Ulnar Neuropathy

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Background

The ulnar nerve is an extension of the medial cord of the brachial plexus. It is a mixed nerve that supplies innervation to muscles in the forearm and hand and provides sensation over the medial half of the fourth and the entire fifth digit of the hand (the ulnar aspect of the palm) and the ulnar portion of the posterior aspect of the hand (dorsal ulnar cutaneous distribution).

The most common site of entrapment is at or near the elbow region, especially in either the region of the cubital tunnel[1] or the ulnar groove. The second most likely location of entrapment is at or near the wrist, especially in the area of the anatomic structure called Guyon's canal.[2] However, entrapment can occur in the forearm between these 2 regions, below the wrist within the hand, or above the elbow.

As diagnostic and surgical methodologies have evolved over the past century, our ability to recognize and describe sites of entrapment has improved. However, the terminology has become confusing due to the fact that not all clinicians utilize uniform terminology.

First, let us examine ulnar nerve entrapment in the elbow region[3] , the most common location. The two most commonly used (and misused) terms for such entrapments are tardy ulnar palsy[4] and cubital tunnel syndrome[5] .

In 1878, Panas first described what we now often call tardy ulnar palsy.[6] He presented 3 cases in which either prior trauma or osteoarthritis gradually caused damage to the ulnar nerve. The basic idea behind using the word tardy was that the problem appeared late after an injury or a long course of osteoarthritis (possibly together with an old injury) as opposed to a more immediate or early palsy in which the ulnar nerve showed dysfunction directly after trauma, such as what might occur in an injury that caused either total or partial transection.

Subsequent to Panas' paper, other case reports appeared. John Murphy published the first case in the American literature in 1914.[7] Walter Brickner reported a case in 1924.[8] The initial cases of tardy ulnar palsy were usually associated with trauma (eg, fractures in the region of the elbow), and the typical site of nerve entrapment was the ulnar groove, ie, the location between the medial epicondyle of the humerus and the olecranon.[9, 10] In addition to a time-based definition (ie, tardy=appears some years after trauma), an anatomical aspect of the term came to pass (ie, tardy=usually in or very near the ulnar groove).[11]

Later, physicians began to recognize ulnar entrapments in the humeroulnar arcade (HUA). This is the region of the aponeurosis of the 2 heads of the flexor carpi ulnaris (FCU) muscle. The aponeurosis is a fibrous or membranous sheet that connects muscles to bones or other structures that the muscles move. The aponeurosis can be thought of as a flattened tendon. The first description of an ulnar nerve entrapped in this region, together with its surgical decompression, was given by Buzzard and Sargent in 1922.[12, 13] The next published description was by Osborne in 1957. In 1958, Feindel and Stratford reported 3 more such cases and coined the term cubital tunnel syndrome to describe the effects of the ulnar nerve entrapment[14] at the HUA. Numerous other reports ensued.

Our current state of knowledge is still rather incomplete, but now we can identify approximately 5 sites in the elbow region at which the ulnar nerve is most likely to be compressed. The word approximately is used deliberately, because some of the sites are so close together that certain authorities categorize them differently to get a different number. This article principally follows the classification of Posner,[15] with some comments about the classification of other authors. The sites, according to Posner, are as follows:

Above the elbow in the region of the intermuscular septum

Halikis et al[16] divides this into 2 regions—the arcade of Struthers[17, 18] and the medial intermuscular septum. Via the standard anatomic definition, the arcade of Struthers is a thin fibrous band that usually extends from the medial head of triceps to the medial intermuscular septum. It is often said to be about 6-10 cm proximal to the medial epicondyle.

Considerable anatomic variation exists and, in fact, there is outright controversy about the arcade of Struthers.[19]

One such controversy is quite trivial, as no evidence exists that Dr. Struthers discovered this structure or was even aware of it. His name was attached to it by Kane et al in their 1973 paper.[20]

An autopsy study by Siqueira of 60 upper limbs found a structure reasonably approximating the definition given above in 8 limbs (13.5%).[19] Ulnar nerve entrapment occurred in none of them (but there was no reason to clinically expect that there might have been).

Bartels et al could not find this structure in their dissections and they doubt that it exists.[21]

Wehrli and Oberlin have described a different structure in the same region, the internal brachial ligament rather than the arcade of Struthers, that might be involved in ulnar entrapment in some cases.[22] Interestingly, Struthers did describe the existence of this structure, but not in relation to ulnar nerve entrapment. Wehrli and Oberlin advocate "cancelling the concept of the arcade of Struthers."

In contrast, von Schroeder and Scheker find yet another structure, a fibrous tunnel in roughly the same region.[23] They say that the ulnar nerve goes through this tunnel and could be trapped therein and are in favor of naming their structure the arcade of Struthers.

Settling this controversy is beyond the scope of this article. Suffice it to say that in rare cases, the ulnar nerve is compressed considerably above the ulnar groove and that surgeons may find it entrapped in a fibrous/ligamentous structure that may correspond to one of the aforementioned terms.

Medial epicondylar region

Ulnar compression[24] in this region is generally from a valgus deformity of the bone. If a patient is placed in standard anatomical position with palms rotated toward front, thumb away from midline, valgus deformity means the elbow would be deformed away from midline of the body.

Epicondylar groove

This is the same as the ulnar groove. It is a bit distal to the medial epicondyle (or at least to the beginning of it).

Using slightly different terminology, Campbell lumps the medial epicondylar region and the epicondylar groove together as the area of the retrocondylar groove.

Halikis et al consider the medial epicondylar region and the epicondylar groove to be the area of the medial epicondyle.[16]

Both the medial epicondylar region and the epicondylar groove are generally considered to be the classical location (or locations) for the tardy ulnar palsy.

In the author’s personal experience, electromyographers and orthopedic surgeons more commonly refer to a tardy ulnar palsy at the retrocondylar groove, thus using the Campbell terminology.

The region of the cubital tunnel

The main source of compression is a thickening of the Osborne ligament.

Campbell's classification is basically the same for this region, except he no longer uses the term cubital tunnel. He refers to this as the region of the HUA, apparently because he believes so many clinicians loosely use the term cubital tunnel to refer to a place anywhere in the elbow.

Halikis et al divide this region into 2 parts—the cubital tunnel and the Osborne fascia.[16] This is a good example of the difficulty with the terminology. Different terms are used for locations that are virtually the same. For all practical purposes, certainly for anything one can distinguish on EMG, Osborne ligament=Osborne fascia=the HUA.

The cubital tunnel is the space bounded by the following:

The region at which the ulnar nerve exits from the FCU at which the usual cause of compression is the deep flexor-pronator aponeurosis

Campbell[25] and Halikis et al[16] also list this as the final site at the elbow. See the image below.


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This is a schematic diagram of the elbow region. The 5 main sites as given by Posner are labeled 1-5. Other sites and structures are also named. The m....

