Sciatic and Posterior Femoral Cutaneous Nerves

Rarely, sciatic neuropathies develop secondary to external pressure, producing a compression injury in comatose or immobilized patients. Very slender individuals who pass out after using toxic substances while seated on a very hard surface, such as a bench or a toilet seat, may develop severe SN damage. If there is significant axonal damage, there may be little chance for nerve recovery over such a long distance. Other traumatic mechanisms leading to a severe SN occur with misplaced injections into the inferior medial quadrant of the buttocks. Fortunately, intramuscular medications are now avoided in this area. Various benign nerve sheath or malignant tumors, such as lymphomas, affect the sciatic nerve in rare instances. Iliac artery aneurysms, systemic vasculitis, or endometriosis are extremely rarely causes of SNs. Congenital fibrous bands may entrap the SN in the midthigh.

Pediatric sciatic neuropathies are primarily related to trauma or iatrogenic orthopedic or miscellaneous surgeries. Other examples of prolonged extrinsic compression leading to sciatic neuropathies include heel compression in an orthopneic child who slept with a foot tucked under his buttock, after prolonged lithotomy surgical positioning, and the consequences of sitting in the lotus posture. The precise mechanism of injury is unclear; these are possibly due to ischemia, stretch, or external compression. Damage to a persistent sciatic artery at the pelvic notch may predispose to sciatic nerve compression and infarction. A variety of tumors affect SN function in children, including neurofibromas, lymphomas, pelvic neuroblastomas, and chloromas. Various vascular lesions occur, including hemophilia, arteriovenous malformations, hypereosinophilic or meningococcemia vasculitis, and hematocolpos. The sciatic nerve is at risk during rare newborn crises, wherein analeptic agents are inadvertently injected into an umbilical artery rather than the umbilical vein. Because the umbilical artery supplies the inferior gluteal artery (IGA), and thus the embryologic-derived sciatic artery, severe IGA vasoconstriction or thromboembolism leads to sciatic nerve ischemia. Congenital iliac anomalies or myofascial bands deep within the thigh are rare causes of a pediatric SN. Occasionally, no specific pathophysiologic mechanism is defined, even in the face of a progressive clinical deficit.

Differential Diagnosis

Nerve root lesions, particularly at L5, S1 or a lumbosacral plexus lesion, provide the primary differential diagnostic consideration in most SNs, when findings clearly encompass not only fibular but also tibial and or proximal sciatic nerve damage. Diminished sensation on the posterior thigh points to a concomitant posterior femoral cutaneous neuropathy near the greater sciatic foramen. Injury to the perineal branches of the sacral plexus nerves leads to sensory loss on the scrotum or labia majora.

Hip extension and abduction, dependent on gluteal nerve and muscle function, are preserved in primary SNs unless there is concomitant involvement of the superior and inferior gluteal nerves. When clinical or EMG evidence defines gluteal muscle involvement, primary lesions adjacent to the pelvis, such as malignant processes—particularly lymphoma or benign tumors, (e.g., schwannomas)—require consideration. The possibility of a piriformis syndrome is mentioned for completeness. It is a poorly defined entity that has no proved clinical definition despite a modest literature on the subject. Objective clinical or electrodiagnostic evidence of sciatic neuropathy is not confirmed in most patients in whom piriformis syndrome is suspected.

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