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Entrapment neuropathies of the lower extremities are less common than those of the upper extremities. The mere existence of several of them, much less their surgical management, is controversial. In this chapter, the more com­mon syndromes as well as their pathophysiology, electrodiagnostic and clinical features, differential diagnoses, and treatment are addressed.

 Lateral Femoral Cutaneous Nerve Entrapment

Clinical Features

Lesions of the lateral femoral cutaneous nerve were first described by Bernhardt and Roth in 1895. The term meralgia paresthetica, previously used to define any pain in the thigh, was applied. This term now refers to a condition that manifests itself as discomfort in the distribution of the lateral femoral cutaneous nerve. This discomfort may be in the form of formication, coldness, burning, or lightning pains, which may progress to hypesthesia or frank aneasthesia. Relief is usually realized by assuming the supine position or by flexing the thigh while in the erect position. The symptoms are usually unilateral. Physical examination reveals only sensory loss over the affected area. The sensory loss occupies a region much less than that usually described for the lateral cutaneous nerve distribution. The area of sensory loss for pin­prick is usually less than that observed with light touch. Importantly, the response to sensory testing may be one of hyperesthesia rather than hypesthesia in some cases.


Ghent described four variations of the course of the lateral femoral cutaneous nerve, each of which may produce the classical picture of this disorder: (1) the nerve passes through the inguinal ligament; (2) nerve deformation by a sharp edge of iliacus fascia lying posterior to a normally placed nerve (compression occurs when the patient is in the supine position); (3) the nerve enters the sartorius muscle near its origin at the anterior superior iliac spine and passes distally in the muscle before emerging beneath the fascia lata; and, (4) the lateral cutaneous nerve enters the thigh, crossing the iliac crest lateral and posterior to the anterior superior iliac spine.  Factors that precipitate symptoms include obesity, adoption of the recumbent position in debilitating disease or following anesthesia, increased intra-abdominal pressure (usually associated with pregnancy, ascites, or tumor), and altered mechanics of the hip joint secondary to intraspinal disease such as a herniated disc).

Differential Diagnosis

Proximal lesions should be ruled out before surgical therapy is considered. The differential diagnosis includes femoral neuropathy and radiculopathy involving the second or third lumbar nerve roots. In these conditions, whether caused by intraspinal or extraspinal disease, motor disability consisting of weakness of the hip flexors or the quadriceps muscle is generally present. A herniated disc at Ll-2 or L2-3 may also mimic meralgia paresthetica. In addition, lesions in the ilium, cecum, sigmoid colon, or any lesion in the upper retroperitoneal space may compress the nerve at the level of the psoas muscle.

Electrodiagnostic evaluation

Electromyographic (EMG) studies of the quadriceps muscle are useful because the diagnosis of meralgia paresthetica is unlikely if abnormalities are found. Sensory action potentials may be abnormal in meralgia paresthetica. It is important to test the asymptomatic thigh to assure the validity of the technique, especially in obesity.


A conservative approach to this mild condition is usually indicated. Initial attempts should include altering physical activity or removing constricting belts, corsets, or binders. If weight gain or pregnancy is a provocative factor, weight reduction or passage of time will often improve matters. If these measures do not relieve the symptoms, local nerve blocks or steroid injections may be helpful. On rare occasions, severe symptoms persist despite attempts at conservative measures. In these cases, surgical decompression may be entertained. The lateral femoral cutaneous nerve is exposed, either through a vertical or horizontal incision. Kempe describes a vertical incision that begins approximately 2.5 cm above and medial to the anterior superior iliac spine and extends caudally. This exposes the interval between the tensor fascia lata and the sartorius muscle. The fascia lata is then incised and retracted, permitting the nerve to be identified. The nerve then can be dissected proximally to the inguinal ligament, where it is released into the subcutaneous tissue. Failures of surgical management are not uncommon, and are sometimes blamed on the difficulties associated with nerve identification and/or the performance of an inadequate decompression. Sectioning of the nerve should be avoided because the symptoms may worsen postoperatively.

Proximal Sciatic Nerve Entrapment

The piriformis syndrome represents a clini­cal entity characterized by neurologic symptoms referable to the distribution of the sciatic nerve. It is one of many pathological processes that may cause symptoms in a sciatic nerve distribution of nonspinal origin. Patients with these symptoms may have associated lumbo­sacral spine disease. The legitimacy of the piriformis syndrome is often questioned. The partial involvement with weakness of any or all of the knee flexors, ankle flexors or extensors, and foot intrinsics may occur. Sensory loss may involve all of the foot except for the small region supplied by the saphenous nerve over the medial malleolus. Pathophysiology and Differential Diagnosis diagnosis of a proximal sciatic nerve lesion is difficult to establish with certainty.

