Carbamazepine (CBZ) selectively suppressed kindled convulsions, whereas ethosuximide (ESM) suppressed spike-wave activity accompanying systemic penicillin epilepsy in cats. Evoked potential data indicated that CBZ acted at the thalamic level, whereas ESM acted at cortex. Reduction of seizures and thalamic or cortical excitability occurred throughout the sleep-wake cycle, but effects were most pronounced in seizure-prone sleep or awakening states. These findings extend previous work showing differential antiepileptic drug (AED) effects on temporal lobe and absence seizures. The results are also consistent with recent work suggesting that thalamocortical pathways provide a final common pathway for the manifestation of sleep and awakening epilepsy and also reflect a chronic, latent pathophysiology.

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