After the ulnar nerve passes distal to the elbow,[26, 27, 7] it makes several important divisions. The first branches to come off are those that go to the FCU. Further distally, the branches to the flexor digitorum profundus muscles of digits 4 and 5 arise.

As the ulnar nerve courses down the forearm toward the wrist, the dorsal ulnar cutaneous nerve leaves the main branch. A little further down, the palmar cutaneous branch takes off. Thus, neither of these 2 branches goes through Guyon canal.[2] The remainder of the ulnar nerve enters Guyon canal at the proximal portion of the wrist. This is bounded proximally and distally by the pisiform bone and the hook of hamate bone. It is covered by the volar carpal ligament and the palmaris brevis muscle. Although the nerve could be injured or entrapped at any point along its course, the 4 most common locations in relation to Guyon canal are shown in the following image.


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This diagram shows the ulnar nerve distal to the elbow region. The dorsal ulnar cutaneous nerve (lavender) branches off the main trunk (blue). Althoug....

Pathophysiology

The nerve, axon, and myelin can be affected. Within the axon, fascicles to individual muscles may be involved selectively. Axonal involvement leads to motor unit loss and amplitude/area reduction. Conduction block implies impaired transmission through a segment of nerve. In the absence of changes indicating axonal damage, conduction block implies myelin damage to the involved segment. Significant slowing of conduction and/or significant spreading out of the temporal profile of the recorded response (ie, abnormal temporal dispersion) with preserved axonal integrity suggests demyelination.

Epidemiology

Frequency

United States

In the general population, abnormalities in the ulnar nerve at the elbow in asymptomatic subjects are common (about 40%).

The elbow is the second most common site of nerve entrapment in the upper extremity, the first being the wrist (ie, carpal tunnel syndrome).

Mortality/Morbidity

Delayed recognition of ulnar neuropathy at the elbow or wrist or unsuccessful surgical intervention can lead to loss of function due to prolonged axonal degeneration.

Sex

No gross anatomical differences in the course of the nerve are noted between the sexes. However, the following have been noted.[28]

Age

According to the older literature, most cases of ulnar compression neuropathy occur in patients older than 35 years.[31] This is consistent with an independent anatomical study of 200 cadavers showing that the ulnar nerve is largest at the entrance to the cubital tunnel and that this enlargement is of maximal size in males older than 35 years.[32] A prospective study of 76 patients showed that increased age is highly correlated with a greater tendency toward ulnar neuropathy.[30]

History

Both the onset and progress of the symptoms can be variable. Although the answer is frequently negative, one should ask specifically about trauma and pressure to the arm and wrist, especially the elbow, the medial side of the wrist, and other sites close to the course of the ulnar nerve.

Many patients complain of sensory changes in the fourth and fifth digits. Rarely, a patient actually notices that the unusual sensations are mainly in the medial side of the ring finger (fourth digit) rather than the lateral side, corresponding to the textbook sensory distribution. Sometimes the third digit is also involved, especially on the ulnar (ie, medial) side. The sensory changes can be a feeling of numbness or a tingling or burning. Pain rarely occurs in the hand. Complaints of pain tend to be more common in the arm, up to and including the elbow area. Indeed, the elbow is probably the most common site of pain in an ulnar neuropathy. Occasionally, patients specifically say “I have pain in my elbow,” “I have pain in my funny bone,” or even “I have pain in this little groove in my elbow,” but usually they are not quite so explicit unless prompted. Patients rarely notice specific muscle atrophy, but when they do, they often complain that their hands "lookolder."

Weakness may also be a presenting complaint, but the complaint may be expressed in subtle ways.

One traditional sign of ulnar neuropathy, Wartenberg sign, is actually a complaint of weakness. The patient complains that the little finger gets caught on the edge of the pants pocket when he or she tries to place the hand into the pocket. At first, that complaint seems surprising because most physicians remember that finger abduction is governed by the ulnar nerve. So the physician might think that with an ulnar neuropathy, the patient would have less tendency to have the little finger abducted and thus caught on the edge of the pocket. But adduction is also mediated by the ulnar nerve. In essence, the patient cannot abduct the fifth digit tightly against the fourth because of weakness of the interosseous muscles.

In addition, the muscle that extends the fifth digit at the metacarpal phalangeal joint (extensor digiti quinti) is radially innervated and it inserts on the ulnar side of the joint. Normally this muscle is opposed by ulnar innervated muscles that flex the joints. But with an ulnar neuropathy, the muscle is relatively unopposed so it pulls the finger up and to the ulnar side. This is the perfect position to catch onto the edge of the pocket.

The patient also may express the complaint of weakness by saying “my grip is weak.” Many of the grip muscles are ulnar. Also, when someone tries to grip powerfully, the hand usually deviates in the ulnar direction under the influence of the flexor carpi ulnaris. If this ulnar deviation is impaired, the grip mechanism does not work optimally even for the muscles that are unimpaired.

Sometimes a patient notices that his pincer grip (pinching with the thumb and index finger) is weak. Two of the key muscles involved in this movement are the adductor pollicis (which adducts the thumb) and first dorsal interosseus, which adducts the index finger. Not only may the pincer grip be weak in an ulnar neuropathy, the median innervated flexor pollicis longus partially compensates for the weakened adductor pollicis and the thumb flexes at the distal joint. Usually a patient does not notice the thumb flexion, but when demonstrated by the examiner, this flexion is considered to be Froment sign.

Physical

On physical examination, numerous findings offer clues to the existence of ulnar compression.

In addition to assessing sensation and testing individual muscle strength, inspection of the hand may reveal a clawed posture (called main en griffe in French).

Several factors contribute to the clawed appearance. Wasting of the intrinsic muscles of the hand makes it look bonier. The fourth and fifth digits extend at the metacarpal phalangeal joint because the extensors at that joint are radially innervated, whereas the flexors are innervated by the ulnar. Also, the fifth digit deviates slightly in the medial direction because, as explained for Wartenberg sign, the muscle that extends the fifth digit at the metacarpal phalangeal joint is radially innervated and it inserts on the ulnar side of the joint.

The fourth and fifth interphalangeal joints flex because for them the extensor muscles are also ulnar and the natural tension of the muscles and tendons in the absence of strong muscle activity in either direction leads to flexion. The first 3 digits are extended at both the metacarpal phalangeal joints and the interphalangeal joints because of the unopposed radial nerve innervation. All these factors make the hand look somewhat like a claw.

A different interpretation of the posture is that it looks like the hand gesture that a priest makes in the process of conferring a blessing, and thus it is sometimes called the benediction sign or the benediction hand.

Froment sign is an observable sign that correlates with the complaint of weakness of the ability to pinch normally between the first and second digits.

This sign is sometimes elicited by asking the patient to grasp a piece of paper between the thumb and index finger. Ordinarily, the grasp is tight and the patient makes heavy use of the adductor pollicis to adduct the thumb and the first dorsal interosseus to move the index finger.

