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Ulnar neuropathy at the elbow and wrist

Ulnar neuropathy at the elbow and wrist
Literature review current through: Jan 2024.
This topic last updated: Jan 12, 2023.

INTRODUCTION — Entrapment or compressive neuropathies are common problems that may lead to functional impairment and disability of the upper limb due to weakness, altered sensation, loss of dexterity, and sometimes pain [1]. Ulnar neuropathy, especially at the elbow, is a common focal neuropathy affecting the upper extremity and is second in frequency only to entrapment of the median nerve at the wrist (the carpal tunnel syndrome). Accurate and timely diagnosis is important for clarifying the presence and severity of nerve injury, determining prognosis, avoiding unnecessary investigation or surgery, and establishing a treatment plan.

This topic will review the clinical features, diagnosis, and treatment of ulnar neuropathy at the elbow and wrist. Other focal neuropathies affecting the arm and hand are discussed separately. (See "Overview of upper extremity peripheral nerve syndromes" and "Brachial plexus syndromes" and "Carpal tunnel syndrome: Clinical manifestations and diagnosis".)

ANATOMY — The ulnar nerve is derived from the anterior rami of the C8 and T1 spinal nerves with a variable contribution from C7 (figure 1). These contributing fibers are initially carried in the lower trunk and medial cord of the brachial plexus with the ulnar nerve arising in the proximal axilla.

Upper arm – In the upper arm, the ulnar nerve lies in close proximity to the brachial artery and the median nerve. It has no motor or sensory branches above the elbow (figure 2). This anatomic feature can lead to challenges in localizing proximal ulnar nerve lesions in some cases.

Midhumeral region – At the midpoint of the upper arm, the ulnar nerve pierces the medial intermuscular septum (the arcade of Struthers) and heads posteriorly where it lies close to the humerus and the medial head of the triceps brachii muscle and tendon. Distal to this segment, the ulnar nerve travels within the retrocondylar groove of the elbow, posteromedial to the medial epicondyle. As the nerve exits the groove, it passes under the aponeurotic arch of the flexor carpi ulnaris muscle, also called the humeroulnar arcade [2], which is formed by attachments of this muscle to the medial epicondyle and olecranon (figure 3). The proximal edge of the arcade lies approximately 1 to 2 cm distal to a line joining the medial epicondyle and olecranon. This is an important structure clinically because it is often implicated as the cause of compressive ulnar neuropathy at the elbow.

Cubital tunnel – After passing underneath the arch, the ulnar nerve travels within the cubital tunnel through the two heads of the flexor carpi ulnaris muscle. The roof of the cubital tunnel is the humeroulnar arcade proximally, and the substance of the two heads of the flexor carpi ulnaris muscle distally. The floor of the tunnel is composed of the medial elbow ligaments proximally and the deep fibers of the flexor carpi ulnaris muscle more distally. The nerve then pierces the aponeurosis lining the deep heads of the flexor carpi ulnaris and runs between the tendons and muscle planes of the medial forearm to the wrist.

Forearm – The ulnar nerve gives off motor branches to the flexor carpi ulnaris in the proximal forearm, distal to the medial epicondyle and just proximal to or within the cubital tunnel (figure 2) [3]. The branch to the ulnar-innervated portion of the flexor digitorum profundus (supplying digits four and five) is given off more distally within the cubital tunnel. The palmar cutaneous branch arises in the midforearm and runs distally over the volar aspect of the forearm and wrist without passing through Guyon's canal. It supplies the cutaneous territory over the proximal border of the ulnar portion of the palm (figure 4). The dorsal cutaneous branch is given off more distally, approximately 5 cm proximal to the wrist, and courses dorsally around the ulna to supply the ulnar side of the dorsum of the hand and dorsal surfaces of the fifth and ulnar half of the fourth digit (figure 4).

Guyon’s canal – At the wrist, the ulnar nerve passes through Guyon's canal (along with the ulnar artery), the floor of which is formed by the transverse carpal ligament and pisohamate ligament. The roof of Guyon's canal consists of the palmar fascia and the palmaris brevis muscle. The ulnar nerve then divides into the superficial and deep terminal branches (figure 5). In the hand, after giving off a branch to the palmaris brevis muscle, the superficial terminal branch supplies the cutaneous ulnar border of the palm and then divides into two digital branches that innervate the palmar or volar surfaces of the fifth and ulnar half of the fourth digit (figure 4). The deep branch pierces and innervates the opponens digiti muscle and then gives off a branch to the remaining hypothenar muscles just after emerging from Guyon's canal. In the palm, the deep branch innervates all of the interossei and the third and fourth lumbricals (figure 2). It then terminates in the thenar eminence where it supplies the adductor pollicis and variable portions of the flexor pollicis brevis muscles.

The anatomy of the ulnar nerve at the elbow requires special mention, given the close relationship between the musculoskeletal structures of this region and the ulnar nerve. With elbow flexion, the distance between the medial epicondyle and olecranon increases by up to 1 cm. This results in tightening of the humeroulnar arcade of the flexor carpi ulnaris over the nerve (figure 6). Also upon flexion, the medial elbow ligaments bulge and flatten the floor of the normally deep retrocondylar groove, while the medial head of the triceps muscle pushes the nerve posteriorly. With complete elbow flexion the nerve is stretched taut around the medial epicondyle, whereas in extension there is redundant length in the nerve allowing for freedom of movement. Intraoperative pressure recordings in patients with ulnar neuropathy have documented increased pressure under the humeroulnar arcade during elbow flexion [4].

LOCALIZATION AND ETIOLOGY — The most common site of focal ulnar entrapment or compression is at the elbow, followed by the wrist.

