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 digit and the entire fifth digit (the ulnar aspect of the palm) and the ulnar portion of the posterior aspect of the hand (dorsal ulnar cutaneous distribution). Entrapment of the ulnar nerve is the second most common entrapment neuropathy in the upper extremity (after entrapment of the median nerve).[1, 2, 3]

The most common site of ulnar nerve entrapment is at or near the elbow region, especially in the region of the cubital tunnel[4] or in the epicondylar (ulnar) groove; the second most likely site is at or near the wrist, especially in the area of the anatomic structure called the canal of Guyon.[1, 5, 6, 7] However, entrapment can also occur in the forearm between these two regions, below the wrist within the hand, or above the elbow.

Pressure on or injury to the ulnar nerve may cause denervation and paralysis of the muscles supplied by the nerve. Affected patients often experience numbness and tingling along the little finger and the ulnar half of the ring finger. This discomfort is often accompanied by weakness of grip and, rarely, intrinsic wasting. One of the most severe consequences is loss of intrinsic muscle function in the hand. When the ulnar nerve is divided at the wrist, only the opponens pollicis, superficial head of the flexor pollicis brevis, and lateral 2 lumbricals are functioning.

Conservative nonsurgical treatment may play a useful role in management. If such treatment fails or the patient has severe or progressive weakness or loss of function, surgical treatment is warranted. Several surgical approaches have been employed, each of which has its advocates; results for all of them appear to be satisfactory.

Anatomy

Course of ulnar nerve

The ulnar nerve is the terminal branch of the medial cord of the brachial plexus and contains fibers from C8, T1, and, occasionally, C7.[8, 9] It enters the arm with the axillary artery and passes posterior and medial to the brachial artery, traveling between the brachial artery and the brachial vein.

At the level of the insertion of the coracobrachialis in the middle third of the arm, the ulnar nerve pierces the medial intermuscular septum to enter the posterior compartment of the arm.[10, 11] Here, the nerve lies on the anterior aspect of the medial head of the triceps, where it is joined by the superior ulnar collateral artery. The medial intermuscular septum extends from the coracobrachialis proximally, where it is a thin and weak structure, to the medial humeral epicondyle, where it is a thick, distinct structure.

The next important site along the course of the ulnar nerve is the arcade of Struthers. This structure is found in 70% of patients, 8 cm proximal to the medial epicondyle, and extends from the medial intermuscular septum to the medial head of the triceps. The arcade of Struthers is formed by the attachments of the internal brachial ligament (a fascial extension of the coracobrachialis tendon), the fascia and superficial muscular fibers of the medial head of the triceps, and the medial intermuscular septum.

It is important to distinguish the arcade of Struthers from the ligament of Struthers, which is found in 1% of the population and extends from a supracondylar bony or cartilaginous spur to the medial epicondyle. This supracondylar spur can be found on the anteromedial aspect of the humerus, 5 cm proximal to the medial epicondyle, and it can often be seen on radiographs. The ligament of Struthers may occasionally cause neurovascular compression, usually involving the median nerve or the brachial artery but sometimes affecting the ulnar nerve.

Next, the ulnar nerve passes through the cubital tunnel, which is the space bounded by the following:

The deep forearm investing fascia of the flexor carpi ulnaris and the arcuate ligament of Osborne, also known as the cubital tunnel retinaculum, form the roof of the cubital tunnel. The cubital tunnel retinaculum is a 4-mm-wide fibrous band that passes from the medial epicondyle to the tip of the olecranon. Its fibers are oriented perpendicularly to the fibers of the flexor carpi ulnaris aponeurosis, which blends with its distal margin.

The elbow capsule and the posterior and transverse portions of the medial collateral ligament form the floor of the cubital tunnel. The medial epicondyle and olecranon form the walls.

O’Driscoll suggested that the roof of the cubital tunnel (ie, the Osborne ligament or fascia), is a remnant of the anconeus epitrochlearis,[12] an aberrant muscle that has been found in 3-28% of cadaver elbows and in as many as 9% of patients undergoing surgery for cubital tunnel syndrome. This muscle arises from the medial humeral condyle and inserts on the olecranon, crossing superficially to the ulnar nerve, where it may cause compression.[13]

O’Driscoll also identified a retinaculum at the proximal edge of the arcuate ligament in all but 4 of 25 cadaveric specimens.[12] He classified this retinaculum into the following four types:

Upon entering the cubital tunnel, the ulnar nerve gives off an articular branch to the elbow. It then passes between the humeral and ulnar heads of the flexor carpi ulnaris and descends into the forearm between the flexor carpi ulnaris and the flexor digitorum profundus. About 5 cm distal to the medial epicondyle, the ulnar nerve pierces the flexor-pronator aponeurosis, the fibrous common origin of the flexor and pronator muscles.

The ligament of Spinner is an additional aponeurosis between the flexor digitorum superficialis of the ring finger and the humeral head of the flexor carpi ulnaris. This septum is independent of the other aponeuroses and attaches directly to the medial epicondyle and the medial surface of the coronoid process of the ulna. With anterior transposition of the ulnar nerve, it is important to recognize and to release this structure to prevent kinking.

In the forearm, the ulnar nerve extends motor branches to the flexor carpi ulnaris and the flexor digitorum profundus of the ring and small fingers. The ulnar nerve may extend as many as 4 branches to the flexor carpi ulnaris, ranging from 4 cm above to 10 cm below the medial epicondyle. Proximal dissection of the first motor branch to the flexor carpi ulnaris from the ulnar nerve may be performed up to 6.7 cm proximal to the medial epicondyle, facilitating anterior transposition of the nerve.

Posterior branches of the medial antebrachial cutaneous nerves cross the ulnar nerve anywhere from 6 cm proximal to 4 cm distal to the medial epicondyle. These branches are often cut in the course of making the skin incision for a cubital tunnel release, creating an area of dysesthesia or resulting in potential neuroma formation.

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 two branches goes through the canal of Guyon.[1] The remainder of the ulnar nerve enters the canal at the proximal portion of the wrist. This is bounded proximally and distally by the pisiform bone and the hook of the hamate bone. It is covered by the volar carpal ligament and the palmaris brevis.

The following two nerve anomalies should be mentioned because they may confuse the diagnosis in the setting of ulnar neuropathy:

Blood supply

The extrinsic blood supply to the ulnar nerve is segmental and involves the following three vessels:

Typically, the inferior ulnar collateral artery (and often the posterior ulnar recurrent artery) is sacrificed with anterior transposition. At the level of the medial epicondyle, the inferior ulnar collateral artery is the sole blood supply to the ulnar nerve. In an anatomic study, no identifiable anastomosis was found between the superior ulnar collateral artery and the posterior ulnar recurrent arteries in 20 of 22 arms; instead, communication between the two arteries occurred through proximal and distal extensions of the inferior ulnar collateral artery.

The intrinsic blood supply is composed of an interconnecting network of vessels that run along the fascicular branches and along each fascicle of the ulnar nerve itself. The surface microcirculation of the ulnar nerve follows an anastomotic stepladder arrangement. The inferior ulnar collateral artery is consistently found 5 mm deep to the leading edge of the medial intermuscular septum on the surface of the triceps.[14]

Sites of nerve entrapment

As diagnostic and surgical methodologies have evolved over the past century, physicians’ ability to recognize and describe sites of entrapment has improved. However, the terminology used to describe ulnar nerve entrapment has become confusing, in that not all clinicians use the same words for the same things. This confusion can be illustrated by examining the terms applied to ulnar nerve entrapment in the elbow region,[15] of which the two most commonly used (and misused) are tardy ulnar palsy[16] and cubital tunnel syndrome.[17]

In 1878, Panas first described what is now often called tardy ulnar palsy, in which either prior trauma or osteoarthritis gradually caused damage to the ulnar nerve.[18] Additional cases were reported over the ensuing decades,[19, 20] usually associated with trauma (eg, fractures in the elbow region) and typically occurring in the epicondylar groove.[21, 22] Initially denoting time (ie, appearing years after trauma), the term came to have an anatomic connotation (ie, usually seen in or very near the epicondylar groove).[23]

From 1922 on, physicians began to recognize ulnar entrapments in the HUA.[24, 25] In 1958, the term cubital tunnel syndrome was coined to describe the effects of the ulnar nerve entrapment[26] at the HUA. Numerous other reports ensued.

Although the current state of knowledge is still incomplete, it is possible to identify approximately five sites in the elbow region at which the ulnar nerve is most likely to be compressed. (Five is not a firm figure; some of the sites are so close together that certain authorities categorize them differently to get a different number.) This article principally follows Posner’s classification,[27] which lists the following sites (see the image below):

Region of intermuscular septum

Halikis et al[28] divided this region into 2 areas, the arcade of Struthers[29, 30] and the medial intermuscular septum. According to the standard anatomic definition, the arcade of Struthers is a thin fibrous band that usually extends from the medial head of the 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.[31] One component of the controversy is quite trivial: There is no evidence that Struthers discovered this structure or was even aware of it; his name was attached to it by Kane et al in a 1973 paper.[32]

Siqueira, in an autopsy study of 60 upper limbs, found a structure reasonably approximating the definition given above in 8 limbs (13.5%).[31] Ulnar nerve entrapment occurred in none of them (but there was no clinical reason to expect that it might have).

Bartels et al could not find the arcade of Struthers in their dissections, and they expressed doubts about its existence.[33]

Wehrli and Oberlin described a different structure in the same region that might be involved in ulnar entrapment in some cases—the internal brachial ligament.[34] This structure was in fact described by Struthers, but not in relation to ulnar nerve entrapment. Wehrli and Oberlin advocated abolishing the concept of the arcade of Struthers.

Von Schroeder and Scheker described yet another structure, a fibrous tunnel in roughly the same region.[35] They maintained that the ulnar nerve goes through this tunnel and could be trapped therein and suggested naming this structure the arcade of Struthers.

Settling this anatomic controversy is beyond the scope of this article. It is sufficient to note that in rare cases, the ulnar nerve may be compressed considerably above the ulnar groove and that surgeons may find it entrapped in a fibrous or ligamentous structure that may correspond to one of the aforementioned anatomic descriptions.

Medial epicondylar region

Ulnar compression[36] in the medial epicondylar region is generally from a valgus deformity of the bone. If a patient is placed in standard anatomic position with the palms rotated toward the front and the thumb away from the midline, a valgus deformity means that the elbow would be deformed away from midline of the body.