In addition to overt weakness of the pinch, the examiner also notes that the thumb flexes at the interphalangeal joint because the flexor pollicis longus activates in an attempt to compensate for the weakness. Thus, in addition to the weakness, the examiner sees the flexion of the tip of the thumb.

Ulnar neuropathy at the elbow

Positive Tinel sign at the elbow

The examiner taps with a reflex hammer over the ulnar nerve in the ulnar groove and a little further distal over the cubital tunnel. The test is positive if the patient experiences definite paresthesias in the ulnar portion of the hand, especially the last 2 digits. This test is not considered highly sensitive, but it is considered to be quite specific if performed properly (eg, not hit too hard). If the examiner hits hard enough, many normal individuals experience paresthesias in the fourth and fifth digits. Assuming the complaint is unilateral, the opposite side is a good control for this. Sometimes palpating the nerve in the ulnar groove may produce a similar result.

Atrophy and muscle weakness

The most important ulnar hand muscles to test are the first dorsal interosseous and the abductor digiti minimi (abductor digiti quinti). In the forearm, the flexor digitorum profundus of the fourth and fifth digits (which flexes the distal phalanges of those fingers) and the flexor carpi ulnaris (flexion at the wrist in the ulnar direction) are valuable to examine. Of these latter 2 muscles, it is not uncommon for the flexor carpi ulnaris to be spared in ulnar lesions near the elbow, especially the lower (more distal) lesion near the elbow. Sparing occurs because the branch to the flexor carpi ulnaris splits off from the main trunk prior to (ie, above or proximal to) the compression.[33]

The ulnar muscles should not be examined in isolation from other muscles. In particular, several key muscles with C8/T1, lower trunk, medial cord innervation should be examined, especially the abductor pollicis brevis (a thenar muscle typically involved with carpal tunnel syndrome, the major compressive median nerve neuropathy) and the median innervated long thumb and index finger flexors.

If both the ulnar intrinsics hand muscles and the ulnar forearm muscles are involved, then an ulnar nerve lesion should be suspected in the region of the elbow (or, very rarely, above the elbow region). If the ulnar forearm muscles are spared, considering the possibility of a lesion at the wrist is reasonable, but extra caution is warranted in this case. Sometimes the forearm muscles are spared with a lesion near the elbow, especially if the lesion is in the lower elbow region in or around the cubital tunnel. Even for higher elbow lesions, there can be considerable selectivity in which muscles are affected because the ulnar nerve is organized into a number of separate fascicles. Sometimes some fascicles are severely affected by whatever is pinching the nerve and other fascicles are unaffected. If other C8/T1, lower trunk, medial cord muscles are affected, a C8/T1 radiculopathy or a brachial plexus lesion may be the cause.

Ulnar neuropathy at or distal to the wrist

Weakness of the interossei and hypothenar muscles only with no sensory loss: This would most likely be due to compression of the deep motor branch in the hand after it had separated from the superficial terminal sensory branch but before the branch to the hypothenar muscles had taken off.

Interosseus weakness only with no sensory loss: This would most likely be due to compression of the deep motor branch after the branch to the hypothenar muscles has taken off.

Weakness of the interossei and hypothenar muscles with sensory involvement in the fifth digit: This would suggest involvement in Guyon canal with compression of both the deep motor branch and the superficial terminal sensory branch. This might be said to be the typical or classical Guyon canal pattern.

Pure sensory loss with normal dorsal ulnar cutaneous sensory nerve, normal palmar cutaneous sensory nerve, and normal motor responses: This would imply injury to the superficial terminal sensory branch alone, probably a compression distal to Guyon canal.

Interossei weakness and sensory loss with preserved function in the hypothenar and dorsal ulnar cutaneous territories: This would imply a compression of the deep motor branch and the superficial terminal sensory branch distal to the point where the sub-branch to the hypothenar area (eg, the ADM) had split off the deep motor branch.

Sensory examination

Adding information from the sensory examination to that of the motor examination helps to localize the ulnar lesion. The image below, which has been discussed earlier in the context of the anatomy of the ulnar nerve, shows the ulnar sensory regions on the hand. Jacob et al have published a beautiful case report, complete with MRI pictures, on such a case.[34]


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This diagram shows the ulnar nerve distal to the elbow region. The dorsal ulnar cutaneous nerve (lavender) branches off the main trunk (blue). Althoug....

Although the area of the palmar cutaneous sensory nerve can extend a bit more proximal than shown, if the sensory involvement extends more than an inch above the wrist crease along the medial aspect of the forearm, the nerve roots (C8/T1) or brachial plexus most likely are involved (but in some cases this could be in addition to an ulnar injury).

As previously noted, both the palmar cutaneous sensory branch of the ulnar and the dorsal ulnar cutaneous branch come off of the main ulnar branch above (proximal to) the wrist. Thus, a lesion exclusively at the wrist (Guyon canal) would miss these branches and the superficial terminal branch would be the only sensory involvement. However, a physician must be cautious in interpretation.

Typically, neuropathic damage, whether generalized or related to nerve compression, affects (or is perceived to affect) the most distal parts of the nerves preferentially. A compression at Guyon canal might be perceived by the patient and might be detectable on examination only in the tips of the fingers. Thus, the compression would appear to be affecting only the superficial terminal branch.[35, 36, 37]

Causes

Ulnar nerve at or near the elbow

Ulnar neuropathy at or distal to the wrist (ie, at Guyon's canal)

Laboratory Studies

Consider the following peripheral neuropathy workup depending on the specific clinical situation:

Imaging Studies

Ultrasonography

Ultrasonographic examination of peripheral nerves may be used to support the clinical and electrophysiologic diagnosis in a compressive neuropathy. It may also be helpful in identifying specific compressive etiologies of nerve injury (tumors, cysts, etc) and in visualizing structural nerve changes. Advantages of ultrasonography include the following:

The ultrasonography finding that seems to be the most useful is a change in the diameter of a nerve at the site of compression. Just proximal to the site of compression, swelling of the nerve can often be seen. One small study hypothesized that using a ratio of the cross-sectional nerve area at the site of maximal enlargement and at an uninvolved site could improve diagnostic accuracy. Using this ratio did not add any diagnostic accuracy to simply looking for the point of maximal swelling; the ratio did, however, help distinguish compressive neuropathies from other systemic processes associated with diffuse nerve enlargement (eg, diabetes, polyneuropathy).[49] More recently, another study[50] examined nerve vascularity in 137 patients afflicted with ulnar neuropathy at the elbow and determined that increased intraneural vascularization seen by ultrasonography was indicative of axonal damage.

