- Author:
Jieun CHOI
1
;
Sookyong KOH
Author Information
- Publication Type:Review ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
- Keywords: Epilepsy; childhood; steroid; cytokine; innate immunity; microglia; astrocytes
- MeSH: Animals; Blood-Brain Barrier; Chronic Disease; Encephalitis/genetics/immunology/metabolism/*pathology; Epilepsy/immunology/metabolism/*pathology/therapy; Gene Expression Regulation; Humans; Nervous System Diseases/immunology/pathology
- From:Yonsei Medical Journal 2008;49(1):1-18
- CountryRepublic of Korea
- Language:English
- Abstract: Inflammation is known to participate in the mediation of a growing number of acute and chronic neurological disorders. Even so, the involvement of inflammation in the pathogenesis of epilepsy and seizure-induced brain damage has only recently been appreciated. Inflammatory processes, including activation of microglia and astrocytes and production of proinflammatory cytokines and related molecules, have been described in human epilepsy patients as well as in experimental models of epilepsy. For many decades, a functional role for brain inflammation has been implied by the effective use of anti-inflammatory treatments, such as steroids, in treating intractable pediatric epilepsy of diverse causes. Conversely, common pediatric infectious or autoimmune diseases are often accompanied by seizures during the course of illness. In addition, genetic susceptibility to inflammation correlated with an increased risk of epilepsy. Mounting evidence thus supports the hypothesis that inflammation may contribute to epileptogenesis and cause neuronal injury in epilepsy. We provide an overview of the current knowledge that implicates brain inflammation as a common predisposing factor in epilepsy, particularly childhood epilepsy.