Ulnar Neuropathy

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). The 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, 4]

The most common site of ulnar nerve entrapment is at or near the elbow region, especially in the region of the cubital tunnel[5] 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, 6, 7, 8]  Entrapment can also occur in the forearm between these two regions, below the wrist (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 grip weakness and, rarely, intrinsic wasting. One of the most severe consequences is losing 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 two lumbricals are functioning.

Conservative nonsurgical treatment may play a beneficial role in management. However, surgical treatment is warranted if such treatment fails or the patient has severe or progressive weakness or loss of function. 

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.[9, 10] 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.[11, 12] Here, the nerve lies on the anterior aspect of the medial head of the triceps, which 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 arcade of Struthers is the next important site along the course of the ulnar nerve. 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 essential 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 medial epicondyle (medial border)

• The olecranon (lateral border)

• The elbow capsule at the posterior aspect of the ulnar collateral ligament (floor)

• The humeroulnar arcade (HUA), or Osborne fascia or ligament (roof)

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 flexor carpi ulnaris aponeurosis fibers, which blend 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,[13] 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, which may cause compression.[14]

O’Driscoll also identified a retinaculum at the proximal edge of the arcuate ligament in all but 4 of 25 cadaveric specimens.[13] He classified this retinaculum into the following four types:

• Absent retinaculum

• Thin retinaculum that becomes tight with full flexion without compressing the nerve

• Thick retinaculum that compresses the nerve between 90° and full flexion

• Accessory anconeus epitrochlearis

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. Finally, about 5 cm distal to the medial epicondyle, the ulnar nerve pierces the flexor-pronator aponeurosis, the common fibrous origin of the flexor and pronator muscles.

The ligament of the 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 the anterior transposition of the ulnar nerve, it is essential to recognize and release this structure to prevent kinking.

In the forearm, the ulnar nerve extends motor branches to the flexor carpi ulnaris, the flexor digitorum profundus of the ring, and small fingers. The ulnar nerve may extend as many as four 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 from 6 cm proximal to 4 cm distal to the medial epicondyle. These branches are often cut when 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. It is bounded proximally and distally by the pisiform bone and the hook of the hamate bone. In addition, 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:

• Martin-Gruber anastomosis in the forearm - In this anomaly, fibers that supply the intrinsic muscles are carried in the median nerve to the middle of the forearm, where they leave the median nerve to join the ulnar nerve; functioning intrinsic muscles could be observed with injury above this anastomosis, though the ulnar nerve dysfunction is proximal

• Riche-Cannieu anastomosis - Median and ulnar nerves are connected in the palm; even with an injury at the wrist, there is some intrinsic function.

Blood supply

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

• Superior ulnar collateral artery

• Inferior ulnar collateral artery

• Posterior ulnar recurrent artery

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.[15]

Sites of nerve entrapment

As diagnostic and surgical methodologies have evolved over the past century, physicians’ ability to recognize and describe entrapment sites has improved. However, the terminology used to describe ulnar nerve entrapment has become confusing because not all clinicians use the exact words for the same things. This confusion can be illustrated by examining the terms applied to ulnar nerve entrapment in the elbow region,[16] of which the two most commonly used (and misused) are tardy ulnar palsy[17] and cubital tunnel syndrome.[18]

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.[19] Additional cases were reported over the ensuing decades,[20, 21] usually associated with trauma (eg, fractures in the elbow region) and typically occurring in the epicondylar groove.[22, 23] 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).[24]

From 1922 on, physicians began to recognize ulnar entrapments in the HUA.[25, 26] In 1958, the term cubital tunnel syndrome was coined to describe the effects of the ulnar nerve entrapment[27] 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 areas are so close together that certain authorities categorize them differently to get a different number.) Therefore, this article principally follows Posner’s classification,[28] which lists the following sites (see the image below):

• Above the elbow in the region of the intermuscular septum

• The medial epicondylar region

• The epicondylar (ie, ulnar) groove

• The region of the cubital tunnel

• The region where the ulnar nerve exits from the flexor carpi ulnaris, at which the usual cause of compression is the deep flexor-pronator aponeurosis

A schematic diagram of the elbow region with 5 main sites (as given by Posner) labeled 1-5; other sites and structures are also named. The main regions of interest are colored circles. 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.

Region of intermuscular septum

Halikis et al[29] divided this region into 2 areas, the arcade of Struthers[30, 31] 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 about 6-10 cm proximal to the medial epicondyle.

Considerable anatomic variation exists; in fact, there is outright controversy about the arcade of Struthers.[32] 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.[33]

In an autopsy study of 60 upper limbs, Siqueira found a structure reasonably approximating the definition given above in 8 limbs (13.5%).[32] 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.[34]

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.[35] This structure was 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.[36] 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. However, 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 previous anatomic descriptions.

Medial epicondylar region

Ulnar compression[37] in the medial epicondylar region is generally from a valgus deformity of the bone. For example, a patient is placed in a standard anatomic position with the palms rotated toward the front and the thumb away from the midline. In that case, a valgus deformity means that the elbow would be deformed away from the body’s midline.

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 its beginning.

