Thalamocortical mechanisms of state-dependent seizures during amygdala kindling and systemic penicillin epilepsy in cats.

Somatomotor system-evoked potential data suggested that thalamus and cortex provide a final common pathway for the timing of generalized seizures in the sleep-wake cycle. Results indicated thalamic mediation of sleep-activated seizures in the amygdala kindling model of secondary generalized epilepsy; in contrast, cortical hyperexcitability was implicated in the timing of seizures with the systemic penicillin model of primary generalized, petit mal epilepsy. Even though thalamic or cortical hyperexcitability peaked during seizure prone sleep or awakening states in the two models, increased, 'subclinical' levels of hyperexcitability persisted during seizure resistant states, notably rapid-eye-movement (REM) sleep. This finding suggested a chronic, if often latent neuropathology for both epilepsy models and upon which the sleep-wake state modulation of seizures is superimposed.