Abstracts

Rationale: Ictal asystole (IA), defined as RR interval greater than 3 sec, is a rare event during VEEG monitoring estimated to occur with an incidence of 0.22-0.4%. It is a malignant condition as it predisposes to severe traumas from falls. IA is thought to occur when the epileptic discharges interferes with the central autonomous system (mesial temporal, insula, cingular and medial prefrontal cortex). However, the intracranial data confirming this theory is scarce due to the rarity of cases. Only two cases with bitemporal implantation and IA have been reported and just one with concomitant insular and mesial temporal electrodes, disposed unilaterally. Our objective is to describe the intracranial activity leading to IA observed in a bitemporal-biinsular exploration from our surgical series. Methods: DG is a 32 years old, right handed, patient suffering from drug resistant epilepsy since the age of 19. She describes focal seizures with a retrosternal aura, aphasia, loss of consciousness, vegetative signs and postictal amnesia, sometimes accompanied by a hypotonic fall. During the VEEG a typical seizure was recorded with a left basal temporal onset followed by a rapid bilateralisation correlated with tachycardia then by bradycardia and 9 sec asystole. As a result a ventricular cardiac pacemaker was implanted to prevent the falls. The 3T IRM revealed a left hippocampal sclerosis and the PET and ictal SPECT were also concordant with an anterior left temporal focus. An invasive exploration was planned due to bilateral EEG abnormalities, ictal amnesia and early aphasia with a rapid EEG ictal bilateralisation. A SEEG with bilateral temporal asymmetric (favoring the left) implantation was performed including electrodes in the left anterior and right middle insular cortex (Fig. 1). Results: 4 seizures were recorded during SEEG with an ictal onset in the left hippocampus. An ictal bradycardia (IB) trigging the pacemaker was recorded (Fig. 2). Its start corresponds to a low voltage fast activity (LVFA) in the infero-anterior left insula synchronized with a widespread LVFA in the left temporal pole, amygdala and hippocampus. The diffusion in the right mesial structures was correlated with the late phase of the IB but was not compulsory for its maintenance as in the seizure 3, IB it was not linked to a significant right spread. The electrodes located in the right insula were not involved. The patient is awaiting for a left temporal lobectomy. Conclusions: To our best knowledge this is the first case report with IA explored by bilateral temporal and insular sampling with depths electrodes. It expands the results of Catenoix et al. 2013 by involving the left antero-inferior insular cortex –first short gyrus (close to the amygdala) as a determinant of IA, along with ipsilateral temporal structures and the reported posterior long gyrus (not explored in this patient). It also confirms the hypothesis that contralateral temporal or insular spread is not necessary for producing this rare sign. Funding: No funding.