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Mechanisms of Action of Antiseizure Medications: Targeting the Excitation–Inhibition Balance
Epileptic seizures arise from a disruption of the delicate balance between neuronal excitation and inhibition. Contemporary antiseizure medications (ASMs) exert their therapeutic effects through diverse molecular targets, including voltage-gated sodium and calcium channels, synaptic vesicle protein 2A (SV2A), GABAergic neurotransmission, and glutamatergic receptors (AMPA and NMDA).
This schematic illustrates the principal mechanisms by which ASMs modulate neuronal excitability: enhancing inhibitory GABAergic signaling (e.g., benzodiazepines, barbiturates, vigabatrin, tiagabine), reducing excitatory glutamatergic transmission (e.g., perampanel, felbamate, topiramate), inhibiting voltage-gated ion channels (e.g., phenytoin, carbamazepine, lacosamide, lamotrigine), or regulating synaptic vesicle release via SV2A binding (e.g., levetiracetam, brivaracetam).
Understanding these pharmacodynamic pathways is essential for rational drug selection, optimization of combination therapy, and the development of precision-based approaches in epilepsy management.
References
1. Schmidt D, Schachter SC. Drug treatment of epilepsy in adults. BMJ. 2014;348:g2546.
06/06/2026