Campbell used slightly different terminology, lumping the epicondylar groove with the medial epicondylar region and labeling the entire region as the area of the retrocondylar groove. Halikis et al. considered the medial epicondylar region and the epicondylar groove to be the medial epicondyle area.[29]

The medial epicondylar region and the epicondylar groove are generally considered the classic locations (or locations, if considered as a single area) for tardy ulnar palsy. However, in the author’s personal experience, electromyographers and orthopedic surgeons 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.[38, 39, 40]

Campbell’s classification was 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 the cubital tunnel and the Osborne fascia.[29] This is an excellent example of the problems with the terminology: Different terms are used for locations that are virtually the same. For all practical purposes—indeed, concerning 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 the ulnar nerve exits from flexor carpi ulnaris

Campbell[41] and Halikis et al[29] 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,[42, 43, 20] 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).

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

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

• Zone 1 (encompassing the area proximal to the bifurcation of the ulnar nerve) - Compression in zone 1 causes combined motor and sensory loss; it is most commonly caused by a fracture of the hook of the hamate or a ganglion

• Zone 2 (encompassing the motor branch of the nerve after it has bifurcated) - Compression in zone 2 causes pure loss of motor function to all of the ulnar-innervated muscles in hand; ganglion and fracture of the hook of the hamate are the most common causes

• Zone 3 (encompassing the superficial or sensory branch of the bifurcated nerve) - Compression in zone 3 causes sensory loss to the hypothenar eminence, the small finger, and part of the ring finger, but it does not cause motor deficits; common causes are an aneurysm of the ulnar artery, thrombosis, and synovial inflammation

As the elbow moves from extension to flexion, the distance between the medial epicondyle and the olecranon increases by 5 mm for every 45° elbow flexion. Elbow flexion places stress on the medial collateral ligament and the overlying retinaculum. In addition, 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.[44, 45] 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 six times normal.[46, 47, 48, 49, 37]

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 a complete 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.[50] The ulnar nerve elongates by 5-8 mm with elbow flexion.

In addition to prior cadaver and surgical studies of ulnar nerve motion, recently developed sonographic methods facilitate monitoring the movement in the intact arm.[51] Interestingly, the nerve is somewhat more motile in patients with ulnar neuropathies than in individuals with normal ulnar nerves.

Within the cubital tunnel, the measured mean intraneural pressure is significantly greater than the mean extraneural pressure at elbow flexion of 90° or more.[52] 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. Therefore, a 45° flexion is considered the optimum position for immobilization of the elbow to decrease the 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°.[53] Of the 325 patients with ulnar nerve subluxation, only 14 had unilateral subluxation. Subluxation does not appear to cause cubital tunnel syndrome. Still, the friction generated with repeated subluxation may cause intraneural inflammation, and the subluxed position may render the nerve more susceptible to accidental trauma.

Sunderland described the internal topography of the ulnar nerve at the medial epicondyle.[54] The sensory 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.[55, 56, 57] The central location protects the motor fibers and explains why weakness of these two muscles is not typically seen in ulnar neuropathy.[58, 59, 28, 60]

Proximal compression of a nerve trunk, such as 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 the disruption of normal axonal transport.[61]

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 the nerve. In the absence of changes indicating axonal damage, conduction block means myelin damage to the involved segment. Significant slowing of conduction or 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:[62]

• Neurapraxia - This is a transient episode of complete motor paralysis with little sensory or autonomic involvement, usually occurring secondary to transitory mechanical pressure; once the pressure is relieved, a total return of function follows

• Axonotmesis - This is a more severe injury involving loss of continuity of the axon with the maintenance of continuity of the Schwann sheath; motor, sensory, and autonomic paralysis is complete, and denervated muscle atrophy can be progressive; recovery can be full but depends on several factors, including timely removal of the compression and axon regeneration; the time necessary to recover function depends on the distance between the denervated muscle and the proximal regenerating axon

• Neurotmesis - This is the most severe level of injury, entailing complete loss of continuity both of the axon and the Schwann sheath; recovery rarely is full, and the amount of loss can only be determined over time; regenerating axons without intact neural tubes reinnervate muscle fibers that were not part of their original network

Sunderland’s classification specifies five degrees of nerve damage.[63] 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. Finally, in a fifth-degree injury, the nerve trunk is severed.

McGowan established the following classification system for ulnar nerve injuries[64] :

• Grade I - Mild lesions with paresthesias in the ulnar nerve distribution and a feeling of clumsiness in the affected hand; no wasting or weakness of the intrinsic muscles

• Grade II - Intermediate lesions with weak interosseous muscles and muscle wasting

• Grade III - Severe lesions with paralysis of the interosseous muscles and marked weakness of the hand

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.[65] There was a high correlation between DASH scores, the severity of symptoms, and functional status. Correlations were identified as significant between DASH and biomechanical measures, but correlation coefficients were lower. All measurements showed significant improvement postoperatively.

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 of. 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.[66, 67, 68]

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

• Compression during general anesthesia

• Blunt trauma

• Deformities (eg, rheumatoid arthritis)

• Metabolic derangements (eg, diabetes)

• Transient occlusion of the brachial artery during surgery[69]

• Subdermal contraceptive implant[70]

• Venipuncture[71]

• Hemophilia[72] leading to hematomas

• Malnutrition leading to muscle atrophy and loss of fatty protection across the elbow and other joints

• Cigarette smoking[73]

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

• Ganglionic cysts

• Tumors

• Blunt injuries, with or without fracture

• Aberrant artery

• Idiopathic

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.[74] This is consistent with an independent anatomic study of 200 cadavers from 1963, which showed that the ulnar nerve is the largest at the entrance to the cubital tunnel and that this enlargement is a maximal size in males older than 35 years.[75] A prospective study of 76 patients published in 2006 showed that increased age correlates with a greater tendency toward ulnar neuropathy.[76]