One specific area in which ultrasonography may be useful is the evaluation of traumatic peripheral nerve injuries. In one interesting study, 20 fresh cadaver arms were disarticulated, and the median, ulnar, or radial nerves were randomly transected in 0-2 locations per arm. Sham incisions were performed throughout the extremity. The peripheral nerves were then systematically scanned by ultrasonographers who were blinded to the sites of transection.

High-resolution ultrasonography was able to identify transected nerves with 89% sensitivity and 95% specificity. The diagnostic accuracy improved throughout the study; with the first 10 arms, the ultrasonographer correctly identified the transection in 77% of cases. With the final 10 arms, the accuracy was 100%.

This suggests that the experience of the ultrasonographer plays a vital role in the use of ultrasonography in peripheral nerve injury. The study suggests that ultrasonography may be useful both in prognostication of nerve injury when an experienced ultrasonographer can assess for a partial versus complete nerve injury, and/or in localizing a nerve transection for possible surgical repair.[51, 52]

Magnetic resonance imaging

MRI is being increasingly used in the evaluation of peripheral neuropathies, including ulnar neuropathy. In most patients, history, physical examination, and electrophysiologic testing are sufficient to make the diagnosis of ulnar neuropathy. However, there may be a subgroup of patients with inconclusive findings on the standard evaluation in whom MRI may be beneficial.

On MRI, normal nerves appear as smooth, round, or ovoid structures that are isointense to surrounding muscles on T1-weighted sequences. There is often a rim of hyperintense signal on T1. On T2-weighted images, the nerve is normally isointense to slightly hyperintense with respect to surrounding muscle. Normal nerves do not enhance after administration of gadolinium.

Possible changes that could be seen in neuropathies include increased signal intensity within the nerve on T2-weighted sequences. Neurogenic muscle edema can be seen as early as 24-48 hours after denervation, and STIR sequences are particularly sensitive for that. This is to be contrasted with electrophysiologic testing, in which changes after denervation are not seen for 1-3 weeks. After months of denervation, fatty muscle atrophy is seen. Changes in the surrounding structures that may be related to the neuropathy in question, such as osteoarthritis, synovitis, or tumors, can be seen with MRI as well.[53]

Several small studies exist that attempt to address the use of MRI in the diagnostic evaluation of ulnar neuropathy. In one study by Vucic et al, 52 patients were identified who met clinical criteria for ulnar neuropathy, based on either sensory symptoms or motor weakness in the distribution of the ulnar nerve. All of these patients underwent electrophysiologic testing. In 63%, the electrophysiologic studies were diagnostic of an ulnar neuropathy at a specific location, commonly at the elbow. In 37%, the EP studies were nonlocalizing based on the criteria of the American Association of Electrodiagnostic Medicine.

All patients subsequently underwent MRI scanning as well, which revealed abnormalities in 90% of patients. In the subgroup of patients who had diagnostic EP studies, 94% had an abnormal MRI; in those who had nondiagnostic EP studies, 84% had an abnormal MRI. The authors' conclusion was that MRI was "more sensitive" than neurophysiologic testing, and that the sensitivity of MRI does not change, regardless of the EP results.[54]

Another study by Andreisek et al looked at 51 patients with clinically evident neuropathies in either the radial, median, or ulnar nerves who were referred to their center for MRI scans of an upper extremity. This study was designed to assess the impact of the MRI results on clinical decision making and patient management. In summary, this study found only a weak/moderate correlation between MRI results and clinical findings, which the authors felt was not surprising given that clinical findings imply physiologic dysfunction of the nerves, whereas MRI findings can evaluate nerve morphology alone. The authors reported that the greatest use of MRI in this study seemed to be in the patients in whom the etiology of their symptoms was unclear; in these cases, the MRI scan was said to have found the etiology of the symptoms in 93% of cases. This resulted in a moderate to major impact on treatment in 84% of patients in this subgroup.[55]

Despite the seemingly positive results of these 2 studies, some caveats should be applied. Firstly, imaging criteria for diagnosing neuropathy on MRI scans are not well-defined. Furthermore, the clinical significance of certain MRI findings has been called into question. A study by Husarik et al took 60 asymptomatic patients and performed MRI scans of their elbows. In these healthy volunteers, 60% had increased signal intensity of their ulnar nerves without accompanying changes in the medial or radial nerves. This study suggests that an increase in signal intensity should not be used as the only criterion when evaluating for possible ulnar neuropathy.[56]

The role of MRI in the evaluation of ulnar and other peripheral neuropathies continues to evolve. At this point, it seems safe to conclude that MRI may be a useful adjunct in select cases, either when a specific compressive lesion such as a mass is suspected, or when a patient with the clinical syndrome of ulnar neuropathy has nondiagnostic electrophysiologic tests. To improve diagnostic accuracy, further research is required to develop standardized criteria to make the diagnosis of ulnar neuropathy on MRI.[55, 56, 57, 58]

Other Tests

Nerve conduction studies

This test measures basic sensory and motor nerve parameters such as latency, amplitude, and conduction velocity.

Electrodes (metallic reusable or pregelled disposable tape) are placed over the main belly of the muscle (active) such as the abductor digitorum quinti (ADQ) or first dorsal interosseous[59] (FDI) and the tendon of the fifth or first digit, respectively.

The ulnar nerve is stimulated at the wrist and above and below the elbow. This helps localize the site of involvement.

Short segment stimulation (also known as the inching technique) can increase the sensitivity of this method and can possibly improve the localization by helping the examiner judge whether a blockage is infracondylar (ie, near the cubital tunnel) or higher, near the ulnar grove (ie, near the location associated with tardy ulnar palsy) (see image below). In fact, one can try to choose one of the 5 or 6 locations previously mentioned; however, the exact course of the ulnar nerve is impossible to know in any given case. Considerable anatomic variation exists from person to person and even controlling the angle of the elbow does not determine exactly where the nerve is running beneath the skin. Thus, one really does not know exactly where the nerve is being stimulated. The take-off point of the impulse may not be exactly under your stimulator.

See the image below.


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An example of the inching technique used to isolate conduction block in the left ulnar nerve. Note the significant amplitude drop at the 305-mm distan....

A good percentage of experienced electromyographers believe that usually the best that can be done is to say whether or not a blockage exists at the elbow. Often even that cannot be done for sure. For a discussion of the anatomic variation, see Campbell, 1991.[25] The reader is invited to try the inching technique and report to the prospective surgeon where he or she thinks the blockage might be with respect to anatomical landmarks. Report this as tentative information, ie, the best you can do but not to be taken as definite, and ask the surgeon to tell you where the blockage actual seemed to be if surgery is performed. Keep track and draw your own conclusions about how accurate this method is in your own hands. Even attempting to use the inching technique may help you by making you more conscious of the anatomy, even if it does not give you the exact localization.

