Bilateral peroneal nerve palsy induced by prolonged squatting

Military Medicine, Mar 2000 by Togrol, Erdem

External or internal pressures on peripheral nerves may result in compression neuropathies. Although compressive common peroneal nerve palsy is well known, to date very few cases with bilateral palsies have been reported. The clinical and electrophysiological manifestations of three patients with bilateral peroneal nerve palsies are reported, and their clinical outcomes are discussed. The first patient's transient bilateral palsy was corrected by conservative means. The second patient, with a more severe axonal lesion, did not improve within 3 months, and nearly complete recovery occurred after operative decompression. For the third patient, who had been suf fering for a long time, no improvement could be hoped for. Prolonged squatting was the etiological factor in all three cases. Bilateral compression neuropathies of the peroneal nerve, like unilateral lesions, may recover spontaneously. Surgical intervention is recommended for patients with predominantly axonal lesions and for those who do not improve within 3 months.

Introducton

Damage to a peripheral nerve by internal or external pressure of various origins causes a "compression neuropathy." At certain sites, the nerve in question is anatomically more vulnerable. Examples of external compression neuropathies are radial nerve palsy caused by misuse of crutches and compression during drunken sleep, ulnar neuropathy from habitual leaning on the elbow, and common peroneal nerve palsy attributable to pressure from a below-knee plaster cast. Alternatively, the nerve may be compressed or stretched by adjacent tissues such as bone, bony callus, synovial thickening, ganglia, tumors, fibrous bands, and muscle.1 It is also known that nerves in particular patients are more sensitive to pressure. These include patients with generalized neuropathy, diabetes mellitus, tomaculous neuropathy, and certain infectious, genetic, and metabolic diseases.

Compressive peroneal nerve palsy is a well-known clinical condition. Usually, the nerve is compressed at the knee as it passes around the head of the fibula along its course, or the nerve's sensory branch may be entrapped over the dorsal side of the foot.2 Bilateral compression of the nerve is quite rare. It may occur as a result of mechanical irritation during prolonged leg crossing and squatting.

Case Reports

Case 1

A 13-year-old male patient was admitted with the complaints of difficulty in walking and moving his feet. He had had no walking problems until 5 days before, when he became aware of a difficulty in walking after he awoke one morning. The next day, he had a stepping gait. He had gone fishing the day before the beginning of his complaints and had been squatting for more than 5 hours. It was noted that the patient was quite slim for his age. His height was 156 cm and his weight was 41 kg. The neurological examination on admission revealed marked weakness in the dorsiflexion at the ankle of both feet and the dorsiflexion of the toes. Plantar flexors and inventors were normal. He had hypesthesia in the common peroneal nerve cutaneous sensation area in both legs. Deep tendon reflexes were mildly reduced, with Achilles reflexes being moderately reduced in both lower extremities.

Electromyography and nerve conduction studies were performed on admission and 10 days later. Lesions of both common peroneal nerves at the head of the fibula were confirmed. The lesion appeared to be predominantly segmental demyelination. No abnormality was found proximal to the lee, and there were no findings suggestive of generalized peripheral neuropathy. Meanwhile, the patient's complaints regressed and the sensory loss in his feet disappeared in 5 days and his gait became more normal.

The patient was told to avoid this posture at all times and was given oral B vitamins, including thiamine, riboflavine, pyridoxine, and cyanocobalamin. His condition improved progressively, and he was followed up on an outpatient basis. All his complaints had disappeared by the second month, and on neurological examination only a minimal weakness in dorsiflexing the toes of both feet was noted. The patient stopped coming for follow-up examinations after the second month.

Case 2

A 20-year-old male patient complained of difficulty in walking and excessive weakness in the dorsiflexion of both feet. He stated that he had remained in a squatting position for more than 6 hours while cutting grass, with almost no changes in this position and never standing up. His complaints started the next day. This happened about 1 month before presentation. The neurological examination on admission showed weakness in the eversion and dorsiflexion at the ankle of both feet and the dorsiflexion of the toes. Plantar flexors and inventors were normal. The patient could not stay on his feet for an extended period of time, and the sensation on the dorsal side of the feet was reduced. There were no other neurological abnormalities. The patient had no known preexisting medical condition, including diabetes or other metabolic problems, but he was extremely slim. His height was 176 cm and his weight was 57 kg on admission. All hematological parameters, including glycemia, blood urea and creatinine, serum electrolytes, bilirubinemia, liver function tests, cholesterol, lipoproteins, triglyceride, and erythrocyte sedimentation rate, were normal. Electromyography and nerve conduction studies were performed 1 month after bilateral development of foot-drop. Lesions of both common peroneal nerves at the head of the fibula were confirmed. These lesions were severe. There were no orthopedic abnormalities proximal to the knee or any signs of generalized peripheral neuropathy. The nerve damage was thought to be attributable to physical pressures. The patient was told to avoid squatting and was prescribed oral B vitamins, including thiamine, riboflavine, pyridoxine, and cyanocobalamin. Two months after his admission, there was no improvement in the foot-drop, and electrophysiological examination revealed predominantly axonal loss rather than segmental demyelination. The patient was operated on, and the nerves were decompressed bilaterally. He benefited greatly from this treatment, and the bilateral palsy regressed. After 15 days, the patient could walk much more easily, and the extension of both feet and their toes was stronger. At his follow-up examination 2 months later, almost complete recovery was observed, with only a mild weakness in the extension of the big toes of both feet.