Sex-related demographics

No gross anatomic differences in the course of the nerve are noted between the sexes. However, the following have been noted:[77]

• Men develop perioperative ulnar neuropathies[28] at the elbow[78] more frequently than women do[76] ; cubital tunnel syndrome is 3-8 times more common in men

• Women have 2-19 times more fat content in the medial elbow overlying the tubercle of the ulnar coronoid process

• The tubercle of the coronoid process is 1.5 times larger in men

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.[77]

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

The following factors are relevant to the prognosis:

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

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

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

• The outcome is not correlated with clinical features noted at baseline or with the duration of symptoms before treatment

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

Unfavorable or poor surgical outcome is associated with the following:

• Age older than 50 years

• Coexisting diabetes or other causes of peripheral polyneuropathy

• Atrophy and ongoing denervation of ulnar-derived muscles

• Absent ulnar sensory responses

• Postoperative position of the ulnar nerve in relation to the medial epicondyle[81, 82, 83]

Bartels et al performed a meta-analysis of the literature from 1970 to 1997, which included 3024 patients. [84] 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 following 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.[85]

Steiner et al. monitored 41 patients who underwent simple ulnar nerve decompression for an average follow-up period of 2 years.[86] Results were good or excellent in 89% of the patients; 8% had no improvement.

Lluch studied 20 patients who underwent decompression in situ through a transverse incision.[87] 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 an excellent 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.[88]

Kaempffe and Farbach reviewed 27 patients who underwent partial medial epicondylectomies and were monitored for an average of 13 months.[89] Subjective improvement was noted in 93% of cases. Results were excellent in 8 patients, good in 10, and fair in 8; 1 had a poor outcome.

To assess factors influencing outcome after medial epicondylectomy, Seradge and Owen studied 160 patients over ten years and monitored them for three years postoperatively.[90] In all, 21 patients had a recurrence—a return of symptoms three months or longer after surgery—and 44% of these recurrences occurred in the fourth decade of life. The recurrence rate was 18% in females and 10% in males. In addition, the recurrence rate was twice as high in patients who did not return to work within three months.

When concomitant ipsilateral carpal tunnel syndrome was present, the recurrence rate was 17%, compared with 9% when this syndrome was absent.[90] When concurrent 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 three months postoperatively.

Seradge also examined the results of medial epicondylectomy in patients on workers’ compensation.[91] These patients stayed out of work longer, used a long 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 monitored for an average of 15 months.[92] In 87% of patients, symptoms resolved or improved. In addition, the 24 patients receiving workers’ compensation had a 33% rate of complete symptom resolution, whereas those not receiving workers’ compensation had a 57% rate of full symptom resolution.

Geutjens et al conducted a prospective study of 52 patients, comparing medial epicondylectomy with anterior transposition.[93] Results were better with medial epicondylectomy: More patients were satisfied, more stated that they would have the operation, and fewer complained of mild pain in their hand postoperatively. However, no follow-up visits or significant differences were present in motor power or nerve conduction rates.

Kleinman and Bishop monitored 47 patients after anterior intramuscular transposition for an average of 28 months.[94] Results were good or excellent in 87%, with the 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 was performed with or without preservation of the extrinsic vasculature.[95] 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, 4fair, 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.[96] 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.[97] 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 parts of their motor and sensory functions.

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 and neurophysiologic improvement. Transposition was associated with a higher incidence of wound infections. [98]

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.[18]

It is crucial to determine when the symptoms began, how long they last, 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.[99, 100]

Pain rarely occurs in hand. Instead, 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 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.” Still, usually, they are not quite so explicit unless prompted. Occasionally, 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 opening jars or turning doorknobs or may experience early fatigue or weakness with work requiring 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 a complaint of weakness. In this scenario, the patient complains that the little finger gets caught on the edge of the pants pocket when they try 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 the 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 inserted on the ulnar side of the joint. Typically, this muscle is opposed by ulnar-innervated muscles that flex the joints. However, in ulnar neuropathy, the muscle is relatively unopposed and pulls the finger up to the ulnar side. This is the perfect position for catching onto the edge of the pocket.

The patient may also express the weakness complaint 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 unimpaired muscles.

Sometimes, a patient notices that the thumb−index finger pincer grip is weak. Two 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 the examiner demonstrates it, it constitutes the Froment sign.

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:

• Check elbow range of motion, and examine the carrying angle; look for areas of tenderness or ulnar nerve subluxation 

• Check for the Tinel sign - This sign is typically present in individuals with cubital tunnel syndrome; however, as many as 24% of the asymptomatic population also present with the sign

• Perform an elbow flexion test - This test, generally considered the best diagnostic test for cubital tunnel syndrome,[101, 102] involves having the patient flex the elbow past 90°, supinate the forearm, and extend the wrist; results are positive if discomfort is reproduced or paresthesia occurs within 60 seconds

• Consider a shoulder internal rotation test - In this test, the upper extremity is kept at 90° of shoulder abduction, maximal internal rotation, and 10° of flexion, with the elbow, flexed at 90°, the wrist in neutral, and the fingers extended; a result is considered positive if any symptom attributed to cubital tunnel syndrome appears within 10 seconds; this test appears specific to cubital tunnel syndrome and may be more sensitive for the syndrome than the 10-second elbow flexion test is[103]

