Epilepsy is the most common neurological illness, with about 50 million people suffering from it globally. The disorder might be caused by a hereditary predisposition or acquired as a result of an acute insult that alters cellular and molecular pathways. Hyperexcitability is a result of an imbalanced state in which increased excitatory glutamatergic and decreased inhibitory GABAergic signalling is thought to be responsible for seizures-related damage, according to the latest and current knowledge in regard to the mechanisms underlying molecular and cellular change. However, the role of neurodegeneration in epileptogenesis is becoming more widely recognised. GABAergic neuronal and receptor modifications, neuroinflammation, axonal transport changes, oxidative stress, excitotoxicity, and other cellular and functional changes are all at the forefront of neurodegenerative changes during epileptogenesis. Vitamin E as an antioxidant, anti-inflammatory, and neuroprotective agent may show to be one of the therapeutic options beneficial in the treatment of epilepsy. We analyse and debate seizure-induced events as a link for the development of epilepsy's neurodegenerative and pathological repercussions in this paper. We also provided an overview of the possible use of vitamin E therapy in the treatment of epilepsy.
