Mechanism of action
Lamotrigine acts primarily via a dose dependent blockade of voltage sensitive sodium channels in their slow inactivated state, thus stabilizing the presynaptic neuronal membrane inhibiting release of excitatory neurotransmitters mainly glutamate. Because of its preferential interaction with sodium channels is slow and inactivated state, it is expected to act selectively against sustained depolarization and high frequency discharges, characteristics of epileptic foci, while leaving normal electrophysiological activity unaffected.