An Experimental Model of Some Varieties of Petit Mai Epilepsy Electrical‐Behavioral Correlations of Acute Bilateral Epileptogenic Foci in Cerebral Cortex

UMMARY This discussion has examined 2 central questions regarding the pathophysiology of petit mal epilepsy. First, what is the locus of the lesion responsible for the bilateral synchronous and symmetrical spike-slow wave discharges and the associated behavioral absence of petit mal epilepsy? We have demonstrated that it is possible to produce an experimental model of petit mal epilepsy in the otherwise intact cat or monkey without the necessity of lesions in the brain stem or diencephalic structures. The essential lesion in this model is solely cortical and bilateral in location. In particular our experiments have involved the production of acute relatively large bilateral and symmetrical cortical epileptogenic foci. The interaction of these foci resulted in the development of synchronous and symmetrical patterns of bilateral discharge resembling the various forms of human primary bilateral synchrony including the 2½-4 c/s spike-slow wave complex. In the monkey, regional variations in capacity for bilateral discharge were noted, related to regional differences in callosal projection. Particularly well regulated bilaterally synchronous and symmetrical bursts of 2½-4 c/s spike-slow wave complexes occurred with bilateral foci in the premotor area of monkey frontal lobe. Studies of behavior and simultaneously recorded electroencephalogram indicated that bilateral synchronous discharges of 3 c/s spike-slow wave complex resulting from bilateral foci in anterior premotor area were closely correlated with short staring spells resembling petit mal (absence) seizures. Second, irrespective of where the responsible lesion(s) may be located, are the brain stem and diencephalic structures essential for the development of these bilateral symmetrical and synchronous discharges of 2½-3 c/s spike-slow wave complexes which are the hallmark of petit mal epilepsy? From the standpoint of the present model, it is demonstrated that section of the corpus callosum in the cat or of all major commissures in the monkey markedly disrupted the synchrony of discharge of bilateral foci. Alternate pathways for coarse synchrony at low rates of discharge were demonstrated. These results should be compared to the high degree of synchrony of bilateral discharge obtained in the cat or monkey preparation in which large blocks of cerebral cortex in each hemisphere were isolated from subcortical structures but remained connected via the corpus callosum. The spike discharges of bilateral foci in this preparation were synchronized within 10–20 msec, well within the limits noted in the intact animal and in the patient with petit mal epilepsy. The patterns of bilateral discharge in this cortical-callosal preparation included bilateral synchronous bursts of 2½-3 c/s spike-slow wave complexes. RESUME Ce travail envisage deux questions essentielles concernant la physiopathologie de l'epilepsie petit mal. Premiere question: Quel est le siege de la lesion responsable des decharges bilaterales, synchrones et symetriques de pointes-ondes qui accompagnent les absences petit mal? Nous avons demontrea ce propos qu'il est possible de reproduire une epilepsie du type petit mal chez un chat ou un singe d'autre part normal independamment de toutes lesions du tronc cerebral ou du diencephale. II suffit de realiser chez ces animaux des lesions corticales bilaterales, notamment des foyeis epileptogenes corticaux aigus, bilateraux et symetriques, assez etendus. L'interaction de ces foyers aboutit a la production de decharges bilaterales synchrones et symetriques ressemblant aux differents types de synchronic bilaterale primaire observee chez FHomme, y compris la pointe-onde a 2½-4 c/s. Chez le singe on observe des variations regionales dans la capacitye de produire des decharges bilaterales qui dependent des differences regionales dans les projections commissurales calleuses; c'est ainsi que les bouffees de pointes-ondes bilaterales synchrones et symetriques a 2½-4 c/s particulierement regulieres, accompagnees de troubles du comportement evoquant une absence, surviennent sous l'effet de foyers bilateraux dans l'aire premotrice des lobes frontaux. Deuxieme question: Quel que soit le siege des lesions responsables, le tronc cerebral et le diencephale sont-ils indispensables pour le developpement des decharges bilaterales synchrones et symetriques de pointes-ondes a 2½-4 c/s qui sont caracte-ristiques des epilepsies petit mal? En ce qui concerne nos propres experiences, il apparait que la section du corps calleux du chat ou celle de toutes les grandes commissures chez le singe altere considerablement la synchronic des decharges de foyers bilateraux. Ces resultats contrasted avec le haut degre de synchronic des decharges bilaterales obtenues dans les larges etendues de cortex cerebral qui, dans chaque hemisphere, sont isolees des structures sous-corticales mais demeurent interconnectees a travers le corps calleux. Dans de telles preparations cortico-callosales, les decharges de pointes des complexes pointes-ondes recueillies dans les foyers bilateraux sont synchronises dans des limites de 10–20 msec qui correspondent a celles observees chez l'animal intact ou chez le sujet humain presentant une epilepsie petit mal.