Clinical Vignette

An 82-year-old frail woman fell in her home. She sustained a hip fracture, which necessitated surgical repair. Postoperatively, she received anticoagulation. Two days later, she had discomfort in her right buttock and hip and foot weakness. Within 24 hours, marked buttock pain and paralysis of all muscles below the right knee and numbness developed. Computed tomographic (CT) scan revealed pelvic hematoma. Despite surgical drainage of 2 L of blood, there was little improvement in sciatic nerve function. Electromyography (EMG) confirmed a primary sciatic neuropathy.

The sciatic nerve is the body’s largest nerve, receiving contributions primarily from the L5, S1, and S2 nerve roots, but also carrying L4 and S3 fibers (Fig. 66-1). It has two primary divisions: the laterally situated more superficial peroneal nerve and the more medially placed tibial nerve (see Fig. 66-1). These separate into two distinct nerves in the mid- to distal thigh. The sciatic nerve and its branches innervate the hamstrings (biceps femoris, semimembranosus, and semitendinosus muscles), distal adductor magnus, anterior and posterior lower leg compartments, and intrinsic foot musculature. Through sensory branches of the tibial nerve (sural, medial and lateral plantar, and calcaneal) and the superficial peroneal nerve, the sciatic nerve also supplies sensation to the skin of the entire foot and the lateral and posterior lower leg.

Figure 66-1 Sciatic, Peroneal, and Tibial Nerves.

Etiology

Sciatic neuropathies can be due to hip arthroplasty, pelvic or femoral fractures, or posterior dislocation of the hip. Like femoral neuropathies, they are sometimes caused by a prolonged lithotomy position, presumably from stretching of the nerve in individuals who are anatomically predisposed. Occasionally, sciatic neuropathies develop from external pressure in patients who are comatose or immobilized for protracted periods such as with drug overdose. They may result from traumatic mechanisms including misplaced injections into the inferior medial quadrant of the buttock. Mass lesions including nerve sheath tumors and external compression from hematoma, aneurysm, endometriosis, and other mechanisms have been described. Sciatic neuropathies may occur in patients with systemic vasculitis.

Clinical Presentation

Acute sciatic neuropathies typically present with distal leg weakness, pain, and sensory loss. Foot pain is a frequent complaint. Because of predominant affliction of the peroneal division, the weakness often manifests itself as foot drop and needs to be differentiated from a common peroneal neuropathy at the fibular head. Weakness of the more proximal muscles (hamstrings) and of foot plantar flexion and inversion (gastrocnemius, tibialis posterior) helps differentiate between the two entities. The ankle jerk and internal hamstring reflex are usually depressed or absent. Sensory loss and dysesthesia of the sole and dorsum of the foot and posterolateral lower leg are common.

Differential Diagnosis

A lumbosacral plexus lesion is the primary consideration in most patients with sciatic neuropathies, when findings clearly encompass a territory outside the peroneal nerve. Diminished sensation on the posterior thigh points to a concomitant neuropathy of the posterior femoral cutaneous nerve, which exits the greater sciatic foramen in proximity to the sciatic nerve. Injury to the perineal branches of this nerve leads to sensory loss on the scrotum or labia majora. Hip extension and abduction should be preserved in sciatic neuropathies. When clinical or EMG evidence suggests gluteal muscle involvement, primary lesions within the pelvis, such as benign tumors, for example, schwannoma, or malignant processes, particularly, lymphoma are considerations.

Piriformis syndrome is a poorly understood disorder that is phenomenologically similar to the thoracic outlet and tarsal tunnel syndromes. The piriformis muscle lies deep to the gluteal muscles; it originates from the sacral spine and attaches to the greater trochanter of the femur. The sciatic nerve passes posterior to the piriformis muscle. It is postulated that acute or chronic injury of the muscle may cause irritation of the sciatic nerve, resulting in posterior thigh and gluteal pain. Patients with an aberrant course of the nerve through the muscle are particularly predisposed to this condition. Objective clinical or electrodiagnostic evidence of sciatic neuropathy is not seen in most patients in whom piriformis syndrome is suspected.