Elbow — Ulnar neuropathy at the elbow was first identified in 1878 within a description of operative treatment for ulnar neuropathy following remote elbow fracture [5]. Broca and Mouchet applied the term "tardy ulnar palsy" to this syndrome in 1899 [6]. This term has subsequently been used inappropriately to describe all cases of ulnar neuropathy at the elbow, as opposed to only those following remote bony injury. Entrapment under the humeroulnar arcade was described in 1922 [7], in what later became known as the cubital tunnel syndrome [8]. This term is also often used inappropriately to describe all causes of ulnar neuropathy at the elbow. However, the clinical features of ulnar neuropathy and the available diagnostic tools are often incapable of localizing the exact site of lesions at the elbow precisely. Therefore, the more generic term "ulnar neuropathy at the elbow" is preferred, as it does not imply a specific site of compression (eg, the cubital tunnel). However, it is important to understand the anatomic structures around the elbow in terms of their role in the pathophysiology of ulnar nerve injury.

The etiology of ulnar nerve lesions at the elbow includes acute trauma (eg, distal humeral fracture, nerve lacerations, perioperative injury) [9] and nerve compression, traction, or friction from leaning on the elbow or from prolonged elbow flexion [9-11]. Intrinsic causes include elbow joint pathology such as osteophytes, arthritis, synovitis, anomalous muscles or fibrous bands, ganglia, and other mass lesions. Subluxation of the ulnar nerve laterally over the medial epicondyle is a potential cause of ulnar neuropathy at the elbow, but its role is often unclear, since it occurs in a substantial proportion of asymptomatic individuals [11,12].

Wrist — The main distal trunk of the ulnar nerve and its two branches, the superficial sensory branch and deep motor branch (figure 5), can be injured around the wrist, although ulnar nerve injury at the wrist is less common than at the elbow. The etiology of distal ulnar lesions can be divided into intrinsic and extrinsic causes. The extrinsic causes include bone fractures (eg, hook of hamate), lacerations, and direct, often repetitive trauma, such as repetitive use of tools in the workplace [13] or propulsion of a manual wheelchair [13-15]. A number of cases have been reported in bicyclists as a result of direct pressure [16-18], sometimes called handlebar palsy [19]. This is uncommon and is usually a mild neurapraxia. Intrinsic causes include ganglia arising from the wrist joint or intraneural ganglia [20]. Many cases are idiopathic [15].

Other — The ulnar nerve, sometimes in combination with the median and radial nerves, can also be compressed in the axilla or upper arm by external structures (eg, crutches, tourniquets, pressure during sleep). However, such injuries to the ulnar nerve are uncommon owing to its reasonably protected position in the upper arm. Compression of the ulnar nerve by internal structures (eg, aneurysms, hematomas, compartment syndromes, bony fragments from humeral shaft fractures) also can result in proximal ulnar nerve lesions. There are case reports of entrapment by the medial intramuscular septum (arcade of Struthers) as the ulnar passes through this structure when traversing from the anterior to posterior compartment of the upper arm, but these presentations are rare in clinical practice [21-25]. Because there are no motor or sensory branches given off by the ulnar nerve in the upper arm, the neurologic deficits related to proximal ulnar nerve injuries in the upper arm or axilla are identical to those caused by more distal ulnar nerve lesions at the elbow. Therefore, one is dependent on the clinical scenario, the presence of proximal pain or a mass, or the involvement of other nerves (median and radial) to aid in localization.

Distal to the elbow, the ulnar nerve rarely can be compressed within the body of flexor carpi ulnaris muscle or where it exits through the deep flexor-pronator aponeurosis [8].

Ulnar nerve mononeuritis can occur with infectious causes (eg, leprosy), hereditary neuropathies, and vasculitis; acromegaly is a rare cause [26,27]. (See "Overview of upper extremity peripheral nerve syndromes", section on 'Etiologies'.)

EPIDEMIOLOGY — Ulnar neuropathy at the elbow is the second most commonly diagnosed focal neuropathy, surpassed only by median neuropathy at the wrist [28,29]. In a study from Italy, the raw annual incidence of ulnar neuropathy at the elbow was 24.7 cases per 100,000 person-years, and the incidence in males was nearly double that of females (32.7 versus 17.2 per 100,000) [30]. In another study from the United Kingdom that analyzed a large general practice database, the annual incidence of ulnar neuropathy (including all anatomic locations) for males and females was 25.2 and 18.9 per 100,000, respectively [31].

Risk factors for ulnar neuropathy are poorly defined because the available data are retrospective, limited, and conflicting. However, a positive association of ulnar neuropathy at the elbow with smoking is supported by two of the larger reports:

In a study that compared 324 subjects with ulnar neuropathy at the elbow with 832 matched control subjects, the condition was associated with smoking (odds ratio 4.1, 95% CI 2.4-7.6) but not with body mass index or alcohol consumption [32].

In a hospital based case-control study that compared 110 patients who had surgical treatment for ulnar neuropathy at the elbow with 192 control patients treated for cervical or lumbar herniated disc, risk factors for ulnar neuropathy at the elbow included smoking, educational level, and work experience; by contrast, sex, body mass index, alcohol consumption, elbow trauma, diabetes, and hypertension were not risk factors [33].

Another retrospective study compared patients with electrodiagnostic studies confirming ulnar neuropathy at the elbow (n = 112) with patients whose studies excluded it (n = 104) and identified male sex and increasing age as risk factors [34].

The incidence and prevalence of ulnar neuropathy at the wrist are unknown, but the incidence is much lower than ulnar neuropathy at the elbow [35,36].

CLINICAL FEATURES — Ulnar lesions at the elbow typically present with numbness and tingling in the fourth and fifth digits, medial elbow pain, nocturnal numbness and paresthesia, and worsening of symptoms with elbow and/or repeated wrist flexion [3]. Ulnar lesions at the wrist typically present with hand weakness and atrophy, loss of dexterity, and variable sensory involvement as outlined below.