Needle electrode examination

Evaluation of motor unit morphology and recruitment patterns

Ascertains ongoing loss of muscle fibers via detection of abnormal spontaneous activity (eg, fibrillation potentials and fasciculations)

Checks the integrity of the muscle membrane to expand differential diagnosis (eg, myotonia, paramyotonia, periodic paralysis) as manifested by increased insertional activity such as complex repetitive discharges, myokymia, and (para)myotonic discharges

Histologic studies

Nerve enlargement in cases of entrapment typically occurs proximal to the point of compression.

Nerve compression leads to a cascade of edema, demyelination, inflammation, axonal loss, fibrosis, and remyelination with subsequent thickening of the perineurium and endothelium.

Martin-Gruber anastomosis

This anatomic variant is seen during routine nerve conduction studies and can pose a diagnostic dilemma if not identified as such. Martin originally described it in 1763. Gruber's paper appeared over a century later in 1870. It is a anomalous pattern of innervation occurring between the median and ulnar nerves in the forearm.[60]

In Martin-Gruber, a crossover of axons from the anterior interosseous nerve (exclusively motor branch of the median) to the ulnar nerve in the forearm usually occurs. In such cases, no sensory fibers are involved in the crossover. However, in a small minority of cases, the crossover can occur from the main median trunk (in which case some sensory nerve fibers may cross over as well).

Martin-Gruber occurs in 10-30% of individuals and 60-70% of those affected show the anomaly bilaterally. In some families, an autosomal dominant inheritance is possible, although a gene controlling this occurrence has not been identified.

The fibers involved are from the C8/T1 nerve roots. Three patterns of Martin-Gruber are commonly recognized. In type II, the most common pattern, the crossover fibers innervate the first dorsal interosseus (FDI). In type I, the next most common pattern, the hypothenar muscles are involved. In type III, the least common pattern, the thenar muscles, typically the adductor pollicis and the flexor pollicis brevis rather than the abductor pollicis brevis, are involved. Sometimes other muscles, including forearm muscles such as the flexor digitorum superficialis and the flexor digitorum profundus, are involved as well. These 3 common types are delineated in the following image.


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The normal median and ulnar pattern are compared with that of the 3 commonly recognized types of the Martin-Gruber anomaly.

In the patient without Martin-Gruber anomaly, stimulating the median nerve at the wrist produces a compound muscle action potential (CMAP) amplitude at the thenar eminence (eg, abductor pollicis brevis [APB]) that is essentially the same size as the thenar CMAP produced by elbow stimulation (the CMAP produced by wrist stimulation could be a bit larger because stimulating further away from the ultimate target muscle gives a little more temporal dispersion of the signal). With the anomaly, however, the wrist response is smaller because many axons from the median nerve have crossed already. Contributions from now median-innervated ulnar intrinsic hand muscles falsely increase the elbow response.

The converse applies with ulnar nerve stimulation, when recording over the hypothenar eminence (ADQ) or FDI, as median nerve fibers are innervating ulnar muscles in the hand, and the elbow response is smaller (see images below). This could be mistaken for a conduction block. Thus, a Martin-Gruber anastomosis should be excluded prior to diagnosing ulnar conduction block.


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The first 3 traces correspond to the ulnar compound muscle action potential (CMAP) amplitude while recording at the abductor digitorum quinti (ADQ) an....


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The first 3 traces correspond to stimulation of the ulnar nerve while recording at the first dorsal interosseous (FDI) muscle at the wrist, below the ....

To see these relationships even more clearly, the image below shows the same anatomical diagrams as the image above, plus the corresponding EMG patterns.


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In people with the Martin-Gruber anomaly who do not otherwise have significant neuropathy or nerve compressions, here is what happens when the relevan....

Table 1 below explains in words why the patterns look the way they do. If you really want to understand this, you may need to print these out and sketch them yourself a few times. This table describes the 3 major types of the Martin-Gruber anastomosis and shows the pattern of CMAP response at the thenar eminence, the FDI, and the hypothenar muscle in people who have the Martin-Gruber anomaly but do not otherwise have significant neuropathy or nerve compressions.

Two potentially important diagnostic implications are associated with this Martin-Gruber anomaly.

First, in cases of carpal tunnel syndrome (ie, median mononeuropathy at the wrist), the larger median CMAP amplitude at the elbow has an initial positive (ie, downward) deflection, which is not seen at the wrist. This is explained by the fact that the median nerve axons are traveling slower through the carpal tunnel so that the median-innervated ulnar hand muscles conduct first, leading to a volume-conducted response that is manifested by a positive deflection. If carpal tunnel syndrome is suspected clinically, the chance of a false-negative result on nerve conduction testing is still about 8-10%. Given that the anomaly exists 15-31% of the time, a chance still exists of diagnosing carpal tunnel syndrome electrically.

Second, in suspected cases of ulnar neuropathy at the elbow or forearm, a reduced-to-absent response would be expected proximally with sparing of the wrist responses, provided that no diffuse severe axon loss has occurred. To disprove a true ulnar neuropathy, stimulation of the median nerve at the elbow would lead to a wrist response that, when added to the response achieved by stimulating the ulnar nerve at the elbow, would equal a difference of less than 20-25% between elbow and wrist, which is acceptable as normal temporal dispersion. Stimulation of the median nerve at the wrist should lead to a small response, as this would represent contributions from ulnar-derived muscles in the thenar eminence.[61, 62, 63, 64]

The table below summarizes tests for Martin-Gruber anastomosis.

Table 1. Martin-Gruber Anastomosis


View Table

See Table

Riche-Cannieu anastomosis

Another anomaly that can complicate diagnostic studies is the Riche-Cannieu anastomosis.

See the image below.


View Image

The Riche-Cannieu anastomosis is a communication between the recurrent branch of median nerve and deep branch of ulnar nerve in the hand. Although it ....

Medical Care

Medical and other nonsurgical treatments can provide significant help in cases of ulnar neuropathy. Vasculitic and metabolic causes can be evaluated and diagnosed to facilitate treatment of the underlying condition.

The physician can address pain or other sensory symptoms using trials of various classes of pain medications including:

Occupational therapy and work hardening programs are also beneficial. Therapists may use and design splints to restrict the range of joint motion and cushions to ameliorate the effects of pressure.[65]

Use of a night splint is a common occupational or physical therapy technique that aims to limit the flexion and extension of the elbow at night. This has shown some efficacy in clinical trials.[66] Therapists also use nerve gliding, sliding, or tensioning exercises which seek to promote smoother movements of the nerve within the cubital tunnel and to reduce adhesions and other causes of physical nerve compression.[67] A randomized, controlled study of conservative methods to treat mild and moderate ulnar neuropathy at the elbow indicated that simply giving patients information about how to avoid injuring the ulnar nerve by avoiding or reducing movements or positions that compromise the nerve produced significant symptomatic improvement. Interestingly, adding splinting or nerve-gliding treatments to the program of providing information did not add a significant additional benefit.[68, 69]

Surgical Care

If nonsurgical methods fail, and in patients with severe and/or progressive weakness/atrophy, specific surgical techniques such as medial epicondylectomy, simple release of the flexor carpi ulnaris aponeurosis, and anterior transposition of the nerve are often beneficial in cases of ulnar neuropathy at the elbow.[70] Entrapments in Guyon canal are also amenable to surgical treatment.[2]

A Cochrane review presented results of 2 meta-analyses of 5 randomized, controlled clinical trials of surgical treatments for idiopathic ulnar neuropathy at the elbow.[68] Four of the studies addressed simple decompression compared with decompression plus transposition.[71, 72, 73, 74] These studies found no significant difference between simple decompression of the nerve and decompression with either submuscular or subcutaneous transposition. This was true both for clinical outcomes and neurophysiological outcomes (ie, nerve conduction and EMG).