Clinical Features

Symptoms are not unlike those associated with a herniated lumbar disc. Sensory and motor deficits are more extensive than those asso­ciated with a single nerve root, however. Complete palsy of the sciatic nerve is unusual. Partial involvement with weakness of any or all of the knee flexors, ankle flexors or extensors, and foot intrinsics may occur. Sensory loss may involve all of the foot except for the small region supplied by the saphenous nerve over the medial malleolus.

Pathophysiology and Differential Diagnosis

Yeoman first stressed the clinical significance of the anatomical relationships of the sciatic nerve and the piriformis muscle. The pathophysiologic mechanisms of nerve irritation or injury by this muscle are still unclear. It is thought that the variable anatomical relationship of the nerve or its branches to the muscle are the principal factors. Pecina examined 130 cadavers and discovered that in 6% the sciatic nerve passed between the two tendinous parts of the piriformis muscle. A high bifurcation of the nerve, with the peroneal portion of the nerve passing through the muscle, was not uncommon. Inward rotation rather than outward rotation of the hip was noted to cause nerve compression by the two tendinous portions of the muscle. However, this anatomical variation is much more common than the existence of the syndrome. Other causes of sciatic nerve entrapment are also rare. A case in which a myofascial band in the distal portion of the thigh trapped the sciatic nerve was reported by Banerjee and Hall. Entrapment has been reported to occur secondary to fibrosis induced by pentazocine injection. Symptomatic compression of the sciatic nerve may be caused by a retroperitoneal hematoma due to a complication of anticoagulant therapy or hip surgery. Sciatic nerve compromise may be caused by the leakage of acrylic into the region posterior to the hip joint during total hip replacement. Abnormal subclinical EMG findings have been observed in the majority of patients undergoing hip replacement. An aneurysm of the iliac artery may also involve the sciatic nerve. Finally, nonstructural etiologies should be considered: diabetic and vascular neuropathies may cause symptoms similar to those mentioned earlier.

Electrodiagnostic and Radiographic Evaluation

The most important role of electrodiagnostic studies is to separate proximal sciatic nerve entrapment from the more common root compression syndromes. EMG studies are invaluable: the proximal paraspinous muscles, as well as the muscles supplied by the inferior and superior gluteal nerves (tensor fascia lata, and the gluteus minimus and medius muscles) are usually abnormal with a root lesion, but normal with a sciatic nerve entrapment. If the superior gluteal nerve is involved, the gluteus minimus and medius muscles and the tensor fascia lata often demonstrate abnormal EMG readings. Somatosensory evoked potentials may be assessed over the gluteal fold, over the spine at L5 region, and over the T12-Ll region. These potentials are thought to respectively originate from the sciatic nerve, the roots of the cauda equina, and the dorsal root entry zone of the spinal cord. Cutaneous sensory action potentials recorded from the sural, peroneal, or plantar nerves may be abnormal with sciatic lesions and normal with root lesions. The H-reflex and F-responses are not useful regarding the differential diagnosis. Abdominal and pelvic computed tomography (CT) may demonstrate structural lesions impinging upon the sciatic nerve. Magnetic resonance imaging (MRI), however, is increasingly being used for this purpose


Since the true etiology of proximal sciatic nerve dysfunction is often in question, a reasonable course of conservative treatment should nearly always precede surgical management. Although this management scheme is nonspecific, a trial with a nonsteroidal anti­inflammatory agent and rest should be the initial therapy in most cases. It consists of the sectioning of the piriformis muscle at its tendinous insertion on the greater trochanter. When sciatic neuropathy is due to hematoma as a complication of anticoagulant therapy, operative exploration may occasionally be appropriate, following correction of the coagulation abnormalities. Fleming demonstrated that, in the setting of postoperative hematomas following hip surgery, neural recovery appears to occur sooner and more completely in those patients who undergo early decompression compared to those who do not.

Posterior Tarsal Tunnel Syndrome

Two forms of the tarsal tunnel syndrome exist, but the posterior form is usually called the tarsal tunnel syndrome and is much more common. The less common anterior tarsal tunnel syndrome involves the deep peroneal nerve.

