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Abstract
Epilepsies bearing some relationship to infections or vaccinations are often encountered clinically. While the onset of epilepsy or aggravation of seizures may follow common infections or vaccinations, complete seizure control has also been observed after infections. However, the true mechanisms underlying the relationship between infections and epilepsies have not been fully elucidated. Recently, advances in immunology have contributed to the study of autoimmune mechanisms in Rasmussen‘s syndrome, a prototype of autoimmune epilepsy related to infections. The roles of autoimmunity, including cytotoxic T cells and autoantibodies against neural molecules, have been demonstrated in Rasmussen‘s syndrome. This review postulates the probable molecular mimicry of microbial and neural components in Rasmussen‘s syndrome and proposes possible autoimmune mechanisms related to the development of symptomatic epilepsies.
Acknowledgements
The author thanks Masayoshi Mishina and Hisashi Mori for their helpful comments, and Shigeko Nishimura and Hisano Tsunogae for technical assistance. This study was funded in part by Research Grants (16A-3) for Nervous and Mental Disorders from the Ministry of Health, Labor and Welfare, grants-in-aid for Scientific Research I No. 15591151, 16590859 and 17591133, Health and Labour Sciences Research Grants for Research on Psychiatry and Neurological Diseases and Mental Health (H17–017) and Research on Children and Families (H16–016) and grants from The Japan Epilepsy Research Foundation.