One difference between the two approaches was that decompression with transposition produced more superficial and deep wound infections.[68] Two additional meta-analyses, using somewhat different meta-analytic methods, have also concluded that they can find no significant differences between the outcomes of simple decompression compared with decompression plus transposition.[75, 76] However, one of these studies, detected a trend in favor of decompression plus transposition, and the authors opined that perhaps a more highly powered study could detect a difference.[76]

The Cochrane review also examined one study that compared epicondylectomy with anterior transposition and concluded that no significant differences could be found in either clinical or neurophysiological outcomes.[68] Interestingly, patient satisfaction was higher in patients treated with epicondylectomy.[77]

Surgery is also valuable for correction or stabilization of traumatic injuries, resection of masses/cysts, and sectioning of fibrous bands.

Much more detail on the surgical approaches to these problems may be found in Ulnar Nerve Entrapment[14] and Cubital Tunnel Syndrome.[78]

Consultations

Depending upon etiology, symptoms, and signs, referral to a neurosurgeon, hand surgeon, pain specialist, internist, physiatrist, rheumatologist, occupational therapist, and/or alternative medicine specialist may be appropriate.

Medication Summary

The goals of pharmacotherapy are to reduce morbidity and prevent complications.

Amitriptyline (Elavil)

Clinical Context:  By inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase their synaptic concentrations in CNS. Dose may be increased slowly up to maximum of 125 mg/d. If no response, different TCA may be of benefit, but more often drugs from different category such as anticonvulsants are preferable.

Nortriptyline (Aventyl HCl, Pamelor)

Clinical Context:  Has demonstrated effectiveness in treatment of chronic pain. By inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal membrane, may increase synaptic concentrations in CNS.

Pharmacodynamic effects, such as desensitization of adenyl cyclase and down-regulation of beta-adrenergic receptors and serotonin receptors, also appear to play role in its mechanisms of action.

Duloxetine (Cymbalta)

Clinical Context:  Indicated for diabetic peripheral neuropathic pain. Potent inhibitor of neuronal serotonin and norepinephrine reuptake.

Class Summary

TCAs are effective in painful paresthesias. While the dosages are similar, the drugs in this category vary in their sedative properties. Amitriptyline can be used if the patient suffers from insomnia, while nortriptyline and desipramine are better choices when sedation becomes a problem.

Mexiletine (Mexitil)

Clinical Context:  An orally active local anesthetic drug structurally related to lidocaine. May operate by reducing spontaneous discharges from damaged primary small nerve fibers; recommended only in intractable cases; can be used for both dysesthetic and paresthetic pain.

Class Summary

Mexiletine, which has been used in various forms as an antiarrhythmic and local anesthetic, tends to blunt some of the stinging and burning of neuropathic pain in some patients. It is categorized as off-label use for diabetic neuropathy.

Morphine sulfate (Astramorph, MS Contin, MSIR, Oramorph)

Clinical Context:  DOC for analgesia due to reliable and predictable effects, safety profile, and ease of reversibility with naloxone.

Various IV doses are used; commonly titrated until desired effect obtained.

Class Summary

Although traditionally narcotics have been avoided in peripheral neuropathies, they are useful in many cases.

Gabapentin (Neurontin)

Clinical Context:  Membrane stabilizer, a structural analogue of inhibitory neurotransmitter GABA, which paradoxically is thought not to exert effect on GABA receptors. Appears to exert action via the alpha(2)delta-1 and alpha(2)delta-2 auxiliary subunits of voltage-gated calcium channels.

Used to manage pain and provide sedation in neuropathic pain.

Pregabalin (Lyrica)

Clinical Context:  Structural derivative of GABA. Mechanism of action unknown. Binds with high affinity to alpha2-delta site (a calcium channel subunit). In vitro, reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium channel function. FDA approved for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

Lamotrigine (Lamictal)

Clinical Context:  Triazine derivative useful in treatment of neuralgia. Inhibits release of glutamate and inhibits voltage-sensitive sodium channels, which stabilizes neuronal membrane. Follow manufacturer's recommendation for dose adjustments.

Topiramate (Topamax)

Clinical Context:  Precise mechanism unknown, but the following properties may contribute to its efficacy: (1) electrophysiological and biochemical evidence showing blockage of voltage-dependent sodium channels, (2) augments the activity of the neurotransmitter GABA at some GABA-A receptor subtypes, (3) antagonizes AMPA/kainate subtype of the glutamate receptor, and (4) inhibits the carbonic anhydrase enzyme, particularly isozymes II and IV.

Levetiracetam (Keppra)

Clinical Context:  Another new anticonvulsant being used to combat pain of peripheral neuropathies. Mechanism that improves condition not known but probably related to fact that anticonvulsants generally reduce nerve irritability. Not FDA approved for this indication.

Phenytoin (Dilantin)

Clinical Context:  Blocks sodium channels nonspecifically and therefore reduces neuronal excitability in sensitized C-nociceptors. Has been demonstrated effective in neuropathic pain but suppresses insulin secretion and may precipitate hyperosmolar coma in patients with diabetes.

Antineuralgic effects may derive from the blocking of posttetanic potentiation by reducing summation of temporal stimulation.

Carbamazepine (Tegretol, Carbatrol, Epitol)

Clinical Context:  A sodium-channel blocker that typically provides substantial or complete relief of pain in 80% of individuals with both idiopathic and MS-associated TN within 24-48 h. Reduces sustained high-frequency repetitive neural firing. Potent enzyme inducer that can induce own metabolism. Due to potentially serious blood dyscrasias, undertake benefit-to-risk evaluation before drug instituted. Therapeutic plasma levels are between 4-12 mcg/mL for analgesic and antiseizure response. Peak serum levels in 4-5 h. Half-life (serum) in 12-17 h with repeated doses. Metabolized in liver to active metabolite (ie, epoxide derivative) with half-life of 5-8 h. Metabolites excreted through feces and urine.

