Abstract
Comorbidities, such as cognitive deficits, which often accompany epilepsies, constitute a basal state, while seizures are rare and transient events. This suggests that neural dynamics, in particular those supporting cognitive function, are altered in a permanent manner in epilepsy. Here, we test the hypothesis that primitive processes of information processing at the core of cognitive function (i.e., storage and sharing of information) are altered in the hippocampus and the entorhinal cortex in experimental epilepsy in adult, male Wistar rats. We find that information storage and sharing are organized into substates across the stereotypic states of slow and theta oscillations in both epilepsy and control conditions. However, their internal composition and organization through time are disrupted in epilepsy, partially losing brain state selectivity compared with controls, and shifting toward a regimen of disorder. We propose that the alteration of information processing at this algorithmic level of computation, the theoretical intermediate level between structure and function, may be a mechanism behind the emergent and widespread comorbidities associated with epilepsy, and perhaps other disorders.
SIGNIFICANCE STATEMENT Comorbidities, such as cognitive deficits, which often accompany epilepsies, constitute a basal state, while seizures are rare and transient events. This suggests that neural dynamics, in particular those supporting cognitive function, are altered in a permanent manner in epilepsy. Here, we show that basic processes of information processing at the core of cognitive function (i.e., storage and sharing of information) are altered in the hippocampus and the entorhinal cortex (two regions involved in memory processes) in experimental epilepsy. Such disruption of information processing at the algorithmic level itself could underlie the general performance impairments in epilepsy.