Clinical Vignette

A 44-year-old woman presented with right foot drop and numbness of the dorsum of the right foot. She had first noted difficulty walking 7 weeks earlier when she tripped over a curb and fell. She had intentionally lost 70 pounds over the last year. To accomplish this, she had done frequent exercises in a squatting position on the floor. There was no history of recent trauma to the back or buttock, or of radicular leg pain.

On examination of the patient, there was tenderness to palpation at the proximal lateral knee, but there was no discrete mass. On motor examination, she had weakness in right toe extension, foot dorsiflexion, and foot eversion. Plantar flexion and inversion of the foot, knee flexion, and hip abduction were preserved. Sensory examination was notable for reduced pinprick and light touch on the dorsum and first web space of the right foot. Muscle stretch reflexes were normal. Nerve conduction studies revealed conduction block on peroneal motor studies across the fibular head; needle electromyography showed a reduced recruitment in peroneal muscles with sparing of the short head of the biceps femoris; this is consistent with a demyelinating peroneal neuropathy. Her weakness improved significantly over the following weeks, and 3 months later, she had recovered completely.

Axons originating from the L4, L5, S1 and S2 roots, primarily L5 nerve root fibers, come together to form the common peroneal nerve. It is one of the two major divisions of the sciatic nerve and separates from it as a distinct nerve in the mid- to distal thigh. It travels through the popliteal fossa and gives off the lateral sural cutaneous nerve, which unites with the medial sural cutaneous nerve (a branch of the tibial nerve) to form the sural nerve. The lateral cutaneous nerve of the calf also branches off in the popliteal fossa. It provides sensation to the skin of the lateral leg just below the knee. On its course around the fibular head, the common peroneal nerve is very superficial and covered only by skin and subcutaneous tissue. It then pierces through a fibrous, sometimes tight opening in the peroneus longus muscle (fibular tunnel) and divides into superficial and deep branches.

Etiology

Common peroneal neuropathy is the most frequent lower extremity mononeuropathy. The common peroneal nerve is most susceptible to external compression at the fibular head, where it is very superficial (Fig. 66-2). Predisposing causes include recent substantial weight loss, habitual leg crossing, or prolonged squatting. External devices such as casts, braces, and tight bandages can also cause peroneal neuropathy. Diabetes mellitus, vasculitis, and rarely hereditary tendency to pressure palsy (HNPP) are other etiologic conditions. An acute anterior or lateral compartment syndrome below the knee can also lead to acute common, deep, or superficial peroneal neuropathies. Patients with insidious onset and progressive course require evaluation for mass lesions, including a Baker cyst or ganglion, osteoma, or schwannoma (Fig. 66-3). The common peroneal nerve is sometimes injured iatrogenically. Knee positioning and padding to decrease pressure on the peroneal nerve in the operating room and intensive care unit are important to prevent an acute compression neuropathy. Rarely, laceration of the peroneal nerve occurs with arthroscopic knee repair or direct penetrating trauma.

Figure 66-2 Peroneal Nerve.

Figure 66-3 Peroneal Nerve Schwannoma.

Isolated superficial peroneal neuropathies are uncommon but can result from lateral compartment syndrome, local trauma, or rarely an isolated schwannoma.

Clinical Presentation

Most peroneal neuropathies involve the common peroneal nerve at the fibular head causing weakness of foot dorsiflexion and eversion (see Fig. 66-1). Ambulation reveals a “steppage gait” with compensatory hip and knee flexion in order to lift the foot off the floor. The foot might hit the floor with a slap, as the patient has poor control over its movements. With the less frequently occurring deep peroneal neuropathies, there is weakness of the tibialis anterior, extensor hallucis, extensor digitorum longus, and extensor digitorum brevis. Primary superficial peroneal neuropathies cause weakness of the peroneus longus and brevis muscles, which are mainly responsible for foot eversion.

Sensory symptoms are limited to the web space between the first and second toes with deep peroneal neuropathies. Superficial peroneal neuropathies can diminish sensation on the dorsum of the foot and lateral distal half of the leg. Common peroneal sensory symptoms occur on the dorsal foot surface extending up the lateral half of the leg.