Oxcarbazepine (Trileptal)

Clinical Context:  Pharmacologic activity primarily by 10-monohydroxy metabolite (MHD). Studies indicate that this drug may block voltage-sensitive sodium channels, inhibit repetitive neuronal firing, and impair synaptic impulse propagation. Anticonvulsant effect also may occur by affecting potassium conductance and high-voltage activated calcium channels. Pharmacokinetics similar in older children (>8 y) and adults. Young children (< 8 y) have 30-40% greater clearance than older children and adults. Children < 2 y have not been studied in controlled clinical trials. Not FDA approved for this indication.

Class Summary

Many anticonvulsants are used to alleviate painful dysesthesias, which frequently accompany peripheral neuropathies. Although they have many different mechanisms of action, their use to alleviate neuropathic pain probably depends on the fact that they generally tend to reduce neuronal excitability.

Prognosis

A motor amplitude of 10% of normal or a greatly reduced recruitment of motor units indicates a low likelihood of significant or full recovery.

Typically, nerves regenerate at a rate of 1 mm/d.

In some cases, regeneration is accompanied by pain and paresthesias, which are thought to be secondary to random ectopic impulse generation of affected nerves.

A diameter greater than 3.5 mm on the initial sonogram of the ulnar nerve at the elbow is associated with persistent symptoms or signs regardless of treatment (ie, conservative treatment or surgical treatment[79] ).

The outcome does not correlate with clinical features at baseline or with the duration of symptoms prior to treatment.

The presence of motor conduction velocity slowing or pure conduction block across the elbow signifies a favorable outcome; these are considered independent prognostic factors[80] .

A favorable surgical outcome is more likely for sensory function than for motor function; however, overall, a favorable outcome occurs in 85-95% of cases.

Unfavorable or poor surgical outcome is characterized by the following:

Author

Charles F Guardia III, MD, Clinical Instructor, Department of Neurology, Dartmouth Hitchcock Medical Center

Disclosure: Nothing to disclose.

Coauthor(s)

Christina J Azevedo MD, Staff Physician, Department of Neurology, Dartmouth-Hitchcock Medical Center

Disclosure: Nothing to disclose.

Stephen A Berman, MD, PhD, MBA, Professor of Neurology, University of Central Florida College of Medicine

Disclosure: Nothing to disclose.

Specialty Editors

Paul E Barkhaus, MD, Professor, Department of Neurology, Medical College of Wisconsin; Director of Neuromuscular Diseases, Milwaukee Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

Neil A Busis, MD, Chief, Division of Neurology, Department of Medicine, Head, Clinical Neurophysiology Laboratory, University of Pittsburgh Medical Center-Shadyside

Disclosure: Nothing to disclose.

Selim R Benbadis, MD, Professor, Director of Comprehensive Epilepsy Program, Departments of Neurology and Neurosurgery, Tampa General Hospital, University of South Florida College of Medicine

Disclosure: UCB Pharma Honoraria Speaking, consulting; Lundbeck Honoraria Speaking, consulting; Cyberonics Honoraria Speaking, consulting; Glaxo Smith Kline Honoraria Speaking, consulting; Sleepmed/DigiTrace Honoraria Speaking, consulting; Sunovion Consulting fee None

Chief Editor

Nicholas Lorenzo, MD, CPE, Chairman and CEO, Neurology Specialists and Consultants; Senior Vice President, Founding Executive Director, Continuing Medical Education, Gannett Education (Division Gannett Healthcare Group)

Disclosure: Nothing to disclose.

Additional Contributors

The authors and editors of Medscape Reference gratefully acknowledge the contributions of previous author, Sandeep K Aggarwal, MD, to the development and writing of this article.

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This is a schematic diagram of the elbow region. The 5 main sites as given by Posner are labeled 1-5. Other sites and structures are also named. The main regions of interest are circled with pastel colored arrows. Sites 2 and 3 are close together and distinguishing them by EMG and nerve conduction studies is not possible. The term ulnar groove or retrocondylar groove are used to describe this location.

This diagram shows the ulnar nerve distal to the elbow region. The dorsal ulnar cutaneous nerve (lavender) branches off the main trunk (blue). Although the course is not followed in detail after that, the lavender region on the sensory dermatome diagram shows where this sensory nerve innervates the skin. Similarly, the palmar cutaneous sensory nerve (yellow) branches off to innervate the skin area depicted in yellow. The superficial terminal branch is mostly sensory (see green colored skin on palmar surface), though it also gives a branch to the palmaris brevis muscle. The deep terminal branch has no corresponding skin area because it is solely motor innervating the muscles shown, as well as some others not explicitly depicted. Of course the nerve could be pinched or injured anywhere, but the sites listed with Roman numerals I-IV are the relatively common sites.

This diagram shows the ulnar nerve distal to the elbow region. The dorsal ulnar cutaneous nerve (lavender) branches off the main trunk (blue). Although the course is not followed in detail after that, the lavender region on the sensory dermatome diagram shows where this sensory nerve innervates the skin. Similarly, the palmar cutaneous sensory nerve (yellow) branches off to innervate the skin area depicted in yellow. The superficial terminal branch is mostly sensory (see green colored skin on palmar surface), though it also gives a branch to the palmaris brevis muscle. The deep terminal branch has no corresponding skin area because it is solely motor innervating the muscles shown, as well as some others not explicitly depicted. Of course the nerve could be pinched or injured anywhere, but the sites listed with Roman numerals I-IV are the relatively common sites.

An example of the inching technique used to isolate conduction block in the left ulnar nerve. Note the significant amplitude drop at the 305-mm distance that correlates with a position 2 cm above the medial epicondyle. This is an example of supracondylar block. Image courtesy of AS Lorenzo, MD.

The normal median and ulnar pattern are compared with that of the 3 commonly recognized types of the Martin-Gruber anomaly.

The first 3 traces correspond to the ulnar compound muscle action potential (CMAP) amplitude while recording at the abductor digitorum quinti (ADQ) and stimulating at the wrist, below the elbow, and above the elbow, respectively. The fourth trace corresponds to stimulation of the median nerve at the elbow while recording at ADQ. Though CMAP amplitude is reduced markedly above the elbow, this is compensated by adding the response seen after stimulating the median nerve; this represents the Martin-Gruber anastomosis.

The first 3 traces correspond to stimulation of the ulnar nerve while recording at the first dorsal interosseous (FDI) muscle at the wrist, below the elbow, and above the elbow, respectively. The fourth trace corresponds to stimulation of the median nerve at the elbow while recording at FDI. This represents the Martin-Gruber anastomosis.

In people with the Martin-Gruber anomaly who do not otherwise have significant neuropathy or nerve compressions, here is what happens when the relevant nerves are stimulated. Median stimulation: Stimulation at the elbow yields a larger compound muscle action potential (CMAP) at the hypothenar muscles, the first dorsal interosseus (FDI), or the thenar muscles (or a combination of these) than does stimulation at the wrist. Ulnar stimulation: Stimulation at the wrist yields a larger CMAP at the hypothenar muscles, the FDI, or the thenar muscles (or a combination of these) than does stimulation at the elbow. Larger and smaller generally means a difference of 1.0 millivolt in amplitude or more.

