Mechanisms of seizure propagation in a cortical model.
We consider a mathematical model of mesoscopic human cortical ictal electrical activity. We compare the model results with ictal electrocortical data recorded from three human subjects and show how the two agree. We determine that, in the model system, seizures result from increased connectivity between excitatory and inhibitory cell populations, or from decreased connectivity within either excitatory or inhibitory cell populations. We compare the model results with the disinhibition and 4-AP models of epilepsy and suggest how the model may guide the development of new anticonvulsant therapies.
Kramer
Mark A
MA
Applied Science and Technology Graduate Group, University of California, Berkeley, CA 94720-1740, USA.
Szeri
Andrew J
AJ
Sleigh
James W
JW
Kirsch
Heidi E
HE
D015761:4-Aminopyridine / Q000494:pharmacology; D000328:Adult; D000927:Anticonvulsants / Q000494:pharmacology; D001569:Benzodiazepines / Q000494:pharmacology; D002540:Cerebral Cortex / Q000503:physiopathology*; D004569:Electroencephalography / Q000706:statistics & numerical data; D004594:Electrophysiology; D005260:Female; D005625:Frontal Lobe / Q000502:physiology; D006801:Humans; D008959:Models, Neurological; D015233:Models, Statistical; D026902:Potassium Channel Blockers / Q000494:pharmacology; D012640:Seizures / Q000503:physiopathology*; D013702:Temporal Lobe / Q000502:physiology
D000927:Anticonvulsants; D026902:Potassium Channel Blockers; D001569:Benzodiazepines; D015761:4-Aminopyridine