Disorders of Peripheral Nerves

First-degree nerve injury

Neurapraxia, or first-degree nerve injury, usually results from brief or mild compression on the nerve that distorts the myelin, resulting in segmental demyelination but leaving the axons intact. The nerve conducts normally distal to but not across the lesion, resulting in conduction block, which is the electrophysiological correlate of neurapraxia. With this type of injury, recovery is usually complete following remyelination that occurs within 1–3 months if the offending cause (such as a compression) is removed.

Second-degree nerve injury

The axonal loss is associated with intact endoneurial tubes as well as intact perineurium and epineurium. These lesions have fairly good prognosis, since nerve regeneration between the site of nerve injury and the target organs is well guided by the intact endoneurial tubes.

Third-degree nerve injury

The axons and endoneurium are damaged while leaving the perineurium and epineurium intact. These lesions have fair prognosis and may require surgical intervention, mostly because of axonal misdirection and formation of neuromas.

Fourth-degree nerve injury

The axons, endoneurium, and perineurium are disrupted, but the epineurium is intact. These lesions have poor prognosis and often require surgical repair.

Fifth-degree nerve injury

Neurotmesis, or fifth-degree nerve injury, is the most severe type of nerve injury. It involves complete disruption of the nerve and all supporting structures. The nerve is transected, with loss of continuity between its proximal and distal stumps.

Entrapment neuropathy is defined as a mononeuropathy caused by focal compression or mechanical distortion of a nerve within a fibrous or fibro-osseous tunnel or less commonly by other structures such as bone, ligament, other connective tissues, blood vessels, or mass lesions. Compression, constriction, angulation, and stretching are important mechanisms that produce nerve injury at certain vulnerable anatomical sites (see Tables 106.3 and 106.5 ). The term entrapment is a useful one in that it implies that compression occurs at particular sites where surgical intervention is often required to release the entrapped nerve, such as in the case of the median nerve at the wrist in moderate to severe CTS. Overuse has been implicated as the cause of entrapment neuropathies in certain occupations, including playing of musical instruments by professional musicians.

In chronic entrapment, mechanical distortion of the nerve fibers leads to focal demyelination or, in severe cases, to wallerian degeneration. Morphological studies show a combination of active demyelination, remyelination, wallerian degeneration, and axonal regeneration at the site of entrapment. Endoneurial swelling, collagen proliferation, and thickening of perineurial sheaths accompany the nerve fiber changes. Ischemia is not a significant contributing factor to nerve fiber damage in chronic compression. In contrast, ischemia plays a more significant role in nerve injury associated with acute compression secondary to space-occupying lesions such as hematoma or compartment syndromes.

The characteristic electrophysiological feature of entrapment neuropathy is either short-segment conduction delay (i.e., focal slowing) or conduction block across the site of entrapment (see Chapter 36 ). In severe cases, wallerian degeneration gives rise to denervation and reinnervation in affected muscles. Nerve conduction studies together with needle EMG are essential for diagnosis and reliable documentation of the site and severity of nerve entrapment. Neuromuscular ultrasound has had an increasing role in the diagnosis of entrapment neuropathies, particularly when EDX studies are more difficult (such as in young children) or show only signs of nonlocalizing axonal loss such as with severe ulnar neuropathies ( ). In contrast, plain radiography, computed tomography (CT), and MRI may be of occasional value in identifying rare structural abnormalities, but these imaging procedures are often not necessary for routine diagnosis.

Applied anatomy

The median nerve, formed from contributions of the lateral cord (C6 and C7 fibers) and medial cord (C8 and T1 fibers) of the brachial plexus, runs into the forearm between the two heads of the pronator teres. It then gives off branches to the pronator teres, flexor carpi radialis, flexor digitorum sublimis, and the palmaris longus muscles, as well as the anterior interosseous nerve. The anterior interosseous nerve is the largest branch of the median nerve and is a pure motor nerve. It arises from the median nerve distal to these motor branches in the upper forearm and innervates the flexor pollicis longus, pronator quadratus, and median part of the flexor digitorum profundus muscles of the index and middle fingers. The median nerve then enters the wrist through the carpal tunnel, formed by the carpal bones and the transverse carpal ligament, the latter forming its roof. Before reaching the wrist, the median nerve gives off the palmar cutaneous sensory branch, which runs subcutaneously (not through the carpal tunnel) to innervate the skin over the thenar eminence. Distal to the carpal tunnel, the median nerve divides into motor and sensory divisions. The motor division innervates the first and second lumbricals and most muscles of the thenar eminence including the opponens pollicis, abductor pollicis brevis, and superficial head of the flexor pollicis brevis. The sensory fibers of the median nerve innervate the skin of the thumb, index, middle, and lateral half of the ring fingers.

Median nerve entrapment at the wrist (carpal tunnel syndrome)

CTS is by far the most common entrapment neuropathy seen in clinical practice. CTS prevalence in a primary care population is about 36 per 10,000 people, with an annual incidence of 19 per 10,000 for men and 36 per 10,000 for women ( ). Both the incidence and prevalence of CTS seem to be increasing.

This entrapment occurs in the tunnel through which the median nerve and long finger flexor tendons pass. Because the transverse carpal ligament is an unyielding fibrous structure forming the roof of the tunnel, tenosynovitis or arthritis in this area often produces pressure on the median nerve. The syndrome is frequently bilateral and usually of greater intensity in the dominant hand.

Symptoms consist of nocturnal pain and paresthesias, most often confined to the thumb, index, and middle fingers, but may be reported to involve the entire hand. Patients complain of tingling numbness, and burning sensations, which often awaken them from sleep. Referred pain may radiate to the forearm and even as high as the shoulder ( ). Symptoms are often provoked after excessive use of the hand or wrist or during ordinary activities such as driving or holding a phone, book, or newspaper, in which the wrist is assumed in either a flexed or extended posture. Objective sensory changes may be found in the distribution of the median nerve, most often impaired two-point discrimination, pinprick and light touch sensation, or occasionally hyperesthesia, in the thumb, index, and middle fingers, most evident in finger tips, with sparing of the skin over the thenar eminence. Thenar (abductor pollicis brevis muscle) weakness and atrophy may be present in advanced cases of CTS ( Fig. 106.6 ). Phalen maneuver (flexing the patient’s hand at the wrist for 1 minute) or reversed Phalen maneuver (hyperextension of the wrist for 1 minute) often reproduces the symptoms; it is present in about 80% of patients, and is rarely false positive ( ). A positive Tinel sign , in which percussion of the nerve at the carpal tunnel causes paresthesias in the distribution of the distal distribution of the median nerve, is present in approximately 60% of affected patients but is not as specific for CTS and may be false positive.