The Riche-Cannieu anastomosis is a communication between the recurrent branch of median nerve and deep branch of ulnar nerve in the hand. Although it is present in 77% of hands, the extent to which it makes a detectable physiological difference is quite variable. In many hands it seems to contribute little and it does not affect the diagnostic findings at all. Probably the most common effect of the anomaly is to give an ulnar innervation to some muscles that are usually innervated by the median nerve and/or vice versa. The most extreme version of this is the very rare all ulnar hand. Two examples of the confusion this might cause are (1) a median lesion could cause denervation in a typical ulnar muscle such as the adductor digiti minimi (ADM, also called adductor digiti quinti [ADQ]) or the first dorsal interosseus and (2) an ulnar lesion could cause denervation in typically median muscles such as the flexor pollicis brevis (FPB) or the abductor pollicis brevis (APB).

This is a schematic diagram of the elbow region. The 5 main sites as given by Posner are labeled 1-5. Other sites and structures are also named. The main regions of interest are circled with pastel colored arrows. Sites 2 and 3 are close together and distinguishing them by EMG and nerve conduction studies is not possible. The term ulnar groove or retrocondylar groove are used to describe this location.

This diagram shows the ulnar nerve distal to the elbow region. The dorsal ulnar cutaneous nerve (lavender) branches off the main trunk (blue). Although the course is not followed in detail after that, the lavender region on the sensory dermatome diagram shows where this sensory nerve innervates the skin. Similarly, the palmar cutaneous sensory nerve (yellow) branches off to innervate the skin area depicted in yellow. The superficial terminal branch is mostly sensory (see green colored skin on palmar surface), though it also gives a branch to the palmaris brevis muscle. The deep terminal branch has no corresponding skin area because it is solely motor innervating the muscles shown, as well as some others not explicitly depicted. Of course the nerve could be pinched or injured anywhere, but the sites listed with Roman numerals I-IV are the relatively common sites.

An example of the inching technique used to isolate conduction block in the left ulnar nerve. Note the significant amplitude drop at the 305-mm distance that correlates with a position 2 cm above the medial epicondyle. This is an example of supracondylar block. Image courtesy of AS Lorenzo, MD.

The normal median and ulnar pattern are compared with that of the 3 commonly recognized types of the Martin-Gruber anomaly.

The first 3 traces correspond to the ulnar compound muscle action potential (CMAP) amplitude while recording at the abductor digitorum quinti (ADQ) and stimulating at the wrist, below the elbow, and above the elbow, respectively. The fourth trace corresponds to stimulation of the median nerve at the elbow while recording at ADQ. Though CMAP amplitude is reduced markedly above the elbow, this is compensated by adding the response seen after stimulating the median nerve; this represents the Martin-Gruber anastomosis.

The first 3 traces correspond to stimulation of the ulnar nerve while recording at the first dorsal interosseous (FDI) muscle at the wrist, below the elbow, and above the elbow, respectively. The fourth trace corresponds to stimulation of the median nerve at the elbow while recording at FDI. This represents the Martin-Gruber anastomosis.

In people with the Martin-Gruber anomaly who do not otherwise have significant neuropathy or nerve compressions, here is what happens when the relevant nerves are stimulated. Median stimulation: Stimulation at the elbow yields a larger compound muscle action potential (CMAP) at the hypothenar muscles, the first dorsal interosseus (FDI), or the thenar muscles (or a combination of these) than does stimulation at the wrist. Ulnar stimulation: Stimulation at the wrist yields a larger CMAP at the hypothenar muscles, the FDI, or the thenar muscles (or a combination of these) than does stimulation at the elbow. Larger and smaller generally means a difference of 1.0 millivolt in amplitude or more.

The Riche-Cannieu anastomosis is a communication between the recurrent branch of median nerve and deep branch of ulnar nerve in the hand. Although it is present in 77% of hands, the extent to which it makes a detectable physiological difference is quite variable. In many hands it seems to contribute little and it does not affect the diagnostic findings at all. Probably the most common effect of the anomaly is to give an ulnar innervation to some muscles that are usually innervated by the median nerve and/or vice versa. The most extreme version of this is the very rare all ulnar hand. Two examples of the confusion this might cause are (1) a median lesion could cause denervation in a typical ulnar muscle such as the adductor digiti minimi (ADM, also called adductor digiti quinti [ADQ]) or the first dorsal interosseus and (2) an ulnar lesion could cause denervation in typically median muscles such as the flexor pollicis brevis (FPB) or the abductor pollicis brevis (APB).

TypeAnatomyMost Characteristic FindingConfirmationAdditional VerificationClinical Confusion
ICrossover fibers innervate hypothenar musclesUlnar stimulation at wrist produces larger hypothenar CMAP than stimulation at elbow.Stimulation of median nerve at elbow produces response at hypothenar muscles.Hypothenar CMAP from ulnar stimulation at wrist = Hypothenar CMAP from ulnar stimulation at elbow, plus hypothenar CMAP from median stimulation at elbow Smaller response from proximal stimulation could be mistaken for conduction block.
IICrossover fibers innervate the FDI.Ulnar stimulation at wrist produces larger FDI CMAP than stimulation at elbow.Stimulation of median nerve at elbow produces response at FDI.FDI CMAP from ulnar stimulation at wrist = FDI CMAP from ulnar stimulation at elbow plus FDI CMAP from median stimulation at elbow. Usually none because FDI is not usually a recording site. If it is used, conduction block could be suspected as in type I.
IIICrossover fibers innervate thenar muscles (typically ADP and FPB).Elbow stimulation of median nerve produces greater thenar response than does wrist stimulation.Ulnar stimulation produces thenar CMAP with initial positive deflection. It is higher with wrist stimulation than with elbow stimulation. For thenar CMAP amplitudes, median elbow stimulation amp = median wrist stimulation amp plus ulnar wrist stimulation amp – ulnar elbow stimulation amp Can complicate median nerve studies, especially involving carpal tunnel syndrome.
Abbreviations: CMAP: Compound motor (or muscle) action potential

FDI: First dorsal interosseus

ADP: Adductor pollicis

FPB: Flexor pollicis brevis

Median stimulation: Stimulation at the elbow yields a larger CMAP at the hypothenar muscles, the FDI, or the thenar muscles (or sometimes in a combination of these) than does stimulation at the wrist.

Ulnar stimulation: Stimulation at the wrist yields a larger CMAP at the hypothenar muscles, the FDI, or the thenar muscles (or sometimes in a combination of these) than does stimulation at the elbow.

Note: Larger and smaller generally means a difference of 1 millivolt in amplitude or more.