• Palpate the cubital tunnel region to exclude mass lesions

• Examine for intrinsic muscle weakness

• Examine for clawing or abduction of the small finger with extension (the Wartenberg sign)

• Assess the ability to cross the index and middle fingers

• Check for the Froment sign with a critical pinch

• Check grip and pinch strength

• Check vibratory perception and light touch with Semmes-Weinstein monofilaments - This is more important than static and moving 2-point discrimination tests, which reflect innervation density, as the initial changes in nerve compression affect threshold

• Check 2-point discrimination

• Evaluate sensation, especially the area on the ulnar dorsum of the hand supplied by the dorsal ulnar sensory nerve - Hypoesthesia in this area suggests a lesion proximal to the canal of Guyon

• Exclude other causes of dysesthesias and weakness along with the C8-T1 distribution (eg, cervical disk disease or arthritis, thoracic outlet syndrome, and ulnar nerve impingement at the canal of Guyon)

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

Several factors contribute to the clawed appearance. Wasting 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 ulnar nerve innervates the flexors. 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 inserted 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 solid muscle activity in either direction, leads to flexion. Because of the unopposed radial nerve innervation, the first three digits are extended at both the metacarpophalangeal joints and the interphalangeal joints. 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 when 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 generally 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 heavily uses the adductor pollicis to adduct the thumb and the first dorsal interosseous muscle to move the index finger.

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

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

Positive Tinel sign at the 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 pretty specific if appropriately performed (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. Palpating the nerve in the ulnar groove may produce a similar result.

Atrophy and muscle weakness

The most crucial 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) ones near 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.[104]

The ulnar muscles should not be examined in isolation from other muscles. In particular, several vital muscles with C8/T1, lower-trunk, and 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.

Suppose both the ulnar intrinsic hand muscles and the ulnar forearm muscles are involved. In that case, an ulnar nerve lesion should be suspected in the elbow region (or, very rarely, above the elbow region). 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. The forearm muscles are sometimes spared 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 several separate fascicles. In some instances, 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 the wrist

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

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

• Interosseous muscle weakness only, with no sensory loss - This would most likely be due to compression of the deep motor branch after the branch to the hypothenar muscles had taken off

• Weakness of the interosseous and hypothenar muscles, with sensory involvement in the fifth digit - This would suggest involvement in the canal of Guyon with compression of both the deep motor branch and the superficial terminal sensory branch (ie, what might be considered the typical or classic Guyon canal pattern)

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

• Interosseous weakness and sensory loss, with preserved function in the hypothenar and dorsal ulnar cutaneous territories - This would imply a compression of the deep motor branch and the superficial terminal sensory branch distal to the point where the subbranch to the hypothenar area (eg, the abductor digit minimi) had split off from the deep motor branch

Sensory examination

Adding information from the sensory examination to the motor examination helps localize the ulnar lesion.[105]

Although in some patients, the area of the palmar cutaneous sensory nerve can extend a bit farther proximally than 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. Again, 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. The patient might perceive compression at the canal of Guyon and might be detectable on examination only in the tips of the fingers. Thus, the compression would affect only the superficial terminal branch.[106, 107, 108]

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

• Complete blood cell (CBC) count

• Urinalysis

• Fasting blood glucose

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

• Hemoglobin A1C[111]

• Antinuclear antibody

• Erythrocyte sedimentation rate

• Renal function tests

• Paraproteinemia workup (serum protein electrophoresis with immunofixation)

• Angiotensin-converting enzyme

• Lyme serology

• Thyroid function tests

• Vitamins B-12, B-1, and B-6

• Folate level

• Methylmalonic acid

• Tissue transglutaminase antibody

• Gliadin antibody

• HIV serology

• Hepatitis serologies

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

Radiographs of both the elbow and wrist radiographs are mandatory in ulnar nerve compression because double-crush syndrome may be present. In addition, 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 soft-tissue masses and calcifications to a lesser extent.

High-resolution ultrasonographic examination of peripheral nerves may be used to support the clinical and electrophysiologic diagnosis of compressive neuropathy. It may also help identify specific compressive etiologies of nerve injury (eg, tumors or cysts) and visualize structural nerve changes. Advantages of ultrasonography include the following:

• Unlike computed tomography (CT) or magnetic resonance imaging (MRI), ultrasonography provides real-time evaluation of nerve displacement or compression during movements of adjacent joints

• Ultrasonography is noninvasive, cheap, portable, and well-tolerated

• Ultrasonography is readily available (though technicians with specific experience in peripheral nerve ultrasonography may not be)

• The peripheral nerve can be followed for much of its course in an extremity[112, 113, 114, 115, 116]

The ultrasonographic finding that seems to be most helpful in this setting is a change in the diameter of a nerve at the site of compression. Just proximal to the site of compression, nerve swelling can often be seen.

A small study suggested that using a ratio of the cross-sectional nerve area at maximal enlargement and an uninvolved site could improve diagnostic accuracy.[117] 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.[118]

Chiou et al used high-resolution ultrasonography and found that the mean value of the ulnar nerve area at the medial epicondyle level in symptomatic patients was significantly more extensive than that of the control group and that of the unaffected, contralateral side.[119] They concluded that if the ulnar nerve area 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 in evaluating 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.[120] Sham incisions were performed throughout the extremity. The peripheral nerves were then systematically scanned by ultrasonographers blinded to the transection sites.