Work-related wrist and hand symptoms (repetitive motion injury) from cumulative trauma in the workplace have received increasing attention by the general public in recent years ( ). Although a proportion of these cases have bona fide CTS, longitudinal natural history data suggest that the majority of industrial workers do not develop symptoms of CTS ( ). Symptoms consistent with hand and wrist arthritis in a variety of occupational settings are now recognized as being much more common than CTS ( ). CTS appears to occur in work settings that include repetitive forceful grasping or pinching, awkward positions of the hand and wrist, direct pressure over the carpal tunnel, and the use of handheld vibrating tools. Increased risk for the syndrome has been found in meat packers, garment workers, butchers, grocery checkers, electronic assembly workers, musicians, dental hygienists, and housekeepers. The highest reported incidence of work-related CTS, based on the number of carpal tunnel surgeries performed, was 15% among a group of meat packers. Though using the computer keyboard may aggravate symptoms of CTS, keyboard use does not increase the risk of developing CTS ( ; ; ).

Diseases and conditions that have been found to predispose to the development of CTS include pregnancy, diabetes, obesity, age, rheumatoid arthritis, hypothyroidism, amyloidosis, gout, acromegaly, certain mucopolysaccharidoses, arteriovenous shunts for hemodialysis, old fractures at the wrist, and inflammatory diseases involving tendons or connective tissues at the wrist level ( ). On rare occasions, CTS may be familial, and some patients with CTS have carpal tunnels that are significantly narrower than average.

The most commonly performed EDX tests for CTS are the median nerve sensory and motor conduction studies, which exhibit delayed sensory or motor latencies across the wrist in about 70% of patients. However, these studies are not sensitive enough in the diagnosis of CTS and fail to detect up to a third of patients with CTS, particularly those with mild and early symptoms. Recording the median latency at short distances over the course of the median nerve from palm to wrist and/or comparing this latency with the latency for the ulnar or radial nerve at the same distance (internal comparison nerve conduction studies) increase the sensitivity of these nerve conduction studies ( ; ; Table 106.4 ) .

Mild CTS must be distinguished from proximal median neuropathies, upper brachial plexopathy, C6 or C7 radiculopathies, and polyneuropathy involving the hands. Occasionally, a transient ischemic attack may mimic the symptoms of CTS.

Ultrasound is increasingly used in the diagnosis of CTS. Thickening of the median nerve, best expressed as an increase in the CSA of the median nerve at the carpal tunnel inlet (more than 13 mm; normal <10–13 mm), or flattening of the nerve at the level of the hamate are the best diagnostic criteria ( Fig. 106.7 ) ( ; ). The majority of studies have found that the diagnostic utility of ultrasound and EDX studies are equal ( ; ). MRI is most useful when a space-occupying lesion, such as ganglion, hemangioma, or bony deformity, is suspected in patients with CTS.

In cases with only mild sensory symptoms, treatment with splints in neutral position, nonsteroidal antiinflammatory drugs (NSAIDs), and local corticosteroid injection often suffice ( ). Local corticosteroid injection is slightly better than splinting ( ). Withdrawal of provoking factors is also important. Although nonoperative treatments have been advocated ( ), a comparison of splinting versus surgery suggested that the latter may have a better long-term outcome than the former ( ). Use of a range of devices and appliances to protect the hand against CTS, including gel-padded gloves, has shown little if any improvement in objective measures of nerve function. There is conflicting evidence that NSAIDs, diuretics, laser, and ultrasound are effective. Exercise therapy is not useful ( ). Methylprednisolone injections for CTS significantly relieve symptoms for a few months and reduce the need for surgery, but a significant number of patients will ultimately need surgical treatment ( ). Oral steroids are also effective but are associated with side effects. Severe sensory loss, thenar atrophy, and active denervation on needle EMG of thenar muscles suggest the need for surgical carpal tunnel release. Open surgical sectioning of the volar carpal ligament or fiberoptic techniques are often successful, with more than 90% of patients having prompt resolution of pain and paresthesias ( ; ). Improvement in distal latencies may lag behind the relief of symptoms. Comparing with preoperative values, nerve conduction studies demonstrate improvement in those with moderate abnormalities preoperatively, whereas patients with severe or no abnormalities on baseline nerve conduction studies have poorer results ( ). A correlation between patients seeking workers’ compensation who hire attorneys and poorer operative outcomes has also been reported ( ). Older individuals may not improve as much as younger patients ( ), and factors such as poor mental health, significant alcohol consumption, longer disease duration, and male gender also portend a poorer outcome. Rarely, symptoms persist after operation. Poor surgical results usually are associated with incomplete sectioning of the transverse ligament, surgical damage of the palmar cutaneous branch of the median nerve by an improperly placed skin incision, scarring within the carpal tunnel, or an incorrect preoperative diagnosis. Surgical re-exploration may be required in certain cases with poor response to the initial operation ( ).

Median nerve compressions at the elbow

Applied anatomy

The ulnar nerve derives its fibers from the C8 and T1 roots via the lower trunk and originates from the medial cord of the brachial plexus, along with the medial brachial and antebrachial cutaneous sensory nerves. The ulnar nerve gives no branches in the arm. At the elbow, the nerve becomes superficial and enters the ulnar groove formed between the medial epicondyle and the olecranon process. Normally, the ulnar nerve remains in the groove, but in some individuals or when there is an unusual degree of physiological cubitus valgus, the nerve may be unduly mobile, tending to slip forward (sublux) over the medial epicondyle when the elbow is flexed. In a small number of individuals, a dense fibrotendinous band and/or an accessory epitrochleoanconeus muscle may be present between the medial epicondyle and the olecranon process. Slightly distal to the groove in the proximal forearm, the ulnar nerve travels under the tendinous arch of the two heads of the flexor carpi ulnaris muscle, known as the humeral-ulnar aponeurosis , which forms the entrance of the cubital tunnel. Muscular branches originate to the flexor carpi ulnaris and the flexor digitorum profundus (ulnar part to the little and ring fingers). The ulnar nerve continues under the flexor carpi ulnaris and then exits in the distal forearm between the deep fascia separating the flexor carpi ulnaris and flexor digitorum profundus. Some 5–8 cm proximal to the wrist, the dorsal ulnar cutaneous sensory branch exits to innervate skin on the dorsal medial hand and the dorsal little and ring fingers. The palmar cutaneous sensory branch originates at the level of the ulnar styloid to supply sensation to the proximal medial palm. The ulnar nerve then enters the wrist through the Guyon canal, which is formed between the pisiform bone and the hook of the hamate and is covered by the volar carpal ligament and the palmaris brevis muscle. Within the Guyon canal, the ulnar nerve divides into its terminal deep palmar and superficial ulnar branches. Because the palmar cutaneous sensory and dorsal cutaneous sensory branches do not pass through the Guyon canal, the deep palmar branch is purely motor and supplies muscular innervation to the hypothenar muscles, the palmar and dorsal interossei, the third and fourth lumbricals, and two muscles in the thenar eminence, the adductor pollicis, and the deep head of the flexor pollicis brevis.

