Abstracts

Rationale: The main purpose of this study is to explore the role of post-ictal generalized EEG suppression (PGES) as a marker of increased risk for sudden unexpected death in epilepsy (SUDEP). In a previously published study, longer PGES duration was found in SUDEP cases compared with living patients who served as controls (1). However, another study directly contradicts this finding, with no difference in PGES between the two groups (2). We compared the duration and association with seizure type of PGES in patients who died from SUDEP with living control patients. In addition, we explored the role of nursing intervention on seizure and PGES duration.Methods: We reviewed 77 total seizures (30 non-convulsive NCS, 47 convulsive seizures CS) in 17 confirmed and probable SUDEP patients and 228 total seizures (142 NCS, 86 CS) from living control patients’ video-EEG recorded between 1992 and 2014. Video EEG was reviewed for presence and duration of PGES, total seizure duration and for control patients with CS: time from seizure onset to first intervention (tactile stimulation, oxygen delivery, suction).Results: Median follow up was significantly longer in living control patients than in SUDEP (1114.1 vs 681 days, Mann-Whitney U test p =0.02). The proportion of PGES after all seizures was not significantly higher in the SUDEP group compared to living controls (20% vs 17% Fisher’s exact, p=0.61). The mean duration of PGES in SUDEP patients was less than 50% of that seen in living controls (22.7 vs 56.2 s, Mann Whitney U test p < 0.001). PGES was observed only after GTCs (40.6% of all GTCs). Nurses intervened in 36 (93%) of the GTCs reviewed, on average 57.4 s after seizure onset. Sooner intervention was associated with shorter total seizure duration (Spearman’s r =0.75 p <0.001). PGES was an inconsistent finding in an individual, seen after all seizures in 10 (43.4%) of 23 patients with multiple CS. PGES consistency was not seen in people with more than 2 recorded CS.Conclusions: We found that PGES is only seen after CS and the duration of PGES after CS is significantly shorter in SUDEP patients compared to living controls, in contrast to prior data. Our data suggests that prolonged PGES cannot be used as a reliable independent marker of increased SUDEP risk. However, the presence of PGES is strongly associated with GTC, which is associated with increased risk for SUDEP. Prompt intervention shortens GTCs duration and may have a protective effect. Further prospective studies are needed to explore the electro-clinical risk factors and markers of SUDEP.