Ephaptic conduction in tonic–clonic seizures

Abstract

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ObjectivesElectroencephalograms (EEGs) or multi-unit activities (MUAs) of tonic–clonic seizures typically exhibit a distinct structure. After a preliminary phase (DC shift, spikes), the tonic phase is characterized by synchronized activity of numerous neurons, followed by the clonic phase, marked by a periodic sequence of spikes. However, the mechanisms underlying the transition from tonic to clonic phases remain poorly understood.MethodsWe employ a simple two-dimensional cellular automaton model to simulate seizure activity, specifically focusing on replicating the tonic–clonic transition. This model effectively illustrates the physical processes during the ictal phase and, more importantly, differentiates the roles of neurons’ activity, identifying their origin as either synaptic or ephaptic.ResultsOur model reveals an intriguing interaction between the synaptic and ephaptic modes of action potential wave conduction. By replicating the EEG and multi-unit activity (MUA) structure of a tonic–clonic seizure and comparing it with real MUA data, we validate the model’s underlying assumption: the transition from tonic to clonic phases is driven by a shift in dominance from synaptic to ephaptic conduction. During synaptic-mode control, neural conduction occurs through synaptic transmission involving chemical substances, while in the ephaptic mode, information transfer occurs through direct Ohmic conduction.SignificanceGaining a deeper understanding of the neuronal electrical conduction transitions during tonic–clonic seizures is crucial for improving the treatment of this debilitating condition.

Keywords

• ephaptic
• tonic–clonic
• seizures
• EEG
• cellular automaton (CA)