ABSTRACT
The current thinking about the pathogenesis of absence seizures dates to the landmark experiments of Jasper and Droogleever-Fortuyn (1947), who demonstrated that 3 c/s stimulation of the midline and intralaminar nuclei of the thalamus in cats could produce bilaterally synchronous SWD in the cortical EEG of those animals. The relevance of this finding to human epilepsy was demonstrated by Williams (1953), who, utilizing depth electrode recordings from the thalamus of a child with absence seizures, demonstrated that bilaterally synchronous 3 c/s SWD arose from that structure. Over the next twenty years, a debate ensued in the literature as to which was preeminent in controlling the bilaterally synchronous SWD that characterized absence seizures: the cortex (Bennett 1953; Marcus and Watson 1966; Marcus et al. 1968), the thalamus (Pollen et al. 1963), or both (Gloor 1968). With the advent of a number of animal models of generalized absence seizures, this controversy has been partially resolved. Moreover, the availability of these models has advanced our understanding of the basic mechanisms of absence seizures considerably (Snead et al. 1999).