EMG involvement of the short head of the biceps femoris is the major distinguishing feature with proximal peroneal division sciatic neuropathies. Biceps femoris function cannot be isolated clinically; therefore, EMG is crucial to diagnosis.

Differential Diagnosis

Differential diagnoses of peroneal neuropathies include anterior horn cell disease, L5 radiculopathy, lumbosacral trunk or plexus lesions, sciatic neuropathy, or rarely neuromuscular junction disorders. Sciatic neuropathies are sometimes mistakenly diagnosed as peroneal neuropathies. The peroneal division of the sciatic nerve is more superficial than its tibial division and therefore external compressive proximal lesions of the sciatic nerve involve the common peroneal nerve more than the tibial nerve. Most sciatic neuropathies also affect some tibial nerve functions with weakness of knee flexion, foot plantar flexion, and foot inversion. The ankle jerk is characteristically depressed or absent if there is involvement of the tibial component of the sciatic nerve, whereas it is typically unaffected in primary peroneal neuropathies. Sensory loss involves the common peroneal territory described above and the plantar and lateral foot surface. L5 radiculopathy remains a consideration in any patient with a foot drop. Back pain is common with nerve root lesions and is uncommon in peroneal neuropathies; the pain is typically radicular, with buttock, thigh, and leg components sometimes aggravated by positional change. The distribution of weakness is very important; involvement of muscles outside the peroneal nerve territory, such as the tibialis posterior or gluteus medius innervated by the L5 root is critical. Isolated weakness of great toe extension occurs with mild L5 radiculopathy but is uncommon in peroneal neuropathy. In moderate–severe L5 radiculopathies, foot inversion will be weak because of involvement of the tibial nerve innervated posterior tibial muscle. Uncommonly, hip abduction weakness due to involvement of gluteus medius, an L5 muscle supplied by the superior gluteal nerve, is noticeable. Careful evaluation of patients with an L5 root lesion should demonstrate these deficits in addition to weakness of the peroneal innervated muscles. The distribution of sensory symptoms in L5 radiculopathies overlaps significantly with peroneal neuropathies, although L5 nerve root sensory loss may extend more proximally onto the lateral leg. Lumbosacral plexus lesions rarely enter the differential diagnosis of peroneal neuropathies but are a consideration in patients who have a foot drop, proximal lower extremity pain, and motor and sensory findings extending beyond a single peripheral nerve or root distribution. Involvement of hip abduction and extension, clinically and/or by EMG, suggests plexus localization. Polyneuropathy is easily distinguished from peroneal neuropathy, the clinical examination and EMG usually reveal bilateral widespread motor and sensory abnormalities, not confined to a particular nerve or root distribution, muscle tendon reflexes are depressed or absent. The possibility of motor neuron disease exists with insidious onset of a foot drop without pain or sensory findings. Motor neuron disease or amyotrophic lateral sclerosis is a slowly progressive disorder and may be associated with evidence of upper motor neuron dysfunction. In patients with myasthenia, a disorder of neuromuscular transmission, unilateral foot drop is not seen. Distal myopathies may produce foot drop but usually do so bilaterally, and there is often evidence of weakness elsewhere. Unilateral foot drop with or without sensory symptoms can occur with disorders of the spinal cord or parasagittal frontal lobe; these conditions are usually associated with hyperreflexia; magnetic resonance imaging (MRI) is useful to diagnose these conditions.

Clinical Vignette

A 39-year-old man presented to the emergency room for severe pain and swelling of the right leg associated with difficulty walking. On neurologic examination, there was weakness of right foot plantar flexion and inversion, and flexion of the toes. The ankle jerk was absent. Doppler ultrasound and an MRI of the right knee revealed a ruptured Baker’s cyst in the popliteal fossa. Surgical removal of the synovial cyst resulted in resolution of the pain and foot weakness.

