Amygdaloid kindling in rhesus monkeys resulted in development of secondarily generalized convulsive seizures in an average of 196 days. Prior pharmacologic (bemegride) kindling accelerated this seizure development in one animal. None of the animals reached the stage 5 primary generalized seizure of baboons (Papio papio), even after 400 daily amygdaloid stimulations. Seizure stage instability, with frequent regression to an earlier stage, and the difficulty of establishing a generalized seizure triggering threshold in most of the rhesus monkeys, contrasts with our experiences in Papio papio. Thus, differences in the speed of kindling and in the quality of kindled convulsion between rhesus monkeys and epileptic baboons probably reflect the presence or absence of an epileptogenic predisposition in these two species. The difficulty of developing convulsive seizure in rhesus monkeys suggests that this species is particularly suited for the study of partial complex seizure. These studies indicate that the abrupt onset of human epilepsy with a fully developed convulsive seizure must represent and overwhelming central pathophysiologic event resulting from an endogenous, exogenous or a combined insult interacting with a genetically predisposed seizure susceptibility.

SUMMARY:In our earlier study of amygdaloid kindling in Papio papio (Pp), the development of partial complex seizure and of focal motor seizure was correlated with bifrontal theta discharge and increasing Rolandic spike discharge respectively and the final stage was characterized by primary generalized convulsive seizure. Since the latter seizure pattern is known to originate from the frontal focus in man, the frontal cortex became suspect in the development of the final stage seizure pattern. Daily prefrontal stimulation showed that Pp can be kindled from this site, culminating in a recurrent spontaneous seizure state identical to that induced by amygdaloid kindling in this species. However, our observation did not support our original assumption regarding the genesis of primary generalized convulsive seizure. Prefrontal and amygdaloid kindling are significantly different with respect to morphology, distribution and propagation of afterdischarge and interictal spike discharge, and speed and pattern of clinical seizure development. Most intriguingly, inter-ictal behavioral aberration associated with depth EEG changes was observed only in the prefrontal animals and not in the amygdaloid animals.

Despite ready bilateralization of ictal and interictal EEG discharge throughout cortical kindling, the rate of convulsive seizure development was slow at both orbital and mesial frontal sites, even in the epileptic baboon. However, convulsive generalization occurred swiftly from the mesial frontal cortical (MF) sites once conjugate head, eye, and body adversion developed in the three primate species examined. Only epileptic baboons developed Stage 5 bisymmetrical and bisynchronous convulsion. Stimulation of the contralateral homotopic mesial cortical site readily produced afterdischarge that remained localized and convulsive seizure development did not occur. The findings suggest that (a) the frontal lobe plays an important role in the generation of nonconvulsive seizures, (b) the frontorolandic cortex plays a unique role in convulsive seizure generalization, (c) the role of the intrinsic (genetic) factor is significant in determining the quality of the kindled seizure, and (d) the development of focal epileptogenesis at one MF site interferes with clinical seizure development at the "mirror focus." Our findings underscore (a) the necessity of the conceptual differentiation between the EEG mirror focus and the epileptogenic focus capable of generating clinical seizures and (b) the importance of dissecting interictal behavior reflecting a "continuous disorder of neuronal function," which may cause symptoms other than seizures.

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We report the rare of occurrence of a medullary venous malformation (MVM) with an arterial component associated with a saccular aneurysm on the opposite side. This 49-year-old male patient was admitted with headache and vomiting. He was diagnosed as having a subarachnoid hemorrhage on the basis of bloody cerebrospinal fluid. Angiography revealed a saccular aneurysm at the junction of the internal carotid and posterior communicating arteries on the left side. A MVM with an arterial component was also seen in the right basal frontal lobe. On the seventh hospital day, the aneurysm was clipped via a left frontotemporal craniotomy. The postoperative course was uneventful. There are many hypotheses concerning cerebral aneurysms; some are thought to derive from persistent primitive arteries in the early fetal period. On the other hand, MVM is thought to be intimately related to arteriovenous malformation, which is believed to develop from the premordial vascular plexus, also in early fetal life.