDI, the most frequently abnormal muscle, and ulnar innervated forearm flexors. If ulnar innervated muscles are abnormal, the examination should be extended to include nonulnar C8/medial cord/lower trunk muscles to exclude brachial plexopathy, and the cervical paraspinals to exclude radiculopathy
The ADM or the FDI for recording may be used; the latter is also useful for identifying lesions of the deep palmar branch. There is value in doing NCV while recording from both the FDI and ADM in order to detect lesions causing selective damage. Although the ADM is more commonly studied, the motor fibers to the FDI are more likely to be abnormal in a lesion at the elbow, and conduction studies are more likely to show conduction block (CB).
After Maynard and Stolov’s influential article on experimental error, a minimum 10 cm across-elbow distance became standard. This article showed specifically how errors in measurement of latency and distance affect calculation of NCV, with errors in latency measurement accounting for 89% of the error, and error from distance measurement accounting for only 11%. A repeat of the same study using computer-automated equipment demonstrated an improvement in latency measurements errors. This improvement in latency measurement, however, did not offset the significantly worsened error, resulting from distance measurements across a nonlinear surface. The distance measurement error for the curved across-elbow segment can be 3 times higher than for a straight-line segment of comparable length. A decrease of greater than 10 m/s between the distal and proximal segments can occur from distance measurement error alone.
Although accepted that longer distance measurements are used to lessen experimental error and improve specificity for diagnosis, focal nerve injuries typically cause abnormalities of nerve conduction over a 1-cm segment. Studying long nerve segments may mask focal slowing by including lengths of normally conducting nerve. Thus, shorter distances are necessary to improve sensitivity. Two independently conducted studies, that equally weighted sensitivity and specificity, concluded that optimal distance to detect focal lesions is approximately 5 cm to 6 cm.
The technical and biologic factors that affect determination of ulnar forearm and across-elbow NCV are different. Technically, the distance measurement for the across-elbow segment is nonlinear and shorter than the forearm segment. Two important biologic variables are body mass index (BMI) and temperature. Each effects NCV determination, but the effects on the across-elbow and forearm segment are different. The across-elbow segment NCV directly correlates with BMI, but the forearm segment does not. As BMI increases, the distance measurement increases and dissociates from the actual nerve distance. Thus, demonstrating a difference in the NCV between the 2 segments is more difficult in those with high BMIs (possible false-negative study) and is easier in those with low BMIs (possible false-positive study).
Ambient temperatures also affect ulnar forearm and across-elbow NCV differently. Low skin temperature causes no appreciable change in forearm NCV but significantly lower across-elbow NCV. The deep location of the forearm segment presumably insulates this segment from surface temperature fluctuations, whereas the superficial location of the across-elbow segment makes it more susceptible to temperature effects. This discrepancy can be seen when there are no other indications from other nerve conduction studies of cool temperature effects (eg, prolonged peak latencies of sensory potentials). Failure to maintain adequate temperature of the across-elbow segment may, therefore, lead to false-positive studies and should be warmed particularly when there are no other clinical or electrodiagnostic findings that support the diagnosis of UNE (cold elbow syndrome). The continued use of the forearm NCV as an internal control variable for diagnosis of UNE should be reconsidered.
All or most cases of UNE demonstrate demyelinating abnormalities. Focal demyelination at the elbow leads to an excessive dispersal of conduction velocities of the motor axons, which produces a low amplitude, long duration, fragmented CMAP on stimulation proximal to the elbow compared with stimulation distal to the elbow. A decline in total area under the CMAP curve correlates better with true CB, but temporal dispersion (TD) is just as suggestive of focal demyelination. A reduction in amplitude of more than 20% or a significant change in CMAP configuration between the BE and AE sites is suggestive of UNE. A reduction in amplitude of more than 25% was the best criterion for localization in one study.
Some patients with UNE have no or minimally detectable conduction velocity abnormalities, the so-called pure axon loss ulnar neuropathy. Sensory and motor studies demonstrate decreased amplitudes and slowing of NCV consistent with axonal loss but no differences between across-elbow and forearm NCVs. In nearly all cases, however, if other muscles are used to measure NCV (ie, FCU or FDI) or short-segment studies are performed, focal demyelination can be disclosed.
The distal sensory nerve action potential (NAP) is a sensitive indicator of ulnar nerve function. Most patients with UNE have a low amplitude or absent NAP, although it is a nonspecific, nonlocalizing, finding. A lesion at the elbow can sometimes be identified by sensory studies using needle electrodes to record possible focal slowing and NAP dispersion at the elbow, especially in patients with only sensory symptoms. Such NAP studies have significant pitfalls and limitations and should only be used if the examiner is fully aware of the technical details and the applicable literature.
Motor conduction studies in patients have shown localizing abnormalities in symptomatic elbows with a sensitivity of 37% to 100%. Eisen demonstrated 53% sensitivity in severe cases and 27% in mild cases. In general, change in the absolute CV is a more sensitive indicator of abnormality than is abnormality of the relative CV. The results of various studies are reviewed in detail by Campbell and colleagues.
An ancillary technique measures ulnar nerve conduction to the FCU. Benecke and Conrad found the technique equally sensitive to motor conduction to the ADM. Payan was able to localize the lesion to the elbow in another 10 of his 50 cases with this method. The technique is limited by the nerve fibers to the FCU tending to be spared in UNE.
Ulnar Neuropathy at the Wrist
Assessment of conduction to the FDI muscle, in addition to the routine motor latencies to the ADM, is integral to the evaluation of distal ulnar neuropathies. Olney and Wilbourn studied conduction to the FDI and ADM in 373 nerves, determining absolute distal motor latency (DML) to the FDI as well as differences between the latency to FDI and the ADM on the same side and differences in the side-to-side FDI latencies. With stimulation at the proximal wrist crease, 5.5 cm to 6.5 cm proximal to the ADM recording site, the upper limit of normal for DML was 3.4 ms to the ADM and 4.5 ms to the FDI. There was an increase of approximately 0.5 ms per decade in the DML to each muscle, but advancing age did not significantly alter the side-to-side latency difference or ipsilateral muscle-to-muscle difference. According to this study, the side-to-side difference in DML should not exceed 1.0 ms for the ADM or 1.3 ms for the FDI. The ipsilateral difference in DML to the ADM versus FDI should not exceed 2.0 ms. A CMAP amplitude less than 6 mV for the FDI and less than 5 mV for the ADM was considered abnormal.
A lesion of the deep palmar branch, beyond the branches to the hypothenar muscles, causes prolongation of the DML to the FDI in the face of a normal motor latency to the ADM and normal sensory studies. Even if the DML is not prolonged, the CMAP may demonstrate fragmentation, dispersion, or CB. Needle electrode examination (NEE) typically shows denervation in all the ulnar intrinsic hand muscles except those of the hypothenar eminence. A sequential assessment of the first through the fourth dorsal interossei can sometimes provide precise localization. When the lesion involves the volar sensory branch alone, only the distal sensory action potentials are abnormal.
As with carpal tunnel syndrome, some ulnar lesions at the wrist cause mild secondary slowing of motor conduction velocity in the forearm segment. Care must be taken in the final assessment to determine the site of most significant slowing, and the final electrophysiologic diagnosis should reflect the perspective of the entire picture.
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