Mononeuropathies of the Lower Extremities

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 prolonged lithotomy positioning, 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 intramuscular injections into the inferior medial quadrant of the buttock. Mass lesions including nerve sheath tumors and external compression from hematoma, aneurysm, endometriosis; other mechanisms also have been described. Sciatic neuropathies due to nerve infarcts 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) help differentiate the two entities. The ankle and internal hamstring reflexes are usually depressed or absent. Sensory loss and dysesthesia of the sole, dorsum of the foot, and posterolateral lower leg are common.

Differential Diagnosis

A lumbosacral plexus lesion is the other primary consideration in most patients with sciatic neuropathies, especially 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, a primary lesion within the pelvis is a consideration. Examples include benign tumors, such as schwannoma, or malignant processes, particularly lymphoma.

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 usually exits inferior to the piriformis muscle but anatomical variations with the nerve piercing through the muscle have been described. 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. Objective clinical or electrodiagnostic evidence of sciatic neuropathy is not seen in most patients in whom piriformis syndrome is suspected. Patients may benefit from intramuscular injections with botulinum toxin, or steroids and lidocaine.

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. 61.2 ). Predisposing causes include recent substantial weight loss, habitual leg crossing, or prolonged squatting. External devices, such as casts, braces, and tight bandages, can 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. 61.3 ). The common peroneal nerve is sometimes injured iatrogenically, such as during arthroscopic knee repair.

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. 61.2 ). 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.

EMG involvement of the short head of the biceps femoris is the major distinguishing feature with proximal peroneal division sciatic neuropathies, but function of this muscle cannot always be isolated clinically. Therefore, EMG is crucial in establishing this 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; therefore external compressive proximal lesions of the sciatic nerve involve the common peroneal more than the tibial divisions. 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 innervated by the L5 root, such as the tibialis posterior or gluteus medius, is critical. Isolated weakness of great toe extension occurs with mild L5 radiculopathy but is uncommon in peroneal neuropathy. In moderate to severe L5 radiculopathies, foot inversion will be weak because of the involvement of the tibial nerve-innervated tibialis posterior muscle. Uncommonly, hip abduction weakness due to the involvement of the gluteus medius, an L5 muscle supplied by the superior gluteal nerve, is noticeable. 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, and muscle tendon reflexes are depressed or absent. The possibility of motor neuron disease or amyotrophic lateral sclerosis exists with insidious onset of a foot drop without pain or sensory findings. In these instances, there may be 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, and magnetic resonance imaging (MRI) is useful to diagnose them.

Proximal Lesions

Proximal tibial neuropathies may result from Baker cysts, ganglia, tumors ( Fig. 61.4 ), 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 nerve injury occurs proximal to the branch points of the gastrocnemius–soleus complex. Sensory loss occurs on the heel and plantar foot surface.