Epicondylar groove

The epicondylar (ulnar) groove is a fibro-osseous tunnel holding the ulnar nerve and its vascular accompaniment. It is slightly distal to the medial epicondyle, or at least to the beginning of it.

Campbell used slightly different terminology, lumping the epicondylar groove together with the medial epicondylar region and labeling the entire region the area of the retrocondylar groove. Halikis et al considered the medial epicondylar region and the epicondylar groove to be the area of the medial epicondyle.[28]

The medial epicondylar region and the epicondylar groove are generally considered to be the classic locations (or location, if considered as a single area) for 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.

Region of cubital tunnel

The cubital tunnel is the passage between the two heads of the flexor carpi ulnaris, which are connected by a continuation of the fibroaponeurotic covering of the epicondylar groove (Osborne ligament). During elbow flexion, the tunnel flattens as the ligament stretches, causing pressure on the ulnar nerve.[37, 38, 39]

Campbell’s classification was basically the same for this region, except that he preferred to call it the region of the HUA, apparently because he believed that too many clinicians loosely used the term cubital tunnel to refer to a place anywhere in the elbow.

Halikis et al divided this region into two parts, the cubital tunnel and the Osborne fascia.[28] This is a good example of the problems with the terminology: Different terms are used for locations that are virtually the same. For all practical purposes—certainly with regard to anything that can be distinguished on electromyography (EMG)—the Osborne ligament is equivalent to the Osborne fascia, and both are equivalent to the HUA.

Region where ulnar nerve exits from flexor carpi ulnaris

Campbell[40] and Halikis et al[28] agreed with Posner in listing this region as the final entrapment site in the elbow area. As the nerve exits the flexor carpi ulnaris, it perforates a fascial layer between the flexor digitorum superficialis and the flexor digitorum profundus. Entrapment can occur here also.

More distal entrapment sites

After the ulnar nerve passes distal to the elbow,[41, 42, 19] it makes several important divisions. The first branches to come off are those that go to the flexor carpi ulnaris. Further distally, the branches to the flexor digitorum profundus muscles of digits 4 and 5 arise.

Although the nerve could be injured or entrapped at any point along its course, four sites have been identified as the most common locations of entrapment in relation to the canal of Guyon (see the image below).


View Image

Diagram shows ulnar nerve distal to elbow region. Dorsal ulnar cutaneous nerve (lavender) branches off main trunk (blue). Although course is not follo....

The canal of Guyon may be conveniently divided into 3 zones as follows:

Pathophysiology

As the elbow moves from extension to flexion, the distance between the medial epicondyle and the olecranon increases by 5 mm for every 45° of elbow flexion. Elbow flexion places stress on the medial collateral ligament and the overlying retinaculum. The shape of the cubital tunnel in cross-section changes from round to oval, with a 2.5-mm loss of height, because the cubital tunnel rises during elbow flexion and the epicondylar groove is not as deep on the inferior aspect of the medial epicondyle as it is posteriorly.

The cubital tunnel’s loss in height with flexion leads to a 55% volume decrease in the canal, which causes the mean ulnar intraneural pressure to increase from 7 mm Hg to 14 mm Hg.[43, 44] A combination of shoulder abduction, elbow flexion, and wrist extension results in the greatest increase in cubital tunnel pressure, with ulnar intraneural pressure increasing to about 6 times normal.[45, 46, 47, 48, 36]

Traction and excursion of the ulnar nerve also occur during elbow flexion, as the ulnar nerve passes behind the axis of rotation of the elbow. With full range of motion of the elbow, the ulnar nerve undergoes 9-10 mm of longitudinal excursion proximal to the medial epicondyle and 3-6 mm of excursion distal to the epicondyle.[49] In addition, the ulnar nerve elongates by 5-8 mm with elbow flexion.

Within the cubital tunnel, the measured mean intraneural pressure is significantly greater than the mean extraneural pressure at elbow flexion of 90° or more.[50] With the elbow flexed 130°, the mean intraneural pressure is 45% higher than the mean extraneural pressure. With this degree of flexion, significant flattening of the ulnar nerve occurs; however, with full elbow flexion, there is no evidence for direct focal compression, which suggests that traction on the nerve in association with elbow flexion is responsible for the increased intraneural pressure.

In addition, studies have shown that the intraneural and extraneural pressures within the cubital tunnel are lowest at 45° of flexion. As a result of these studies, 45° of flexion is considered to be the optimum position for immobilization of the elbow to decrease pressure on the ulnar nerve.

Subluxation of the ulnar nerve is common. Childress, in a study of 2000 asymptomatic elbows, found that although none of the patients were aware of ulnar nerve subluxation, 16.2% had this condition after flexion past 90°.[51] Of the 325 patients with ulnar nerve subluxation, only 14 had unilateral subluxation. Subluxation does not appear to cause cubital tunnel syndrome, but the friction generated with repeated subluxation may cause intraneural inflammation, and the subluxed position may render the nerve more susceptible to inadvertent trauma.

Sunderland described the internal topography of the ulnar nerve at the medial epicondyle.[52] The sensory fibers and intrinsic muscle nerve fibers are located superficially. In contrast, the motor fibers to the flexor carpi ulnaris and the flexor digitorum profundus are located deep within the nerve.[53, 54, 55] The central location protects the motor fibers and explains why weakness of these two muscles is not typically seen in ulnar neuropathy.[56, 57, 27, 58]

Proximal compression of a nerve trunk, such as occurs with cervical radiculopathy, may lead to increased vulnerability to nerve compression in a distal segment. This "double crush" condition can affect the ulnar nerve and results from disruption of normal axonal transport.[59]

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 or significant spreading out of the temporal profile of the recorded response with preserved axonal integrity suggests demyelination.

Various systems have been proposed for classifying nerve injuries. Seddon in 1972 and Sunderland in 1978 took similar approaches to this classification. Seddon stratified nerve injuries into the following three levels[60] :

Sunderland’s classification specifies five degrees of nerve damage.[61] The first degree corresponds to neurapraxia in Seddon’s schema; the second corresponds to axonotmesis; and the third, fourth, and fifth correspond to increasingly severe levels of neurotmesis. In a Sunderland third-degree injury, axons and Schwann sheaths are disrupted within intact nerve fascicles. In a fourth-degree injury, the perineurium surrounding the fascicles is damaged, as is the endoneurium. In a fifth-degree injury, the nerve trunk is severed.

McGowan established the following classification system for ulnar nerve injuries[62] :

In a study of the validity of the Disabilities of Arm, Shoulder and Hand (DASH) questionnaire for elbow ulnar neuropathy, Zimmerman et al found that the DASH questionnaire accurately reflected the clinical staging of ulnar neuropathy.[63] There was a high correlation between DASH scores, severity of symptoms, and functional status. Correlations were identified as significant between DASH and biomechanical measures, but correlation coefficients were lower. All measures showed significant improvement postoperatively.

Etiology

Cubital tunnel syndrome may be caused by constricting fascial bands, subluxation of the ulnar nerve over the medial epicondyle, cubitus valgus, bony spurs, hypertrophied synovium, tumors, ganglia, or direct compression. Occupational activities may aggravate cubital tunnel syndrome secondary to repetitive elbow flexion and extension. Certain occupations are associated with the development of cubital tunnel syndrome; however, a definite relation to occupational activities is not well defined.[64, 65, 66]

Factors that may cause ulnar neuropathy at or near the elbow include the following:

Factors that may cause ulnar neuropathy at or distal to the wrist (ie, at the canal of Guyon) include the following:

Epidemiology

United States statistics

The elbow is the second most common site of nerve entrapment in the upper extremity, the first being the wrist (ie, carpal tunnel syndrome). In the general population, abnormalities in the ulnar nerve at the elbow in asymptomatic subjects are common (about 40%).

Age-related demographics

The older literature indicated that most cases of ulnar compression neuropathy occur in patients older than 35 years.[72] This is consistent with an independent anatomic study of 200 cadavers from 1963, which showed 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.[73] A prospective study of 76 patients published in 2006 showed that increased age is highly correlated with a greater tendency toward ulnar neuropathy.[74]

Sex-related demographics

No gross anatomic differences in the course of the nerve are noted between the sexes. However, the following have been noted[75] :

Contreras et al suggested that the coronoid process may be a potential site for ulnar nerve compression in men and that the increased subcutaneous fat around the ulnar nerve in women may provide a protective advantage against acute ulnar neuropathy.[75]

Prognosis

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

The following factors are relevant to the prognosis:

Unfavorable or poor surgical outcome is associated with the following:

Bartels et al performed a meta-analysis of the literature from 1970 to 1997, which included 3024 patients.[82] Irrespective of preoperative status, simple decompression had the best outcomes, and subcutaneous and submuscular transposition had the worst. For severe compression (McGowan grade III), anterior intramuscular transposition had the best outcome, and simple decompression and submuscular transposition had the next best outcomes.

Heithoff reviewed 14 clinical studies, covering 516 patients, in which a simple decompression was performed for cubital tunnel syndrome. Results were satisfactory in 75-92% of the patients.[83]

Steiner et al monitored 41 patients who underwent simple ulnar nerve decompression for an average follow-up period of 2 years.[84] Results were good or very good in 89% of the patients; 8% of the patients had no improvement.

Lluch studied 20 patients who underwent decompression in situ through a transverse incision.[85] A retrospective review of 22 patients noted a 24% incidence of complications from unsightly scarring and injury to the posterior branches of the medial antebrachial cutaneous nerve. To avoid this complication, a transverse incision was used for decompression in 20 patients, allowing easier identification and protection of the nerve branches. No problems with dysesthesia or amputation neuromas occurred, and a good cosmetic result was obtained.

Heithoff and Millender reviewed 12 clinical studies involving 350 patients in which a medial epicondylectomy was performed for cubital tunnel syndrome. Results were satisfactory in 72-94% of the patients.[86]

Kaempffe and Farbach reviewed 27 patients who underwent partial medial epicondylectomies and were monitored for an average of 13 months.[87] Subjective improvement was noted in 93% of cases. Results were excellent in 8 patients, good in 10, and fair in 8; 1 patient had a poor result.

To assess factors influencing outcome after medial epicondylectomy, Seradge and Owen studied 160 patients over a 10-year period and monitored them for 3 years postoperatively.[88] In all, 21 patients had a recurrence—defined as a return of symptoms 3 months or longer after surgery—and 44% of these recurrences occurred in the fourth decade of life. The rate of recurrence was 18% in females and 10% in males. The rate of recurrence was twice as high in patients who did not return to work within 3 months.