Ulnar neuropathy at the elbow — The clinical features of ulnar neuropathy at the elbow are understood based upon knowledge of the motor and sensory distribution of the ulnar nerve and its major branches. Sensory symptoms of numbness or paresthesiae in the ulnar nerve distribution are the most frequent initial complaints [1]. It is the author's impression that patients usually experience the sensory symptoms over the volar aspect of the fourth and fifth digits and ulnar aspect of the hand. The presence of sensory symptoms in the dorsal ulnar or palmar cutaneous territory (figure 4) is helpful in localizing the lesion proximal to the distal forearm or wrist, but these complaints are not always present. As an example, in one study of 25 patients with ulnar neuropathy at the elbow, sensory symptoms involved the digital terminal branches, the palmar cutaneous territory, and the dorsal cutaneous territory in 92, 80, and 72 percent of patients, respectively [37]. Some patients with severe and persistent numbness have sensory symptoms that split the ring finger. Medial elbow pain or aching is common, and many patients report referred pain along the medial forearm.

Sensory symptoms from ulnar neuropathy at the elbow are often brought on by sustained elbow flexion (eg, when talking on the phone or lying on one's side with the elbow flexed). Symptoms can also be provoked by leaning on the elbow or when performing activity that requires sustained or repetitive grip, or repeated forearm pronation and supination.

Motor symptoms in ulnar neuropathy at the elbow are less common than sensory symptoms, but range from mild weakness of intrinsic hand muscles to severe wasting and claw hand deformity (picture 1). Some patients will report only mild weakness and clumsiness of the hand during activities requiring dexterity and fine control such as buttoning or typing. Loss of dexterity due to ulnar neuropathy is usually indicative of weakness of the intrinsic hand muscles (ie, the lumbricals and interossei), in contrast to mild median nerve injury, where loss of dexterity is most often related to sensory loss. More significant involvement of the ulnar-innervated forearm muscles, primarily flexor digitorum profundus to the fourth and fifth digits, leads to complaints of grip weakness and difficulty lifting and carrying. In a report of 25 patients with ulnar neuropathy at the elbow, weakness of the first dorsal interosseous, abductor digiti minimi, flexor digitorum profundus, and flexor carpi ulnaris was present in 84, 76, 56, and 20 percent of patients, respectively [37]. This distribution is consistent with our clinical experience.

Ulnar neuropathy at the wrist — Ulnar neuropathy at the wrist typically presents with hand weakness and atrophy, loss of dexterity, and variable sensory involvement. The extent of clawing of digits four and five (picture 1) can be worse with lesions at the wrist than at the elbow as a result of sparing of the flexor digitorum profundus and weakness of the third and fourth lumbricals, resulting in greater muscle imbalance.

Injury to the terminal branches of the ulnar nerve at the wrist (figure 5) is often divided into four sites and their associated clinical scenarios:

(1) Injury to the main trunk of the nerve proximal to or within Guyon's canal. These lesions will produce sensory symptoms in the distribution of the superficial terminal branches and motor involvement of all ulnar innervated intrinsic hand muscles (hypothenar muscles, interossei, lumbricals three and four, and the adductor pollicis).

(2) Injury to the deep terminal motor branch of the ulnar nerve proximal to the branches supplying the hypothenar muscles. This will again produce motor symptoms in all of the ulnar-innervated intrinsic hand muscles but no sensory symptoms.

(3) Injury to the deep motor branch distal to the hypothenar muscles will spare the hypothenar muscles and result in no sensory symptoms, but the remainder of the ulnar-innervated intrinsic hand muscles will be affected.

(4) Injury to the superficial terminal branch supplying the superficial sensory branches will result in sensory involvement of the digital branches but no motor involvement. Clinically detectable dysfunction of the palmaris brevis muscle innervated by this branch is unlikely.

While this classification makes sense anatomically, the actual anatomic site of the lesion does not reliably correlate with the clinical features of ulnar neuropathy at the wrist. As an example, a lesion within Guyon's canal can spare the hypothenar branch or deep motor branch. This is a result of the fascicular arrangement of the nerve and the typically incomplete involvement of all fascicles with injury or compression at a given level, especially with lesions of the main trunk of the nerve within Guyon's canal. Nevertheless, this approach provides a framework for clinical assessment prior to further investigation.

DIAGNOSIS — The clinical diagnosis of ulnar neuropathy at the elbow or ulnar neuropathy at the wrist should be reasonably straightforward from a careful history, clinical examination, and knowledge of the anatomy underlying the peripheral motor and sensory symptoms. In most cases, the diagnosis of ulnar neuropathy can be confirmed by electrodiagnostic testing (see 'Electrodiagnostic confirmation' below) or imaging (see 'Imaging for patients with atypical features' below) when suspected on the basis of clinical symptoms or signs.

Clinical evaluation — The clinical diagnosis of ulnar neuropathy at the elbow is likely if typical symptoms of intermittent numbness and paresthesia in the fourth and fifth digits are present, often brought on by pressure or flexion of the elbow. However, the diagnosis can be challenging due to the potential for selective fascicular involvement of the motor and sensory fibers and the presence of comorbid conditions such as carpal tunnel syndrome, generalized polyneuropathy, radiculopathy, or referred pain from musculoskeletal problems such as tendonitis. Ulnar lesions in the upper arm can mimic ulnar lesions at the elbow or wrist, and one is often dependent on the clinical scenario or the presence of motor and sensory deficits secondary to coexisting median or radial nerve injuries to aid in localization. Therefore, further diagnostic tools are often required, as discussed below.

Examination — Physical examination should include a careful inspection of the limb for any evidence of muscle wasting, particularly in the interossei and hypothenar eminence. It is important to make side-to-side comparisons, looking for any asymmetry. Deformity of the elbow or wrist may be associated with previous trauma or degenerative or inflammatory arthritis. The ulnar nerve should be palpated along its course in the retrocondylar groove and above the elbow for any evidence of masses or swelling. In the author's clinical experience, it is useful to examine for the presence of ulnar nerve subluxation laterally over the medial epicondyle; this is especially relevant when present only on the affected side. Motor examination should focus on a careful assessment of the ulnar-innervated intrinsic and extrinsic muscles. An assessment of radial- and median-innervated forearm and hand muscles is necessary to exclude more proximal lesions of the C8 or T1 roots, the brachial plexus, or a more generalized motor neuron disorder.

