Abstract
The epilepsies are a heterogeneous group of disorders characterized by the propensity to experience spontaneous recurrent seizures. Epilepsies can be genetic or acquired, and the underlying mechanisms of seizure initiation, seizure propagation, and comorbid conditions are incompletely understood. Metabolic changes including the production of reactive species are known to result from prolonged seizures and may also contribute to epilepsy development. In this review, we focus on the evidence that metabolic and redox disruption is both cause and consequence of epileptic seizures. Additionally, we discuss the promise of targeting redox processes as a therapeutic option in epilepsy.
Highlights
IntroductionEpilepsy is the fourth most common neurological condition, affecting approximately 65 million people worldwide [1]
Epilepsy is the fourth most common neurological condition, affecting approximately 65 million people worldwide [1]. It is a complex spectrum of disorders defined by the tendency to experience abnormal, highly synchronous brain activity known as a seizure
Epilepsy syndromes that are associated with genetic mutations are relatively rare, representing only a small fraction of all cases; this number is likely to increase as genetic testing becomes more commonplace
Summary
Epilepsy is the fourth most common neurological condition, affecting approximately 65 million people worldwide [1]. It is a complex spectrum of disorders defined by the tendency to experience abnormal, highly synchronous brain activity known as a seizure. Available therapeutics include those that target ion channels or neurotransmitter systems [2]. These types of medications are effective at controlling seizure activity in about 60% of people with epilepsy but provide merely symptomatic relief, are ineffective in roughly 40% of people, and have the potential to exacerbate comorbidities [2,3]. We will discuss the evidence suggesting the role of metabolic and redox alterations in genetic and acquired epilepsies
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