Joon Y Kang1, Amin H Rabiei2, Leslie Myint3, Maromi Nei2. 1. Johns Hopkins School of Medicine, United States. Electronic address: Jkang50@jhmi.edu. 2. Thomas Jefferson University Hospital, United States. 3. Department of Biostatistics, Johns Hopkins Bloomberg School of Public Health, United States.
Abstract
PURPOSE: Our objective was to determine the significance of PGES as a possible EEG marker of increased risk for SUDEP and explore factors that influence PGES. METHODS: We identified 17 patients who died due to definite or probable SUDEP and 52 living control patients with drug resistant focal epilepsy who underwent EEG monitoring and least one seizure recorded on EEG. We reviewed 305 seizures on EEG and when available, on video, for presence or absence of PGES, the duration of PGES immediately after seizure end, seizure type, state seizure occurred (sleep vs. wake), tonic duration and time from seizure onset to initial nursing intervention. We noted that majority (93% in SUDEP group and 83% living controls) with PGES had additional brief bursts of suppression. We measured the time from the end of seizure to end of last brief suppression to determine the time to final PGES. RESULTS: SUDEP patients had statistically significant shorter PGES duration compared to living controls (unadjusted: -32.8s, 95%CI[-54.5, -11.2], adjusted: -39.5s, 95% CI[-59.4, -19.6]). SUDEP status was associated with longer time to final PGES compare to living controls, but this was not statistically significant. Earlier nursing intervention was associated with shorter seizure duration. PGES occurred only after GCS. Time to nursing intervention, tonic duration or state did not have a statistically significant effect on PGES. CONCLUSIONS: PGES is an equivocal marker of increased SUDEP risk. Earlier nursing intervention is associated with shorter seizure duration and may play a role in reducing risk of SUDEP.
PURPOSE: Our objective was to determine the significance of PGES as a possible EEG marker of increased risk for SUDEP and explore factors that influence PGES. METHODS: We identified 17 patients who died due to definite or probable SUDEP and 52 living control patients with drug resistant focal epilepsy who underwent EEG monitoring and least one seizure recorded on EEG. We reviewed 305 seizures on EEG and when available, on video, for presence or absence of PGES, the duration of PGES immediately after seizure end, seizure type, state seizure occurred (sleep vs. wake), tonic duration and time from seizure onset to initial nursing intervention. We noted that majority (93% in SUDEP group and 83% living controls) with PGES had additional brief bursts of suppression. We measured the time from the end of seizure to end of last brief suppression to determine the time to final PGES. RESULTS: SUDEP patients had statistically significant shorter PGES duration compared to living controls (unadjusted: -32.8s, 95%CI[-54.5, -11.2], adjusted: -39.5s, 95% CI[-59.4, -19.6]). SUDEP status was associated with longer time to final PGES compare to living controls, but this was not statistically significant. Earlier nursing intervention was associated with shorter seizure duration. PGES occurred only after GCS. Time to nursing intervention, tonic duration or state did not have a statistically significant effect on PGES. CONCLUSIONS:PGES is an equivocal marker of increased SUDEP risk. Earlier nursing intervention is associated with shorter seizure duration and may play a role in reducing risk of SUDEP.
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