Mapping of limbic seizure progressions utilizing the electrogenic status epilepticus model and the 14C-2-deoxyglucose method.
We have previously described a model of limbic status epilepticus in which chronic prolonged seizure states of immobile, exploratory, minor convulsive or clonic convulsive behavior are induced by intracerebral electrical stimulation; these states appear to belong to the same behavioral progression as kindled seizures. We postulated that the underlying seizure substrates, as mapped by the 14C-2-deoxyglucose method, should reflect a corresponding anatomic progression of discharge spread. Status epilepticus was induced in rat by pulsed-train current delivered for up to 90 min to one of several subcortical areas. Autoradiographs revealed that most of the observed patterns of seizure-induced metabolic activation comprised a hierarchical sequence, such that progressively more extensive patterns subsumed anatomic territories activated in less extensive patterns, thus allowing inferences as to the progression of discharge spread. In this sequence, the basolateral amygdala ipsilateral to the induction electrode was among the first structures to be activated. In successively larger activation patterns a small unilateral network related to basolateral amygdala was involved; this evolved through a transitional state to a unilateral extensive limbic pattern; which in turn was succeeded by bilateral extensive limbic activation. This hierarchical sequence culminated in a neocortical activation pattern, in which most of the forebrain was involved in intense seizure-induced activation. Seizure behaviors increased in severity in correspondence with the underlying seizure-activated anatomic substrate. In contrast, patterns of seizure activation were observed which did not fit within the early stages of the above sequence, although analysis indicates that the later stages of spread may be shared. The study of these patterns and those reported in the literature indicates that although limbic seizure networks may be anatomically distinct at their origination, further expansion is characterized by overlap; upon assumption of extensive patterns of activation the number of nuclei participating is so vast that the identity of the limbic originator is lost and common convulsive manifestations occur.
Handforth
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A
Department of Neurology, UCLA School of Medicine, Reed Neurological Research Center 90024, USA.
Ackermann
R F
RF
D000679:Amygdala / Q000378:metabolism / Q000502:physiology; D000818:Animals; D001345:Autoradiography; D001931:Brain Mapping; D002250:Carbon Radioisotopes; D003847:Deoxyglucose / Q000378:metabolism; D004569:Electroencephalography; D007839:Functional Laterality / Q000502:physiology; D006624:Hippocampus / Q000378:metabolism / Q000502:physiology; D007696:Kindling, Neurologic / Q000378:metabolism* / Q000502:physiology; D008032:Limbic System / Q000378:metabolism* / Q000502:physiology; D008297:Male; D009434:Neural Pathways / Q000378:metabolism / Q000502:physiology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013226:Status Epilepticus / Q000378:metabolism* / Q000503:physiopathology
D002250:Carbon Radioisotopes; D003847:Deoxyglucose