Authors :
Presenting Author: Shelly Degani Schwalm, MD – Rabin Medical Center
Nir Cafri, PhD – Tel-Aviv University
felix Benninger, MD – Felsenstein Medical Research Center, Rabin Medical Center
Oded Schor, PhD – Felsenstein Medical Research Center
Rationale:
Cenobamate (CNB) is a third-generation anti-seizure medication with a dual mechanism—positive allosteric modulation of GABA-A receptors and selective enhancement of the inactivated state of voltage gated Na+ channels yielding robust anti-seizure efficacy in drug resistant focal epilepsy. Yet Its EEG-level pharmacodynamic effects remain under-characterized, especially for paroxysmal slow-wave events (PSWEs), transient cortical slow bursts linked to disease burden and post-first-seizure epilepsy risk. We hypothesized that CNB would reduce PSWE burden and interictal epileptiform discharge (IED) rates on routine scalp EEG.
Methods:
Single-center retrospective intraindividual comaprison study. Adults (≥18 y) who initiated CNB and had ≥1 scalp EEG within pre-CNB and another post-CNB were included. EEG preprocessing (0.5–40 Hz) and automated PSWE detection followed the original algorithm.
Results:
Primary outcome: change in PSWE events/min between last pre-CNB and first post-CNB EEG. Secondary outcomes: change in IEDs/min and correlation of EEG changes with clinical seizure-frequency reduction. Paired Wilcoxon tests evaluated within-subject differences; negative-binomial models summarized seizure counts.
97 CNB-treated adults screened and met the EEG criteria. Early signals suggest CNB reduces PSWE burden and IED rates on routine scalp EEG, with effect sizes that appear to track clinical improvement
Conclusions:
If confirmed in the full cohort, ΔPSWE may serve as a practical pharmacodynamic biomarker to monitor CNB response alongside seizure counts.
Funding: no