Abstract
Currently, an epileptic seizure is considered to involve a temporary network that exists for a finite period of time. Formation of this network evolves through spread of epileptiform activity from a seizure onset zone (SOZ). Propagation of seizures evoked by kainic acid injection in hippocampus to different brain areas was analyzed at macro- and micro-intervals. The mean latency of seizure occurrence in different brain areas varied between 0.5 sec and 85 sec (mean 14.9 ± 14.5 (SD)), and it increased after each consecutive seizure in areas located contralateral to the area of injection, but not in the ipsilateral sites. We have shown that only 41% of epileptic individual events in target brain areas were driven by epileptic events generated in the SOZ once the seizure began. Fifty-nine percent of epileptiform events in target areas occurred one millisecond before or after events in the SOZ. These data illustrate that during seizure maintenance, only some individual epileptiform events in areas outside of SOZ could be consistently triggered by the SOZ; and the majority must be triggered by a driver located outside the SOZ or brain areas involved in ictal activity could be coupled to each other via an unknown mechanism such as stochastic resonance.
Highlights
An epileptic seizure is considered to involve a temporary network that exists for a finite period of time
We provide results of analysis of propagation of epileptiform events generated in an acute epileptic focus created by intrahippocampal injection of kainic acid (KA)
Some properties of seizures induced by KA injection and their relation to spontaneous seizures where described in our previous publications[16,17,18]
Summary
An epileptic seizure is considered to involve a temporary network that exists for a finite period of time Formation of this network evolves through spread of epileptiform activity from a seizure onset zone (SOZ). In addition to visual estimation of propagation of epileptiform events from the area of occurrence at “macro” intervals, we analyzed the relationship between the SOZ and its potential targets at “micro” intervals, once the seizure began. This analysis was based on event by event measurements of the temporal relationships between the SOZ and its potential targets. Non-synaptic mechanisms, and that the latency of epileptiform events in target brain areas depends on the physical distance between these areas and SOZ
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