Tibial nerve fibers arise primarily from L5, S1 and S2 nerve roots with some contributions from L4 and S3. The tibial nerve leaves the sciatic nerve in the mid- to distal thigh (see Fig. 66-1). The medial sural cutaneous nerve comes off in the popliteal fossa and joins the lateral sural cutaneous nerve (a branch of the common peroneal nerve) in the distal calf to form the sural nerve, which supplies the skin of the lateral aspect of the foot and the posterior lower leg to a variable degree. After innervating the gastrocnemius and soleus muscles, the nerve travels distally between the tibialis posterior and gastrocnemius muscles. It sends branches to the tibialis posterior, flexor digitorum longus, and flexor hallucis longus before entering the tarsal tunnel under the flexor retinaculum. Here, the tibial nerve typically divides into the medial plantar, lateral plantar, and medial calcaneal nerves. Although the medial calcaneal nerve is a purely sensory branch to the medial heel, the medial and lateral plantar nerves are mixed nerves innervating the intrinsic foot muscles as well as the skin of the sole.

Proximal Lesions

Proximal tibial neuropathies may result from Baker’s cysts, ganglia, tumors (Fig. 66-4), or rarely indirectly from severe ankle strains, the latter presumably resulting from traction injury. They rarely occur in isolation. They are characterized by weakness of foot plantar flexion and inversion; although flexion, abduction, and adduction of the toes may be affected, these latter functions are difficult to evaluate clinically. The ankle jerk is absent if the neuropathy occurs proximal to the branch points of the gastrocnemius-soleus complex. Sensory loss occurs on the heel and plantar foot surface.

Figure 66-4 Posterior Tibial Neurofibroma.

Tarsal Tunnel Syndrome

Tarsal tunnel syndrome (TTS), a distal tibial neuropathy, presents primarily with sensory symptoms. It is classified as an entrapment neuropathy of the posterior tibial nerve and of its primary branches, the medial and lateral plantar nerves, at the ankle (See Fig. 66-3). Although well described, there is controversy regarding its prevalence as electrophysiological documentation is infrequent. Whether this reflects its uncommon occurrence or the inadequate sensitivity of diagnostic procedures is unclear. Fractures, ankle sprain, foot deformities due to rheumatoid arthritis or other conditions, varicose veins, tenosynovitis and fluid retention have been implicated as possible etiologies. Patients typically present with burning pain and numbness on the sole of one or both feet. Symptoms may occur while weight bearing and are often exacerbated at night. In well-established instances, examination may disclose intrinsic plantar surface muscle atrophy. However, weakness of these muscles is difficult to appreciate because the more proximal long toe flexors in the leg mask weakness from the involved short toe flexors within the foot. Toe abduction weakness occurs early but is difficult to assess even in healthy individuals. Sensory loss is confined to the sole of the foot; there is sparing of the lateral foot (sural distribution), the dorsum of the foot (peroneal territory), and the instep (saphenous nerve). Muscle stretch reflexes are unaffected. A Tinel sign elicited from the tibial nerve at the ankle is supportive, although not confirmatory.

If TTS results from nerve entrapment, simulating carpal tunnel syndrome, EMG should demonstrate demyelination via prolongation of the distal latencies. However, prolonged tibial motor and mixed nerve distal latencies from the medial and lateral plantar nerves are rarely seen in patients with suspected TTS. Absent mixed nerve responses from the plantar nerves may be seen, but have limited localizing value because they also occur in some seemingly healthy elderly individuals and in those with an underlying polyneuropathy. Fibrillation potentials in tibial innervated foot muscles must be interpreted with similar caution. Imaging in suspected TTS includes radiographs to detect osseous abnormalities involving the tarsal tunnel region and CT, if severe ankle osteoarthritic changes and exostosis are considered.

Initial treatment of TTS is nonoperative, consisting of footwear modification, particularly avoidance of high-heeled and poorly fitting footwear. Anti-inflammatory medications may help. Steroid injections, augmented with lidocaine, can be helpful if flexor tenosynovitis is suspected. Care is taken to avoid an intraneural injection with the unlikely possibility of causing local nerve sclerosis. Hind foot valgus deformities may benefit from orthoses. When nonoperative measures fail in TTS, surgical intervention may be considered. The results of surgical decompression are not always rewarding. Release of the flexor retinaculum and fibrous origin of the abductor hallucis muscle is required. Local flexor tenosynovitis is resected with radical tenosynovectomy. Enlarged and varicose veins are ligated and resected. Postoperatively, an open shoe is used with partial weight bearing for 2 weeks.

