Abstract

Patients with focal temporal lobe seizures often experience transient episodes of impaired awareness with behavioural arrest, but the precise mechanism remains unknown. The Blumenfeld hypothesis attributes these deficits to a loss of cholinergic input to the cortex. This is presumed to result from increased activation of inhibitory regions that suppress subcortical arousal, giving rise to slow wave activity. To investigate this hypothesis – and more specifically, to characterize the relationship between propagated discharge, cortical slow waves and behavioural arrest – we performed kindling studies in rats. We found that seizure discharge took longer to spread from the amygdala than the hippocampus, and took more kindling stimulations to elicit behavioural arrest. In addition, the onset of propagated discharge in subcortical and cortical sites did not always match with the onset of behavioural arrest. Importantly, the activity seen in the cortex did not resemble the slow waves seen in deep sleep. Together, these findings suggest an additional mechanism – other than the Blumenfeld hypothesis – to explain how temporal lobe seizures may produce behavioural arrest and impair awareness.

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