Sensation should be tested to pinprick and light touch in all three major ulnar sensory territories, which are innervated by the following branches (figure 4):

Superficial terminal branch (digital branch)

Palmar cutaneous nerve

Dorsal cutaneous nerve

The presence of deficits in the palmar and dorsal cutaneous territories is helpful in ruling in a lesion proximal to the distal forearm, but their absence does not rule out ulnar neuropathy at the elbow, as some patients may experience deficits in only the digital tips of the fourth and fifth digits or may have no demonstrable sensory loss resulting from selective fascicular injury.

Provocative tests — There are a number of provocative maneuvers for ulnar neuropathy, including Tinel test, elbow flexion, pressure (compression), combined elbow flexion with pressure, and palpation for local nerve tenderness and nerve thickening. Unfortunately, the sensitivity and specificity of these provocative tests for ulnar neuropathy appear to be suboptimal. Nevertheless, these tests may be helpful when interpreted in the proper clinical context.

The Tinel test at the elbow is performed by firm percussion over the ulnar nerve in the ulnar groove and a bit further distally over the cubital tunnel. Percussion over Guyon's canal can be performed for assessment of ulnar neuropathy at the wrist. In addition, percussion can be applied in the upper arm 7 to 10 cm proximal to the medial epicondyle to evaluate for ulnar neuropathy along the medial intermuscular septum [25]. The elbow flexion test involves sustained maximal elbow flexion for one minute with the wrist in a neutral position, while the pressure test is carried out by applying sustained manual pressure over the ulnar nerve in the ulnar groove. These tests are considered positive when they result in paresthesia or pain in ulnar-innervated regions of the hand, particularly the fourth and fifth digits (figure 4).

The available data are limited and inconsistent but suggest that clinical utility of provocative tests for ulnar neuropathy is inadequate.

One of the highest-quality prospective studies evaluated 192 patients suspected of having ulnar neuropathy at the elbow, including 137 patients with a final diagnosis of the condition [38]. The sensitivities and specificities were as follows: Tinel test, 62 and 53 percent; combined elbow flexion, 61 and 40 percent; palpation for nerve thickening, 28 and 87 percent; and palpation for nerve tenderness, 32 and 80 percent. Thus, none of the evaluated provocative tests had both good sensitivity and good specificity. Combinations of two or more tests did not improve the diagnostic accuracy because of a substantial loss of specificity.

By contrast, another prospective study compared a group of 32 subjects who had clinical and electrophysiologic evidence of ulnar neuropathy at the elbow with 33 control subjects [39]. The sensitivities were good for Tinel test (70 percent) and the combined pressure flexion test (91 percent), but sensitivities were low for elbow flexion (32 percent) and pressure provocation (55 percent). While specificities were high (95 to 99 percent) for all tests, this observation likely relates to the severity of the group examined in this small study.

Clinical experience suggests that the presence of a Tinel sign with percussion of the ulnar nerve at the elbow is common in asymptomatic individuals. However, its presence unilaterally with light tapping of the nerve may suggest the presence of ulnar neuropathy. Some investigators stress that Tinel test should be considered positive only when there is marked tingling and local sensitivity on light tapping or palpation, since mild paresthesia are often elicited in normal individuals [40].

Electrodiagnostic confirmation — Electrodiagnostic testing, typically involving nerve conduction studies and sometimes needle electromyography (EMG), is a standard part of the evaluation for ulnar neuropathy, even in seemingly straightforward cases where suspicion is high. These tests are useful to confirm the diagnosis, establish baseline results, determine severity, and rule out other potential causes [41]. They are particularly helpful when the clinical presentation is not straightforward, such as in cases complicated by associated musculoskeletal pain, coexisting carpal tunnel syndrome, or radiculopathy.

Ulnar neuropathy at the elbow — In the evaluation of suspected ulnar neuropathy at the elbow, the goal of electrodiagnostic studies is to localize the lesion to the ulnar nerve at the elbow, determine the character and severity of the injury, aid in prognosis, and examine for the presence or absence of alternative diagnoses [41]. Typically, motor nerve conduction studies are obtained, recording from either the hypothenar eminence or first dorsal interosseous muscles, with stimulation at the wrist, below the elbow, and above the elbow [42]. The amplitude of the maximum compound muscle action potential in response to the distal site of stimulation at the wrist is a reasonable indication of the number of functioning motor axons, at least with acute or subacute presentations prior to reinnervation via collateral reinnervation. Focal slowing or conduction block across the elbow provides the most compelling evidence of a localized lesion (figure 7). In the absence of focal conduction block or slowing, one cannot be definite as to the presence of ulnar neuropathy at the elbow [43].

Some authors are proponents of short-segment incremental studies, or so-called "inching," an electrodiagnostic technique that is performed by stimulating short intervals of the ulnar nerve, typically at successive 1 cm increments, in order to more precisely localize the lesion [44,45]. As an example, one such study reported that short-segment inching technique distinguished focal slowing in the retrocondylar groove from slowing in the humeroulnar arcade/cubital tunnel in 80 percent of cases based upon comparison with intraoperative electrodiagnostic studies [44].

Sensory nerve conduction studies that record the sensory nerve action potential from the ulnar-innervated fourth or fifth digits provide evidence of sensory axonal involvement. Segmental sensory studies can also be used to look for evidence of conduction slowing across the elbow. However, these studies can be technically challenging in the setting of moderate to severe axon loss. The presence of a normal or absent dorsal ulnar cutaneous sensory response is helpful in localizing lesions to the elbow or wrist, especially when the response is normal on the unaffected side.