Clinical Vignette

A 63-year-old man with hemophilia presented with right knee buckling a week after a motor vehicle accident. He also complained of dull pain in the right flank radiating into the thigh and knee. He could not raise his right leg off the bed. There was no back pain or sphincter dysfunction. The neurologic examination revealed weakness of the right iliopsoas and quadriceps muscles, an absent right quadriceps muscle stretch reflex, and diminished sensation to touch and pinprick over the anterior thigh and medial leg below the knee. Pelvic CT demonstrated a hemorrhage of the right iliacus and psoas muscles in the pelvis. Surgery revealed a large hematoma compressing the femoral nerve. This was successfully drained. Postoperatively, the patient gradually improved, regaining significant function within a week.

The femoral nerve comes off the lumbar plexus and is formed by the posterior divisions of the L2–L4 roots (Fig. 66-5). It travels between two important hip flexors, the iliopsoas and iliacus muscles, which it innervates. Approximately 4 cm proximal to the inguinal ligament, the femoral nerve is covered by a tight fascia at the iliopsoas groove. It exits the pelvis by passing beneath the medial inguinal ligament to enter the femoral triangle just lateral to the femoral artery and vein. Here, the nerve separates into the anterior and posterior divisions. The anterior division innervates the sartorius muscle and the anteromedial skin of the thigh via the medial cutaneous nerve of the thigh. The posterior division gives off muscular branches to the pectineus and quadriceps femoris muscles as well as the saphenous nerve, a cutaneous branch to the skin of the inner calf. The nerve can be compressed anywhere along its course, but it is particularly susceptible within the body of the psoas muscle, at the iliopsoas groove, and at the inguinal ligament.

Figure 66-5 Femoral Nerve and Lateral Cutaneous Nerve of Thigh.

Etiology

Femoral mononeuropathies are infrequent. Historically, diabetic femoral neuropathies were considered common, although most of these were actually diabetic radiculoplexopathies in which the femoral component dominated. They may represent an autoimmune process, perhaps with a vasculitic component. Vasculitis, such as polyarteritis nodosa, may manifest as mononeuritis multiplex, with acute involvement of the femoral nerve.

Femoral neuropathies occasionally follow prolonged surgeries or childbirth in the lithotomy position, presumably from anatomic predisposition to kinking beneath the inguinal ligament. Iliacus hematoma or abscess, misplaced attempts at femoral artery or vein puncture, or iatrogenic injury after nephrectomy or hip arthroplasty are other recognized causes. Tumors, benign and malignant, may rarely cause femoral neuropathy (Fig. 66-6). Isolated saphenous nerve injuries may result from knee arthroscopy, femoral–popliteal artery bypass surgery, and in the course of coronary artery bypass graft surgery.

Figure 66-6 Femoral Nerve Neurofibromas in Neurofibromatosis (arrows).

Clinical Presentation

When the more proximal femoral nerve is involved, weakness of the iliopsoas manifests as limited hip flexion. Mild hip flexion weakness may also occur with more distal femoral nerve involvement from poor function of the rectus femoris, the only head of the quadriceps muscle originating within the pelvis and contributing to hip flexion. Patients with severe quadriceps weakness are unable to extend the leg or lock the knee; when severe, this often interferes with or precludes walking. Initially, mild femoral neuropathies may present with difficulty going down stairs because the knee buckles from mild quadriceps weakness. Eversion of the thigh might be impaired because of sartorius weakness. The patellar muscle stretch reflex is almost always diminished or absent in femoral neuropathies. Groin and thigh pain are frequent presenting symptoms. When patients experience sensory symptoms, these typically involve the anteromedial thigh, and medial lower leg. A pure motor syndrome with quadriceps weakness and atrophy can result from lesions distal to the branching of the saphenous nerve in the thigh.

Differential Diagnosis

A nerve root lesion at L3–L4 is the most common consideration. Unlike L5–S1 radiculopathies, a herniated nucleus pulposus infrequently involves the level L3–L4. Lumbosacral plexus lesions primarily affecting the lumbar nerves may also mimic femoral neuropathies.

