Rather than discussing in detail each of these presentations, we wish to re-examine two central questions regarding the pathophysiology of petit ma1 epilepsy, in the light of some of our own recent experimental data. The answers, we believe may be relevant to each of the preceding presentations.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 ma1 epilepsy? Precisely where is the lesion located: in the cerebral cortex; in the nonspecific thalamic system or in the mesencephalic reticular formation? Perhaps the lesion affects all of these structures in a diffuse manner. The necessarily rare and limited neuropathological examination does not provide a clear-cut answer. We should indicate at the onset that it is evident that nonspecific thalamic system, specific thalamic systems and mesencephalic reticular formation may modify on-going normal and abnormal cerebral electrical activity (17, 29, 30, 35, 38). The demonstration of such a role of subcortical systems, however, does not necessarily localize the basic lesions to these structures. Moreover, there is some clinical and experimental evidence that the pathology may involve the cerebral cortex ( I , 10, 16, 21, 34, 37).Second, irrespective of where the responsible lesion(s) may be located; are the brain stem and diencephalic structures essential for the development of the bilateral symmetrical and synchronous discharges of spike-slow wave or polyspike-slow wave complexes which are the hallmark of petit ma1 epilepsy and of the other varieties of primary bilateral synchrony?In attempting to answer the first question, what is the location of the lesion responsible for spike-wave and absence seizure phenomenon, we have tested the hypo-