Bilateral peroneal nerve palsy induced by prolonged squatting

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.

Case 3

This 47-year-old male patient had become a private in the Turkish Army after serving a long (civilian) prison sentence. He complained of difficulty in walking, inability to dorsiflex the right foot and excessive weakness in the dorsiflexion of the left foot, inability in the eversion and inversion of both feet, and inability to dorsiflex the toes of the right foot. He could not stand on his heels, but he could stand on his toes. He also complained of frequently tripping. He explained that his complaints had started 16 years before, during his prison sentence, after prolonged squatting and physical trauma from other prisoners. His neurological examination on admission revealed bilateral atrophy in both tibialis anterior muscles, although this was more advanced on the right side. Dorsifiexion, eversion, and inversion at the ankle were not present in the right foot, and dorsiflexion was minimal on the left side. The toes could not be dorsiflexed. The plantar flexion of the feet and toes was normal. The patient presented a bilateral foot-drop with a bilateral stepping gait. The Achilles reflex was absent on both sides. A hypesthesia on the dorsal side of the left foot and anesthesia on the right foot was noted. There were no other neurological abnormalities.

The electrophysiological examination (electromyography and nerve conduction studies) revealed excessive partial axonal lesions in both peroneal nerves. The findings were more advanced on the right side. There was an axonal lesion in the branch of the right deep peroneal nerve innervating the right tibialis anterior muscle. All hematological parameters, including glycemia, blood urea and creatinine, serum electrolytes, bilirubinemia, liver function tests, cholesterol, lipoproteins, triglyceride, and erythrocyte sedimentation rate, were normal; creatinine kinase was found to be mildly elevated. Yet, when the test was repeated 1 week later, no abnormality could be shown, and this was accepted as an occasional finding.

Because this condition had been present for more than 16 years, no operation was planned. The patient was discharged, and his military service was brought to an end.

Discussion

Although peroneal nerve compression palsy is a well-documented and investigated clinical condition, very few individual cases with bilateral compression of the peroneal nerve have been reported. The large series of 60 patients with peroneal nerve entrapment reported by Fabre et al. includes only two patients with bilateral involvement.l It has been described in bedridden patients and in patients who undergo prolonged hospitalization, after squatting, as a result of ganglia and other space-occupying lesions, in habitual leg crossing, especially after weight loss, and in anorexia nervosa,.3-6 Rarely, the lesions may also develop after pelvic surgery in the lithotomy position.7

Prolonged squatting is the most frequent cause of peroneal nerve palsy. It was the etiological factor in all three cases presented here. Another finding that was present in all three patients was their being slim; the third patient probably was in a state of malnutrition at the time of the lesion. The relationship between anorexia nervosa and peroneal nerve palsies is mentioned in the literature, and several mechanisms have been proposed to explain this phenomenon.6,8 The loss of subcutaneous tissue and the decrease of fat around the head of the fibula could render the common peroneal nerve more sensitive to mechanical irritations, minor injuries, and direct pressures. Vitamin B deficiency of malnutrition could also be a secondary predisposing factor. These mechanisms may also apply to the cases presented in this paper.

As observed with patient l, peroneal neuropathies may be reversible. Kern and Cholewicki have described this condition as a transient conduction block of motor axons.4 But as seen in patient 3, the pathology may be permanent, as a result of an irreversible damage to the motor axons.

The policy of treatment must be conservative and supportive in the beginning, the main principle being protection of the nerve from further injury and compression. In cases with severe axonal degeneration and cases in which the symptoms do not respond to treatment within an interval of 2 or 3 months, the surgical approach is recommended.9,10 Thus, permanent functional disability like that present in patient 3 can be prevented.

Comments

Bilateral peroneal nerve palsy may occur after prolonged squatting, crossing of legs, or by other actions or means that cause the compression of the nerve in its course around the fibula. Several factors may cause this condition, including malnutrition, vitamin deficiency, loss of subcutaneous tissue and decrease of fat, and various metabolic conditions. Treatment is usually supportive and conservative. However, if the electrophysiological study shows a total axonal lesion or if palsies persist in spite of conservative measures for 2 or 3 months, the surgical approach should be chosen.

References

1. Fabre T. Piton C, Andre D, Lasseur E, Durandeau A: Peroneal nerve entrapment. J Bone Joint Surg Am 1998: 80: 47-53.

2. Dellon AL: Deep peroneal nerve entrapment on the dorsum of the foot. Foot Ankle 1990; 11: 73-80.

3. Khairallah EW, Weinberg MJ, Mahoney J: Acute common peroneal nerve palsy caused by hemorrhage into a recurrent ganglion. Can J Plast Surg 1995; 3: 3-6. 4. Kern RZ, Cholewicki J: Squatting-induced common peroneal neuropathy: serial

electrophysiological studies. Abstracts of the American Association of Electromyography and Electrodiagnosis Meeting, September 15-16. 1989. Muscle Nerve 1989; 2: 763.

5. Uncini A, Di Muzio A, Awad J, Gambi D: Compressive bilateral peroneal neuropathy: serial electrophysiologic studies and pathophysiological remarks. Acta Neurol Scand 1992; 85: 66-70.

6. Kershenbaum A, JafFa T, Zeman A, Boniface S: Bilateral foot-drop tn a patient with anorexia nervosa. Int J Eating Disord 1997; 22: 335-7.

7. Jacobs D, Azagra JS, Delauwer M, Bain H, Vanderheyden JE: Unusual complication after pelvic surgery: unilateral Lower limb crush syndrome and bilateral common peroneal nerve paralysis. Acta Anaesthesiol Belg 1992; 43: 139-43.

8. Lutte I, Rhys C, Hubert C, Brion F. Boland B, Peeters A, van den Bergh P, Lambert M: Peroneal nerve palsy in anorexia nervosa. Acta Neurol Belg 1997; 97: 251-4.

9. Goudamzi YM, Khodadadyan C, Leuenberger D: Bilaterale lasion des nerves peronaeus mit lasion der linksseitigen need medianus and ulnaris bei multiplen osteocartilaginaren exostosen. Chirurg 1995; 66: 1158-61.

10. Mont MA, Dellon AL. Chen F, Hungerford MW, Krackow KA. Hungerford DS: The operative treatment of peroneal nerve palsy. J Bone Joint Surg Am 1996; 78: 863-9.

Guarantor: Commander Erdem Togrol

Contributors: Commander Erdem Togrol*; Major Ahmet Colak^; Major Murat Kutlay+; Major Mehmet Saracoglu*;*; Captain Nevzat Akyatan*; Colonel Osman Niyazi Akin^

*Department of Neurology and tDepartment of Neurosurgery, Gulhane Military Medical Academy, Haydarpasa Training Hospital, Istanbul, Turkey.

This manuscript was received for review in December 1998. The revised manuscript was accepted for publication in May 1999.

Reprint & Copyright by Association of Military Surgeons of U.S., 2000.

Copyright Association of Military Surgeons of the United States Mar 2000
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