Abstracts

Rationale: Increasing interest in the dynamics of the post-ictal state is motivated by the potential association of post-ictal generalized EEG suppression (PGES) and SUDEP. Localization of the epileptogenic zone may be another rationale for examining the post-ictal intracranially recorded EEG. A recent study of the dynamics of the post-ictal state using intracranial EEG recordings identified intracranial post-ictal attenuation (IPA) as a very common finding after bilateral tonic-clonic seizures (Bateman et al., 2019). Interestingly, Bateman et al also identified post-ictal increased gamma power - relative to the pre-ictal baseline - in association with IPA. This study aims to replicate these results, and demonstrate the connection, if any, with the seizure onset zone (SOZ). Methods: FBTCS are analyzed from patients undergoing presurgical evaluation with stereotactic EEG (S-EEG). Ictal and post-ictal clinical behaviors and EEG are characterized, with particular attention to the dynamics of the post-ictal state. The post-ictal EEG is evaluated for the presence of IPA - meeting the previously defined threshold of <= 50 (µV) peak-to-peak (Bateman et al., 2019) - and for gamma activity. Both IPA and gamma are correlated with post-ictal clinical findings and with ictal seizure localization. Results: IPA is identified in all 9 seizures from 6 patients undergoing S-EEG evaluation, though it did not always involve all electrodes. We confirm the previously established dynamics of the post-ictal state: IPA, followed by discontinuous slowing (DS), followed by continuous slowing (CS). In all seizures (n=9), IPA is associated with post-ictal immobilization. Resumption of motor activity correlates with discontinuous slowing. The SOZ region is involved in prolonged IPA in at least 6 seizures (67%). The presence of low amplitude (10-20µV) post-ictal gamma (25-80Hz), occurs in all seizures. The gamma activity appears shortly after the start of the post-ictal period, and is not always continuous, often occurring in brief bursts, lasting 2-3 seconds - even while IPA is sustained. Gamma activity does not appear specific to the SOZ, with a rather broad area of distribution involving cortical contacts. Gamma activity strongly correlates with IPA, only occurring during periods of attenuation. Gamma activity attenuates with transition to the burst phase of post-ictal discontinuous slowing (DS) -however tends to recur during periods of inter-burst attenuation.  Conclusions: IPA is present in most, but not all, S-EEG electrodes and correlates with post-ictal immobilization. While initial findings suggest a relationship between IPA duration and the SOZ, further cases need to be analyzed to confirm this relationship, which may facilitate localization of the SOZ in seizures with more diffuse onsets. We also replicate the presence of post-ictal gamma activity - an intermittent neocortical activity of uncertain significance. It could represent a resting cortical brain rhythm that is only active during periods of low cortical activity, as it attenuates with high amplitude slowing. It is doubtful as a manifestation of residual ictal activity as it is not clearly co-localized with the SOZ. One limitation of our study is that coverage is not of the whole brain, but rather of candidate seizure onset regions.  Funding: No funding