Clinical and Electrodiagnostic Features

Patients with posterior tarsal tunnel syndrome present with a slow and insidiously progressive course of burning pain and paresthesias involving the plantar surface of the foot and toes. The distribution of involvement depends on which branch of the posterior tibial nerve is involved. Occasionally, the pain radiates proximally into the leg. The pain is usually exacerbated by standing and/or activity and is relieved by rest and/or by rubbing the foot. Symptoms are often worse at night. The heel is frequently spared because the calcaneal branch more often arises proximal to the flexor retinaculum and, hence, is less frequently involved. Clinical signs of the posterior tarsal tunnel syndrome are frequently difficult to detect. The intrinsic foot musculature may be weak and atrophied; it is best evaluated by examining toe plantar flexion strength, especially in the lateral toes. Intrinsic muscle weakness leads to a change in conformation of the foot and to instability of the phalanges, which impairs the pushing-off phase of walking. This motor disturbance may lead to a pes cavus deformity, with clawing of the toes. A flat-foot gait with a short stride length may result. The sensory loss is dependent on which of the branches is involved. The sensory examination is also difficult because of the thickness of the skin on the plantar surface of the foot. Hypesthesia along the medial surface of the foot, if present, is easier to detect. A positive Tinel's sign may be present with distal paresthesias and pain occurring following gentle percussion over the tarsal tunnel. This is located inferior and posterior to the medial malleolus. A Tinel's sign may also be present over the course of each of the plantar nerves. Electrodiagnostic studies are often useful. Baylen found an abnormal EMG in 11 of 48 patients with rheumatoid arthritis. Only 2 had symptoms of the posterior tarsal tunnel syndrome. When conduction latencies are performed, they should be determined in both plantar nerves in order to increase the accuracy of pathology detection. Sensory action potentials recorded proximal to the flexor retinaculum may be abnormal and are more sensitive than motor conduction velocities for detecting pathology. Motor conduction latencies, recorded distally following stimulation proximal to the flexor retinaculum, are considered abnormal when prolonged more than 1 millisecond (comparing the two feet). prolonged distal motor latency to the abductor hallucis is indicative of involvement of the medial plantar branch, while prolonged latency to the abductor digiti quinti represents involvement of the lateral branch. Typically, the conduction velocities in the posterior tibial nerve in the leg are normal. EMG has been infrequently reported because of difficulty in testing the intrinsic foot musculature.


The posterior tarsal tunnel syndrome is the counterpart of the carpal tunnel syndrome. The site of compression is located posterior and inferior to the medial malleolus. The roof of the tarsal tunnel is comprised of the flexor retinaculum and the floor comprised of the bones of the ankle. Numerous structures are present within this tunnel, including tendons, synovial sheaths, and neurovascular structures. Any or all of the three terminal branches of the posterior tibial nerve (the medial and lateral planter and the calcaneal nerve) may lie within the tunnel. The tarsal tunnel also differs from the carpal tunnel in that numerous fibrous septa connect the roof of the tunnel and the floor. Fifty percent of patients presenting with symptoms of the posterior tarsal tunnel syndrome have a history of trauma. However, the symptoms may develop some time after injury. Symptoms may be due to intraneural scarring or to nonspecific scarring of the surrounding osseous and soft tissue structures. prolonged standing and venous stasis also have been reported to be associated with this syndrome. The etiology may be a nonspecific tenosynovitis or venous congestion within the tunnel. The tarsal syndrome has been reported in association with rheumatoid arthritis, and in hyperlipidemias, where the etiology is lipid deposition within the tunnel.


Conservative treatment should begin by minimizing local trauma and/or by bracing the foot with a medial arch support. An arch support immobilizes the affected region, similar to the use of a wrist splint in the carpal tunnel syndrome. Nonsteroidal anti-inflammatory agents may be beneficial in the presence of a local phlebitis or tenosynovitis. A block of the posterior tibial nerve with a local anesthetic agent just proximal to the flexor retinaculum may relieve symptoms and aid in predicting a favorable operative result. Operative treatment should be performed only following failure of conservative management, and in patients in whom the clinical features are typical and the electrodiagnostic studies support the diagnosis. Wilemon reported that fewer than 200 patients with tarsal tunnel syndrome had been reported prior to 1979; only about 60% underwent surgery. The surgical approach is usually through a curvilinear incision 1. 5 cm behind and below the medial malleolus. The incision may be extended proximally to identify the posterior tibial nerve in the distal calf. Following incision of the flexor retinaculum, most authors recommend external neurolysis of both branches, which may be bound by the numerous fibrous bands and septations that exist in this region.