Ulnar nerve entrapment at the elbow

Ulnar mononeuropathy is the second most common entrapment or compression mononeuropathy, although it is considerably less common than CTS. Compression of the ulnar nerve by a thickened, fibrotic flexor carpi ulnaris aponeurosis (humeral-ulnar aponeurosis) at the entrance of the elbow’s cubital tunnel is a common cause of ulnar neuropathy (cubital tunnel syndrome) . Patients with a subluxed ulnar nerve are at high risk for compression at the elbow. Also, prolonged and frequent resting of the flexed elbow on a hard surface such as a desk or armchair may result in external pressure to the nerve (ulnar groove syndrome) . Occupations involving repeated flexion of the elbow may on occasion cause symptoms of ulnar neuropathy. A flexed elbow position increases both the intraneural and extraneural pressure on the nerve. The nerve at the site of repeated compression is associated with fibrous thickening, when a spindle-shaped swelling may be felt. Other possible sources of injury of the ulnar nerve at the elbow include direct compression when the patient uses the arms to raise up in bed following surgical operations ( ) or after periods of prolonged unconsciousness. The ulnar nerve at the elbow may be acutely injured as a result of fracture or dislocation involving the lower end of the humerus and the elbow joint. Occasionally, however, the nerve becomes chronically compressed years after such an injury, which often has led to cubitus valgus deformity (“tardy ulnar palsy”) . The nerve may be damaged by osteophyte outgrowths resulting from arthritis of the elbow joint, by a ganglion or lipoma, by a Charcot elbow, and by the epitrochleoanconeus muscle and/or its dense fibrotendinous band. The ulnar nerve may also be involved in conditions that are known to increase the susceptibility of nerves to compression, such as DM or HNPP. Ulnar neuropathy at the elbow segment may also occur without any apparent cause.

Ulnar nerve lesions at the elbow result in numbness and tingling of the little and ring fingers, with variable degrees of hand weakness. Less commonly, patients present with weakness and wasting with no clear sensory symptoms. There is also variable weakness of the flexor carpi ulnaris and the flexor digitorum profundus of the ring and little fingers (ulnar part). Grip strength is reduced secondary to weakness of the adductor pollicis, flexor pollicis brevis, and palmar and dorsal interosseous muscles. To compensate for adductor pollicis weakness during an attempt to pinch a piece of paper between the thumb and index fingers, the flexor pollicis longus, a median nerve-innervated muscle, becomes involuntarily active and flexes the distal phalanx of the thumb (Froment sign) . Weakness of the interossei muscles results in an inability to forcefully extend the interphalangeal joints, as is necessary in finger-flicking movements. Prominent atrophy of hand muscles ensues and is most noticeable at the first dorsal interosseous muscle. Lumbrical weakness leads to clawing of the fourth and fifth fingers and flexion of the proximal and distal interphalangeal joints, with secondary hyperextension of the metacarpophalangeal joints (benediction posture or ulnar clawing) . Weakness of the third palmar interosseous muscle results in abduction of the little finger, which may get caught when the patient tries to put the hand in a pocket (Wartenberg sign) . In chronic ulnar neuropathies, the weakness and atrophy of small muscles of the hand is always more severe than the weakness and atrophy of the forearm muscles. Sensory loss or hypoesthesia involves the fifth finger, part of the fourth finger, and the hypothenar eminence and includes the dorsum of the hand but does not extend above the wrist level. Pain around the elbow and tenderness of the ulnar nerve with deep palpation is common, but distal hand or finger pain is rare. A Tinel sign at the elbow may be elicited, but this sign as well as provocative tests (flexion compression test, palpating for local ulnar nerve tenderness and nerve thickening) have poor diagnostic values ( ).

Ulnar nerve lesions at the elbow should be distinguished from ulnar nerve lesions at the wrist, lower brachial plexus lesions (lower trunk or medial cord), and C8 radiculopathy. Confirmed sensory loss that extends more than 3 cm above the wrist into the medial forearm and arm, the territories of the medial brachial and antebrachial cutaneous nerves, is inconsistent with an ulnar neuropathy at the elbow and suggests a more proximal lesion of the lower plexus or C8 or T1 roots. Similarly, weakness of median and radial innervated C8 muscles such as the flexor pollicis longus or the long finger extensors points to a plexopathy or radiculopathy.

Compared to evaluating other entrapment neuropathies such as CTS, the EDX studies used to confirm and localize ulnar nerve entrapment at the elbow are more challenging. Localizing ulnar neuropathy at the elbow relies upon the demonstration of focal demyelination across the elbow, namely slowed motor conduction velocity (>10–15 m/sec) or conduction block (localized reduction in CMAP amplitude and area of >20%–30%) or both. Focal slowing or conduction block may be found in the elbow segment in more than 75% of cases ( ). Performing an additional ulnar motor conduction study, recording the first dorsal interosseous muscle in addition to recording the abductor digiti minimi muscle, increases the yield of finding focal slowing or conduction block. In the remaining patients, localization becomes less precise because of predominant axonal loss. To provide the extra nerve length needed during elbow flexion, the ulnar nerve is anatomically redundant in the ulnar groove when the elbow is extended, and this can cause measurement errors. A flexed position of the elbow (70–90 degrees) is preferred to the extended position when doing ulnar motor conduction studies to localize an ulnar lesion at the elbow.

