Functional mapping of limbic seizures originating in the hippocampus: a combined 2-deoxyglucose and electrophysiologic study.
The pathways by which seizures spread from the hippocampus were studied both with multiple electroencephalographic recordings and 2-deoxyglucose autoradiography. The rapid kindling model described in the previous report was employed to compare mild versus severe limbic seizures. Seizures were accompanied by an increased glucose utilization in localized brain areas. The transition from mild to severe limbic seizures involved a greater spatial extent of paroxysmal electroencephalographic activity and metabolic signals. However, electrical recordings proved more sensitive in mapping seizures, as regions shown to be involved in mild or severe limbic seizures with electrical recordings did not necessarily show an increased glucose metabolism. Three types of circuits are important in dissemination of these seizures: interhippocampal connections, pathways leading out of the hippocampus to other limbic regions, and connections to certain extralimbic areas. The nucleus accumbens, amygdala, and substantia nigra emerge as important relay points in the spread of hippocampal-based seizures.
D000818:Animals; D001345:Autoradiography; D001479:Basal Ganglia / Q000503:physiopathology; D002540:Cerebral Cortex / Q000503:physiopathology; D003847:Deoxyglucose / Q000378:metabolism; D004569:Electroencephalography; D004833:Epilepsy, Temporal Lobe / Q000503:physiopathology*; D006624:Hippocampus / Q000503:physiopathology; D008032:Limbic System / Q000503:physiopathology*; D051381:Rats; D013378:Substantia Nigra / Q000503:physiopathology
D003847:Deoxyglucose