Clinical Vignette

A 38-year-old woman presented with pain and numbness of the left thigh in her seventh month of pregnancy. She described a burning discomfort extending from the hip to the lateral aspect of the thigh, intensified by standing or walking. There was associated cutaneous hypersensitivity with an aversion to having clothes or bed sheets rub against her. She was unaware of any other precipitating events. Examination demonstrated an elliptically shaped area of sensory loss on the distal half of the left anterolateral thigh. She had no atrophy, weakness, or reflex loss. The symptoms gradually improved in the months following the delivery of a healthy baby.

The lateral femoral cutaneous nerve (LFCN) arises from the second and third lumbar roots and travels through the retroperitoneum. After traversing the psoas muscle, the nerve reaches the iliacus muscle (see Fig. 66-4). Medial to the anterior superior iliac spine, it exits the pelvis under or through the inguinal ligament, the presumed usual site of entrapment. Subsequently, it supplies sensation to the anterolateral thigh.

Etiology

Meralgia paresthetica is an entrapment mononeuropathy of the lateral femoral cutaneous nerve (Fig. 66-7). Cadaver studies suggest that meralgia paresthetica is primarily an entrapment neuropathy due to “kinking” of the nerve as it passes through the inguinal ligament. Like many mononeuropathies, it is more common in people with diabetes. Meralgia paresthetica often occurs in overweight individuals, especially after sudden gain in weight, or in individuals wearing tight belts and garments. It is usually unilateral. Occasionally, the nerve is injured within the thigh secondary to blunt or penetrating trauma (e.g., a misplaced injection), or rarely, by a soft tissue sarcoma within the thigh.

Figure 66-7 Lateral Femoral Cutaneous Nerve.

Clinical Presentation

Often aggravated by standing or walking, symptoms include an uncomfortable positive component (burning, hypersensitivity) and negative features (numbness). Typically, the area of demonstrable sensory loss on examination is smaller than the lateral femoral cutaneous nerve territory in most anatomic diagrams, likely due to significant overlap with adjacent nerves. Because the LCFN is a purely sensory nerve, there are no associated reflex or motor abnormalities, helping to distinguish meralgia from other disorders that deserve diagnostic consideration.

Differential Diagnosis

Although uncommon, L2 radiculopathy of any etiology, evidenced as weakness and denervation of L2-innervated hip flexors and adductors, is a differential consideration. Sensory symptoms and signs extend over the anterior and medial aspects of the thigh. Lumbar spinal stenosis also tends to be exacerbated by prolonged standing or walking, although it does not cause numbness in this specific distribution.

Disorders of the lumbosacral plexus may mimic meralgia, particularly in patients having insidious onset of invasive or compressive disorders in which pain and other sensory symptoms have no obvious motor component. Retroperitoneal neoplasms or hematomas and abdominal surgery might affect the LCFN; however, they are unlikely to cause isolated meralgia. Instead, concomitant involvement of adjacent nerves usually leads to widespread motor, reflex, and sensory loss, indicating that there may be a plexus lesion rather than a single nerve problem.

Isolated femoral neuropathies are uncommon and unlikely to be confused with meralgia because of the type and distribution of abnormalities. Sensory symptoms involve the anterior and medial thigh and extend to the medial surface of the leg. Weakness of the quadriceps muscle and loss of its stretch reflex are other objective and distinguishing features.

Although the LFCN can be tested by nerve conduction studies in the thigh distal to the inguinal ligament, technical difficulties interfere with detection of mild demyelinating injuries. A response cannot be obtained from all individuals and is particularly difficult to record in overweight individuals who are most susceptible to this syndrome. Nerve conduction studies of the LFCN are of greatest value when a normal response is readily obtained from the asymptomatic side and a low-amplitude or absent response is obtained from the symptomatic side. In patients with atypical symptoms, thigh MRI is indicated to exclude primary lesions such as soft tissue sarcoma. MRI and CT of the retroperitoneum and pelvis should be considered in patients with unexplained LFCN neuropathy. Fasting blood glucose measurement is appropriate in acute-onset, painful LFCN neuropathies without alternative explanation.