Reference values to determine absolute across-elbow ulnar motor conduction velocity slowing or relative slowing in across-elbow versus forearm conduction velocities have varied depending on study design and population studied. In addition, the optimal distance for measuring ulnar motor NCV around the flexed elbow continues to be debated between 6 and 10 cm ( ). To improve diagnostic accuracy and reduce false-positive and false-negative results, different diagnostic criteria are advocated for patients with different pre-test probability of ulnar neuropathy across the elbow ( ). Patients with high pre-test probability of ulnar neuropathy across the elbow (i.e., with typical clinical symptoms and signs) should have less stringent diagnostic criteria (for example >14 m/sec velocity difference or <47 m/sec velocity), while those with low pre-test probability of ulnar neuropathy across the elbow (i.e., with atypical or inconsistent clinical symptoms and signs) should have more strict diagnostic criteria (such as >23 m/sec velocity difference and <38 m/sec velocity). Short-segment incremental studies (“inching”) by stimulating the ulnar nerve in successive 1- or 2-cm increments across the elbow, looking for either an abrupt drop in amplitude or increase in latency, are useful techniques that help to precisely localize the ulnar nerve lesion ( ; ). Electrophysiological tests are helpful in differentiating between an ulnar neuropathy and a C8 nerve root or brachial plexus lesion. Ulnar sensory nerve conduction sparing points to C8 radiculopathy and normal needle EMG of C8 muscles innervated by the median nerve (e.g., abductor pollicis brevis, flexor pollicis longus) and radial nerve (e.g., extensor indicis proprius) help exclude a C8 root lesion or a lower brachial plexopathy.

High-resolution ultrasonography at the elbow is also useful by accurately detecting enlargement of the ulnar nerve at the elbow ( ). MRI of the elbow may reveal a space-occupying lesion or anomalous structures impinging on the nerve or demonstrate nerve enlargement and increased signal intensity, even in the absence of localizing electrophysiological abnormalities ( ).

Conservative treatment should be attempted in patients with mild or intermittent sensory symptoms or in those with symptoms brought on by occupational causes. Avoidance of repetitive elbow flexion and extension or direct pressure on the elbow may alleviate the symptoms. Elbow protectors are helpful in patients with a history of excessive elbow leaning. Conservative treatment should be continued for at least 3 months before surgery is considered. Several surgical approaches to an ulnar nerve lesion at the elbow are possible, each with its proponents and critics. Techniques include simple release of the flexor carpi ulnaris aponeurosis, anterior transposition of the nerve trunk, and resection of the medial epicondyle. The choice of procedure should be tailored to the specific lesion found at surgery and may be assisted by short-segment incremental electrophysiological studies (“inching”). Transposition of the nerve trunk carries a higher rate of complications than ulnar neurolysis ( ). Depending on the type of surgery and the severity and duration of neuropathy, response to these procedures will vary. Only about 60% of patients, especially those with symptoms of less than 1 year’s duration, benefit from surgery; some experience worsening of symptoms. It appears that those with more thickening of the nerve at the time of diagnosis (as determined by sonography) have a more unfavorable outcome, and those with electrophysiological signs of demyelination across the elbow, specifically significantly greater than 50% conduction block, have a more favorable course ( ; ).

Ulnar nerve entrapment at the wrist

Distal entrapment of the ulnar nerve at the wrist (Guyon canal) or hand is a relatively uncommon condition. Ulnar nerve entrapment in the Guyon canal occurs much less frequently than at the elbow. Aside from direct trauma and laceration, the most common cause is a ganglion cyst. Other usual causes are chronic or repeated external pressure by hand tools, bicycle handlebars, the handles of canes, or excessive push-ups. Compression also may be caused by degenerative wrist joint changes, rheumatoid arthritis, or distal vascular anomalies.

Ulnar nerve entrapment at the wrist may present with a confusing array of sensory and motor symptoms or both, depending on which branches of the nerve are involved. Most cases of ulnar nerve entrapment at the Guyon canal, however, involve solely motor fibers and present with painless unilateral hypothenar and interossei weakness or atrophy. Because the palmar cutaneous and dorsal cutaneous branches leave the ulnar nerve in the distal forearm and do not enter the Guyon canal, sensation in the proximal hypothenar region and the dorsum of the little and ring fingers is not impaired in all cases of ulnar nerve lesions at the wrist or hand. The sensory loss, if present, is confined to the palmar surface of the ulnar-innervated fingers (the little finger and usually the ulnar half of the ring finger) and the distal hypothenar region. Compression at the distal portion of the Guyon canal (also referred to as the pisohamate hiatus ) results in selective involvement of the deep motor branch, with interossei weakness and atrophy and complete or relative sparing of the hypothenar muscles as well as sensation ( ).

The diagnosis is confirmed by EDX studies, often by demonstrating low amplitude (with or without prolonged distal motor latencies) to the first dorsal interosseous or abductor digiti minimi muscles or both, along with denervation of the ulnar-innervated hand muscles that parallels the clinical manifestations. Ulnar SNAP may or may not be abnormal. These EDX studies are also important in excluding an ulnar neuropathy at the elbow. Several features on the EDX examination are inconsistent with an ulnar neuropathy at the wrist: low amplitude or absent dorsal ulnar SNAP, focal slowing or conduction block across the elbow, or denervation of the flexor carpi ulnaris or the flexor digitorum profundus (ulnar portion).

Plain radiograph of the wrist may reveal a fracture of the pisiform or hook of the hamate bone. Neuromuscular ultrasound or MRI is extremely helpful and may demonstrate a structural lesion such as a ganglion cyst. Sources of occupational or recreational trauma should be eliminated. In patients with fractures, ganglia, or mass lesions, surgical intervention is necessary. The prognosis is usually good after surgical decompression with effective reinnervation.

Applied anatomy

The radial nerve is the largest nerve in the upper extremity. In the arm, lying medial to the humerus, the radial nerve innervates all three heads of the triceps muscle and the anconeus muscle. The nerve passes obliquely behind the humerus and then through the spiral groove, a shallow groove formed deep to the lateral head of the triceps muscle. Before entering the spiral groove in the midarm, it gives three sensory branches: the posterior cutaneous nerve of the arm (which innervates a strip of skin overlying the triceps muscle), the lower lateral cutaneous nerve of the arm (which innervates the lateral half of the arm), and the posterior cutaneous nerve of the forearm (which innervates the skin of the extensor surface of the forearm). In the anterior compartment of the arm, the radial nerve, lying lateral to the humerus, innervates the brachioradialis and the extensor carpi radialis longus. The nerve then passes anterior to the lateral epicondyle and innervates the extensor carpi radialis brevis and supinator. The “radial tunnel” is a space (not an anatomical tunnel) where the radial nerve travels in the upper forearm from the humeroradial joint past the supinator muscle. Within that space, the radial nerve divides into its terminal branches, the superficial radial and posterior interosseous nerves (PINs). The PIN, a terminal pure motor branch, passes under the proximal edge of the supinator muscle (arcade of Frohse) and travels in the forearm and innervates all the remaining wrist and finger extensors. The superficial radial nerve is a terminal pure sensory nerve and innervates the skin of the proximal two-thirds of the extensor surfaces of the thumb, index, and middle fingers, and half of the ring finger, along with the corresponding dorsum of the hand.