Anterior Tarsal Tunnel Syndrome

Clinical Features

The anterior tarsal tunnel syndrome refers to compression of the deep peroneal nerve at the ankle. The clinical features are mainly sensory, with numbness and paresthesias in the first dorsal web space. Occasionally, complaints relate to aching and tightness around the ankle and dorsum of the foot with centripetal radiation up the entire peroneal trunk. Pain increases with certain positions and with inactivity, often awakening the patient from sleep. This syndrome has been reviewed extensively by Barges et al. There are, however, very few reports and little investigation regarding the syndrome's frequency, etiology, or electrophysiologic features. Barges et al, in an autopsy study, demonstrated that the deep peroneal nerve was flattened and widened by the overlying extensor retinaculum. This study demonstrated that firm plantar flexion at the ankle with dorsiflexion of the toes stressed the nerve to the maximum degree. This is the same position that is induced by wearing high-heel shoes. The position of the nerve at the dorsum of the ankle also makes it susceptible to compression, for example by tight shoes.


If the patient does not experience relief with rest, removal of possible external aggravating pressure, or anti-inflammatory medication, operative intervention may be necessary. Decompression is undertaken in a similar manner to that performed for the posterior syndrome. During decompression of the nerve, a branch of the superficial peroneal nerve should not be mistaken for a parallel branch of the deep peroneal nerve. The nerve also should be traced proximally to exclude a lesion in the ankle region.

Peroneal Nerve Entrapment

Clinical and Electrodiagnostic Features

Peroneal neuropathy is a common and well­known clinical entity. It is manifested as paralysis or weakness of the foot dorsiflexors and as weakness of foot eversion. A steppage gait may be present. The peroneal nerve, as well as its superficial and deep branches, may be affected by compression. Superficial branch compression, however, is more common. The lateral surface of the leg, the lateral malleolus, the dorsum of the foot, and the web interspaces of the second and third toes are usually hypesthetic. The superficial branch also innervates the peroneus longus and brevis muscles. This leads to weakness of foot eversion. If the deep branch is affected, motor involvement is more prominent because of the innervation of the anterior tibial muscles, as well as the extensors of all the toes. The deep branch provides sensation to a relatively small area between the first and second toes and the adjacent portion of the dorsum of the foot. The branch to the extensor digitorum brevis is observed to be weak early in the course when nerve damage occurs. It is consequently important to examine the activity of this muscle. Although the extensor digitorum brevis muscle may receive innervation from both branches, it is innervated by the deep peroneal nerve in 72% of cases. When the common peroneal nerve is compressed, clinical features attributable to both the deep and superficial branches may be present. The clinical features of peroneal entrapment vary, depending on the nature of the condition. Acute compressive lesions tend to be associated with more motor than sensory involvement. More chronic forms of compression, such as those caused by cysts or tumors, may be associated with radiating pain and subsequent progressive motor and sensory disturbances. An electrodiagnostic evaluation is useful diagnostically, and for establishing a prognosis. If the motor conduction velocity is normal or nearly normal, the prognosis for recovery is excellent. The prognosis is poor if the conduction velocity is slow. Motor nerve conduction velocities are measured from the tibialis anterior muscle with stimulation at the ankle, lateral popliteal fossa, and below the fibular head. Recording from the tibialis anterior rather than the extensor digitorum brevis muscles may be more useful because of the frequent presence of complete denervation when the extensor digitorum is involved. The loss of amplitude of the compound motor action potential is also a useful observation regarding motor nerve conduction studies. Again, recording from the tibialis anterior muscle is more beneficial than from the extensor digitorum muscle for the same reason. Distal stimulation at the ankle, with nerve action potential recording distal and proximal to the fibular head, is more accurate than motor conduction velocity regarding identification of focal slowing. In fact, absolute focal slowing of sensory conduction is a more sensitive measurement with fewer false positives than relative focal sensory conduction slowing, decrease of sensory action potential, and dispersal of the sensory action potential. Axonal features are more common than features associated with demyelination. EMG readings are frequently abnormal, but may be confusing because of the tendency of proximal lesions to involve the peroneal innervated muscles. However, EMG of the peroneal innervated muscles is a good indicator of recovery because reinnervation occurs prior to clinical recovery.