When concomitant ipsilateral carpal tunnel syndrome was present, the recurrence rate was 17%, compared with 9% when this syndrome was absent.[88] When concomitant thoracic outlet syndrome was present, the recurrence rate was 20%, compared with 9% when this syndrome was absent. In conclusion, Seradge and Owen noted a high recurrence rate after medial epicondylectomy in middle-aged women with ipsilateral carpal tunnel syndrome or thoracic outlet syndrome who did not return to work within 3 months postoperatively.

Seradge also examined the results of medial epicondylectomy in patients on workers’ compensation.[89] These patients stayed out of work longer, used a longer period of conservative treatment without a positive impact on surgical outcome, had a less favorable surgical result, and had a higher recurrence rate.

Glowacki and Weiss reviewed the results of anterior intramuscular transpositions in 45 patients who were monitored for an average of 15 months.[90] In 87% of patients, symptoms resolved or improved. The 24 patients receiving workers’ compensation had a 33% rate of complete symptom resolution, whereas those who were not receiving workers’ compensation had a 57% rate of complete symptom resolution.

Geutjens et al conducted a prospective study of 52 patients, comparing medial epicondylectomy with anterior transposition.[91] Results were better with medial epicondylectomy: More patients were satisfied, more stated that they would have the operation again, and fewer complained of mild pain in their hand postoperatively. No significant differences were present in motor power or nerve conduction rates at follow-up visits.

Kleinman and Bishop monitored 47 patients after anterior intramuscular transposition for an average of 28 months.[92] Results were good or excellent in 87%, with return of normal grip strength and two-point discrimination. None of the patients required a repeat operation.

Asami et al monitored 35 patients for an average of 70-72 months after anterior intramuscular transposition performed with or without preservation of the extrinsic vasculature.[93] Nerve conduction velocities and clinical results were better in the group whose extrinsic vessels were preserved. When the extrinsic vessels were sacrificed, 3 excellent, 3 good, 4 fair, and no poor results were obtained; when they were preserved, 16 excellent, 12 good, 3 fair, and no poor results were obtained.

Nouhan and Kleinert monitored 33 limbs in 31 patients who underwent anterior submuscular transposition for an average of 49 months.[94] A flexor-pronator Z-lengthening technique was performed without internal neurolysis and yielded 36% excellent, 61% good, and 3% poor results.

Tsujino et al followed 16 patients after cubital tunnel reconstruction for ulnar nerve neuropathy in osteoarthritic elbows.[95] A simple decompression with resection of the osteophytes from the epicondylar groove was performed. Patients were monitored for an average of 36 months. All patients were relieved of their preoperative discomfort and recovered all or some part of their motor and sensory function.

In a 2011 Cochrane review, Caliandro et al found no difference in clinical outcomes between simple decompression and transposition of the ulnar nerve in terms of both clinical improvement and neurophysiologic improvement. Transposition was associated with a higher incidence of wound infections.[96]

History

A careful clinical history is imperative. Both the onset and the progress of the symptoms can be variable. Presenting symptoms of ulnar nerve entrapment can range from mild transient paresthesias in the ring and small fingers to clawing of these digits and severe intrinsic muscle atrophy.[17]

It is important to determine when the symptoms began, how long they are lasting, whether they are transient or continuous, and whether they are related to work, sleep, or recreation. In addition, although the answer will frequently be 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 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 include numbness, tingling, or burning. If the patient rests on the elbows at work, increasing numbness and paresthesias may be noticed throughout the day.[97, 98]

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. On occasion, severe pain at the elbow or wrist may radiate into the hand or up into the shoulder and neck.

Patients rarely notice specific muscle atrophy, but when they do, they often complain that their hands “look older.”

Weakness may also be a presenting complaint. For example, patients may report difficulty in opening jars or turning doorknobs or may experience early fatigue or weakness with work that requires repetitive hand motions.

The complaint of weakness may also be expressed in more subtle ways. For example, one traditional sign of ulnar neuropathy, the Wartenberg sign, is actually a complaint of weakness. In this scenario, 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, this complaint may be surprising, because most physicians, remembering that finger abduction is governed by the ulnar nerve, are probably inclined to assume that a patient who has an ulnar neuropathy would be less, rather than more, likely to have the little finger abducted and thus caught on the edge of the pocket. However, 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.

Furthermore, the muscle that extends the fifth digit at the metacarpal phalangeal joint (the extensor digiti quinti) is radially innervated and inserts on the ulnar side of the joint. Normally, this muscle is opposed by ulnar-innervated muscles that flex the joints. In the setting of an ulnar neuropathy, however, the muscle is relatively unopposed and thus pulls the finger up and to the ulnar side. This is the perfect position for catching 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 the thumb−index finger pincer grip is weak. Two of the key muscles involved in this movement are the adductor pollicis (adducting the thumb) and the first dorsal interosseous muscle (adducting the index finger). In addition to the weak pincer grip, the median-innervated flexor pollicis longus partially compensates for the weakened adductor pollicis, and the thumb flexes at the distal joint. This flexion usually goes unnoticed by the patient, but when it is demonstrated by the examiner, it constitutes the Froment sign.

Physical Examination

Typically, the clinical examination begins at the neck and shoulder and moves down the affected extremity to the elbow. The physical examination should include the following steps:

In addition to assessing sensation and testing individual muscle strength, inspection of the hand may reveal a clawed posture (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 nerve. Also, the fifth digit deviates slightly in the medial direction because the muscle that extends the fifth digit at the metacarpophalangeal joint is radially innervated and inserts on the ulnar side of the joint.

The fourth and fifth interphalangeal joints flex because the extensor muscles for these joints are also ulnar and because the natural tension of the muscles and tendons, in the absence of strong muscle activity in either direction, leads to flexion. The first three digits are extended at both the metacarpophalangeal 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. For this reason, it is sometimes called the benediction sign or the benediction hand.

The Froment sign is an observable sign that correlates with the complaint of a weakened 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 interosseous muscle 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 flexion of the tip of the thumb.

If a Martin-Gruber anastomosis in the forearm or a Riche-Cannieu anastomosis in the palm is present, the examiner may be deceived by the apparent functioning of ulnar-innervated muscles.

Ulnar neuropathy at elbow

Positive Tinel sign at elbow

To test for the Tinel sign, the examiner taps with a reflex hammer over the ulnar nerve in the ulnar groove and a little further distally over the cubital tunnel. The test is considered to yield a positive result if the patient experiences definite paresthesias in the ulnar portion of the hand, especially in the last two digits.

This test is not regarded as highly sensitive, but it is quite specific if performed properly (ie, if the examiner does not hit too hard). With a sufficiently hard tap, many normal individuals will experience paresthesias in the fourth and fifth digits. On the assumption that the complaint is unilateral, the opposite side serves as 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 muscle 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 (which controls flexion at the wrist in the ulnar direction) are valuable to examine.

It is not uncommon for the flexor carpi ulnaris to be spared in ulnar lesions near the elbow, especially in lower (more distal) lesions close to the elbow. Sparing occurs because the branch to the flexor carpi ulnaris splits off from the main trunk before (ie, above or proximal to) the compression.[102]

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 intrinsic hand muscles and the ulnar forearm muscles are involved, then an ulnar nerve lesion in the region of the elbow (or, very rarely, above the elbow region) should be suspected. If the ulnar forearm muscles are spared, it is reasonable to consider the possibility of a lesion at the wrist, 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 regarding which muscles are affected because the ulnar nerve is organized into a number of separate fascicles. In certain cases, some fascicles are severely affected by whatever is pinching the nerve while other fascicles remain 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 wrist

The following physical findings are significant with respect to ulnar neuropathy at or distal to the wrist:

Sensory examination

Adding information from the sensory examination to that of the motor examination helps to localize the ulnar lesion.[103]

Although in some patients, the area of the palmar cutaneous sensory nerve can extend a bit farther proximally than is usual, if the sensory involvement extends more than 2.5 cm above the wrist crease along the medial aspect of the forearm, involvement of the nerve roots (C8/T1) or the brachial plexus is likely (possibly in addition to an ulnar injury).

As noted (see Anatomy), both the palmar cutaneous sensory branch of the ulnar nerve and the dorsal ulnar cutaneous branch come off the main ulnar branch above (proximal to) the wrist. Thus, a lesion exclusively at the wrist (at the canal of Guyon) would miss these branches, and the only sensory involvement would be in the superficial terminal branch. 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 the canal of Guyon 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.[104, 105, 106]

Laboratory Studies

Routine studies for ulnar nerve entrapment are ordered to rule out anemia, diabetes mellitus, and hypothyroidism and include the following:

Depending on the specific clinical situation, the following tests may be considered as well:

Radiography

Radiographs of the neck should be obtained if cervical disk disease is suspected and to rule out cervical ribs. Radiographs of the chest should be obtained if Pancoast tumor or tuberculosis is suspected.

Radiographs of both the elbow and the wrist are mandatory in ulnar nerve compression because double-crush syndrome may be present. Entrapment of the ulnar nerve may occur at more than one level.

Radiographs of the elbow reveal abnormal anatomy, such as a valgus deformity, bone spurs or bone fragments, a shallow olecranon groove, osteochondromas, and destructive lesions (eg, tumors, infections, or abnormal calcifications). If there is a history of trauma or arthritis, a cubital tunnel projection radiograph should be obtained to exclude medial trochlear lip osteophytes. If a supracondylar process on the medial aspect of the humerus is suspected, an elbow radiograph should be obtained 5 cm proximal to the medial epicondyle.

Radiographs of the wrist reveal fractures of the hook of the hamate, dislocations of the wrist bones, and, to a lesser extent, soft-tissue masses and calcifications.

Ultrasonography

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

The ultrasonographic finding that seems to be most useful in this setting 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.

A small study suggested 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.[115] Using this ratio did not improve diagnostic accuracy over what could be achieved simply by looking for the point of maximal swelling; however, the ratio did help distinguish compressive neuropathies from other systemic processes associated with diffuse nerve enlargement (eg, diabetes and polyneuropathy).

