The active role of non-synaptic electromagnetic induction in modulating absence epilepsy: a kinetic modeling study.

We propose a novel computational model incorporating simplified representations of the basal ganglia, cortex, and thalamus (SGGCT network), and systematically investigate the regulatory and control mechanisms underlying typical absence seizures in the cortex under memristive electromagnetic induction. Spike-and-wave discharges (SWDs, 2-4 Hz), a hallmark of absence epilepsy, are successfully reproduced in the SGGCT model by modulating the coupling strengths of two excitatory output projections to the thalamic specific relay nuclei (SRN). Our findings highlight the critical role of both the direct glutamatergic cortico-pallidal and cortico-nigral pathways in seizure regulation, acting through distinct inhibitory routes: the globus pallidus interna (GPi)-SRN pathway and the GPi-thalamic reticular nucleus (TRN) pathway, respectively. The cortex emerges as a promising target for electrical stimulation to suppress SWDs. We observe that applying memristive electromagnetic induction to the cortex significantly reduces the parameter space conducive to SWDs generation. Furthermore, electromagnetic induction enhances the ability of basal ganglia pathways to inhibit SWDs. Specifically, electromagnetic induction can transform previously unsuppressible SWDs regimes into suppressible ones. It also alters the operational mode of basal ganglia pathways in controlling seizure dynamics. Notably, the suppression efficacy can be optimized by tuning the memristor's control parameters. These results provide computational evidence supporting the potential of electromagnetic induction as a neuromodulatory strategy, which might offer testable hypotheses for future clinical interventions in epilepsy treatment.