The investigators found that high-resolution ultrasonography could identify transected nerves with 89% sensitivity and 95% specificity.[120] 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 can distinguish between partial and complete injury, in localizing a nerve transection for possible surgical repair, or in both.[120, 121]

A further consideration is the comparison of the localizations derived from sonographic and electrophysiological methods. Simon et al compared the lesion localization obtained by careful short-segment neurophysiological inching studies with that obtained by ultrasonographic methods.[122] For the larger segment across the entire elbow, the overall drop in conduction velocity correlated well with the maximum cross-sectional area (CSA) and maximal degree of the hypoechoic fraction. However, on the short segments in patients whose lesion was apparently at the medial epicondyle as judged by neurophysiological methods, the maximal sonographic abnormalities were detected both slightly proximally and distally to the medial epicondyle. It was concluded, therefore, that the ultrasonographic images may see secondary changes adjacent to the primary site of damage.

MRI is increasingly used to evaluate peripheral neuropathies, including ulnar neuropathy.[123] In most patients, history, physical examination, and electrophysiologic (EP) testing are sufficient to diagnose ulnar neuropathy, and MRI is not necessary. However, there may be a subgroup of patients with inconclusive findings on the standard evaluation for whom MRI may benefit.[124]

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 usually is isointense to slightly hyperintense to surrounding muscle. Normal nerves do not enhance after the 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.

Neurogenic muscle edema can be seen as early as 24-48 hours after denervation, and short T1 inversion recovery (STIR) sequences are susceptible to that. It contrasts 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 also be seen with MRI.[125]

Several small studies have attempted to address the use of MRI in the diagnostic evaluation of ulnar neuropathy. For example, Vucic et al identified 52 patients who met clinical criteria for ulnar neuropathy based on either sensory symptoms or motor weakness in the ulnar nerve distribution; all underwent EP testing.[126] In 63%, the EP studies were diagnostic of ulnar neuropathy at a specific location, commonly at the elbow. In 37%, the studies were non-localizing according to the American Association of Electrodiagnostic Medicine criteria.

All 52 patients also underwent MRI scanning, which revealed abnormalities in 90%.[126] 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.

Andreisek et al. assessed 51 patients with clinically evident neuropathies in the radial, median, or ulnar nerve, which were referred to their center for MRI scans of an upper extremity.[127]  This study aimed 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. In contrast, MRI findings can evaluate nerve morphology alone.[127] The most effective 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. In addition, it 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, the 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 nerve. This study suggests that increased signal intensity should not be the sole criterion in evaluation for possible ulnar neuropathy.[128]

Britz et al examined the use of MRI with a STIR sequence to diagnose cubital tunnel syndrome.[129] 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%.

Diffusion-tensor imaging (DTI) is an advanced quantitative MRI technology.[130] This has previously been used mainly to image central myelin tracts, but it is also applicable to peripheral myelin. As with central myelin, quantitative measures of MRI parameters, including fractional anisotropy (FA), can be obtained. For example, qualitative FA maps of nerve tracts allow observers to detect peripheral neuropathy with a sensitivity of 80% and a specificity of 83%, which are high enough to make them quite useful. A prospective study of 39 patients showed a positive correlation between the clinical findings, electrodiagnostic tests, and DTI parameters in carpal tunnel syndrome patients.[131] . Neuropathic segments typically show lower FA values compared to healthy nerve segments.[132, 133]

The role of MRI in the evaluation of the ulnar and other peripheral neuropathies continues to evolve. At this point, it is reasonable to conclude that MRI may be a helpful 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 a nondiagnostic EP test. Further research is required to develop standardized criteria for diagnosing ulnar neuropathy on MRI, to improve the diagnostic accuracy.[127, 128, 129, 134]

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 a double-crush syndrome.[135, 136, 137, 138] In recent entrapments of the ulnar nerve, motor and sensory conduction velocities are more valuable, whereas, in chronic neuropathies, conduction velocities and EMG are helpful 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.[139]

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)[109] and the tendon of the fifth or first digit. The ulnar nerve is stimulated at the wrist, 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.)

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.

Findings are considered 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 elbow angle does not determine precisely where the nerve is running beneath the skin. Thus, the examiner does not know exactly where the nerve is being stimulated. In addition, the takeoff point of the impulse may not be precisely 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. Often, even that cannot be accomplished with certainty. The relevant anatomic issues have been discussed more fully by Campbell.[41]

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:

• After performing the inching technique, report to the prospective surgeon where you think the blockage might be with respect to anatomic landmarks

• Make it clear that this is a tentative assessment (ie, done to the best of your ability but not to be taken as definite)

• Ask the surgeon to tell you where the blockage actually seemed to be after surgery was performed

• Keep track of your findings compared with surgical findings, and draw your own conclusions about how accurate the inching method is in your own hands.

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 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. A unique innervation pattern occurs between the forearm's median and ulnar nerves.[140]

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):

• Type I (second most common pattern) - The hypothenar muscles are involved

• Type II (most common pattern) - The crossover fibers innervate the first dorsal interosseous muscle

• Type III (least common pattern) - The thenar muscles, typically the adductor pollicis and the flexor pollicis brevis rather than the abductor pollicis brevis, are involved; sometimes other muscles, including forearm muscles such as the flexor digitorum superficialis and the flexor digitorum profundus, are involved as well

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

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), 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 signal dispersion.)

