Seizures and risk of epilepsy in anti-NMDAR, anti-LGI1, and anti-GABABR encephalitis

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Abstract

Background: Accumulating data have suggested seizures occur frequently in patients with neuronal surface antibody-mediated autoimmune encephalitis. We aimed to evaluate seizure outcomes and potential factors associated with the development of epilepsy in patients with anti-N-methyl-D-aspartate receptor (NMDAR), anti-leucine-rich glioma-inactivated 1 (LGI1), and anti-gamma-aminobutyric-acid B receptor (GABABR) encephalitis. Methods: Patients with anti-NMDAR, anti-LGI1, and anti-GABABR encephalitis were prospectively recruited from 2014 to June 2019, with a median follow-up period of 30.5 months (range 8–67 months). Seizure outcomes were assessed and risk factors of epilepsy were analyzed. Results: A total of 119 patients with anti-NMDAR, anti-LGI1, and anti-GABABR encephalitis were included, and 83 (69.7%) of them developed new-onset seizures. By the end of follow-up, 17 (21.3%) of 80 patients had seizure relapses after intermittent seizure remission or exhibited uncontrolled seizure episodes, contributing to epilepsy. Immunotherapy delay and interictal epileptic discharges (IEDs) were identified to be associated with the development of epilepsy in patients with anti-NMDAR, anti-LGI1, and anti-GABABR encephalitis, particularly anti-NMDAR encephalitis. Furthermore, multivariate logistic regression analysis demonstrated that immunotherapy delay was an independent predictor for epilepsy. Conclusion: Our study suggested that immunotherapy delay and IEDs were associated with the development of epilepsy in patients with anti-NMDAR, anti-LGI1, and anti-GABABR encephalitis. Early diagnosis and treatment were required, and particular consideration should be given to patients with these risk factors.

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Shen, C. H., Fang, G. L., Yang, F., Cai, M. T., Zheng, Y., Fang, W., … Ding, M. P. (2020). Seizures and risk of epilepsy in anti-NMDAR, anti-LGI1, and anti-GABABR encephalitis. Annals of Clinical and Translational Neurology, 7(8), 1392–1399. https://doi.org/10.1002/acn3.51137

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