Subsequently, another study examined nerve vascularity in 137 patients afflicted with ulnar neuropathy at the elbow and determined that increased intraneural vascularization visualized by ultrasonography was indicative of axonal damage.[116]

Using high-resolution ultrasonography, Chiou et al found that the mean value of the area of the ulnar nerve at the level of the medial epicondyle in symptomatic patients was significantly larger than that of the control group and that of the unaffected, contralateral side.[117] They concluded that if the area of the ulnar nerve was greater than 0.075 cm2, at the level of the medial epicondyle, the patient probably had cubital tunnel syndrome.

An area in which ultrasonography may be particularly useful is evaluation of traumatic peripheral nerve injuries. In one study, 20 fresh cadaver arms were disarticulated, and the median, ulnar, or radial nerves were randomly transected in zero, one, or two locations per arm.[118] Sham incisions were performed throughout the extremity. The peripheral nerves were then systematically scanned by ultrasonographers who were blinded to the sites of transection.

The investigators found that high-resolution ultrasonography was able to identify transected nerves with 89% sensitivity and 95% specificity.[118] The diagnostic accuracy improved throughout the study: With the first 10 arms, the ultrasonographer correctly identified the transection in 77% of cases, whereas with the final 10 arms, the accuracy was 100%.

These findings suggest that the experience of the ultrasonographer has a vital effect on the diagnostic utility of ultrasonography in peripheral nerve injury. Thus, ultrasonography may be useful in determining the prognosis for nerve injury when an experienced ultrasonographer is available to distinguish between partial and complete injury, in localizing a nerve transection for possible surgical repair, or in both.[118, 119]

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 (EP) testing are sufficient to make the diagnosis of ulnar neuropathy, and MRI is not necessary. However, there may be a subgroup of patients with inconclusive findings on the standard evaluation in whom MRI may be beneficial.[120]

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. On MRI, increased signal intensity is a better indicator of ulnar nerve entrapment than enlargement of the nerve is.

Neurogenic muscle edema can be seen as early as 24-48 hours after denervation, and short T1 inversion recovery (STIR) sequences are particularly sensitive for that. This is to be contrasted with EP 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.[121]

Several small studies have attempted to address the use of MRI in the diagnostic evaluation of ulnar neuropathy. Vucic et al identified 52 patients who met clinical criteria for ulnar neuropathy on the basis of either sensory symptoms or motor weakness in the distribution of the ulnar nerve; all underwent EP testing.[122] In 63%, the EP studies were diagnostic of an ulnar neuropathy at a specific location, commonly at the elbow. In 37%, the studies were nonlocalizing according to American Association of Electrodiagnostic Medicine criteria.

All 52 patients subsequently underwent MRI scanning as well, which revealed abnormalities in 90%.[122] Of those patients who had diagnostic EP studies, 94% had an abnormal MRI; of those who had nondiagnostic EP studies, 84% had an abnormal MRI. The authors concluded that MRI was “more sensitive” than neurophysiologic testing and that the sensitivity of MRI did not change, regardless of the EP results.

A study by Andreisek et al assessed 51 patients with clinically evident neuropathies in the radial, median, or ulnar nerve who were referred to their center for MRI scans of an upper extremity.[123] The aim of this study was to assess the impact of the MRI results on clinical decision making and patient management.

Andreisek et al found only a weak-to-moderate correlation between MRI results and clinical findings—not surprisingly, given that clinical findings imply physiologic dysfunction of the nerves, whereas MRI findings can evaluate nerve morphology alone.[123] The greatest use of MRI in this study seemed to be in cases where the cause of the symptoms was unclear; in this situation, MRI reportedly identified the symptom etiology in 93% of cases. This resulted in a moderate-to-major impact on treatment in 84% of the patients in this subgroup.

These seemingly positive results notwithstanding, some caveats remain. First, criteria for diagnosing neuropathy on MRI scans are not well defined. Second, the clinical significance of certain MRI findings has been questioned. Husarik et al performed MRI elbow scans in 60 asymptomatic patients and found that 60% had increased ulnar-nerve signal intensity without concomitant changes in their medial or radial nerves. This study suggests that increased signal intensity should not be the sole criterion in evaluation for possible ulnar neuropathy.[124]

Britz et al examined the use of MRI with a STIR sequence to diagnose cubital tunnel syndrome.[125] They studied 31 elbows with documented ulnar nerve entrapment and found increased signal intensity in the ulnar nerve in 97% of cases and enlargement of the ulnar nerve in 75%.

The role of MRI in the evaluation of ulnar and other peripheral neuropathies continues to evolve. At this point, it is reasonable to conclude that MRI may be a useful adjunct in select cases, either when a specific compressive lesion (eg, a mass) is suspected or when a patient with the clinical syndrome of ulnar neuropathy has nondiagnostic EP tests. To improve diagnostic accuracy, further research is required to develop standardized criteria for making the diagnosis of ulnar neuropathy on MRI.[123, 124, 125, 126]

Electromyography and Nerve Conduction Studies

Electromyography (EMG) and nerve conduction studies are indicated to confirm the area of entrapment, document the extent of the pathology, and detect or rule out the possibility of double-crush syndrome.[127, 128, 129, 130] In recent entrapments of the ulnar nerve, motor and sensory conduction velocities are more useful, whereas in chronic neuropathies, conduction velocities and EMG are useful because EMG is capable of showing axonal degeneration.

EMG is not essential when the diagnosis of cubital tunnel syndrome is obvious on clinical examination; a false test result can be misleading and hinder rather than aid diagnosis. However, it is important to perform EMG when the diagnosis of cubital tunnel syndrome is unclear or when it is necessary to determine the efficacy of conservative treatment.[131]

Basic sensory and motor nerve parameters measured in nerve conduction studies include latency, amplitude, and conduction velocity. Electrodes (metallic reusable or pregelled disposable tape) are placed over the main belly of the active muscle (eg, the abductor digiti quinti or the first dorsal interosseous muscle)[107] and the tendon of the fifth or first digit. 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), in which the nerve is stimulated over 1- to 2-cm intervals, can increase the sensitivity of the procedure and may improve localization by helping the examiner judge whether a blockage is infracondylar (ie, near the cubital tunnel) or higher (ie, near the ulnar or epicondylar groove, the location associated with tardy ulnar palsy). (See the image below.)


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Inching technique used to isolate conduction block in left ulnar nerve. Note significant amplitude drop at 305 mm, which correlates with position 2 cm....

Findings are considered to be positive for cubital tunnel syndrome when the motor conduction velocity across the elbow is less than 50 m/s or when the difference between the motor conduction velocity across the elbow and that below the elbow exceeds 10 m/s.

If the point of maximum conduction delay and drop in amplitude of the compound muscle action potential (CMAP) is at or just proximal to the medial epicondyle, compression of the ulnar nerve is probably at the level of the epicondylar groove. If the point of maximum conduction delay and drop in CMAP amplitude is 2 cm distal to the medial epicondyle, compression is probably in the cubital tunnel. Unfortunately, false-positive results are obtained in 15% of cases.

It should be kept in mind that in any given case, it is impossible to know the exact course the ulnar nerve follows. 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, the examiner does not know precisely where the nerve is being stimulated. The takeoff point of the impulse may not be exactly under the stimulator.

A good percentage of experienced electromyographers believe that in many if not most cases, the best that can be done is to establish whether a blockage exists at the elbow, and often, even that cannot be accomplished with certainty. The relevant anatomic issues have been discussed more fully by Campbell.[40]

Reservations aside, the reader is invited to try the inching technique and make an individual assessment of its potential utility in his or her own situation. This might include the following steps:

Even if the inching technique does not yield the exact localization of the lesion, the attempt to use it may be helpful in and of itself insofar as it makes the clinician more conscious of the anatomy.

Martin-Gruber anastomosis

The anatomic variant known as Martin-Gruber anastomosis is seen during routine nerve conduction studies and can pose a diagnostic dilemma if not identified as such. It is an anomalous pattern of innervation occurring between the median and ulnar nerves in the forearm.[132]

In a Martin-Gruber anastomosis, a crossover of axons from the anterior interosseous nerve (the exclusively motor branch of the median nerve) 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).

The Martin-Gruber anomaly 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, though a gene controlling this occurrence has not been identified.

The fibers involved are from the C8/T1 nerve roots. Three patterns of Martin-Gruber anastomosis are commonly recognized, as follows (see the image below):

In a patient who does not have a Martin-Gruber anastomosis, stimulating the median nerve at the wrist produces a CMAP amplitude at the thenar eminence (eg, abductor pollicis brevis) 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.)

In a patient who does have 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 is true with ulnar nerve stimulation during recording over the hypothenar eminence (abductor digiti quinti) or the first digital interosseous muscle; median nerve fibers are innervating ulnar muscles in the hand, and the elbow response is smaller (see the images below). This could be mistaken for a conduction block. Accordingly, a Martin-Gruber anastomosis should be excluded before an ulnar conduction block is diagnosed.


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First 3 traces correspond to ulnar compound muscle action potential (CMAP) amplitude during recording at abductor digiti quinti (ADQ) and stimulating ....


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First 3 traces correspond to stimulation of ulnar nerve during recording at first dorsal interosseous (FDI) muscle at wrist, below elbow, and above el....

These relations can be visualized even more clearly by considering the characteristic EMG patterns with respect to the corresponding anatomy (see the image below).


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In those with Martin-Gruber anomaly who have no other significant neuropathy or nerve compression, stimulation of specific nerves at different sites y....

The distinctions between the three major types of the Martin-Gruber anastomosis, the tests performed to confirm them, and the possible areas of clinical confusion are summarized in the Table below.

Table. Types of Martin-Gruber Anastomosis


View Table

See Table

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. The explanation is 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; this would represent contributions from ulnar-derived muscles in the thenar eminence.[133, 134, 135, 136]

Riche-Cannieu anastomosis

Another anomaly that can complicate diagnostic studies is the Riche-Cannieu anastomosis (see the image below).


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

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

Approach Considerations

Nonsurgical therapy may be helpful in many cases of ulnar neuropathy. If conservative therapy fails, surgical treatment is warranted, typically involving one of the following procedures[133, 137, 138, 139, 140, 141, 142] :

More specifically, indications for surgery for ulnar nerve entrapment include the following:

If a fracture of the hook of the hamate is noted in the wrist, cast immobilization or splinting is required for 4-6 weeks. Surgery is indicated if symptoms progress during this time. On the other hand, as swelling subsides, pressure on the nerve may abate and symptoms may disappear. Nonsteroidal anti-inflammatory drugs (NSAIDs) are also valuable for reducing swelling in the tunnel.