Routine nerve conduction studies for the diagnosis of ulnar neuropathy at the elbow typically include the following [46]:

Ulnar motor study recording from the abductor digiti minimi, stimulating at the wrist, below the elbow, and above the elbow with the elbow in a moderately flexed position

Median motor study recording from the abductor pollicis brevis while stimulating at the wrist and elbow

Ulnar sensory response recording digit five while stimulating at the wrist

Median sensory response recording digit two or three while stimulating at the wrist

Additional comparison studies should be considered if the ulnar neuropathy is not localizable [46]:

Repeat motor studies recording the first dorsal interosseous

Motor inching across the elbow

Sensory or mixed-nerve studies across the elbow

Recording bilateral dorsal ulnar cutaneous sensory nerve action potential

Recording bilateral medial antebrachial cutaneous sensory nerve action potential if sensory loss extends above the wrist on clinical examination, or if there is a suggestion of lower brachial plexus lesion by history

Needle EMG is helpful in determining the presence or absence of acute or chronic motor axonal involvement. In particular, the presence on needle EMG of abnormalities in the ulnar innervated forearm muscles, and the absence of abnormalities in the median and radial distribution, is helpful in localizing a lesion proximal to wrist or forearm. However, one cannot definitively exclude ulnar neuropathy at the elbow when ulnar-innervated forearm muscles are normal due to possible sparing of the fascicles supplying these muscles.

One suggested protocol for EMG evaluation of suspected ulnar neuropathy at the elbow involves needle examination of the following ulnar-innervated muscles [46]:

Distal to the wrist – First dorsal interosseous or abductor digiti minimi

In the forearm – Flexor digitorum profundus (digit five) and flexor carpi ulnaris

Additional muscles are investigated if any of the ulnar muscles are abnormal to rule out a lower brachial plexopathy, polyneuropathy, or radiculopathy of C8 or T1 [46]:

Two or more nonulnar lower trunk/C8-T1 muscles (eg, abductor pollicis brevis, flexor pollicis longus, extensor indicis proprius)

C8 and T1 paraspinal muscles

The precise sensitivities and specificities of electrodiagnostic tests for ulnar neuropathy at the elbow are uncertain because existing studies are generally limited by small numbers of patients with known ulnar neuropathy, as opposed to examination of a larger group of patients that may or may not have the disorder. These reports are also inconsistent with respect to the relative utility of motor conduction, sensory conduction, and mixed motor-sensory conduction studies for ulnar neuropathy at the elbow.

One of the largest studies evaluated 109 affected arms (n = 102 patients) with a clinical diagnosis of ulnar neuropathy at the elbow, including 38 arms with purely sensory signs and 71 arms with both sensory and motor signs (none had motor signs alone) [47]. The sensitivity of motor conduction studies for localizing the ulnar neuropathy at the elbow was 78 percent, and there was no significant difference in sensitivity between those who had sensory signs only compared with those who had both sensory and motor signs (79 versus 76 percent).

In a report that evaluated 21 patients with suspected ulnar neuropathy, the sensitivities for the diagnosis of it based upon motor conduction slowing across the elbow when recording from first dorsal interosseous and abductor digiti minimi (quinti) were 81 and 71 percent, respectively [48]. By contrast, the sensitivity of the ulnar mixed motor-sensory study was only 57 percent.

In a case-control study, 43 patients referred for evaluation of ulnar neuropathy were divided into those with ulnar neuropathy at the elbow considered either clinically definite (n = 21) or possible (n = 22) [49]. Based upon segmental motor slowing, the diagnostic yield was 67 percent in the definite group and only 9 percent in the possible group. These values were increased to 86 percent and 68 percent, respectively, by the addition of segmental sensory or mixed nerve studies.

Ulnar neuropathy at the wrist — The electrodiagnostic localization of ulnar neuropathy at the wrist is based upon the detection of focal motor or sensory nerve conduction slowing or block with stimulation at the wrist and no evidence of more proximal block or slowing. A normal dorsal ulnar cutaneous sensory potential is helpful in ruling out more proximal lesions, as is the presence of normal needle EMG findings in the flexor carpi ulnaris and flexor digitorum profundus muscles. Unfortunately, in some cases where there is only chronic motor and sensory involvement affecting ulnar-innervated intrinsic hand muscles and the digital sensory branches, there is no way to be precise in electrodiagnostic localization.

Routine nerve conduction studies for the diagnosis of ulnar neuropathy at the wrist typically include the following [46]:

Ulnar motor study recording from the abductor digiti minimi while stimulating at the wrist, below the elbow, and above the elbow, with the elbow in the flexed position

Ulnar motor study (bilateral) recording from the first dorsal interosseous while stimulating at the wrist

Median motor study recording from the abductor pollicis brevis while stimulating at the wrist and elbow

Ulnar sensory response recording digit five while stimulating at the wrist

Median sensory response recording digit two or three while stimulating at the wrist

Dorsal ulnar cutaneous sensory response (bilateral)

One suggested protocol for needle EMG evaluation of suspected ulnar neuropathy at the wrist involves examination of the following ulnar-innervated muscles [46]:

Deep palmar – First dorsal interosseous

Hypothenar – Abductor digiti minimi

Forearm – Flexor carpi ulnaris and flexor digitorum profundus (digit five)

Additional muscles are investigated if any of the ulnar muscles are abnormal to rule out a lower brachial plexopathy, polyneuropathy, or radiculopathy of C8 or T1 [46]:

Two or more nonulnar lower trunk/C8-T1 muscles (eg, abductor pollicis brevis, flexor pollicis longus, extensor indicis proprius)

C8 and T1 paraspinal muscles

Imaging for patients with atypical features — Imaging studies are warranted when electrodiagnostic studies are nonlocalizing or when symptoms suggest a mass or compressive lesion, such as with the presence of swelling or severe pain or when symptoms occur in the setting of trauma. Both magnetic resonance imaging (MRI) and ultrasonography are useful diagnostic tests for ulnar neuropathy at the elbow or wrist [50-55].

