The role of inflammation in epilepsy

A Vezzani, J French, T Bartfai, TZ Baram - Nature reviews neurology, 2011 - nature.com
Nature reviews neurology, 2011nature.com
Epilepsy is the third most common chronic brain disorder, and is characterized by an
enduring predisposition to generate seizures. Despite progress in pharmacological and
surgical treatments of epilepsy, relatively little is known about the processes leading to the
generation of individual seizures, and about the mechanisms whereby a healthy brain is
rendered epileptic. These gaps in our knowledge hamper the development of better
preventive treatments and cures for the≈ 30% of epilepsy cases that prove resistant to …
Abstract
Epilepsy is the third most common chronic brain disorder, and is characterized by an enduring predisposition to generate seizures. Despite progress in pharmacological and surgical treatments of epilepsy, relatively little is known about the processes leading to the generation of individual seizures, and about the mechanisms whereby a healthy brain is rendered epileptic. These gaps in our knowledge hamper the development of better preventive treatments and cures for the ≈30% of epilepsy cases that prove resistant to current therapies. Here, we focus on the rapidly growing body of evidence that supports the involvement of inflammatory mediators—released by brain cells and peripheral immune cells—in both the origin of individual seizures and the epileptogenic process. We first describe aspects of brain inflammation and immunity, before exploring the evidence from clinical and experimental studies for a relationship between inflammation and epilepsy. Subsequently, we discuss how seizures cause inflammation, and whether such inflammation, in turn, influences the occurrence and severity of seizures, and seizure-related neuronal death. Further insight into the complex role of inflammation in the generation and exacerbation of epilepsy should yield new molecular targets for the design of antiepileptic drugs, which might not only inhibit the symptoms of this disorder, but also prevent or abrogate disease pathogenesis.
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