The role of free radical-mediated reactions in human neuropathology continues to attract significant interest.
Oxidative injury produced by free radicals may play a role in the initiation and progression of epilepsy and, therapies
aimed at reducing oxidative stress may ameliorate tissue damage and favorably alter the clinical course. The prevalence of
epilepsy increases with age, and mitochondrial oxidative stress is a leading mechanism of aging and age-related degenerative
disease, signifying a further involvement of mitochondrial dysfunction in seizure generation. Oxidative stress occurs
when the generation of reactive oxygen species in a system exceeds the body's ability to neutralize and eliminate them,
thus creating an imbalance or over abundance of free radicals. Therefore, it is imperative to maintain oxidative balance
and control in the brain, and this is tightly regulated by antioxidants. In the last two decades, there has been an explosive
interest in the role of antioxidants or neuroprotectants in clinical as well as experimental models of epilepsy. In this regard,
the present review is intended to discuss the current state of knowledge pertaining to neuroprotection in epileptic
conditions by employing diverse chemical agents including conventional as well as novel anti-epileptic drugs, and to
highlight the efficacy of distinct neuroprotective strategies for preventing or treating epilepsy.