Radial nerve compression in the arm

Radial nerve compression in the arm often occurs at the spiral groove of the humerus during drunken sleep wherein the arm is draped over a chair (Saturday-night palsy) ( ). The radial nerve may also be injured following fractures of the humerus. Radial nerve lesions at the axilla are much less common; they may result from misuse of crutches or from the weight of a sleeping partner’s head (honeymoon palsy) or follow shoulder joint replacement. The radial nerve is also often involved in isolation or in combination with other single nerves in MMN with conduction block.

In radial nerve lesions in the spiral groove or midarm, there is weakness of the brachioradialis, wrist, and finger extensors, while the triceps is spared. Sensory abnormalities may occur over the dorsum of the hand, thumb, index finger, and middle finger. In lesions at the axilla, there is additional weakness of the triceps, and the sensory loss may extend into the extensor surface of the forearm and lateral half of the arm and over to the triceps owing to involvement of the posterior cutaneous nerve of the forearm and the lower lateral cutaneous and posterior cutaneous nerve of the arm.

The EDX studies are essential in confirming the site and extent of the lesion, excluding other causes of wrist drop, and estimating severity and prognosis. Low-amplitude or absent radial SNAP is common except when the pathology at the spiral groove is purely demyelinating. Conduction block across the spiral groove is seen in segmental demyelinating lesions, or the radial motor responses are low in amplitude in axon-loss lesions. Mixed lesions are also common. Needle EMG reveals denervation of all finger and wrist extensors, as well as the extensor carpi radialis and the brachioradialis. The triceps and anconeus are spared in midarm lesions and denervated in axillary lesions. Ultrasonography is a useful additional tool to electrodiagnosis for diagnosing radial neuropathy across the spiral groove. Enlarged radial nerve as determined by CSA above at 5.75 mm ² is a highly specific finding ( ).

As with other peripheral nerve lesions, the prognosis depends on the primary pathology. Radial nerve lesions due to demyelinative conduction block, such as in most cases of Saturday-night palsy, usually improve in 6–8 weeks. Axon-loss lesions such as those often associated with humeral fracture, however, have a less favorable prognosis, with a protracted course and often incomplete recovery.

Posterior interosseous neuropathy

Lesions of the PIN are uncommon and usually occur in association with trauma, fracture, soft-tissue masses (e.g., lipomas, gangliomas), or exuberant synovium motor neuropathy (i.e., rheumatoid arthritis). Occasionally, a PIN lesion, in isolation or in combination with other single nerves is a manifestation of neuralgic amyotrophy, with acute arm pain followed within a few days by weakness ( ). The clinical manifestations of a PIN lesion are dropped fingers and inability to extend them at the metacarpophalangeal joints. Radial deviation of the wrist on wrist extension is often pathognomonic and is due to weakness of the extensor carpi ulnaris muscle with sparing of the extensor carpi radialis muscle, the latter innervated by the main trunk of the radial nerve. EMG study confirms the diagnosis by demonstrating normal radial SNAP and denervation of the muscles supplied by the PIN, with sparing of more proximal radial-innervated muscles including the brachioradialis, extensor carpi radialis, and triceps muscles.

In rheumatoid arthritis, local injection of corticosteroids may be helpful. If the syndrome is progressive, surgical exploration, including synovectomy or decompression of the PIN, may become necessary ( ).

Radial tunnel syndrome

Patients with persistent tennis elbow (lateral epicondylitis) are sometimes given a diagnosis of radial tunnel syndrome, an extremely rare and highly controversial entrapment of the radial nerve or its posterior interosseous branch within the radial tunnel ( ). The nerve appears most vulnerable to entrapment at the level of the supinator muscle. These patients present with forearm pain and tenderness at the lateral epicondyle and slightly distally into the forearm, with no associated muscle weakness or sensory loss in the radial or PIN distribution. Pain is induced by extension of the middle finger or supination with the elbow extended. The EMG study, including radial nerve conduction studies recording the extensor digitorum communis and extensor indicis proprius, is almost always normal. Local steroid injection may temporarily relieve symptoms. In patients with persistent pain, surgical division of the supinator muscle has been advocated, with variable results.

Superficial radial sensory neuropathy (cheiralgia paresthetica)

Cheiralgia paresthetica is a mononeuropathy of the superficial dorsal sensory branch of the radial nerve. It occurs as a result of trauma from tight wristbands or handcuffs, or may result from intravenous cannulation, fracture of the wrist, or wrist surgery (e.g., plating of forearm bones after fracture). The use of one-way (only tighten) ratcheting mechanism of handcuffs increases the risk of cheiralgia paresthetica ( ). In up to 50% of nontraumatic cases, it is also associated with de Quervain tenosynovitis , an inflammatory condition of thumb extensor muscles, predominantly extensor pollicis brevis ( ). In de Quervain tenosynovitis, there is tenderness of the anatomical snuffbox and thumb extensor tendons with forced ulnar deviation while holding the thumb wrapped in the palm (Finkelstien sign). Paresthesias and pain in the distribution of the superficial sensory branch of the radial nerve characterize this benign self-limiting condition. A small area of hypoesthesia in the dorsoradial aspect of the hand is frequently identified. Nerve conduction study often shows a low-amplitude or absent dorsal radial SNAP with normal needle EMG including all radial innervated muscles.

Applied anatomy

The sciatic nerve is formed from nerve roots L4 through S3 and is composed of two distinct nerves, the common peroneal (renamed the fibular nerve by the Federative Committee on Anatomical Terminology [FCAT], owing to confusion between the terms peroneal and perineal ) and tibial nerves, which share a common sheath from the pelvis to the popliteal fossa. Usually the sciatic nerve emerges from the pelvis by passing beneath the piriformis muscle, but sometimes the fibular division only passes through or above the piriformis muscle. The sciatic nerve innervates all the hamstring muscles via the tibial nerve except the short head of the biceps femoris, which is innervated by the common fibular nerve. The common fibular and tibial nerves separate completely in the upper popliteal fossa or slightly above.

