Abstracts

Rationale: The post ictal generalized EEG suppression is seen after an event of the secondary generalized seizure. During the suppression phase, electrocortical activities are diffusely attenuated while the exact mechanism has not been completely elucidated. The observation of the post-ictal suppression is comparable with pharmacologically induced EEG suppression by mesohextal in which inhibitory GABA activity is excessively emphasized. In the mesohextal suppression, the most potent epileptogenic focus will come back first in suppression phase, and it identifes the primary epileptogenic focus. We report that observation of emerging DC current shift in post-ictal suppression phase recorded in subdural grid recording. Methods: We encountered a case of intractable seizure with daily aura and frontal disinhibiting symptoms due to congenital right hemispheric stroke and encephalomalacia. This 23 year old woman had phase I evaluation in which there was no IID in non-invasive recording. In the phase II evaluation, subdural grid electrodes were placed in temporal neocortex, perisyluvian, prefrontal and orbitofrontal on the pathologic non-dominant hemisphere. Multiple IID foci were identified in temporal lobe but the primary epileptogenic zone was not clear. The patient experienced a secondary generalized seizure attack and post-ictal suppression, which revealed several noteworthy findings which resulted in successful surgical intervention. Results: Multi-focal interinctal discharges is the baseline description of the interictal subdural grid recordings. The post-ictal generalized suppression was induced by a seizure originating from perisylvian posterior frontal neocortical seizure. During the suppression phase, the first time of the reemerging ictal phenomena was not sharp acivity but DC current shift in orbito-frontal cortex, which propagated posteriorly and induced high amplitude spike epileptiform discharges in the temporal neocortex with 0.7 second latency. Subsequently, resection of the orbito-frontal lobe and temporal lobe were resected. The patient subsequently became seizure free and mood swing symptom has disappeared. Conclusions: These clinical findings suggests (1) DC current shift in the post-ictal suppression may be useful indicator of ictogenic cortex, (2) DC current shift may induce epileptiform discharges in remote cortex which suggests inerhemispheric connections, and (3) virulent focus comes back first in post-ictal suppression that is comparable with the mesohextal suppression test. The returning activity could be DC current shift from irritable cortex outside of the epileptogenic cortex. It is suspected that DC current shift is more resistant to the mechanism of post-ictal suppression than epileptiform discharges.