Pathophysiology

Epilepsy’s pathophysiology is complex, primarily characterized by neuronal hyperexcitability and hypersynchronization. The intricate mechanisms behind this neurological disorder involve several key factors:

– Neuronal Hyperexcitability:

    – Enhanced predisposition of neurons to depolarize and discharge upon stimulation.

    – Alterations in ion channels like K+, Na+, Ca2+, and Cl− play a significant role.

    – Medications targeting these ion channels, such as carbamazepine, phenytoin, and benzodiazepines, validate their role in epilepsy.

– Genetic Factors:

    – Mutations in ion channels are linked to various types of epilepsies.

    – These genetic changes lead to distinct characteristics among different genetic epilepsies.

– Epileptogenesis and Neuronal Networks:

    – Alterations in vesicle trafficking and neurotransmitter release contribute to the disease.

    – Targeting of synaptic vesicle protein 2A (SV2A) by certain ASMs.

    – Changes in neurotransmitter systems, exemplified by the mechanism of vigabatrin.

– Neuronal Synchronization and Epileptiform Activity:

    – Synchronization of excessive neuronal firing is necessary for seizure generation.

    – Specific brain regions, like the hippocampus, neocortex, and thalamus, are prone to epileptiform activity.

    – Modifications in the ratio and function of inhibitory circuits in these areas are critical in promoting epileptogenesis.