Abstract
An insult to the brain (such as the first seizure) causes excitotoxicity, neuroinflammation, and production of reactive oxygen/nitrogen species (ROS/RNS). ROS and RNS produced during status epilepticus (SE) overwhelm the mitochondrial natural antioxidant defense mechanism. This leads to mitochondrial dysfunction and damage to the mitochondrial DNA. This in turn affects synthesis of various enzyme complexes that are involved in electron transport chain. Resultant effects that occur during epileptogenesis include lipid peroxidation, reactive gliosis, hippocampal neurodegeneration, reorganization of neural networks, and hypersynchronicity. These factors predispose the brain to spontaneous recurrent seizures (SRS), which ultimately establish into temporal lobe epilepsy (TLE). This review discusses some of these issues. Though antiepileptic drugs (AEDs) are beneficial to control/suppress seizures, their long term usage has been shown to increase ROS/RNS in animal models and human patients. In established TLE, ROS/RNS are shown to be harmful as they can increase the susceptibility to SRS. Further, in this paper, we review briefly the data from animal models and human TLE patients on the adverse effects of antiepileptic medications and the plausible ameliorating effects of antioxidants as an adjunct therapy.
Highlights
Epilepsy is a serious neurological disorder manifested by recurrence of unprovoked seizures resulting in devastating effects on patients and the caregivers
We provide the information from animal models and human patients on the harmful role of ROS/RNS that are generated as a consequence to seizure and discuss the role of gliosis, adverse effects of antiepileptic drugs (AEDs), and potential benefits of antioxidant supplements in temporal lobe epilepsy (TLE)
Oxidative stress plays a key role in epileptogenesis after the first seizure
Summary
Epilepsy is a serious neurological disorder manifested by recurrence of unprovoked seizures resulting in devastating effects on patients and the caregivers. Depending on the severity of the first insult, a varying period of latent period was reported during which a cascade of neurobiological changes takes place These neurobiological changes culminate in the development of spontaneous recurrent seizures (SRS) resulting from synaptic reorganization into hyperexcitable and hypersynchronous neural networks [4]. Considering the severe brain pathology associated with generalized convulsive SE, any seizure lasting for more than 5 min is treated as an emergency in clinics [6, 7]. It has been reported that some patients show nonconvulsive SE where EEG abnormalities are associated with impairment of consciousness that lasts at least 30 min without any obvious convulsive seizures [8]. We provide the information from animal models and human patients on the harmful role of ROS/RNS (reactive oxygen species/reactive nitrogen species) that are generated as a consequence to seizure and discuss the role of gliosis, adverse effects of AEDs, and potential benefits of antioxidant supplements in TLE
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