Management

The natural history of meralgia varies, but most patients become asymptomatic within 2 years. Others have a more protracted and chronic course. Conservative management includes weight loss and avoidance of tight garments. Medications such as amitriptyline, carbamazepine, gabapentin, and venlafaxine may diminish pain intensity. Injections of local anesthetics and steroids near the anterior superior iliac spine may serve diagnostic and therapeutic roles and are sometimes “curative.” Exploration at the presumed entrapment site is used in particularly intractable and lifestyle-altering cases.

Clinical Vignette

A 35-year-old woman presented with pain in the right medial thigh and difficulty walking. This had begun 6 months prior, immediately after the delivery of her son. After 8 hours of labor complicated by fetal failure to progress, she had eventually undergone an emergent cesarean section. On neurologic examination she had weakness of the right thigh adductors and a patch of numbness and dysesthesia on the medial surface of the thigh.

The obturator nerve originates from the anterior rami of the L2, L3, and L4 nerve roots (Fig. 66-8). After its course through the pelvis, the nerve exits through the obturator canal and separates into the anterior and posterior divisions. The anterior division supplies the adductor longus, adductor brevis and gracilis muscles, whereas its terminal branch provides sensation to the distal medial thigh. The posterior division innervates the obturator externus, the superior portion of the adductor magnus, and sometimes the adductor brevis.

Figure 66-8 Obturator Nerve.

Etiology

Obturator neuropathies may be caused by pelvic masses, difficult parturition, or obturator hernias or may be complications of hip arthroplasty or pelvic surgery.

Clinical Presentation

Obturator neuropathies are exceedingly uncommon focal nerve lesions that typically present with hip instability. Weakness and denervation are confined to the large hip adductors. Occasionally, they present with pain and sensory symptoms in the medial thigh without obvious weakness.

Iliohypogastric Nerve

The iliohypogastric nerve arises from the T12–L1 nerve roots. Like the ilioinguinal nerve, it supplies the internal oblique and transversus abdominis muscles. Weakness of these muscles, however, is difficult to demonstrate on physical examination. The iliohypogastric nerve divides in lateral and anterior cutaneous branches. Iliohypogastric neuropathies thus produce sensory symptoms in two distinct areas, the lateral aspect of the iliac crest and the suprapubic region. The anterior branch is most commonly injured by lower abdominal surgery with a lateral incision site extending to the internal oblique muscle, and the lateral branch is most commonly injured by major pelvic surgery. The prognosis for recovery is generally good in both.

Ilioinguinal Nerve

This nerve arises from the L1 nerve root. Loss of sensation along the inguinal ligament, over the pubic symphysis and the anterior scrotum or mons pubis, with or without associated pain, characterizes ilioinguinal neuropathies. Ilioinguinal neuropathies most frequently result from lower abdominal surgeries, bone graft harvesting from the iliac crest, and parturition. Rarely, nerve entrapment occurs as it passes through the abdominal wall, causing groin pain relieved by hip flexion.

Genitofemoral Nerve

The genitofemoral nerve is supplied by fibers originating from the L1 and L2 nerve roots. It separates into genital and femoral branches. Genitofemoral neuropathy presents with pain, numbness, and paresthesias of the labia majora or scrotum as well as the proximal anterior thigh, lateral to the sensory territory of the ilioinguinal nerve. Standing or hip extension may exaggerate symptoms. Surgical procedures such as inguinal herniorrhaphies or appendectomies are common causes of genitofemoral neuropathy. The genitofemoral nerve has a motor branch innervating the cremaster muscle. Unfortunately, the cremasteric reflex is not a reliable diagnostic clue.

Diagnosis

As the sensory territories of these three nerves overlap, their mononeuropathies are difficult to distinguish by clinical examination alone. The ilioinguinal, iliohypogastric, and genitofemoral nerves are inaccessible to nerve conduction techniques. Therefore, EMG is of limited value and mainly serves the purpose to rule out differential diagnoses, such as L1 or L2 radiculopathies or proximal lumbar plexopathies. Local injections of anesthetics not only provide symptomatic relief but may also be diagnostically helpful. Retroperitoneal and pelvic MRI and CT are indicated when a progressive ilioinguinal, iliohypogastric, or genitofemoral neuropathy develops without obvious cause.