MRI – On MRI, features of the condition include nerve enlargement and increased signal intensity on T2-weighted or short T1 inversion recovery (STIR) sequences [51]. In one prospective study examining a group of 27 patients (35 arms) meeting typical clinical criteria, increased signal of the ulnar nerve on MRI was found on STIR sequences in 97 percent of cases and enlargement of the nerve in 74 percent [56]. Electrodiagnostic testing in this study was positive in 77 percent of cases. Another study of 52 patients with clinical evidence of ulnar neuropathy at the elbow reported a similarly high sensitivity of MRI for the condition in comparison with nerve conduction studies (90 versus 65 percent) [57]. The MRI was particularly useful for those with nonlocalizing electrodiagnostic studies (n = 19), where MRI detected evidence of ulnar neuropathy at the elbow in 16 patients (84 percent). MRI is also useful for suspected ulnar neuropathy at the wrist, particularly in examining for the presence of ganglia or cysts resulting in external compression of the nerve (image 1).

Ultrasound – On ultrasonography, features of ulnar neuropathy at the elbow include thickening of the nerve (quantified by measures such as increased cross-sectional area) and altered echogenicity (image 2). At the elbow, the normal ulnar nerve diameter is 9 to 10 mm [58]. At the wrist, the upper limit of normal ulnar nerve diameter is 8 mm [59]. The usefulness of ultrasonography for the diagnosis of ulnar neuropathy at the elbow was demonstrated in a prospective study that evaluated 123 patients who had suspected ulnar neuropathy at the elbow, with a final diagnosis of it in 84 [60]. The sonographic diagnosis of ulnar neuropathy at the elbow, based upon the presence of a larger nerve diameter in comparison with control patients, yielded a sensitivity and specificity of 80 and 91 percent compared with the diagnosis made by standard clinical and electrophysiologic criteria. Among 20 cases with nonlocalizing electrodiagnostic findings of ulnar neuropathy but clear clinical evidence of ulnar neuropathy at the elbow, ultrasonography confirmed the diagnosis of ulnar neuropathy at the elbow in 17 (85 percent); in 37 patients who had evidence of motor conduction velocity slowing across the elbow without conduction block, ultrasonography confirmed the diagnosis of ulnar neuropathy at the elbow in 32 cases (86 percent). In another study that evaluated 41 nerves, the ultrasonographic diagnosis of ulnar neuropathy at the elbow, based upon the largest nerve cross-sectional area measurement, yielded a sensitivity and specificity of 95 percent and 71 percent, respectively, compared with electrodiagnostic diagnosis of the condition [58].

DIFFERENTIAL DIAGNOSIS — The differential diagnosis of ulnar neuropathy at the elbow and ulnar neuropathy at the wrist includes proximal lesions of the C8 or T1 roots and the lower trunk/medial cord of the brachial plexus (figure 1). These disorders often differ clinically with sensory involvement extending proximal to the wrist in the distribution of the medial cutaneous nerve of the forearm, and motor involvement of nonulnar innervated muscles such as flexor pollicis longus, extensor pollicis, and the thenar muscles. True paresthesia or numbness of the medial forearm in the distribution of the medial cutaneous nerve of the forearm should alert the clinician to a more proximal lesion of the C8 or T1 roots, or to a lesion of the lower trunk or medial cord of the brachial plexus. (See "Brachial plexus syndromes" and "Clinical features and diagnosis of cervical radiculopathy".)

Central lesions can rarely present as ulnar neuropathy at the elbow. Weakness and wasting in the ulnar distribution in the absence of sensory symptoms is suggestive of amyotrophic lateral sclerosis or the more benign monomelic amyotrophic form of motor neuron disease. (See "Diagnosis of amyotrophic lateral sclerosis and other forms of motor neuron disease" and "Diagnosis of amyotrophic lateral sclerosis and other forms of motor neuron disease", section on 'Monomelic amyotrophy'.)

Cervical syringomyelia can present with focal wasting of intrinsic hand muscles; however, the motor involvement is rarely confined to the ulnar distribution, and the sensory symptoms are more generalized. (See "Disorders affecting the spinal cord", section on 'Syringomyelia'.)

Small subcortical brain infarcts may present with focal hand weakness, but the deficits are not typically confined to the ulnar distribution.

MANAGEMENT — Management options for ulnar neuropathy at the elbow or wrist include conservative and surgical intervention. Recommendations are based primarily on clinical experience as limited data exist. A 2016 Cochrane review found insufficient evidence to recommend a best treatment among conservative or surgical options [61].

Initial conservative treatment — We suggest conservative treatment rather than surgery as the initial treatment for most patients with ulnar neuropathy. Exceptions include those with moderate to severe ulnar neuropathy due to a structural cause, those who have failed conservative treatment, or those with progressive symptoms. (See 'Surgery for refractory or severe symptoms' below.)

There are no well-defined, evidence-based methods to determine the severity of ulnar neuropathy or to choose between conservative and surgical management [35].

Behavioral and mechanical techniques — A variety of mechanical and behavioral options for symptomatic relief are available, but data to guide among options to treat ulnar neuropathy at the elbow or wrist are unavailable.

Activity modification is suggested when the presumed cause is repetitive compression or trauma.

For patients with ulnar neuropathy at the elbow, the following measures may be helpful:

Patients should avoid leaning on the elbows when seated or driving and should avoid prolonged elbow flexion [62]. Practical suggestions include using the other hand or a headset when on the telephone and avoiding sitting with the arms crossed.

The use of a soft foam elbow pad may reduce inadvertent compression of the ulnar nerve at the elbow. To prevent excessive or prolonged elbow flexion, splints that limit flexion to 45 to 90 degrees can be used at night, although patient compliance is often suboptimal [63].