Sciatic neuropathy at the sciatic notch

The sciatic nerve is occasionally vulnerable to entrapment as it crosses over the sciatic notch leaving the pelvis. Most sciatic nerve lesions are complications of hip replacement surgery ( ; ). Traumatic lesions include bullet and stab wounds, fractures, dislocations, hematomas in the posterior thigh compartment, and misplaced intramuscular injections. Recurrent sciatic mononeuropathy may be caused by endometriosis involving the nerve at the sciatic notch. Direct compression of the sciatic nerve is rare but occasionally occurs during coma, anesthesia, or prolonged sitting on a hard surface (“toilet seat palsy”) . Either or both divisions of the nerve may be compressed by a Baker cyst in the popliteal fossa.

A complete sciatic nerve lesion results in weakness of knee flexors and all muscles below the knee, as well as sensory loss of the entire foot and leg below the knee except for a region supplied by the saphenous nerve over the medial leg. The fibular division is more commonly involved than the tibial in proximal lesions of the sciatic nerve. Partial sciatic nerve lesions often affect the fibular nerve more than the tibial nerve and may mimic a more distal common fibular neuropathy. This is explained by the fewer fascicles with limited supportive tissue within the fibular nerve, which is also taut and secured at the sciatic notch and fibular neck. In such patients, evidence of denervation in the short head of the biceps femoris and tibialis posterior muscles and abnormal sural or medial plantar SNAPs help localize partial proximal sciatic nerve lesions ( ). Occasionally, the common fibular nerve gets injured selectively ( ). Young age, lack of severe initial weakness, and recordable distal motor or sensory responses are predictors of favorable outcome ( ; ).

Piriformis syndrome

On rare occasions, the piriformis muscle may entrap the sciatic nerve trunk as it passes through or over the piriformis muscle. Since the term was coined in 1947 by Robinson, the piriformis syndrome has been subject to controversy ( ; ). The syndrome fell out of fashion with the advancement of radiological techniques (myelography, CT, MRI) that often demonstrate that most patients with sciatica have nerve root compression and occasionally lesions of the sacral plexus or sciatic nerve at other locations.

The typical patient with piriformis syndrome has a history of buttock trauma and experiences maximal buttock pain during prolonged sitting (e.g., driving, biking), bending at the waist, or activity that requires hip adduction and internal rotation (e.g., cross-country skiing) ( ). The neurological and EDX examinations are usually normal. A bedside test maneuver in which the hip is placed passively in adduction, internal rotation, and flexion of the hip (AIF maneuver) may reproduce the pain and is considered diagnostic. Imaging is usually normal but occasionally shows hypertrophy of the piriformis muscle or abnormal vessels or bands in the region of the piriformis muscle. MR neurography may show sciatic nerve hyperintensity at the sciatic notch, a more specific sign of nerve entrapment ( ). Treatment consists of exercises that include prolonged stretching of the piriformis muscle by flexion, adduction, and internal rotation of the hip. CT- or MRI-guided corticosteroid injection into the piriformis muscle may alleviate the symptoms; a positive response is used as a confirmatory test. Surgical sectioning of the piriformis muscle is indicated in cases resistant to conservative therapy. Although good outcome is expected in carefully selected patients ( ), severe postoperative sciatic nerve injury was recently reported as a serious complication ( ).

Applied anatomy

As noted earlier, the confusing similarity between peroneal and perineal led FCAT to rename the peroneal nerve the fibular nerve . Soon after the sciatic nerve divides close to the popliteal fossa, the common fibular nerve gives off the lateral cutaneous nerve of the calf, which innervates the skin over the upper third of the lateral aspect of the leg, and the fibular communicating nerve which joins the sural nerve. The common fibular nerve then winds around the fibular neck and passes through the origin of the peroneus longus muscle (“fibular tunnel”). Near that point, the common fibular nerve divides into its terminal branches, the deep and superficial fibular nerves. The deep fibular nerve traverses the lateral and then anterior leg compartments and innervates the tibialis anterior, extensor hallucis longus, peroneus tertius, and extensor digitorum longus. It then divides close to the ankle joint to innervate the extensor digitorum brevis and the skin of the web space between the first and second toes. The superficial fibular nerve innervates the peroneus longus and brevis and the skin of the lower two-thirds of the lateral aspect of the leg and the dorsum of the foot (except for the first web space). An accessory deep fibular nerve, seen in up to 28% of individuals, arises from the superficial fibular nerve, passes behind the lateral malleolus, and innervates the lateral part of the extensor digitorum brevis.

Common fibular (peroneal) neuropathy at the fibular neck

Compression of the common fibular nerve is the most frequent compressive neuropathy in the lower extremity. This nerve is particularly vulnerable to direct pressure in the region of the fibular neck as it passes through the origin of the peroneus longus muscle. Intraoperative compression due to improper positioning or padding during anesthesia is the leading cause of acute common fibular neuropathy at the fibular neck ( ). Weight loss, habitual leg crossing, or unrecognized pressure on the nerve in hospitalized critically ill, debilitated, or unconscious patients may also be responsible for this nerve injury ( ; ). Devices that may compress the fibular nerve include casts, orthoses, pneumatic compression, antithrombotic stockings, bandages, and straps. Fibular nerve stretch injury may result from an acute forceful foot inversion or prolonged squatting (strawberry pickers palsy). Blunt trauma (e.g., post fibular fracture, knee dislocation) and open injury (e.g., lacerations) account for a significant number of cases. Postpartum peroneal neuropathy may be due to stirrups compression, prolonged squatting, or direct hand compression. Fibular nerve injury is also a known complication of knee surgery, including arthroscopic surgery and lateral meniscus repair. Up to half of patients without a clear cause of fibular mononeuropathy across the fibular head have intraneural ganglia ( ). These are formed when disruption of the capsule of the superior tibiofibular joint results in dissection of synovial fluid along the articular branch of the fibular nerve into the tibialis anterior motor branch ( ). Other mass lesions such as osteochondromas or schwannomas are much less common.

A common fibular nerve lesion leads to weakness of foot and toe extension and foot eversion, with a foot drop and steppage gait. Sensory impairment is found over the lateral aspect of the lower two-thirds of the leg and the dorsum of the foot. Foot eversion and sensory loss may be spared (except for the first web space of the foot) when the lesion is selective, involving the deep fibular nerve. Pain is rare except with intraneural ganglia.