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

Follow-up after surgery for ulnar nerve entrapment should take place at 1 month, 3 months, 6 months, and 1 year.

With appropriate decompression performed in a timely manner, the result of surgery for ulnar nerve entrapment should be a return to normal function. If decompression in situ is performed appropriately, return to normal function is almost immediate. With transposition of the nerve following decompression, postoperative immobilization, and the rehabilitative process, 3-6 months may pass before the patient regains normal function.

In chronic palsy (lasting >3-4 months) associated with pain, muscle weakness, or atrophy, surgical outcome is less certain. The duration of entrapment and the severity of numbness and muscle weakness are key factors influencing the prognosis. In these chronic cases, improvement may be limited or even absent after decompression and transposition, but further progression can be halted with proper decompression.

An important pitfall in treatment is to lead the patient to believe that full recovery can be expected in cases where recovery is actually uncertain. Of course, few doctors today promise perfection, and physicians often downplay the likelihood of complete recovery so as not to raise expectations unduly. Even so, many physicians, even neurologists and physiatrists, do not realize that an operation for ulnar entrapment has much less chance of a highly satisfactory result than an operation for carpal tunnel syndrome does. The reason for this is unclear.

Nonsurgical Therapy

Medical and other nonsurgical treatments can provide significant help in cases of ulnar neuropathy. Conservative measures are most likely to be successful when paresthesias are transient and caused by malposition of the elbow or blunt trauma. 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 by trying various pain medications, including the following:

Oral vitamin B-6 supplements may be helpful for mild symptoms. This treatment should be carried out for 6-12 weeks, depending on patient response.

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.[143] They may also use nerve gliding, sliding, or tensioning exercises aimed at promoting smoother movement of the nerve within the cubital tunnel and reducing adhesions and other causes of physical nerve compression.[144]

With nonoperative treatment, strengthening the elbow’s flexors and extensors both isometrically and isotonically within 0-45° of range of motion is helpful. To avoid ulnar nerve impingement in the cubital tunnel, the arc of elbow motion should be limited to an extended range.[145, 146] The patient should be advised to decrease repetitive activities that may exacerbate symptoms. The ulnar nerve should be protected from prolonged elbow flexion during sleep and protected during the day through avoidance of direct pressure or trauma.

For initial conservative treatment of cubital tunnel syndrome, use of an elbow pad or night splinting for a 3-month trial period is recommended.[147, 148] If symptoms do not improve with splinting, daytime immobilization for 3 weeks should be considered. Surgical release may be warranted if the symptoms do not improve with conservative treatment. If the symptoms do improve, conservative treatment should be continued for at least 6 weeks beyond symptom resolution to prevent recurrence.[149]

For mild cubital tunnel symptoms, a reversed elbow pad that covers the antecubital fossa, rather than the olecranon, helps remind the patient to maintain the elbow in an extended position and to avoid pressure on the nerve. At night, a pillow or folded towel may be placed in the antecubital fossa to keep the elbow in an extended position. Another option is to apply a commercial soft elbow splint, with a thermoplastic insert, for persistent symptoms.

For constant pain and paresthesia, one should consider using a rigid thermoplastic splint positioned in 45° of flexion to decrease pressure on the ulnar nerve. Initially, patients should wear this splint at all times; as symptoms subside, they can wear it only at night.

Patient education and insight are important. Resting on elbows at work, using elbows to lift the body from bed, and resting elbows on car windows while driving all are causes of paresthesia that can be corrected without surgical treatment. Patient education, anterior elbow extension splinting (if necessary), and correction of ergonomics at work should correct these transient palsies.

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 led to significant symptomatic improvement.[96, 150] It is noteworthy that in this study, adding splinting or nerve-gliding treatments to the program of providing information did not yield a significant further benefit.

Options for Surgical Intervention

If nonsurgical methods fail and the patient has severe or progressive weakness or atrophy, specific surgical techniques (eg, decompression in situ, decompression with anterior transposition, and medial epicondylectomy) are often beneficial in cases of ulnar neuropathy at the elbow.[151, 152] Entrapments in the canal of Guyon are also amenable to surgical treatment.[1] Surgery is also valuable for correction or stabilization of traumatic injuries, resection of masses or cysts, and sectioning of fibrous bands.

Preoperatively, appropriate blood work, chest radiography (if indicated), and a careful clinical examination are required (see Presentation and Workup). The usual surgical preparation of the affected extremity from fingers to neck is indicated. This is followed by the application of a tourniquet, if necessary.

Indications for ulnar nerve decompression in situ at the elbow are as follows:

Indications for ulnar nerve decompression with anterior transposition include the following:

Indications for medial epicondylectomy include the following[155, 156] :

Contraindications for the various operative procedures used to decompress the ulnar nerve are as follows:

A Cochrane review examined two meta-analyses of five randomized, controlled clinical trials of surgery for idiopathic ulnar neuropathy at the elbow,[96] four of which compared simple decompression with decompression plus transposition.[157, 158, 159, 160] These studies found no significant difference between simple decompression of the nerve and decompression with either submuscular or subcutaneous transposition.

The inability to detect a significant difference between simple decompression and decompression with transposition applied both to clinical outcomes and to neurophysiologic outcomes (ie, nerve conduction studies and EMG).[96] However, one difference between the two surgical approaches was that decompression with transposition produced more superficial and deep wound infections.

Two additional meta-analyses, using somewhat different methods, were also unable to find any significant differences between the outcomes of simple decompression and those of decompression plus transposition.[133, 161] However, one of these studies detected a trend in favor of decompression plus transposition, and the authors raised the possibility that a more highly powered study might be able to detect a difference.[133]

The aforementioned Cochrane review also examined one study that compared medial epicondylectomy with decompression plus anterior transposition and concluded that no significant differences could be found with respect to either clinical or neurophysiologic outcomes.[96] However, patient satisfaction was higher in patients treated with epicondylectomy.[91]

Decompression in Situ

Decompression in situ is essentially a localized decompression of the nerve, accomplished by incising the Osborne ligament and opening the tunnel beneath the two heads of the flexor carpi ulnaris by incising the fascia holding them together. It is easy to perform, and the complication rate is low. In contrast to other methods, ulnar nerve decompression in situ avoids damage to the vascular supply of the nerve. It is less traumatic to the patient than other decompression procedures, and it has been shown to be equally successful.[162, 138, 163]

The main advantage of decompression in situ is the ability to release the ulnar nerve in areas of compression with minimal disturbance of the blood supply. This procedure avoids subluxation of the ulnar nerve, which may lead to a recurrence of symptoms secondary to repeated contusion of the nerve as it snaps over the medial epicondyle.

The disadvantages of simple decompression are the potentially higher recurrence rate and the risk of continued subluxation of the ulnar nerve over the medial epicondyle, if that was present preoperatively.

An incision about 6-10 cm in length is made along the course of the ulnar nerve, midway between the medial epicondyle and the tip of the olecranon. This posterior incision is recommended to avoid damage to the medial brachial and medial antebrachial cutaneous nerves,[164] which must be identified and protected if encountered.

Tourniquet control is employed to facilitate visualization of the nerve. The ulnar nerve is identified proximally. The medial intermuscular septum is released; in some cases, it may be advisable to excise part of the thickened distal medial intermuscular septum to prevent kinking.

The cubital tunnel retinaculum is sharply divided in a proximal-to-distal direction. The ulnar nerve is exposed as it passes between the two heads of the flexor carpi ulnaris. The fascia over the flexor carpi ulnaris is incised, and the nerve is exposed as it passes through the muscle. The deep flexor-pronator aponeurosis is released. Neurolysis is not necessary.

The elbow is taken through its range of motion (ROM), and the ulnar nerve is examined for subluxation; if subluxation is noted, medial epicondylectomy or decompression with anterior transposition should be considered. The tourniquet is dropped, and hemostasis is obtained. Subcutaneous and skin layers are closed. A simple soft compressive dressing is applied. Postoperatively, no or only minimal immobilization is needed, and early active use of the extremity is encouraged.

Some, out of concern over possible resultant subluxation and new compression, believe that the nerve should not be decompressed proximally.[165] The risk of these adverse outcomes can be greatly reduced by limiting the decompression distal to a line drawn from the medial epicondyle to the tip of the olecranon. Proximal decompression is recommended when compression is secondary to a hypertrophied medial head of the triceps or to a snapping of the medial head of the triceps with elbow flexion.

Decompression With Anterior Transposition

Decompression with anterior transposition is usually the operation of choice for ulnar nerve compression at the elbow. Its main advantage is that it moves the ulnar nerve from an unsuitable bed to one that is less scarred. The nerve is effectively lengthened a few centimeters with transposition, and this decreases the tension placed on the nerve with elbow flexion.[37]

The primary disadvantage of an anterior transposition is that it is more technically demanding than a simple ulnar nerve decompression. The risk of complications is increased when the nerve is moved from its natural bed, and there is a potential for devascularization of the ulnar nerve.

There are three types of anterior transposition, as follows:

Each type has its advocates, and specific indications, advantages, and disadvantages differ from one type to the next.

Subcutaneous transposition

Subcutaneous transposition is the most commonly used method of transposition. It may be the procedure of choice in athletes who throw and do not have muscular atrophy. These athletes may lose forearm strength from a submuscular transposition and a simple decompression may not provide adequate relief of symptoms.

The main advantage of a subcutaneous transposition is that it is easy to perform. It is a good procedure when subluxation and traction on the nerve are contributing to the patient’s symptoms.[166] The primary disadvantage is that the nerve may be hypersensitive after surgery because of its new superficial location. The potential exists for disruption of the ulnar nerve blood supply with the transposition.

A longitudinal incision approximately 15 cm in length is made over the course of the ulnar nerve. Once the nerve is visualized from about 8 cm proximal to the medial epicondyle to 6 cm distal to the epicondyle, the distal portion of the medial intermuscular septum, the fibroaponeurotic roof of the epicondylar groove, the Osborne ligament, and the flexor carpi ulnaris fascia are incised, freeing the nerve. About 3-4 cm of the medial intermuscular septum proximal to the medial epicondyle is excised to prevent postoperative kinking of the nerve.

Distally, the additional common aponeurosis between the flexor digitorum superficialis to the ring finger and the humeral head of the flexor carpi ulnaris is sought and, if present, excised to prevent kinking. Motor branches to the flexor carpi ulnaris and flexor digitorum profundus are identified, protected, and preserved. The first motor branch to the flexor carpi ulnaris from the ulnar nerve proper is dissected out if necessary to prevent kinking.