Patients may wrap the affected elbow with a towel at night to limit flexion, since a towel wrap is usually better tolerated than more rigid braces. In our experience, these simple measures often result in improvement of milder intermittent symptoms and can also aid in resolution of those with moderate presentations (eg, conduction block on electrodiagnostic testing).

For ulnar neuropathy at the wrist, padded gloves can be used for protection with occupational or recreational activities (eg, bicycling, gardening). In addition, handlebar padding and frequent changes in hand position while cycling may reduce the frequency and severity of handlebar palsy.

Specific conservative therapies were not beneficial for ulnar neuropathy at the elbow in the only relevant randomized trial identified by a systematic review [61]. In that trial, 70 patients with mild or moderate symptoms of cubital tunnel syndrome were randomly assigned to night splinting, stretching exercises, or control groups [64]. All patients received written information regarding avoidance of movements and positions that provoke symptoms of ulnar neuropathy. At six months, there were no significant differences among the groups in any of the outcome measures. While a few prospective studies have reported that various conservative measures were associated with improved outcome of ulnar neuropathy at the elbow, the strength of these reports is limited by methodologic issues including small patient numbers and lack of a control group [62,65,66].

Uncertain benefits of pharmacotherapy — We do not use pharmacologic therapies including oral medications or local injections for most patients with ulnar neuropathy. Available data are limited to small series and suggest modest benefits appear to be temporary.

Medications used for symptomatic management of neuropathic pain syndromes have not been studied in patients with isolated ulnar neuropathy. Oral agents may be tried for selected patients with painful paresthesias who are unable to adhere to or tolerate behavioral and mechanical techniques. However, symptomatic improvement that does not address the cause of the nerve entrapment may mask the extent and progression of underlying nerve dysfunction.

Very limited data are available regarding the use of local injections for ulnar neuropathy. A small observational study that included 10 patients with ulnar neuropathy at the elbow found that patients treated with a single injection of triamcinolone with lidocaine had improved symptoms and cross-sectional area on ultrasound at one- and four-week follow-ups [67]. However, in a small trial of 36 patients with ulnar neuropathy at the elbow who were treated with either glucocorticoid or dextrose injections, symptomatic improvement was similar at one-month follow-up but lower in the glucocorticoid-treated groups at three-, four-, and six-month follow-up [68]. In another trial that included 55 patients, patients assigned to a single injection of glucocorticoids showed improved ulnar cross-sectional areas at three-month follow-up, but symptomatic improvement was similar between groups [69]. The use of local injections comes with a risk of worsening symptoms due to inadvertent puncture of the nerve [70,71].

Surgery for refractory or severe symptoms — The two common surgical approaches to patients with severe or progressive ulnar neuropathy at the elbow are decompression and transposition.

Indications — We suggest surgical intervention for the initial management of patients with moderate to severe ulnar neuropathy at the elbow caused by trauma, structural abnormality, or nerve compression. In addition, we suggest surgical treatment for patients with ulnar neuropathy of less than six months' duration related to any cause who have moderate to severe continued or progressive signs and symptoms despite conservative measures.

In such cases, there should be convincing clinical and electrophysiologic evidence (eg, clear weakness, sensory loss, and significant axon loss on electrodiagnostic testing) of ulnar neuropathy at the elbow.

The selection of patients for surgery is based on limited data from case series as there are no trials comparing surgical intervention with nonoperative conservative management or sham surgery for ulnar neuropathy at the elbow.

Ulnar decompression for most patients — We suggest open in situ decompression over transposition for most patients who undergo surgery for severe or progressive ulnar neuropathy at the elbow. Decompression of the ulnar nerve at the elbow may be more effective than transposition of the nerve [72]. Additionally, some studies suggest that there is a higher complication rate with transposition, in part because simple decompression is a faster procedure that is technically less demanding [61,73].

In a network meta-analysis involving several open and endoscopic operative approaches to decompression or transposition, patient symptoms were likelier to improve with decompression techniques over transposition [72]. For example, patients who underwent open in situ decompression with epicondylectomy were 13 percent more likely to improve compared with those who underwent subcutaneous transposition (95% CI 1.01-1.25). Overall, post-operative complications were uncommon, occurring in 3 percent of patients, but were least frequent among those who underwent in situ decompression. Additionally, open decompression was associated with the lowest risk of reoperation.

Decompression is usually performed by cutting the flexor carpi ulnaris aponeurosis (the humeroulnar arcade) to decompress the ulnar nerve [40]. The procedure can be performed by open or endoscopic approaches [72,74]. Endoscopic decompression has some potential advantages over open decompression (smaller incision, earlier recovery); however, it is more costly and requires specific training. Small case series are encouraging, but a randomized controlled trial comparing the endoscopic approach with open decompression is required [75]. Open decompression may also include medial epicondylectomy, which is performed by removing the humeral medial epicondyle after making an incision in the humeroulnar arcade [76]. This has been the generally accepted approach in the setting of significant skeletal deformity or trauma.

Including epicondylectomy with open in situ decompression added modest benefits in efficacy and reduced complication rates compared with decompression alone but requires longer operative time and is a more complex procedure.

Other surgical techniques

Transposition of the ulnar nerve – Transposition of the nerve at the elbow can be achieved by first slitting the humeroulnar arcade, mobilizing the ulnar nerve from the retrocondylar groove, and then moving the nerve anteriorly. This may be performed open or endoscopically with either submuscular or subcutaneous nerve transposition [72]. As discussed above, this technique appears to be somewhat less efficacious than decompression techniques.

Anterior interosseous-to-ulnar nerve transfer – In cases of severe ulnar nerve injury with substantial axonal loss and denervation of intrinsic hand muscles, there may be benefit of attempting to augment recovery with end-to-side anterior interosseous-to-ulnar nerve transfer [77-79].

Decompression at the ulnar tunnel – For the less common condition of ulnar neuropathy at the wrist, surgery consists of decompression of the ulnar tunnel (ie, Guyon's canal) by an experienced hand surgeon.

