The Role of Neuroinflammation in Pathogenesis of Epilepsy

Inflammation is a biological response of the immune system that can be mediated by different factors, such as pathogens, damaged cells and toxic compounds. These factors may induce acute and/or chronic inflammatory responses in the heart, pancreas, liver, kidney, lung, intestinal tract, reproductive system and brain potentially leading to tissue damage or disease. Immune and inflammatory reactions occur in brain invarious central nervous system (CNS) diseases such as depression, autism, schizophrenia, anxiety and epilepsy. Materials and Methods: In this review abstract, Scopus, PubMed, Science Direct and Google Scholar databases were searched for inflammation, seizure, epilepsy, brain, nervous system, neuroinflammation key words from 2015 to 2018. Results: Studies have shown that neuroinflammation is inflammation of the nervous tissue. It may be initiated in response to a variety of cues, including infection, traumatic brain injury, toxic metabolites, or autoimmunity. Since epilepsy, a neurological disease characterized by recurrent seizures, is often associated with a history of previouslesions in the nervous system. Impaired regulation of the activation and resolution of inflammatory cells and molecules in the injured neuronal tissue such as elevated IL-1β, TNF-α, IL-6 transcript levels are critical factors to the development of epilepsy. Also, bloodbrain barrier breakdown, EP2-COX2 upregulation and TLR pathways are important in this phenomenon.Conclusion: Peripheral and central inflammations allow for the breakdown of the blood–brain barrier due to the upregulation of inflammatory mediators, BBB breakdown permits leukocyte infiltration which generates neuronal hyper-excitability.