In a patient with the anomaly, however, the wrist response is smaller because many axons from the median nerve have already crossed. 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 innervate ulnar muscles in hand, and the elbow response is smaller (see the images below). Again, this could be mistaken for a conduction block. Accordingly, a Martin-Gruber anastomosis should be excluded before an ulnar conduction block is diagnosed.

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.

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

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 the median nerve, stimulation at the 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 the wrist. With the ulnar nerve, stimulation at the wrist yields larger CMAP at hypothenar muscles, FDI muscle, or thenar muscles (or combination thereof) than does stimulation at the elbow. In this context, "larger" and "smaller" generally refer to amplitude differences ≥1.0 mV.

The distinctions between the three major types of 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 (Open Table in a new window)

Two potentially critical 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 travel 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%. However, 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, representing contributions from ulnar-derived muscles in the thenar eminence.[141, 142, 143, 144]

Riche-Cannieu anastomosis

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

Riche-Cannieu anastomosis is communication between the recurrent branch of the median nerve and the deep branch of the ulnar nerve in the 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. The most common effect is probably to give ulnar innervation to some muscles usually innervated by the median nerve, median innervation to muscles usually innervated by the ulnar nerve, or both. The most extreme version is the so-called all-ulnar hand (very rare). Two examples of confusion this might cause are as follows: (1) a median lesion could cause denervation in typically ulnar muscle, such as adductor digiti minimi (adductor digiti quinti) or first dorsal interosseous muscle, and (2) an ulnar lesion could cause denervation in typically median muscle, such as flexor pollicis brevis or abductor pollicis brevis.

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.

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[141, 145, 146, 147, 148, 149, 150] :

• Decompression in situ

• Decompression with anterior transposition (subcutaneous, intramuscular, or submuscular) 

• Medial epicondylectomy

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

• No improvement in presenting symptoms after 6-12 weeks of conservative treatment

• Progressive palsy or paralysis

• Clinical evidence of a long-standing lesion (eg, muscle wasting or clawing of the fourth and fifth digits)

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 diminish, 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 occur at 1 month, 3 months, 6 months, and 1 year.

With appropriate decompression performed on time, the result of surgery for ulnar nerve entrapment should return to normal function. If decompression in situ is performed appropriately, a return to normal function is almost immediate. With the transposition of the nerve following decompression, postoperative immobilization, and the rehabilitative process, 3-6 months may pass before the patient regains normal function.[151]

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

An essential pitfall in treatment is to lead the patient to believe that full recovery can be expected in cases where recovery is uncertain. Of course, few doctors today promise perfection, and physicians often downplay the likelihood of complete recovery so as not to raise expectations. Even so, many physicians, 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. The reason for this is unclear.

Medical and other nonsurgical treatments can significantly help in cases of ulnar neuropathy. Conservative measures are most likely 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 the treatment of the underlying condition.

The physician can address pain or other sensory symptoms by trying various pain medications, including the following:

• NSAIDs

• Tricyclic (and related) antidepressants

• Anticonvulsants

• Narcotics (generally considered to be a last resort)

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

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 alleviate pressure effects.[152] They may also use nerve gliding, sliding, or tensioning exercises to promote the nerve's smoother movement within the cubital tunnel and reduce adhesions and other causes of physical nerve compression.[153]

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, limit the elbow motion arc to an extended range.[154, 155] The patient should be advised to decrease repetitive activities that may exacerbate symptoms. In addition, the ulnar nerve should be protected from prolonged elbow flexion during sleep and saved during the day by avoiding direct pressure or trauma.

For initial conservative treatment of cubital tunnel syndrome, an elbow pad or night splinting for a 3-month trial is recommended.[156, 157] If symptoms do not improve with splinting, daytime immobilization for three weeks should be considered. Surgical release may be warranted if the symptoms do not improve with conservative treatment. If the symptoms improve, conservative treatment should be continued for at least six weeks beyond symptom resolution to prevent a recurrence. [158]

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 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 at 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 essential. Resting on elbows at work, using elbows to lift the body from the 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 preventing or reducing movements or positions that compromise the nerve led to significant symptomatic improvement.[98, 159] 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.

Suppose nonsurgical methods fail and the patient has severe or progressive weakness or atrophy. In that case, specific surgical techniques (eg.decompression in situ, decompression with anterior transposition, and medial epicondylectomy) are often beneficial in ulnar neuropathy at the elbow.[160, 161] Entrapments in the canal of Guyon are also amenable to surgical treatment.[1] Surgery is also valuable for correcting or stabilizing traumatic injuries, resectioning masses or cysts, and sectioning fibrous bands.

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

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

• Mild ulnar nerve compression

• Documented mild slowing on electromyography (EMG) as the ulnar nerve passes into and through the proximal flexor carpi ulnaris

• Absence of pain around the medial epicondyle

• Nerve that does not sublux with elbow flexion

• Normal osseous anatomy and epicondylar (ulnar) groove at the elbow and findings at surgery that is consistent with compression under the fibrous arcade[162]

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

• Unsuitable bed for the nerve secondary to the presence of osteophytes

• Tumor

• Ganglion

• Accessory anconeus epitrochlearis

• Heterotopic bone

• Significant bursal tissue or other mass

• Significant tension on the ulnar nerve as indicated by a positive elbow flexion test result or symptoms aggravated by activities requiring flexion

• Subluxation of the ulnar nerve with elbow flexion

• Deformity at the elbow secondary to a valgus elbow or a tardy ulnar palsy[163, 3]

• Valgus instability at the elbow

Indications for medial epicondylectomy include the following:[164, 165]

