Clinical and experimental data hints that prolonged and repeated epileptic seizures can lead to molecular, biochemical, metabolic, and structural changes in the brain, a continuous process of chronic brain injury that ultimately leads to neuronal death. The histological characteristics of hippocampal structure determine its high sensitivity to excitotoxicity and present different types of neuronal death, including apoptosis, necroptosis, autophagy, pyroptosis, and ferroptosis. Hippocampal neuronal death promotes the progression of epileptogenesis, seizures, and epilepsy and is closely related to the impairment of cognitive function. Massive evidence indicates that oxidative stress plays a critical role in different forms of neuronal death induced by epileptic seizures. The brain is particularly vulnerable to damage caused by oxidative stress, and an increase in oxidative stress biomarkers was found in various epilepsy types. The purpose of this review is to elucidate the molecular mechanism of neuronal death and explore the moderating effect of oxidative stress on epileptic seizure-induced neuronal death patterns so as to find potential intervention targets for neuroprotective treatment after epileptic seizures.