Chapter 10 - Inflammation and epilepsy
Section snippets
Clinical evidence
Clinical evidence supporting a role for inflammation in tissue epileptogenicity stems from three main findings. (1) Various markers of inflammation have been measured in epileptogenic tissue from surgically treated pharmacoresistant patients, namely in malformations of cortical development (ganglioglioma, neuroepithelial tumors, focal cortical dysplasia, tuberous sclerosis) (Maldonado et al., 2003, Ravizza et al., 2006a, Boer et al., 2008), in temporal lobe epilepsy with hippocampal sclerosis (
Experimental studies
The experimental studies addressed three main questions related to: (1) the causes of brain inflammation with a special focus on the involvement of seizures, cell death, or their association as triggering factors; (2) the possibility that a proinflammatory state in the brain can precipitate or predispose to seizures; (3) whether pharmacological or genetic interference with specific inflammatory pathways in the brain can modify seizure frequency or duration, neuronal survival, and
Concluding remarks
The hypothesis that brain inflammation is a significant contributor to seizures and their detrimental consequences, such as neuronal cell loss and BBB damage, is strongly supported by experimental findings and corroborated by clinical observations. Recent findings suggest that chronic inflammation may also contribute to epileptogenesis, thus predisposing the brain to the development of recurrent seizures. Ravizza et al., 2011 Importantly, several inflammatory mediators act as transcriptional
Acknowledgments
The authors thank all colleagues who collaborated with them to originate some of the data described in this chapter, in particular Dr. T.Z. Baram, Dr. E. Aronica, Dr. T. Bartfai, Dr. S.L. Moshé, Dr. B. Viviani, and Dr. M.G. De Simoni. They also thank their sources of support: Dana Foundation, Negri-Weizmann Foundation, Epicure (LSH-CT-2006-037315).
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