The nerve is transposed into the subcutaneous plane. A search is made for any remaining sites of constriction or tethering. Several different modifications are used to maintain the ulnar nerve in the transposed position. One is to hold the nerve to the muscle fascia with a few sutures through the epineurium. However, the more popular approach is to use some form of sling.[167, 168] .

A commonly used technique involves the creation of a fasciodermal sling. A 1- to 1.5-cm square flap of antebrachial fascia based on the apex of the medial epicondyle is raised and reflected medially. The nerve is transposed anterior to this flap, and the apex is then sutured to the dermal tissue approximately 1 cm anterior to the medial epicondyle.

Another technique is to use a subcutaneous-to-fascial sling. About 2 cm of the subcutaneous fascia of the anterior skin flap is sutured to the flexor-pronator fascia, just anterior to the epicondyle, to keep the nerve in the transposed position.

A third technique is to create a fascial sling by using the medial intermuscular septum. The intermuscular septum is divided 3-4 cm proximal to its insertion on the medial epicondyle, with the distal attachment kept intact. The nerve is transposed. The septum is then used as either a myofascial or a fasciodermal sling to prevent posterior subluxation of the nerve. Care must be taken to prevent kinking of the nerve at the sling. Finally, a simple soft compressive dressing is applied, and early active ROM is instituted.

Postoperatively, the elbow must be immobilized in 45° of flexion for 2 weeks. Active mobilization with muscle stretching and strengthening is then carried out for 2-3 months.

Intramuscular transposition

Intramuscular transposition is the least popular decompression method. It yields the lowest rate of excellent results and is associated with the most recurrences with severe ulnar nerve compression.

The main advantage of an intramuscular transposition is that it buries the nerve deeply while providing a tunnel through which the nerve can pass. It also allows the nerve to be entirely surrounded by vascularized muscle tissue. The primary disadvantage is that it is a complicated procedure, involving substantial soft-tissue dissection. The risk of perineural scarring is increased, and the procedure may expose the nerve to repeated muscular contractions.

A longitudinal incision 15-20 cm in length is made over the course of the ulnar nerve, and the nerve is decompressed in the same manner as for subcutaneous transposition. The proximal border of the pronator teres and the medial intermuscular septum are excised from the midhumerus to the elbow. The nerve is then temporarily transposed, and the position of the nerve on the flexor-pronator mass is noted.

The ulnar nerve is replaced in the epicondylar groove, and a 5 mm deep trough is made in line with the nerve in its transposed position on the flexor-pronator mass. The fibrous septum separating the flexor-pronator muscles is then excised to provide a soft vascularized muscle bed. The nerve is transposed. The flexor-pronator fascia is closed over the nerve with the forearm fully pronated and the elbow flexed 90°. Finally, a simple soft compressive dressing is applied.

Postoperative management involves 3 weeks of immobilization at 90° of elbow flexion with the forearm in full pronation. This is followed by gradual active ROM exercises, stretching, and muscle strengthening.

Submuscular transposition

A submuscular transposition offers the best results with the fewest recurrences with severe ulnar nerve compression.[169] It is the best salvage procedure when previous surgery has failed because it places the nerve in an unscarred bed. It also works well for patients who are very thin, in whom a subcutaneous transposition may result in an area of hypersensitivity over the transposed nerve. Many consider an anterior submuscular transposition the procedure of choice for symptomatic athletes who throw.

The disadvantage of a submuscular transposition is that it is a technically demanding procedure. Because of the extensive dissection involved, postoperative recovery is more difficult, and there is a 5-10% risk of elbow flexion contracture. Patients may also develop extensive scar formation from the procedure, and revision is difficult if the patient has a recurrence.

In a submuscular transposition, the origin of the flexor-pronator muscle group must be released. This can be accomplished in a number of ways, and the most important part of any of these releases is to be able to reattach the muscle origin securely. Once the nerve has been transposed to its new bed deep to the flexor-pronator muscle group and on the brachialis, the flexor carpi ulnaris fascia is closed, as is the roof of the epicondylar groove.

A longitudinal incision 15-20 cm in length is made over the course of the ulnar nerve, and the nerve is decompressed in the same manner as for subcutaneous transposition. The anterior skin flap is raised until the bicipital aponeurosis is visualized. The overlying fascia is incised, with care taken to identify and protect the median nerve. Because of the extensive venous system in this area, meticulous hemostasis is important.[170]

With the nerves protected, the margins of the flexor-pronator mass are delineated. A plane is developed with blunt dissection between the flexor-pronator mass and the flexor digitorum superficialis and the ulnar collateral ligament. A hemostat is passed in this plane, with care taken to protect the nerves. The flexor-pronator mass is incised in a Z-cut fashion 1-2 cm distal to the medial epicondyle, and then reflected distally. The ulnar collateral ligament must be protected.

The tourniquet is then released and hemostasis obtained. The ulnar nerve is transposed adjacent and parallel to the median nerve. The lengthened flexor-pronator mass is reattached with nonabsorbable sutures with the elbow flexed and the arm pronated.

Postoperatively, the elbow is immobilized in a post mold or cast in 45° of flexion, with slight pronation and the wrist in neutral position, for 3-4 weeks. Active ROM exercises, stretching, and strengthening are then carried out for 3-4 months.

Surgical outcomes

In a retrospective study by Charles et al, 49 patients who underwent ulnar nerve transposition were followed to assess clinical sensory and motor recovery in cubital tunnel syndrome and to determine whether recovery is influenced by such factors as preoperative McGowan stage, age, and symptom duration.[137] Submuscular transposition was used in 25 patients, and subcutaneous transposition was applied in 24 patients.

Obvious improvement was reported in 20 of the 25 patients in the submuscular group and in 17 of the 24 patients in the subcutaneous group.[137] Both groups showed significant improvement in sensory and motor function, with 17 patients in each group recovering sensory function and 19 in each group recovering motor function. Patients with symptoms lasting longer than 6 months had a poor prognosis, regardless of the surgical technique used.

Jaddue et al compared operative technique (incision length and operating time), postoperative care (postoperative pain and complications), and outcome between subcutaneous and submuscular surgical techniques for anterior transposition of the ulnar nerve after decompression in moderate cubital tunnel syndrome.[171] Subcutaneous transposition was found to be associated with a shorter incision, reduced operating time, less postoperative pain, fewer postoperative complications, and better outcome.

Medial Epicondylectomy

Medial epicondylectomy is another technique for releasing pressure on the ulnar nerve at the elbow. Removal of the epicondyle removes a compressive area. Excision of the proper amount of bone is critical to the success of the procedure. If too much bone is excised, damage to the medial collateral ligament of the elbow with valgus instability may occur; if too little is removed, the procedure fails because the compressive area remains.

The main advantage of medial epicondylectomy is that it provides a more thorough decompression of the ulnar nerve than a simple release does. This results in a minitransposition of the ulnar nerve. Compared with decompression plus anterior transposition, medial epicondylectomy better preserves the blood supply to the nerve, causes less injury to the nerve, and preserves the small proximal nerve branches that might be sacrificed with an anterior transposition.[172]

The primary disadvantage is that it allows greater migration of the ulnar nerve with elbow flexion. There is a potential for elbow instability if the collateral ligaments are damaged. Bone pain and nerve vulnerability at the epicondylectomy site may occur. Compared with simple decompression, medial epicondylectomy is more likely to result in elbow stiffness or an elbow flexion contracture. In addition, it is often a poor choice for athletes who throw because of the significant stresses placed on the medial aspect of the elbow joint.

A longitudinal incision 10-15 cm in length is made over the course of the ulnar nerve, centered 1 cm anterior to the tip of the medial epicondyle.[173] The posterior branches of the medial brachial and antebrachial cutaneous nerves are identified and protected, and the nerve is decompressed as previously described.

A longitudinal incision is made over the medial epicondyle, which is then exposed by means of subperiosteal dissection. The flexor-pronator origin is detached from the epicondyle and reflected distally. With care taken to protect the nerve, the medial epicondyle, or a portion of it, is removed with an osteotome. It is important not to enter the elbow joint or cut the ulnar collateral ligament. Sharp edges of bone are smoothed with a rongeur or rasp.

The periosteum is then closed to prevent tethering of the nerve to the raw bone surface. The flexor-pronator origin is reattached with the elbow in extension to help prevent the development of a flexion contracture. The ulnar nerve is allowed to slide anteriorly.[174] Finally, a simple soft compressive dressing is applied.

No postoperative immobilization is necessary, and active ROM exercises are started as soon as the patient is able to tolerate them. Within 1-2 months, normal activities should be resumed.

Surgical outcomes

Seradge found flexion contractures after medial epicondylectomy in 5% of patients who started rehabilitation at an average of postoperative day 3 and in 52% of patients who started rehabilitation at an average of postoperative day 14.[88, 89] Patients in the early mobilization group returned to work twice as early as those in the late mobilization group did, and they experienced no adverse effects on their grip strength or other hand functions.

Weirich studied 36 patients who underwent subcutaneous transposition and found no differences in pain relief, weakness, patient satisfaction, grip strength, lateral pinch, or two-point discrimination between patients who were started on immediate active ROM exercises and those who started rehabilitation an average of 14 days postoperatively.[175] Patients in the immediate-mobilization group returned to work and performed activities of daily living earlier (median, 1 month) than those in the delayed-mobilization group (median, 2.75 months).

Endoscopic Cubital Tunnel Release

Endoscopy of nonjoint cavities is widely performed, and endoscopic carpal tunnel release is a popular, though still debated, method of releasing the median nerve at the wrist.[38] With this experience in mind, some authors have attempted endoscopic cubital tunnel release. This technique allows local decompression while offering the ability to decompress the nerve at all potential sites of compression. The possible advantages of this technique include limited invasiveness, reduced complication rates, and quicker rehabilitation.[176, 177]

Tsu-Min Tsai et al, after performing an endoscopic cubital tunnel release on 85 elbows in 76 patients and monitoring them for an average of 32 months, found that 42% had excellent results, 45% had good results, 11% had fair results, and 2% had poor results.[178] These results are comparable to those achieved with the other decompressive techniques, for which the overall rate of good-to-excellent results is 85-90%.

