Disulfiram-induced convulsions without challenge by alcohol.

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Abstract
A 50 yr old woman alcoholic with no history of seizures was hospitalized following a grand-mal convulsion. She had been abstinent 9 mo. and taking 500 mg of disulfiram a day. Two months prior to admission her family noted marked personality changes and, although the disulfiram dosage had been lowered to 250 mg 1 wk prior to admission, her clinical condition worsened, with increasingly florid paranoid delusions, suicidal ideation, markedly loosened association, increased confusion and further impairment of memory. At admission, the results of routine laboratory tests and physical and neurological examinations were all within normal limits. Blood alcohol concentration was zero. Her mental status examination showed evidence of an acute delirium. An EEG 2 days after admission showed fast spikey background activity suggestive of a drug effect. Four major seizures occurred on the day of admission and 1 the following day. They were preceded by 10-15 min of poor verbal communication. The seizures were bilateral and typical tonic-clonic generalized grand-mal convulsions which ceased spontaneously after 3 min. Disulfiram was discontinued and phenytoin and phenobarbital administered and her cognitive functioning gradually improved. EEG taken 6 and 30 days after admission were normal. Ten days after admission the Halstead-Reitan neuropsychological battery showed evidence of diffuse cortical dysfunction; at 30 days considerable improvement had occurred. Six months postdischarge, and without any medications, the woman had no further seizures. The mechanism of seizure induction by disulfiram is unknown but may be related to inhibition of tissue uptake of oxygen or to inhibition of dopamine .beta.-hydroxylase. The latter leads to a decrease in the brain norepinephrine:dopamine ratio, which has been postulated to lower the seizure threshold.

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