Epileptic seizures result from excessive discharge in a population of hyperexcitable neurons. Excessive production of ROS (reactive oxygen species) is thought to contribute to epilepsy, and there is a potential connection between ROS and mitochondrial dysfunction in epilepsy. Free radical generation can also induce seizure activity by direct activation of glutamine synthatase, thereby permitting an abnormal buildup of glutamic acid, the excitatory neurotransmitter. The brain is extremely susceptible to oxidative damage induced by these ROS because it generates extremely high levels of ROS due to its very high aerobic metabolism and blood perfusion, and it has a relatively poor enzymatic antioxidant defense. Recent research on vitamin C (ascorbic acid, or ascorbate) has pointed out novel mechanisms of its action such as that of neuromodulator in addition to its well-known antioxidant activity. In the current study, I review the dose-dependent effects of ascorbate in intracellular signaling pathways of oxidative stress in epilepsy, focusing on its modulation of neuronal survival. I also focus on ascorbic acid deficiency and treatments in intracellular signaling pathways in the brain as well as in dietary requirements, and I discuss the effects of antiepileptic drugs on plasma ascorbate levels. I conclude with a note on the putative protective role of vitamin C in the neurodegenerative process as well as in epileptic diseases.