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