Management

Most patients with postoperative neuropathies experience full recovery; persistent symptoms typically are seen only in those with unrepaired nerve transection or injury to the lumbosacral plexus. Medications such as amitriptyline, carbamazepine, gabapentin, and venlafaxine may diminish pain intensity in all mononeuropathies.

Diagnostic Approach to Mononeuropathies

Electrodiagnosis is a primary means of assessing a suspected mononeuropathy. EMG helps to differentiate other lesions that mimic mononeuropathies, particularly at the respective plexus or nerve root level. Besides providing anatomic localization, EMG helps to assess prognosis. A specific etiology is rarely revealed, even with abnormal EMG. Demonstration of a predominantly demyelinating lesion provides the primary basis for localization, but this is generally not possible in sciatic, femoral, and obturator neuropathies, as conduction studies of these nerves are limited by technical factors.

Further testing is sometimes indicated, depending on the index of suspicion regarding causation. Plain radiographs can assess possible bone spurs or exostoses, arthritides, congenital deformities, fractures, or bony tumors that may contribute to nerve injury. MRI and occasionally ultrasonography are useful in assessing soft tissue lesions or sometimes localizing areas of entrapment and in providing a spatial image of the nerve and its surrounding structures. However, when EMG indicates a defined localization without clinical evidence or imaging studies of a specific mechanism, surgical exploration is an important diagnostic tool that sometimes also offers a therapeutic option. Acute axonal nerve lesions are characterized by a hyperintense signal on T2-weighted MRI. Thus, MRI can demonstrate the site of nerve injury when localization by EMG is difficult. Furthermore, MRI might be able to identify traumatic nerve lesions with the potential of axonal regeneration, and unnecessary surgical explorations could be avoided. Occasionally, an elevated ESR provides a clue to an underlying vasculitis. Fasting serum glucose levels may help to identify previously undiagnosed diabetes mellitus presenting with a possible femoral neuropathy. Rarely, CSF examination is indicated to distinguish an inflammatory or carcinomatous polyradiculopathy from a mononeuropathy.

Management and Prognosis of Mononeuropathies

When a definable entrapment mechanism, a mass causing nerve compression, or a nerve laceration exists, surgery is indicated. If the neuropathy resulted from nerve traction from excessive squatting or compression from habitual leg crossing, the primary treatment is discontinuation of these activities. If a cast or brace is compressing the nerve, for example the peroneal nerve at the fibular head, it must be modified to protect the nerve. Nerve injury from an acute compartment syndrome is a surgical emergency and necessitates fasciotomy.

Foot drop can be effectively treated by an ankle–foot orthosis, its primary goal being the prevention of falls. Patients also state that their walking endurance improves with this device. An ankle–foot orthosis should be prescribed cautiously in patients with significant quadriceps weakness. It may destabilize a patient’s marginally compensated technique of “knee locking” and weight bearing, thus increasing the risk of falling.

Recovery depends on the nature, location, severity, and persistence of the injury and patients’ underlying health and age. An optimistic prognosis can be expected with a primary demyelinating lesion. Demyelinating lesions secondary to monophasic external compression or stretch typically recover within weeks to months. However, when evidence of significant axonal damage exists, reinnervation, a process that progresses at a rate of 1 mm/day or approximately 1 inch/month, must occur. A longer period (months to years) is therefore required. The degree of axon loss and distance from the site of injury to the target site of reinnervation determine outcome.

Future Directions

Future directions will involve improved diagnosis through more sensitive neurophysiologic and neuroimaging techniques, and more effective nerve repair and treatment of neuropathic pain. Despite improved surgical techniques, functional outcome after severe traumatic nerve injuries is often unsatisfactory. Autografts serve to bridge nerve gaps with limited success. An understanding of the molecular mechanisms of axonal regeneration including the role of Schwann cells, growth factors, and the extracellular environment is essential for the development of better treatment options. Nerve conduits manufactured from synthetic or natural materials are being studied as scaffolds in lieu of nerve grafts and can deliver nerve growth factors. Laser phototherapy has been shown to promote nerve regeneration and is used for pain relief. Stem cell and progenitor cell differentiation might also offer treatment options in the future.