Complications of Surgical Intervention

The most serious complications of surgical decompression of the ulnar nerve are the following[179] :

The creation of a new compressive site at the time of surgery can occur with any of the decompressive methods.[180, 181] Injury to the posterior branches of the medial antebrachial cutaneous nerves at dissection is common. This nerve laceration results in loss of sensibility in an area of skin posterior and distal to the incision. Some patients develop a resultant dysesthesia in the nerve distribution; others develop an amputation neuroma.

Recurrent ulnar nerve subluxation and elbow instability can result from damage to the elbow collateral ligaments.[182] A postoperative flexion contracture can occur, most commonly following a submuscular transposition; it is seen after 5-10% of submuscular transpositions. Medial epicondylitis can occur from detachment of the flexor-pronator mass or as a result of a medial epicondylectomy. In addition, the symptoms may recur after an incomplete anterior transposition. Infection can occur with any surgical procedure.

After decompression with anterior transposition, complications can include recurrent subluxation of the ulnar nerve. Incomplete release of fascial slings may result in new areas of compression. In one series of subcutaneous transpositions, 90% of the failures were secondary to incomplete release of the medial intermuscular septum. An ineffective sling may not maintain the position of the transposed nerve and prevent resubluxation.

In addition, scarring may occur in the new muscular channel for the nerve. Perineural fibrosis may result from an intraneural injury or from a nerve transfer to a hypovascular bed. Injury to the flexor carpi ulnaris motor branches during nerve mobilization may result in weakness. Ligation of the posterior ulnar recurrent artery during nerve mobilization may result in nerve devascularization. A postoperative elbow flexion contracture may occur.

After medial epicondylectomy, medial instability may occur. To prevent this complication, the flexor-pronator origin is carefully detached to preserve the fibers of the medial collateral ligament. According to O’Driscoll et al, excision of more than 20% (1-4 mm) of the width of the medial epicondyle in the coronal plane violates the important anterior band of the ligament.[12]

Removal of the optimal amount of medial epicondyle, without creating instability, also improves results. Heithoff and Millender found in their series that a complete osteotomy resulted in 81% good and excellent results.[86] A partial osteotomy yielded a 67% rate of good or excellent results, and a minimal osteotomy yielded a 50% rate of good or excellent results.

Tenderness at the operative site can occur after medial epicondylectomy, sometimes resulting in prolonged and persistent discomfort during bone healing. In addition, loss of the protection afforded by the medial epicondyle may render the ulnar nerve more susceptible to trauma. To prevent the nerve from adhering to the osteotomy site postoperatively, it is important to preserve and close the periosteum at the end of the procedure.

Detachment of the flexor-pronator origin can result in weakness. Patients may develop an elbow flexion contracture that is often attributed to reattachment of the flexor-pronator muscle origin while the elbow is flexed or to delayed or inadequate postoperative mobilization.

Finally, postoperative ulnar neuropathies frequently give rise to lawsuits. Although such neuropathies appear to be most common after cardiac procedures, a Mayo Clinic study cited a rate of 0.5% even after noncardiac procedures.[183] Often, the neuropathy does not appear immediately after the operation, which suggests that the nerve trauma may occur in the postoperative period. Careful attention to protecting the ulnar nerve both during and after the procedure may reduce both the injury rate and the number of ensuing legal claims.

Medication Summary

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

Amitriptyline

Clinical Context:  Amitriptyline inhibits reuptake of serotonin and norepinephrine by the presynaptic neuronal membrane and thus may increase their synaptic concentrations in the central nervous system (CNS). The dosage may be increased slowly up to maximum of 125 mg/day. If no response is obtained, a different TCA may provide some benefit, but more often, it is preferable to use a drug from a different category (eg, an anticonvulsant).

Nortriptyline (Pamelor)

Clinical Context:  Nortriptyline has demonstrated effectiveness in the treatment of chronic pain. It inhibits reuptake of serotonin and norepinephrine by the presynaptic neuronal membrane and thus may increase their synaptic concentrations in the CNS. The pharmacodynamic effects of nortriptyline (eg, desensitization of adenyl cyclase and downregulation of beta-adrenergic receptors and serotonin receptors) also appear to play role in its mechanisms of action.

Desipramine (Norpramin)

Clinical Context:  Desipramine is a neurotransmitter reuptake inhibitor for norepinephrine and serotonin. It inhibits reuptake by the neuronal membrane, and it may also down-regulate beta-adrenergic receptors and serotonin receptors.

Duloxetine (Cymbalta)

Clinical Context:  Duloxetine is indicated for diabetic peripheral neuropathic pain. It is a potent inhibitor of neuronal serotonin and norepinephrine reuptake.

Class Summary

Tricyclic antidepressants (TCAs) are effective in painful paresthesias. Whereas the drugs in this category are administered in similar dosages, their sedative properties vary. Amitriptyline may be given if the patient suffers from insomnia, whereas nortriptyline and desipramine are better choices when sedation becomes a problem.

Mexiletine

Clinical Context:  Mexiletine is an orally active local anesthetic that is structurally related to lidocaine. It may operate by reducing spontaneous discharges from damaged primary small nerve fibers. Mexiletine is recommended only in intractable cases and 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 used off label for diabetic neuropathy.

Morphine sulfate (Astramorph, MS Contin, Avinza, Kadian, Oramorph)

Clinical Context:  Morphine sulfate is the drug of choice for analgesia in ulnar neuropathy because of its reliable and predictable effects, its good safety profile, and the ease with which its effects can be reversed with naloxone. Various intravenous dosages are used; the dosage is commonly titrated until the desired effect is obtained.

Class Summary

Traditionally, narcotics have been avoided in patients with peripheral neuropathies; however, they are useful in many cases.

Gabapentin (Neurontin)

Clinical Context:  Gabapentin (Neurontin, Gralise)

Gabapentin is a membrane stabilizer, a structural analogue of the inhibitory neurotransmitter gamma-aminobutyric acid (GABA); paradoxically, it is thought not to exert an effect on GABA receptors. It appears to act via the alpha2-delta1 and alpha2-delta2 auxiliary subunits of voltage-gated calcium channels. Gabapentin is used to manage pain and provide sedation in neuropathic pain.

Pregabalin (Lyrica)

Clinical Context:  Pregabalin is a structural derivative of GABA. Its mechanism of action is unknown; it is known to binds with high affinity to alpha2-delta subunits of calcium channels. In vitro, pregabalin reduces calcium-dependent release of several neurotransmitters, possibly by modulating calcium-channel function. It is approved by the US Food and Drug Administration (FDA) for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia and as adjunctive therapy in partial-onset seizures.

Lamotrigine (Lamictal)

Clinical Context:  Lamotrigine is a triazine derivative useful in the treatment of neuralgia. It inhibits release of glutamate and inhibits voltage-sensitive sodium channels, which stabilizes neuronal membrane. The manufacturer's recommendation for dosage adjustments should be followed.

Topiramate (Topamax, Qudexy XR, Topiragen, Trokendi XR)

Clinical Context:  The precise mechanism by which topiramate acts is unknown, but the following properties may contribute to efficacy: (1) electrophysiologic and biochemical evidence showing blockage of voltage-dependent sodium channels, (2) augmentation of GABA activity at some GABA-A receptor subtypes, (3) antagonism of the AMPA/kainate subtype of the glutamate receptor, and (4) inhibition of carbonic anhydrase, particularly isozymes II and IV.

Levetiracetam (Keppra, Keppra XR)

Clinical Context:  Levetiracetam is another new anticonvulsant being used to combat pain of peripheral neuropathies. The mechanism by which it alleviates pain is not known but is probably related to the fact that anticonvulsants generally reduce nerve irritability. Levetiracetam is not FDA-approved for this indication.

Phenytoin (Dilantin, Phenytek)

Clinical Context:  Phenytoin blocks sodium channels nonspecifically and therefore reduces neuronal excitability in sensitized C-nociceptors. It is effective in neuropathic pain but suppresses insulin secretion and may precipitate hyperosmolar coma in patients with diabetes. Its antineuralgic effects may derive from the blocking of posttetanic potentiation by reducing summation of temporal stimulation.

Carbamazepine (Tegretol, Carbatrol, Epitol, Equetro)

Clinical Context:  Carbamazepine is a sodium-channel blocker that typically provides substantial or complete relief of pain in 80% of individuals with both idiopathic and multiple sclerosis−associated trigeminal neuralgia within 24-48 hours. It reduces sustained high-frequency repetitive neural firing and is a potent enzyme inducer that can induce own metabolism. Because of the risk of potentially serious blood dyscrasias, a benefit-to-risk evaluation should be undertaken before administration of the drug is initiated.

Therapeutic plasma levels are between 4 and 12 µg/mL for analgesic and antiseizure response. Peak serum levels are reached in 4-5 hours. The serum half-life is 12-17 hours with repeated doses. Carbamazepine is metabolized in the liver to its active metabolite (ie, epoxide derivative) with a half-life of 5-8 hours. Metabolites are excreted via feces and urine.

Oxcarbazepine (Trileptal, Oxtellar XR)

Clinical Context:  The pharmacologic activity of oxcarbazepine is primarily exerted by the 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 are similar in older children (>8 years) and adults; young children (< 8 years) have 30-40% greater clearance than older children and adults. Children younger than 2 years have not been studied in controlled clinical trials. Oxcarbazepine is 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 for alleviating neuropathic pain probably depends on their general tendency to reduce neuronal excitability.

Author

Charles F Guardia III, MD, Instructor in Neurology, Department of Neurology, Dartmouth Hitchcock Medical Center, Geisel School of Medicine at Dartmouth

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

Chief Editor

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

Disclosure: Nothing to disclose.

Additional Contributors

Sandeep K Aggarwal, MD Clinical Assistant Professor of Neurology, Department of Neurology, Northwestern University Medical School

Disclosure: Nothing to disclose.

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

Christina J Azevedo MD is a member of the following medical societies: American Academy of Neurology

Disclosure: Nothing to disclose.

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

Paul E Barkhaus, MD is a member of the following medical societies: American Academy of Neurology, American Association of Neuromuscular and Electrodiagnostic Medicine, and American Neurological Association

Disclosure: Nothing to disclose.

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

Neil A Busis, MD is a member of the following medical societies: American Academy of Neurology and American Association of Neuromuscular and Electrodiagnostic Medicine

Disclosure: Nothing to disclose.

