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Sci Rep. 2018 Jan 23;8(1):1423. doi: 10.1038/s41598-018-19675-6.

Seizure development in the acute intrahippocampal epileptic focus.

Author information

1
Department of Neurology, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA.
2
I.M. Sechenov First Moscow State Medical University, Moscow, Russia.
3
Department of Neurology, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. engel@mednet.ucla.edu.
4
Department of Neurobiology, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. engel@mednet.ucla.edu.
5
Department of Psychiatry and Biobehavioral Sciences, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. engel@mednet.ucla.edu.
6
Brain Research Institute, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. engel@mednet.ucla.edu.
7
Department of Neurology, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. abragin@mednet.ucla.edu.
8
Brain Research Institute, David Geffen School of Medicine at University of California Los Angeles, 710 Westwood Plaza, Los Angeles, CA, 90095, USA. abragin@mednet.ucla.edu.

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.

PMID:
29362494
PMCID:
PMC5780458
DOI:
10.1038/s41598-018-19675-6
[Indexed for MEDLINE]
Free PMC Article

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