Ischaemic lateral popliteal nerve palsy due to ergot intoxication

Abstract

SYNOPSIS A patient with ergot intoxication due to medication for migraine developed lateral popliteal nerve palsy. This is attributed to recurrent ischaemia caused by ergotamine.Although the development of diffuse peripheral paraesthesiae and numbness is a recognized complication of ergot intoxication, an isolated lateral popliteal nerve palsy has not been described previously in this situation. The purpose of this paper is to record such a case in a patient with evidence of severe arterial spasm in the lower limbs, and to point to some analogies with those cases of isolated lateral popliteal palsies secondary to atherosclerotic disease. CASE REPORTThe patient (MV 76725), a Greek woman aged 30 years, was first admitted in August 1973. She had a four year history of migraine, responding poorly to ergotamine tartrate, 2 mg (Lingraine) and clonidine. For three months she had been using Cafergot suppositories (ergotamine tartrate 2 mg, caffeine 100 mg, belladonna alkaloids 0-25 mg, isobutylallyl barbituric acid 100 mg) up to four times in an attack and 12 times per week.One week before admission, and 24 hours after using suppositories, she awoke with an intense burning pain, associated with numbness, over the dorsum of the right foot and had difficulty in moving the toes. The symptoms persisted.On admission, the peripheries were warm, and all pulses were present. The blood pressure was 140/90 mmHg. Neurological examination showed abnormalities confined to the right leg, where there was impaired sensation to all modalities over the dorsum of the foot, and slight weakness of dorsiflexion of the foot and hallux. The tendon reflexes were present and symmetrical.The following investigations were normal-full blood count, fasting blood sugar, serum urea, electrolytes, cholesterol, uric acid, calcium, phosphorus, and alkaline phosphatase. Successive erythrocyte sedimentation rates (ESR) were 28, 32, 36, and 30 mm in the first hour. The cerebrospinal fluid had no cells, and a protein content of 50 mg/dl. Serology was negative. Radiography of the chest and lumbar spine, and myelography were normal. On electromyography, performed at normal skin temperature, the distal motor latency to extensor digitorum brevis on stimulation of the right lateral popliteal nerve was 4-3 ms with motor nerve conduction velocity (knee-ankle) 48 m/s. The amplitude of the muscle action potential from stimulation at the knee was 100 ,uV and from the ankle, 250 ,V. The ascending nerve action potential, recording with needle electrodes at the knee and stimulating at the ankle, was absent. Distal motor latency to extensor digitorum brevis on stimulating the left lateral popliteal nerve was 3-5 ms with conduction velocity (knee-ankle) 50 m/s. The amplitude of the evoked muscle action potential from stimulation at the knee was 5 mV and from the ankle 6 mV. The ascending nerve action potential had an amplitude of 12 ,uV, with a latency to peak of 7 ms.During this first admission the right foot was noted to be occasionally warmer than the left. Intradermal ...

Acute bilateral anterior tibial compartment syndrome after Caesarian section in a diabetic.

“…Likewise, a focal drug-induced myopathy seems unlikely although it is noted that ergotamine has been reported to cause an ischaemic lateral popliteal nerve lesion. 4 Anterior compartment syndromes may arise from a variety of vascular causes. Commonly, these are either embolic or arteriosclerotic5 but vascular trauma or arteritis may also be responsible.6 7 Interestingly, the site of the causative lesion may be considerably proximal to the origin of the anterior tibial artery, at either knee or pelvis.7 ' This patient underwent uncomplicated pelvic surgery.…”