PROGNOSIS — The natural history of ulnar neuropathy at the elbow is largely unknown, and the available data are sparse. This is not surprising given the complexity of case definition, lack of standardized outcomes, and variable electrodiagnostic approaches used. As an example, one retrospective study followed 22 patients who did not have surgical treatment for ulnar neuropathy at the elbow involving 24 affected arms [80]. At a mean follow-up of 13 months, the outcome was considered improved, unchanged, or worse for 12, 7, and 5 affected arms, respectively. The strength of this study is limited by methodologic issues that include small patient numbers and outcome assessment based entirely upon subjective reporting for approximately one-half of the subjects. The same investigators had previously shown poor correlation between subjective symptoms and electrodiagnostic criteria for ulnar neuropathy at the elbow [81].

Knowledge of the natural history of ulnar neuropathy is crucial, however, when considering the relative merits of various conservative treatments and surgery. Clinical experience suggests that patients with mild ulnar neuropathy, who typically present with intermittent sensory symptoms and electrodiagnostic features of conduction slowing across the elbow, often improve with conservative measures or remain stable over years. In all probability, many such patients do not seek medical attention for these symptoms.

Patients with persistent sensory loss and weakness without wasting often present acutely (sometimes with a preexisting history of mild intermittent symptoms) and commonly have features of both conduction block and slowing on electrodiagnostic testing. This group often improves over the course of three to six months, based upon clinical and electrodiagnostic measures.

Those with persistent symptoms of weakness and numbness beyond six months should be referred for consideration of surgical intervention (see 'Surgery for refractory or severe symptoms' above). Patients with severe weakness, wasting, and persistent sensory loss due to ulnar neuropathy at the elbow or wrist will typically show evidence of axonal injury on electrodiagnostic testing

The outcome with nonoperative management of ulnar neuropathy at the elbow may depend upon the clinical severity of the condition at presentation. This conclusion is suggested by the results of a prospective study of conservative treatment for 128 patients, including 43 with bilateral involvement [62]. At a mean follow-up of 59 months, a successful outcome (defined as not having surgical treatment for ulnar neuropathy at the elbow) for patients with mild, moderate, and severe presentations was reported for 89, 67, and 38 percent, respectively, and the differences between these groups were statistically significant. One weakness of this study was the limited use of electrodiagnostic tests, which were completed at baseline in only a portion of subjects and were not part of the longitudinal assessment. Moreover, these data may be most applicable to patients referred for surgery, who probably represent a more severe end of the clinical spectrum. Thus, the results may not be generalizable to all patients with ulnar neuropathy at the elbow.

SUMMARY AND RECOMMENDATIONS

Localization – The most common site of focal ulnar nerve entrapment or compression is at the elbow, followed by the wrist. Compression in the axilla or upper arm by external structures (eg, crutches, tourniquets, pressure during sleep) is uncommon (figure 2). (See 'Anatomy' above and 'Localization and etiology' above.)

Clinical features – Ulnar lesions at the elbow typically present with numbness and tingling in the fourth and fifth digits (figure 4), elbow pain, nocturnal awakening, and worsening of symptoms with prolonged elbow flexion (figure 6). Ulnar lesions at the wrist typically present with hand weakness and atrophy (picture 1), loss of dexterity, and variable sensory involvement. (See 'Clinical features' above and 'Ulnar neuropathy at the elbow' above and 'Ulnar neuropathy at the wrist' above.)

Diagnosis – The clinical diagnosis of ulnar neuropathy can be confirmed by electrodiagnostic testing with or without neuroimaging. (See 'Diagnosis' above.)

Electrodiagnostic testing, typically involving nerve conduction studies and sometimes needle electromyography (EMG), is a standard part of the evaluation for ulnar neuropathy. (See 'Electrodiagnostic confirmation' above.)

Magnetic resonance imaging and/or ultrasonography are typically used when electrodiagnostic testing is nonlocalizing or when atypical features suggest the presence of structural abnormalities associated with ulnar neuropathy (image 2 and image 1). (See 'Imaging for patients with atypical features' above.)

Differential diagnosis – The differential diagnosis of ulnar neuropathy includes proximal lesions of the C8 or T1 roots and the lower trunk/medial cord of the brachial plexus and central nervous system lesions (rarely) such as motor neuron disease, cervical syringomyelia, and small subcortical infarctions. (See 'Differential diagnosis' above.)

Management

Initial conservative treatment for most patients – For patients with mild to moderate ulnar neuropathy who have intermittent or persistent sensory loss and weakness without wasting, we suggest conservative management (Grade 2C). In addition, for patients who have moderate to severe but stable ulnar neuropathy of less than six months' duration, we suggest conservative treatment rather than surgery as the initial treatment (Grade 2C). (See 'Management' above and 'Initial conservative treatment' above.)

Surgical treatment for severe or refractory symptoms – For patients with convincing clinical and electrodiagnostic evidence of moderate to severe ulnar neuropathy at the elbow who have persistent weakness and numbness beyond six months that is refractory to conservative therapy or those who have moderate to severe progressive symptoms and signs of less than six months' duration despite conservative measures, we suggest surgical treatment with ulnar nerve decompression or transposition rather than conservative therapy (Grade 2C). However, for older adults or medically unwell patients and for patients with chronic (two years or longer) severe involvement, the benefit of surgical intervention is doubtful. (See 'Management' above and 'Surgery for refractory or severe symptoms' above.)

We suggest open in situ decompression over transposition for most patients who undergo surgery for severe or progressive ulnar neuropathy at the elbow (Grade 2C). Decompression of the ulnar nerve at the elbow may be more effective than transposition of the nerve. (See 'Ulnar decompression for most patients' above.)

Prognosis – The natural history of ulnar neuropathy at the elbow is largely unknown, and the available data are sparse. (See 'Prognosis' above.)

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Topic 14172 Version 21.0

References

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