Harris Gellman, MD Consulting Surgeon, Broward Hand Center; Voluntary Clinical Professor of Orthopedic Surgery and Plastic Surgery, Departments of Orthopedic Surgery and Surgery, University of Miami, Leonard M Miller School of Medicine

Harris Gellman, MD is a member of the following medical societies: American Academy of Medical Acupuncture, American Academy of Orthopaedic Surgeons, American Orthopaedic Association, American Society for Surgery of the Hand, and Arkansas Medical Society

Disclosure: Nothing to disclose.

Mark D Lazarus, MD Associate Professor of Orthopedic Surgery, Medical College of Pennsylvania-Hahnemann University, Chief of Shoulder and Elbow Service, Department of Orthopedic Surgery, Hahnemann University Hospital

Disclosure: Nothing to disclose.

Andrew K Palmer, MD Chair, Professor, Department of Orthopedics, State University of New York-Upstate Medical University

Andrew K Palmer, MD is a member of the following medical societies: American Osteopathic College of Physical Medicine and Rehabilitation

Disclosure: Del Palma Orthopedics Salary Board membership

Joseph E Sheppard, MD Professor of Clinical Orthopedic Surgery, Chief of Hand and Upper Extremity Service, Department of Orthopedic Surgery, University of Arizona Health Sciences Center, University Physicians Healthcare

Joseph E Sheppard, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Society for Surgery of the Hand, and Orthopaedics Overseas

Disclosure: Nothing to disclose.

Scott P Steinmann, MD Assistant Professor of Orthopedics, Mayo Medical School; Consulting Staff, Department of Orthopedic Surgery, Mayo Clinic of Rochester

Scott P Steinmann, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Society for Surgery of the Hand, and Minnesota Medical Association

Disclosure: Nothing to disclose.

Mark Stern, MD Former Chief, Department of Orthopedic Surgery, Cedars-Sinai Medical Center

Mark Stern, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, California Medical Association, and Western Orthopaedic Association

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

James R Verheyden, MD Consulting Surgeon, Department of Orthopedic Surgery, The Orthopedic and Neurosurgical Center of the Cascades

James R Verheyden, MD is a member of the following medical societies: American Academy of Orthopaedic Surgeons, American Medical Association, and American Society for Surgery of the Hand

Disclosure: Nothing to disclose.

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Schematic diagram of elbow region, with 5 main sites (as given by Posner) labeled 1-5; other sites and structures are also named. Main regions of interest are circled with pastel-colored arrows. Sites 2 and 3 are close together and cannot be distinguished by means of electromyography and nerve conduction studies. This location is referred to as ulnar (or epicondylar) groove.

Diagram shows ulnar nerve distal to elbow region. Dorsal ulnar cutaneous nerve (lavender) branches off main trunk (blue). Although course is not followed in detail after that, lavender region on sensory dermatome diagram shows where this sensory nerve innervates skin. Similarly, palmar cutaneous sensory nerve (yellow) branches off to innervate skin area depicted in yellow. Superficial terminal branch is mostly sensory (see green-colored skin on palmar surface), though it also gives off branch to palmaris brevis. Deep terminal branch has no corresponding skin area, because it is solely motor-innervating muscles shown, as well as others not explicitly depicted. Nerve could be pinched or injured anywhere, but sites labeled I-IV are more commonly involved.

Inching technique used to isolate conduction block in left ulnar nerve. Note significant amplitude drop at 305 mm, which correlates with position 2 cm above medial epicondyle. This is example of supracondylar block. Image courtesy of A S Lorenzo, MD.

Normal median and ulnar patterns are compared with those of 3 commonly recognized types of Martin-Gruber anomaly.

First 3 traces correspond to ulnar compound muscle action potential (CMAP) amplitude during recording at abductor digiti quinti (ADQ) and stimulating at wrist, below elbow, and above elbow, respectively. Fourth trace corresponds to stimulation of median nerve at elbow during recording at ADQ. Although CMAP amplitude is reduced markedly above elbow, this is compensated for by adding response seen after stimulation of median nerve; this represents Martin-Gruber anastomosis.

First 3 traces correspond to stimulation of ulnar nerve during recording at first dorsal interosseous (FDI) muscle at wrist, below elbow, and above elbow, respectively. Fourth trace corresponds to stimulation of median nerve at elbow during recording at FDI muscle; this represents Martin-Gruber anastomosis.

In those with Martin-Gruber anomaly who have no other significant neuropathy or nerve compression, stimulation of specific nerves at different sites yields differing results. With median nerve, stimulation at elbow yields larger compound muscle action potential (CMAP) at hypothenar muscles, first dorsal interosseous (FDI) muscle, or thenar muscles (or combination thereof) than does stimulation at wrist. With ulnar nerve, stimulation at wrist yields larger CMAP at hypothenar muscles, FDI muscle, or thenar muscles (or combination thereof) than does stimulation at elbow. In this context, "larger" and "smaller" generally refer to amplitude differences ≥1.0 mV.

Riche-Cannieu anastomosis is communication between recurrent branch of median nerve and deep branch of ulnar nerve in hand. Although it is present in 77% of hands, it yields highly variable degrees of detectable physiologic difference; in many hands, it contributes little and does not affect diagnostic findings at all. Most common effect is probably to give ulnar innervation to some muscles usually innervated by median nerve, median innervation to muscles usually innervated by ulnar nerve, or both. Most extreme version is so-called all-ulnar hand (very rare). Two examples of confusion this might cause are as follows. (1) Median lesion could cause denervation in typically ulnar muscle, such as adductor digiti minimi (adductor digiti quinti) or first dorsal interosseous muscle. (2) Ulnar lesion could cause denervation in typically median muscle, such as flexor pollicis brevis or abductor pollicis brevis.

Schematic diagram of elbow region, with 5 main sites (as given by Posner) labeled 1-5; other sites and structures are also named. Main regions of interest are circled with pastel-colored arrows. Sites 2 and 3 are close together and cannot be distinguished by means of electromyography and nerve conduction studies. This location is referred to as ulnar (or epicondylar) groove.

Diagram shows ulnar nerve distal to elbow region. Dorsal ulnar cutaneous nerve (lavender) branches off main trunk (blue). Although course is not followed in detail after that, lavender region on sensory dermatome diagram shows where this sensory nerve innervates skin. Similarly, palmar cutaneous sensory nerve (yellow) branches off to innervate skin area depicted in yellow. Superficial terminal branch is mostly sensory (see green-colored skin on palmar surface), though it also gives off branch to palmaris brevis. Deep terminal branch has no corresponding skin area, because it is solely motor-innervating muscles shown, as well as others not explicitly depicted. Nerve could be pinched or injured anywhere, but sites labeled I-IV are more commonly involved.

Inching technique used to isolate conduction block in left ulnar nerve. Note significant amplitude drop at 305 mm, which correlates with position 2 cm above medial epicondyle. This is example of supracondylar block. Image courtesy of A S Lorenzo, MD.

Normal median and ulnar patterns are compared with those of 3 commonly recognized types of Martin-Gruber anomaly.

First 3 traces correspond to ulnar compound muscle action potential (CMAP) amplitude during recording at abductor digiti quinti (ADQ) and stimulating at wrist, below elbow, and above elbow, respectively. Fourth trace corresponds to stimulation of median nerve at elbow during recording at ADQ. Although CMAP amplitude is reduced markedly above elbow, this is compensated for by adding response seen after stimulation of median nerve; this represents Martin-Gruber anastomosis.

First 3 traces correspond to stimulation of ulnar nerve during recording at first dorsal interosseous (FDI) muscle at wrist, below elbow, and above elbow, respectively. Fourth trace corresponds to stimulation of median nerve at elbow during recording at FDI muscle; this represents Martin-Gruber anastomosis.

In those with Martin-Gruber anomaly who have no other significant neuropathy or nerve compression, stimulation of specific nerves at different sites yields differing results. With median nerve, stimulation at elbow yields larger compound muscle action potential (CMAP) at hypothenar muscles, first dorsal interosseous (FDI) muscle, or thenar muscles (or combination thereof) than does stimulation at wrist. With ulnar nerve, stimulation at wrist yields larger CMAP at hypothenar muscles, FDI muscle, or thenar muscles (or combination thereof) than does stimulation at elbow. In this context, "larger" and "smaller" generally refer to amplitude differences ≥1.0 mV.

Riche-Cannieu anastomosis is communication between recurrent branch of median nerve and deep branch of ulnar nerve in hand. Although it is present in 77% of hands, it yields highly variable degrees of detectable physiologic difference; in many hands, it contributes little and does not affect diagnostic findings at all. Most common effect is probably to give ulnar innervation to some muscles usually innervated by median nerve, median innervation to muscles usually innervated by ulnar nerve, or both. Most extreme version is so-called all-ulnar hand (very rare). Two examples of confusion this might cause are as follows. (1) Median lesion could cause denervation in typically ulnar muscle, such as adductor digiti minimi (adductor digiti quinti) or first dorsal interosseous muscle. (2) Ulnar lesion could cause denervation in typically median muscle, such as flexor pollicis brevis or abductor pollicis brevis.

Type Anatomy Most Characteristic Finding Confirmation Additional Verification Potential Clinical Confusion
ICrossover fibers innervate hypothenar musclesUlnar stimulation at wrist* produces larger hypothenar CMAP than stimulation at elbowStimulation of median nerve at elbow† produces response at hypothenar musclesHypothenar CMAP from ulnar stimulation at wrist is equal to 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 FDI muscleUlnar stimulation at wrist produces larger FDI CMAP than stimulation at elbowStimulation of median nerve at elbow produces response at FDIFDI CMAP from ulnar stimulation at wrist is equal to FDI CMAP from ulnar stimulation at elbow plus FDI CMAP from median stimulation at elbow Usually none, because FDI muscle is not usually 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 wrist stimulationUlnar 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 is equal to median wrist stimulation amplitude plus ulnar wrist stimulation amplitude minus ulnar elbow stimulation amplitude Can complicate median nerve studies, especially when carpal tunnel syndrome is involved
ADP—adductor pollicis; CMAP—compound motor (or muscle) action potential; FDI—first dorsal interosseous; FPB—flexor pollicis brevis.

*Ulnar stimulation at wrist yields larger CMAP at hypothenar muscles, FDI, or thenar muscles (or sometimes combination of these) than does stimulation at elbow.

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

Note: “Larger” and “smaller” generally mean amplitude difference ≥1.0 mV.