• Nonunion of an epicondyle fracture with ulnar nerve symptoms (best indication)

• Poor bed for the ulnar nerve in the epicondylar groove

• Ulnar nerve subluxation

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

• Decompression in situ - This procedure should not be used in cases of severe posttraumatic neuropathy with scarring, chronic subluxation, or dislocation of the ulnar nerve from the epicondylar groove and soft-tissue masses in the epicondylar groove

• Decompression with anterior subcutaneous transposition - This procedure does not release the ulnar nerve completely, leaving the distal course from the cubital tunnel as a possible site of compression; thus, it may not be the best choice for transposition in a thin person who lacks significant adipose tissue at the site of transposition, because of the possibility of repeated trauma to the nerve at the elbow[19]

• Decompression with anterior intramuscular transposition - This is the most controversial of the procedures because of the claim of severe postoperative scarring

• Decompression with anterior submuscular transposition - This procedure is contraindicated in the presence of scarring of the joint capsule or irregularity of the elbow joint due to malunited fracture, severe arthritis, or previous excisional arthroplasty

• Medial epicondylectomy - This procedure is not used when double-crush syndrome with entrapment at the distal end of the cubital tunnel or soft-tissue masses in the epicondylar groove is suspected

A Cochrane review examined two meta-analyses of five randomized, controlled clinical surgery trials for idiopathic ulnar neuropathy at the elbow,[98] four of which compared simple decompression with decompression plus transposition.[166, 167, 168, 169] 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 transposition decompression is applied to clinical outcomes and neurophysiologic outcomes (ie, nerve conduction studies and EMG).[98] 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.[141, 170] 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.[141]

The previous Cochrane review also examined one study that compared medial epicondylectomy with decompression plus anterior transposition. It concluded that it could not find significant differences concerning clinical or neurophysiologic outcomes.[98] However, patient satisfaction was higher in patients treated with epicondylectomy.[93]

A more recent study of 480 patients reported in 2014 showed that both approaches effectively improved clinical outcomes for ulnar nerve compression at the cubital tunnel.[171] However, the decompression (neurolysis) alone showed greater effectiveness in relieving pain at the elbow.

Decompression in situ is essentially a localized decompression of the nerve. It is 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 is equally successful.[172, 146, 173]

The main advantage of decompression in situ is the ability to release the ulnar nerve in compression areas with minimal blood supply disturbance. In addition, 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 would be the potentially higher recurrence rate and the risk of continued subluxation of the ulnar nerve over the medial epicondyle if that were 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,171, 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 extremity use is encouraged.

Out of concern over possible resultant subluxation and new compression, some believe that the nerve should not be decompressed proximally.[174] The risk of these adverse outcomes can be significantly 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 a snapping of the medial head of the triceps with elbow flexion.

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 lengthened a few centimeters with transposition, decreasing the tension placed on the nerve with elbow flexion.[38]

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

There are three types of anterior transposition, as follows:

• Subcutaneous

• Intramuscular

• Submuscular

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. However, these athletes may lose forearm strength from a submuscular transposition, and a simple decompression may not relieve symptoms adequately.

The main advantage of a subcutaneous transposition is that it is easy to perform. Therefore, it is a suitable procedure when subluxation and nerve traction contribute to the patient’s symptoms.[175] The primary disadvantage is that the nerve may be hypersensitive after surgery because of its new superficial location. In addition, the potential exists for disruption of the ulnar nerve blood supply with the transposition.

A longitudinal incision approximately 15 cm in length is made throughout 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 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 a sling.[176, 177]

A commonly used technique involves the creation of a fasciodermal sling. First, a 1- to 1.5-cm square flap of antebrachial fascia based on the apex of the medial epicondyle is raised and reflected medially. Next, the nerve is transposed anterior to this flap, and the apex is 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 creating a fascial sling 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 avoid 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 at 45° of flexion for two weeks. Then, active mobilization with muscle stretching and strengthening is 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 surrounded by vascularized muscle tissue. The primary disadvantage is that it is a complicated procedure involving substantial soft-tissue dissection. In addition, the risk of perineural scarring increases, and the procedure may expose the nerve to repeated muscular contractions.

A longitudinal incision 15-20 cm in length is made throughout the ulnar nerve, and the nerve is decompressed similarly for subcutaneous transposition. The proximal border of the pronator teres and the medial intermuscular septum is excised from the mid humerus 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 excised to provide a soft vascularized muscle bed. The nerve is transposed. The flexor-pronator fascia is closed over the nerve, the forearm fully pronated, and the elbow flexed 90°. Finally, a simple soft compressive dressing is applied.

Postoperative management involves three 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.[178] 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 very thin patients, in whom a subcutaneous transposition may result in an area of hypersensitivity over the transposed nerve. Finally, 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. In addition, because of the extensive dissection involved, the postoperative recovery is more complex, and there is a 5-10% risk of elbow flexion contracture. Patients may also develop extensive scar formation from the procedure, and revision is complex 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 several ways, and the most crucial part of any of these releases is 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 throughout the ulnar nerve, and the nerve is decompressed similarly 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.[179]

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, 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 is 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 at 45° of flexion, with slight pronation and the wrist in a neutral position, for 3-4 weeks. Then, active ROM exercises, stretching, and strengthening are 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 such factors influence recovery as preoperative McGowan stage, age, and symptom duration.[145] Submuscular transposition was used in 25 patients, and subcutaneous transposition was applied in 24 patients.