Fibular mononeuropathy is most often confused with other causes of unilateral foot drop, including L5 radiculopathy, sciatic nerve lesions (especially when predominantly affecting the common fibular nerve), and lumbosacral plexopathy (particularly when involving the lumbosacral trunk). A fibular nerve lesion must be differentiated from anterior tibial compartment syndrome , in which the deep fibular nerve is compressed by muscle swelling within the anterior compartment secondary to injury, heavy exercise, trauma, or ischemia. This results in an acute syndrome of severe lower leg pain, swelling, and weakness of foot and toe extensors. The anterior tibial compartment must be decompressed rapidly by fasciotomy to prevent irreversible nerve and muscle damage.

EDX studies are useful for localizing lesions and may provide clues to the underlying cause and a guide to prognosis. Although it is often possible by nerve conduction studies to demonstrate focal conduction block across the fibular head, contrary to common belief, the most frequent pathophysiological process is axonal loss, regardless of the cause ( ). Axon-loss lesions reveal diffusely low or absent fibular motor and sensory amplitudes. In contrast to ulnar lesions across the elbow and CTS, localized slowing in the region of the fibular head is not common. Needle EMG demonstrates denervation in common fibular-innervated muscles but not in the short head of the biceps femoris (innervated by the common fibular division of the sciatic nerve in the thigh), in the L5 nerve root-innervated muscles, such as the tibialis posterior, flexor digitorum longus, tensor fascia lata and gluteus medius, or the low lumbar paraspinal muscles.

Ultrasound and MRI are effective in visualizing intraneural ganglia and other soft-tissue masses or tumors. Ultrasound is slightly more accurate than MRI in compressive fibular neuropathies ( ). It shows thickened fibular nerve (cross-sectional area >8 mm ² ) in about 70% of patients ( ), and establishes involvement of the anterior fascicles (corresponding to fibers for the deep fibular nerve) in the majority of compressive fibular neuropathies ( ).

The prognosis is uniformly good in cases of acute demyelinating lesions, whereas recovery is delayed in those with axonal lesions and stretch injuries. The distal fibular motor amplitude recording tibialis anterior serves as an accurate estimate of the extent of axonal loss and a good prognostic indicator of foot drop. Hence, fibular nerve studies should be performed bilaterally and compared. Bracing with a custom-made plastic ankle-foot orthosis is necessary to improve the gait in the presence of severe foot drop. The few patients who do not improve spontaneously after 3 months, or those who have pain or a slowly progressive fibular nerve lesion, may require MRI studies and surgical exploration ( ).

Applied anatomy

The tibial nerve innervates all the hamstring muscles except the short head of the biceps femoris. It then separates from the common fibular nerve, usually in the upper popliteal fossa, and gives off the sural sensory nerve, which is often joined by a branch from the common fibular nerve, the sural communicating nerve, to innervate the skin over the lateral aspect of the lower leg and foot, including the little toe. In the upper calf, the tibial nerve passes underneath the soleus muscle and innervates the gastrocnemius, soleus, tibialis posterior, flexor digitorum profundus, and flexor hallucis longus. At the ankle, the tibial nerve passes under the laciniate ligament, which covers the tarsal tunnel through which the nerve passes together with the tendons of the tibialis posterior, flexor digitorum longus, and flexor hallucis longus muscles and the tibial artery and veins.

Tarsal tunnel syndrome

Entrapment of the tibial nerve occurs behind and immediately below the medial malleolus. Burning pain is experienced in the toes and the sole of the foot. If the calcaneal sensory branches are involved, pain and numbness also involve the heel. Examination usually reveals plantar sensory impairment and wasting of the intrinsic foot muscles. Percussion at the site of nerve compression or eversion of the foot often elicit pain and paresthesias. EDX study results should confirm entrapment of the tibial nerve at the tarsal tunnel by demonstrating slowing of motor fibers to the abductor hallucis and/or abductor digiti minimi muscles, as well as involvement of the medial and/or lateral plantar mixed potentials fibers, with sparing of the sural nerve sensory action potential. Unfortunately, medial and/or lateral plantar mixed (or sensory) potentials are technically very difficult and may be unelicitable in normal subjects with plantar calluses, foot edema, previous surgical procedures in the foot, or in adults over the age of 45. Needle EMG shows denervation of the abductor hallucis and/or abductor digiti minimi muscles and normal S1-innervated and proximal muscles such as the gastrocnemius, soleus, biceps femoris, and gluteus maximus muscles. The majority of suspected cases of tarsal tunnel syndrome, particularly when symptoms are bilateral, turn out to have generalized peripheral neuropathy, S1 radiculopathy, or non-neurological foot pain such as plantar fasciitis, stress fracture, arthritis, or bursitis. Ultrasound plays an important role in identifying the cause ( ). This is particularly useful in elderly or patients with foot edema, calluses, or previous surgery as EDX studies may be difficult to perform or interpret.

Local injection with corticosteroids underneath the laciniate ligament may temporarily relieve symptoms. Surgical decompression is needed for permanent results in those rare cases in which objective evidence of this syndrome exists.

Applied anatomy

The femoral nerve is formed in the pelvis from the posterior divisions of the ventral rami of L2, L3, and L4 spinal roots, where it innervates the psoas muscle. It then passes within the iliacus compartment and innervates the iliacus muscle via a motor branch that originates 4–5 cm before the nerve crosses underneath the inguinal ligament. In the anterior thigh, the femoral nerve innervates the quadriceps and sartorius muscles and the skin of the anterior thigh and gives off the saphenous sensory nerve, which innervates the skin of the medial surface of the knee and medial leg.

Femoral nerve lesions

The majority of femoral nerve lesions are iatrogenic ( ). Pelvic lesions follow a variety of gastrointestinal, vascular, urological, or gynecological operations such as abdominal hysterectomy, radical prostatectomy, renal transplantation, and abdominal aortic repair. During these procedures, the femoral nerve becomes compressed between the lateral blade of the retractor and the pelvic wall. Risk factors include the use of self-retaining retractors, a thin body habitus, and transverse abdominal incision ( ). Acute retroperitoneal hematoma is often iatrogenic following anticoagulant therapy, pelvic operations, or femoral vessel catheterization such as for cardiac catheterization. At the inguinal ligament, the femoral nerve may become kinked during lithotomy positioning, particularly when the leg is held in extreme hip flexion and external rotation, used during vaginal delivery, vaginal hysterectomy, prostatectomy, and laparoscopy. Total hip replacement, particularly surgical revisions and complicated reconstructions, may result in femoral nerve injury.

