The administration of neurotoxin thiolactone homocysteine in rats with cobalt-induced epileptogenic focus in the sensomotor cortical region led to the development of secondary generalized convulsions and epileptic state. The pattern was analogous to the manifestation of convulsions in epileptic state in humans. Fenitoin (50 mg/kg) inhibited the development of convulsions, arrested the epileptic state, reduced the number and duration of the secondary generalized tonic--clonic attacks, decreased the behavioral manifestations (focal convulsions, lateral position etc.), normalized EEG, and prevented fatal outcome. An increase in the fenitoin dose to 100 mg/kg decreased the antiepileptic activity, enhanced side effects, and increased the lethality in test animals.
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