Disorders of Peripheral Nerves

Median Nerve Entrapment at the Wrist (Carpal Tunnel Syndrome).

Carpal tunnel syndrome (CTS) is by far the most common entrapment neuropathy. 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, often awakening them from sleep. Referred pain may radiate to the forearm and even as high as the shoulder (Stevens et al., 1999). 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, 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. 107.6). Flexing the patient's hand at the wrist for 1 minute (Phalen maneuver) or hyperextension of the wrist (reversed Phalen maneuver) often reproduces the symptoms, 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 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 (Thomsen et al., 2002). 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 (Nathan et al., 1998). Symptoms consistent with hand and wrist arthritis in a variety of occupational settings are now recognized as being much more common than CTS (Dillon et al., 2002). 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. Although computer keyboard use has long been thought to be related to developing carpal tunnel symptoms, recent data provide no convincing correlation between intensive keyboard use and the subsequent development of CTS (Papanicolaou et al., 2001; Stevens et al., 2001).

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 (Becker et al., 2002). On rare occasions, CTS may be familial, and some patients with CTS have carpal canals 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 (Stevens, 1997) (Table 107.5).

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 cross-sectional area 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 (Tai et al., 2012). Comparing the sensitivity of ultrasound versus electrodiagnostic studies in the diagnosis of CTS has been difficult since the electrodiagnostic studies have long been considered the gold standard. However, the majority of studies have found that the diagnostic utility of these two modalities are equal (Mondelli et al., 2008). 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 anti-inflammatory drugs (NSAIDs), and local corticosteroid injection often suffice. Withdrawal of provoking factors is also important. Although nonoperative treatments have been advocated (Osterman et al., 2002), a comparison of splinting versus surgery suggested that the latter may have a better long-term outcome than the former (Gerritsen et al., 2002). 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 nonsteroidal anti-inflammatory agents, diuretics, laser and ultrasound are effective. Exercise therapy is not useful (Piazzini et al., 2007). 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 (Atroshi et al., 2013). 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 (Mirza and King, 1996). 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 (Bland, 2001). A correlation between patients seeking workers' compensation who hire attorneys and poorer operative outcomes has also been reported (Katz et al., 2001a). Older individuals may not improve as much as younger patients (Porter et al., 2002), 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 diagnostically certain cases with poor response to the initial operation (Steyers, 2002).

Isolated acute involvement of the anterior interosseous nerve is often a partial neuralgic amyotrophy (idiopathic brachial plexus neuropathy, Parsonage-Turner syndrome) (England and Sumner, 1987; Katirji,1986). The majority of these lesions are fascicular lesions of the median nerve in the arm involving the anterior interosseous nerve fascicle selectively (Pham et al., 2014). Fascicular torsion of the anterior interosseous fascicle in the lower arm has also been advocated to be due to the high mobility of the anterior interosseous nerve fascicles during elbow flexion leading to torsion injury or inflammation/edema followed by intraneural adhesions. These cases showed good recovery after interfascicular neurolysis. In chronic lesions, a restricted form of multifocal motor neuropathy with conduction block should be considered and a careful and detailed electrophysiological study may reveal involvement of other nerves. The anterior interosseous nerve may be externally compressed following anterior elbow dislocations or complex elbow fractures, or rarely by fibrous bands attached to the flexor digitorum superficialis muscle, an anomalous muscle such as accessory head of the flexor pollicis longus (Gantzer muscle).

Patients often complain of an acute or subacute onset of pain in the forearm or elbow. The patient is unable to flex the distal phalanges of the thumb and index finger, making it impossible to form a circle with those fingers (pinch or O sign). Sensory and motor nerve conduction studies of the median nerve are usually normal. Needle EMG reveals denervation in muscles innervated by the anterior interosseous nerve, including the flexor pollicis longus, pronator quadratus, and flexor digitorum profundus muscles of the index and middle fingers. Spontaneous recovery usually occurs within 3 to 12 months, and therefore surgery may not be necessary unless penetrating injury, fracture, or progressive deterioration and weakness are detected.

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 can often 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 (Stewart and Shantz, 2003) 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 diabetes mellitus 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 (Beekman et al., 2009).

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 meters per second) 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 (Azrieli et al., 2003). 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 to 90 degrees) is preferred to the extended position when doing ulnar motor conduction studies to localize an ulnar lesion at the elbow. Short-segment incremental studies (“inching”) by stimulating the ulnar nerve in successive 1-cm increments across the elbow, looking for either an abrupt drop in amplitude or increase in latency, is a useful technique that helps to precisely localize the ulnar nerve lesion (Visser et al.,2005). Electrophysiological tests are helpful in differentiating between an ulnar neuropathy and a C8 nerve root or brachial plexus lesion. Ulnar sparing in ulnar sensory studies points to C8 radiculopathy, and 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) helps exclude a C8 root lesion or a lower brachial plexopathy. 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 (Vucic et al., 2006). High-resolution sonography at the elbow is also useful by accurately detecting thickening of the ulnar nerve at the elbow (Beekman et al., 2004).

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 (Biggs and Curtis, 2006). 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 significant >50% conduction block, have a more favorable course (Beekman et al., 2004; Dunselman and Visser et al., 2008).

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. The majority of cases of ulnar nerve entrapment at Guyon's 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 (Katirji and Dokko,1996).

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. MRI or ultrasound through the Guyon canal 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.

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) (Spinner et al., 2002). The radial nerve may be also injured following fractures of the humerus. Radial nerve lesions at the axilla are much less common and may result from crutches or from the weight of a sleeping partner's head (honeymoon palsy). The radial nerve is also often involved in isolation or in combination with other single nerves in multifocal motor neuropathy 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.

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 to 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 posterior interosseous nerve (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). On rare occasions, a PIN lesion is a manifestation of neuralgic amyotrophy, with acute arm pain followed within a few days by weakness (Hashizume et al., 1996). 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 pathognomic 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 posterior interosseous nerve, 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 posterior interosseous nerve, may become necessary (Shergill et al., 2001).

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 (Rosenbaum, 1999). 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 (Grant and Cook, 2000). 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 (Lanzetta and Foucher, 1995). 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. 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.

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 result from trauma such as bullet and stab wounds, fractures, dislocations, hematomas in the posterior thigh compartment, misplaced intramuscular injections, and complications of hip replacement surgery (Plewnia et al., 1999). 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 (Yuen and So, 1999). Occasionally, the common fibular nerve gets injured selectively (Katirji and Wilbourn, 1994).

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 (Fishman and Schaeffer, 2003; Stewart, 2003). 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) (Kirschner et al., 2009). 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 (Filler et al., 2005). 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 (Filler et al., 2005), severe postoperative sciatic nerve injury was recently reported (Justice et al., 2012).

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 (Katirji and Wilbourn, 1988). 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 (Aprile et al., 2005; Katirji, 1999). 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 (Young et al., 2009). 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 (Hebert-Blouin et al., 2010). 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 (Katirji and Wilbourn, 1988). 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. MRI and ultrasound are effective in visualizing intraneural ganglia and other soft-tissue masses or tumors.

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 (Kim and Kline, 1996).

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 involves 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 turn out to have generalized peripheral neuropathy, S1 radiculopathy, or non-neurological foot pain such as plantar fascitis, stress fracture, arthritis, or bursitis.

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.

Femoral Nerve Lesions.

The majority of femoral nerve lesions are iatrogenic (Al-Hakim and Katirji, 1993). 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; the incidence of these lesions is significantly reduced when self-retractors are avoided. 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 (Kuntzer et al., 1997). 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.

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) (Sorenson et al., 2002).

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.