Femoral nerve injury due to spontaneous retroperitoneal hematoma may occur in hemophiliacs, patients with blood dyscrasias, or following a ruptured abdominal aortic aneurysm. Pelvic lymphadenopathy, primary malignancy of the colon or rectum, and neurofibromas or schwannomas are rare causes of femoral neuropathies. Hip hyperextension, such as in dancers or during Yoga exercise, may also cause a femoral stretch injury.

Femoral nerve lesions manifest with acute thigh weakness and anterior thigh and medial leg numbness. Thigh weakness often leads to falls. Pain is usually absent except in cases due to retroperitoneal hematomas. On examination, there is weakness of knee extension, with absent or depressed knee jerk. Thigh adduction is normal. Hip flexion is usually weak when the lesion is within the pelvis, although it may be difficult to assess hip flexion in the setting of severe quadriceps weakness.

Needle EMG reveals denervation of the quadriceps muscle. The iliacus muscle is often normal in inguinal lesions but shows denervation in femoral nerve lesions in the pelvis. Needle EMG of the thigh adductor muscles, innervated by the L2, L3, L4 roots via the obturator nerve, helps distinguish femoral nerve lesions from upper lumbar radiculopathy or plexopathy. Nerve conduction studies have prognostic value, since the amplitude and area of the femoral CMAP is a very good quantitative measure of motor axonal loss ( ). CT or MRI of the pelvis are urgently indicated in patients with suspected retroperitoneal hematoma or pelvic mass lesion.

Apart from patients with confirmed retroperitoneal hematoma who may require emergent drainage, most other femoral nerve lesions are treated conservatively. A knee or knee-ankle-foot orthosis is helpful for patients with unilateral severe weakness of the quadriceps and will assist in walking and prevent falls. Prevention of femoral nerve injury is of paramount importance. The surgeon should limit hip flexion, abduction, and external rotation during lithotomy positioning, particularly when “candy cane” stirrups are used. The incidence of femoral nerve lesions after pelvic and gynecological operations is significantly reduced when self-retractors are avoided; the retracting blades should also cradle the rectus muscle without compressing the psoas muscle ( ).

Lateral femoral cutaneous nerve entrapment (meralgia paresthetica)

The lateral femoral cutaneous nerve, which is a pure sensory nerve, passes medial to the anterior superior iliac spine under the inguinal ligament to enter the thigh under the fascia lata that it penetrates to supply the skin of the anterolateral part of the thigh. The site of entrapment is usually at the level of the inguinal ligament. Rarely, the nerve may be affected in its proximal segment by retroperitoneal tumors or be injured during appendectomy. The disorder occurs in about 4 per 10,000 individuals. It is most often seen in association with obesity, diabetes, and advancing age ( ). It is a common entrapment neuropathy during pregnancy, particularly the third trimester, and usually recovers after delivery. It may occur with ascites, or in other conditions that increase intraabdominal pressure. Direct compression by a belt, corset, beeper, or cellular phone; fracture of the anterior portion of the ilium; or pelvic tilt causing undue stresses on the abdominal musculature are other causes.

Patients develop numbness, painful burning, and itching over the anterolateral thigh. Pressure at the inguinal ligament medial to the anterior superior iliac spine may elicit referred pain and dysesthesias. Some patients report relief of pain when assuming a supine position.

Lateral femoral cutaneous nerve SNAP is technically difficult to measure and may be absent in healthy subjects, particularly women and obese individuals. Asymmetrical low-amplitude or absent potential on the symptomatic side is a confirmatory finding. Electrophysiological studies of the femoral nerve and quadriceps femoris and iliacus muscles are normal, which helps exclude lumbar radiculopathy and plexopathy. A local anesthetic nerve block may have diagnostic value ( ). Treatment consists of symptomatic measures such as rest, analgesics, and weight loss. Postural abnormalities should be corrected. Neurolysis is rarely beneficial.

Ilioinguinal neuropathy

The ilioinguinal nerve is analogous to an intercostal nerve. Muscle branches innervate the lower portion of the transverse abdominal and internal oblique muscles. The cutaneous sensory nerve supplies the skin over the inguinal ligament and the base of the scrotum or labia. As the nerve takes a zigzag course, passing through the transverse abdominal and internal oblique muscles, it is subject to mechanical compression such as with a direct inguinal hernia. Trauma, surgical procedures, scar tissue, and increased abdominal muscle tone caused by abnormal posture are frequently responsible. Pain is referred to the groin, and weakness of the lower abdominal wall may result in the formation of an asymmetrical bulging of the lower abdominal wall.

Conservative treatment includes rest and NSAIDs. Neurolysis may be required in refractory cases when a mechanical lesion is suspected.

Obturator neuropathy

The obturator nerve is vulnerable to entrapment as it passes through the obturator canal (e.g., by an obturator hernia or osteitis pubis). An obturator neuropathy is most often associated with pelvic malignancies (prostate, cervical, or uterine cancers). It can also be seen with trauma and synovial cyst of the hip or as a surgical complication, especially with extensive retroperitoneal surgeries or laparoscopic pelvic lymphadenectomies and during total hip replacement.

Entrapment produces radiating pain from the groin down the inner aspect of the thigh, often difficult to distinguish from the pain of a recent procedure or trauma. There is weakness of hip adduction and sensory impairment in the upper medial thigh. Many patients appear to have hip-flexor weakness as a false localizing sign. Although this phenomenon may be explained by pain, it is more likely due to mechanical disadvantage of the hip flexors in the presence of weak thigh adductors. CT or MRI scanning of the pelvis is helpful in finding primary or metastatic pelvic tumors. EMG testing is essential for diagnosis by detecting selective denervation of the thigh adductor muscles, with normal quadriceps and iliacus muscles, thus excluding other causes of hip weakness including femoral nerve lesions, upper lumbar (L2, L3, or L4) radiculopathy or plexopathy, and diabetic amyotrophy (diabetic proximal neuropathy or radiculoplexopathy) ( ).

This entrapment neuropathy is treated conservatively, which often provides good results, especially in those with acute onset of symptoms. If such treatment fails or if symptoms progress to involve other nerves in the region, a careful search for occult pelvic or retroperitoneal malignancy must be pursued.