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

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.

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