Localization of the epileptogenic network from scalp EEG using a patient-specific whole-brain model

Computational modeling is a key tool for elucidating the neuronal mechanisms underlying epileptic activity. Despite considerable progress, existing models often lack realistic accuracy in representing electrophysiological epileptic activity. In this study, we used a comprehensive human brain model based on a neural mass model, which is tailored to the layered structure of the neocortex and incorporates patient-specific imaging data. This approach allowed the simulation of scalp EEGs in an epileptic patient suffering from type 2 focal cortical dysplasia (FCD). The simulation specifically addressed epileptic activity induced by FCD, faithfully reproducing intracranial interictal epileptiform discharges (IEDs) recorded with electrocorticography. For constructing the patient-specific scalp EEG, we carefully defined a clear delineation of the epileptogenic zone by numerical simulations to ensure fidelity to the topography, polarity, and diffusion characteristics of IEDs. This nuanced approach improves the accuracy of the simulated EEG signal, provides a more accurate representation of epileptic activity, and enhances our understanding of the mechanism behind the epileptogenic networks. The accuracy of the model was confirmed by a postoperative reevaluation with a secondary EEG simulation that was consistent with the lesion’s removal. Ultimately, this personalized approach may prove instrumental in optimizing and tailoring epilepsy treatment strategies.

This study aimed to create a neurophysiologically grounded computer model of focal epilepsy. This is a feature frequently lacking to simulations in this domain, making the translation from in silico to in vivo results questionable and difficult to understand for clinical electrophysiologists. We adapted a whole-brain neuronal mass model for EEG generation in various conscious states to replicate the EEG patterns of a type 2 focal cortical dysplasia (FCD), a condition associated with epilepsy. Our model successfully simulated both intracranial and scalp EEGs of a complex patient with type 2 FCD, who was later cured through surgery. Importantly, the simulated lesion location matched the patient’s epileptogenic zone, and removing this area in the model eliminated epileptic activity in the EEG, demonstrating the model’s accuracy.