Peroneal palsies are relatively common, but true entrapment neuropathies are uncommon. The fibular tunnel syndrome is an entrapment­phenomenon in which the peroneal nerve is compressed against the fibula by the tendinous edge of the peroneus longus muscle, which originates at the neck of the fibula. External compression of the peroneal nerve at the fibular head can occur secondary to a number of processes, however: plaster casts, tight stockings, bandages, and garters may cause compression. External compression may also occur in a patient who is stuporous or in a coma secondary to drug ingestion, with the leg laying against a protruding object. It also may occur when a patient is under general anesthesia or in the lithotomy position. A number of masses, including ganglia, nerve tumors, or tumors of neighboring structures have been noted to lead to compression neuropathy. Peroneal nerve compression has also been associated with increased intra-articular pressure within the knee, which leads to herniation of synovial tissue posteriorly. This may manifest as fullness or swelling and pain in the posterior aspect of the knee. In some instances, surgical exploration may be required to differentiate entrapment from external nerve compression from a variety of masses, including ganglia or tumors. Occupational practices such as prolonged kneeling or squatting may also predispose to a peroneal compression neuropathy. Compression is thought to occur at the tendon of the posterior border of the peroneus longus muscle at the level of the head of the fibula. Peroneal palsy may develop following loss of a large amount of weight. This most probably is related to an increased susceptibility of the nerve to trauma at the fibular head.

Differential Diagnosis

A complete palsy of the foot dorsiflexors is strongly suggestive of a peroneal nerve palsy. Most radiculopathies partially spare these muscles due to overlap of nerve root innervation. An L5 radiculopathy resembles a peroneal palsy, but is differentiated from it by: (1) weakness of foot inversion, (2) sensory loss occurring well above the midpoint of the calf, (3) more weakness of the extensor hallucis than of the anterior tibialis muscle (which receives more L4 innervation than does the ex­tensor hallucis muscle and is, thus, less involved), and (4) back pain. The peroneal nerve may be damaged at different levels below the knee. The deep peroneal nerve may be injured by an anterior compartment syndrome with resultant foot­drop, but with sparing of the foot evertors. The distal deep peroneal nerve may be involved in an anterior tarsal tunnel syndrome. This may produce asymptomatic atrophy of the extensor digitorum brevis as well as a sensory loss in the web space between the first and second toes. A sciatic nerve lesion may present with predominantly peroneal signs because of the more frequent and severe involvement of the peroneal nerve compared to the tibial nerve. The additional absence of the ankle reflex, atrophy or weakness of the hamstring or calf muscles, or sensory loss on the sole of the foot may indicate that the sciatic nerve is affected. Peripheral neuropathies may also cause peroneal nerve dysfunction. The common peroneal nerve is also a frequent site of involvement of diabetic peripheral neuropathy.


Patients who experience a chronic progressive course of pain and sensory and/or motor loss should be considered to have an entrapment neuropathy tumor, or ganglion cyst. Early exploration is indicated, since little will be gained from waiting. Those patients with an acute compressive lesion due to the more common etiologies should be treated expectantly with alteration of behavioral patterns that predispose to the neuropathy. A brace should be used to provide stability to the ankle during ambulation.

Saphenous Nerve Entrapment Syndrome

The saphenous nerve is the largest cutaneous sensory branch of the femoral nerve. It is a pure sensory nerve with two terminal branches. The infrapatellar branch supplies the anteromedial aspect of the knee, while the descending branch supplies the anteromedial aspect of the leg and ankle.

Clinical Features and Anatomy

The saphenous nerve originates just below the inguinal ligament. It then enters the adductor canal (Hunter's canal), crosses the femoral artery from lateral to medial and leaves the canal by piercing its roof together with the descending genicular artery. The nerve penetrates the subsartorial fascia, the roof of the canal. It is here that the site of entrapment is thought to occur, approximately 10 cm above the medial condyle of the femur. After piercing the deep fascia, the nerve branches into its two terminal branches. Physical examination reveals tenderness over the point of emergence of the nerve from the subsartorial canal. A Tinel's sign may be noted at this point, as well as along the course of the nerve. Sensory loss usually occurs along the medial aspect of the knee and/or leg. The saphenous nerve may be injured during vascular surgical procedures (arterial and venous) or by lacerations. The infrapatellar branch may be injured during knee surgery, with numbness occurring over the region of the patellar tendon.


If the syndrome remains refractory to conservative measures, neurolysis should be performed at the point of penetrance through the roof of Hunter's canal. This is carried out via an incision centered at the nerve's point of emergence from the canal. The deep fascia along the anterior border of the sartorius muscle is then incised. The sartorius muscle is retracted medially to identify the roof of Hunter's canal. The point of emergence is then identified, as well as its association with the descending genicular artery. Finally, the fascia should be widely opened.

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