[Generalization mechanisms of limbic seizures].

It is well known that complex partial seizures of temporal origin may evolve into secondarily generalized convulsive seizures. For this reason, amygdaloid kindling, which begins with limbic seizures and culminates in secondarily generalized convulsions, is considered to be a useful model for examination of mechanisms underlying the development of convulsive seizures originating from a non-motor structure such as the amygdala. Recent observations made in our laboratory are relevant to anatomic network underlying expression and the generalization of amygdala-onset seizures. Specifically, functional roles played by the substantia innominata, massa inter-media of the thalamus and caudate-putamen in secondary generalization were examined in rats. Obtained results suggest: (1) the substantia innominata may mediate ictal linkage between the kindled amygdala and the iplilateral cortical motor mechanism, with secondary recruitment of the contralateral cortical motor mechanism, although the kindled amygdala can directly gain access to the contralateral hemispheric motor mechanism without participation of the substantia innominata; (2) the thalamus may be conceived to be a direct extension of the cortical motor mechanism; and (3) the caudate-putamen regulates the function of cerebral motor mechanisms responsible for the expression of generalized convulsive seizures, although the caudate-putamen may partly participate in the termination of seizures.