Ongoing intracortical neural activity predicts upcoming interictal epileptiform discharges in human epilepsy.

ABSTRACT

Interictal epileptiform discharges (IEDs) are a hallmark of focal epilepsies. Most previous studies have focused on whether IED events increase seizure likelihood or, on the contrary, act as a protective mechanism. Here, we study instead whether IED events themselves can be predicted based on measured ongoing neural activity. We examined local field potentials (LFPs) and multi-unit activity (MUA) recorded via intracortical 10 × 10 (4 × 4 mm) arrays implanted in two patients with pharmacologically resistant seizures. Seizures in one patient (P1) were characterized by low-voltage fast-activity (LVFA), and IEDs occurred as isolated (100 - 200 ms) spike-wave events. In the other patient (P2), seizures were characterized by complex spike-wave discharges (2 - 3 Hz) and IEDs consisted of bursts of ~ 2 - 3 spike-wave discharges each lasting ~ 300 - 500 ms. We used extreme gradient boosting (XGBoost) classifiers for IED prediction. Inputs to the classifiers consisted of LFP power spectra; In addition, counts of MUA (1-ms and 100-ms time bins) and envelope, as well as leading eigenvalues/eigenvectors of MUA correlation matrices were used as features. Features were computed from moving short-time windows (1 second) immediately preceding IED events (0.3 - 0.5 preictal gap). Classifiers allowed successful IED prediction in both patients, with better results in the case of IED occurring in the LVFA case (area under ROC curve 0.86). In comparison, LFP features performed comparatively for P1 datasets, while MUA appeared not predictive in the case of P2. Our preliminary results suggest that features of ongoing activity, predictive of upcoming IED events, can be identified based on intracortical recordings, and warrant further investigation in larger datasets. We expect this type of prediction analyses to contribute to a better understanding of the mechanisms underlying the generation of IED events and their contribution to seizure onset.