Oxidative stress in epilepsy

ABSTRACT

Introduction: The brain is particularly susceptible to oxidative stress being the most aerobically active organ in the body due to its high metabolic demands. There is evidence that neuronal hyperexcitability and oxidative injury produced by an excessive production of free radicals may play a role in the initiation and progression of epilepsy. Understanding the role of oxidative stress in epileptogenesis is essential to delineate appropriate therapeutic strategies. Neuroprotectant or antioxidant compounds may exert positive effects when associated with antiepileptic drugs (AEDs).

Areas covered: This review aims to outline the current state of knowledge on the relationship between oxidative stress and epilepsy. The role of neuroprotectants in the therapeutic strategy to prevent or treating epilepsy is also discussed. PubMed/Medline database was searched for relevant articles on the relation between oxidative stress and epilepsy and on antioxidant strategies for epilepsy management.

Expert commentary: Therapeutic intervention with antioxidants may represent a key strategy to counteract the epilepsy-related neurodegenerative process. However, in spite of the incredible development of new drugs for epilepsy treatment, definitive evidence about the neuroprotective ability of the existing compounds is still lacking. Therefore, there is great need for clinical trials to evaluate new antioxidant compounds specifically on epileptic patients.

KEYWORDS:

• Epilepsy
• oxidative stress
• antiepileptic drugs
• antioxidants

Declaration of interest

The authors have no relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript. This includes employment, consultancies, honoraria, stock ownership or options, expert testimony, grants or patents received or pending, or royalties. Peer reviewers on this manuscript have no relevant financial or other relationships to disclose.

Additional information

Funding

This paper was not funded.