Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2018 May 15;15(1):144.
doi: 10.1186/s12974-018-1192-7.

The role of inflammation in the development of epilepsy

Affiliations
Review

The role of inflammation in the development of epilepsy

Amna Rana et al. J Neuroinflammation. .

Abstract

Epilepsy, a neurological disease characterized by recurrent seizures, is often associated with a history of previous lesions in the nervous system. Impaired regulation of the activation and resolution of inflammatory cells and molecules in the injured neuronal tissue is a critical factor to the development of epilepsy. However, it is still unclear as to how that unbalanced regulation of inflammation contributes to epilepsy. Therefore, one of the goals in epilepsy research is to identify and elucidate the interconnected inflammatory pathways in systemic and neurological disorders that may further develop epilepsy progression. In this paper, inflammatory molecules, in neurological and systemic disorders (rheumatoid arthritis, Crohn's, Type I Diabetes, etc.) that could contribute to epilepsy development, are reviewed.Understanding the neurobiology of inflammation in epileptogenesis will contribute to the development of new biomarkers for better screening of patients at risk for epilepsy and new therapeutic targets for both prophylaxis and treatment of epilepsy.

Keywords: Blood–brain barrier (BBB) breakdown; Epileptogenesis; Inflammation; Neurological disorders; Systemic inflammatory disorders.

PubMed Disclaimer

Conflict of interest statement

Ethics approval and consent to participate

Not applicable.

Competing interests

The authors declare that they have no competing interests.

Publisher’s Note

Springer Nature remains neutral with regard to jurisdictional claims in published maps and institutional affiliations.

Figures

Fig. 1
Fig. 1
Sources and targets of unregulated and overlapped components of inflammation in epileptogenesis. Brain injury induces central inflammation and aberrant neuronal connectivity within the hippocampus. Systemic inflammatory disorders generate peripheral inflammation which can further contribute to the buildup of inflammatory mediators. Peripheral and central inflammation 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 and further upregulates inflammatory mediators. Unregulated peripheral and central inflammation and breakdown of the blood–brain barrier lead to morphological synaptic changes within the hippocampus and ultimately, the development of epilepsy

References

    1. Laxer K, Trinka E, Hirsch L, et al. The consequences of refractory epilepsy and its treatment. Epilepsy Behav. 2014;37:59–70. - PubMed
    1. Rakhade SN, Jensen FE. Epileptogenesis in the immature brain: emerging mechanisms. Nat Rev Neurol. 2009;5(7):380. - PMC - PubMed
    1. Chung S. Febrile seizures. Korean J Pediatr. 2014;57(9):384–395. - PMC - PubMed
    1. Musto A, Gjorstrup P, Bazan N. The omega-3 fatty acid-derived neuroprotectin D1 limits hippocampal hyperexcitability and seizure susceptibility in kindling epileptogenesis. Epilepsia. 2011;52(9):1601–1608. - PubMed
    1. Walker LE, Janigro D, Heinemann U, Riikonen R, Bernard C, Patel M. WONOEP appraisal: molecular and cellular biomarkers for epilepsy. Epilepsia. 2016;57:1354–1362. - PMC - PubMed

MeSH terms

Substances