Noticeable improvement was reported in 20 of the 25 patients in the submuscular group and 17 of the 24 patients in the subcutaneous group.[145] 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 six 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 procedures for anterior transposition of the ulnar nerve after decompression in moderate cubital tunnel syndrome.[180] Subcutaneous transposition was associated with a shorter incision, reduced operating time, less postoperative pain, fewer postoperative complications, and better outcomes.

Medial epicondylectomy is another technique for releasing pressure on the ulnar nerve at the elbow. Removal of the epicondyle removes a compressive area. The excision of the proper amount of bone is critical to the procedure's success. 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. This results in a mini transposition of the ulnar nerve. Compared with decompression plus anterior transposition, medial epicondylectomy better preserves the blood supply to the nerve causes minor injury to the nerve and preserves the small proximal nerve branches that might be sacrificed with an anterior transposition.[181]

The primary disadvantage is that it allows more significant migration of the ulnar nerve with elbow flexion. As a result, there is a potential for elbow instability if the collateral ligaments are damaged. In addition, bone pain and nerve vulnerability at the epicondylectomy site may occur. As a result, medial epicondylectomy is more likely to result in elbow stiffness or an elbow flexion contracture than simple decompression. 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 throughout the ulnar nerve, centered 1 cm anterior to the tip of the medial epicondyle.[182] 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 through 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. Avoiding entering the elbow joint or cutting the ulnar collateral ligament is essential. Sharp edges of bone are smoothed with a rongeur or rasp.

The periosteum is then closed to prevent the tethering of the nerve to the raw bone surface. Next, the flexor-pronator origin is reattached with the elbow in extension to help prevent the development of a flexion contracture. Next, the ulnar nerve is allowed to slide anteriorly.[183] Finally, a simple soft compressive dressing is applied.

No postoperative immobilization is necessary, and active ROM exercises are started as soon as the patient can tolerate them. Within 1-2 months, regular 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.[90, 91] Patients in the early mobilization group returned to work twice as early as those in the late mobilization group. In addition, 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 began rehabilitation with an average of 14 days after postoperatively.[184] Patients in the immediate-mobilization group returned to work and performed activities of daily living earlier (median, one month) than those in the delayed-mobilization group (median, 2.75 months).

Endoscopy of nonjoint cavities is widely performed, and endoscopic carpal tunnel release is popular, though still debated, method of releasing the median nerve at the wrist.[39] 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 compression sites. The possible advantages of this technique include limited invasiveness, reduced complication rates, and quicker rehabilitation.[185, 186]

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 and 45% had good, 11% had fair results, and 2% had poor results.[187] 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%. 

The most severe complications of surgical decompression of the ulnar nerve are the following:[188]

• Failure to decompress the nerve adequately, causing a new area of entrapment with the decompression

• Injury to the nerve during decompression or transposition

• Neuromata of the medial antebrachial cutaneous nerve

• Failure to recognize a double-crush syndrome

• Infection, failure to heal, thrombophlebitis, atelectasis, and failure of the operation due to an unknown cause 

Creating a new compressive site at the time of surgery can occur with any of the decompressive methods.[189, 190] 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.[191] 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 the 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 ulnar nerve subluxation. 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 the insufficient 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 a nerve transfer to a hypovascular bed. Damage to the flexor carpi ulnaris motor branches during nerve mobilization may result in weakness. Ligating 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.[13]

Removing the optimal amount of medial epicondyle without creating instability also improves results. For example, Heithoff and Millender found in their series that a complete osteotomy resulted in 81% good and excellent results.[88] 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. Therefore, 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 often attributed to reattachment of the flexor-pronator muscle origin. In contrast, 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.[192] Often, the neuropathy does not appear immediately after the operation, suggesting that nerve trauma may occur in the postoperative period. Careful attention to protecting the ulnar nerve both during and after the procedure may reduce the injury rate and the number of ensuing legal claims.

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

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.

Amitriptyline

Amitriptyline inhibits the reuptake of serotonin and norepinephrine by the presynaptic neuronal membrane and thus may increase their synaptic concentrations in the central nervous system (CNS). Therefore, the dosage may be increased slowly up to a 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 another category (eg, an anticonvulsant).

Nortriptyline (Pamelor)

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

Desipramine (Norpramin)

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, Irenka)

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

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.

Mexiletine

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

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

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

Morphine sulfate is the drug of choice for analgesia in ulnar neuropathy because of its reliable and predictable effects, good safety profile, and 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

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.

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. Instead, it acts 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)

Pregabalin is a structural derivative of GABA. Its mechanism of action is unknown; it is known to bind with high affinity to alpha2-delta subunits of calcium channels. In vitro, pregabalin reduces the 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)

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

Topiramate (Topamax, Qudexy XR, Trokendi XR)

The precise mechanism by which topiramate acts is unknown. Still, 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)

Levetiracetam is another new anticonvulsant used to combat the 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)

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 blocking post-tetanic potentiation by reducing the summation of temporal stimulation. 

Carbamazepine (Tegretol, Carbatrol, Epitol, Equetro)

Carbamazepine is a sodium-channel blocker that typically provides substantial or complete relief of pain in 80% of individuals with 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 drug administration 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)

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, inhibiting repetitive neuronal firing and impairing synaptic impulse propagation. The 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 two years have not been studied in controlled clinical trials. Oxcarbazepine is not FDA-approved for this indication.