Relapsing Anti-NMDAR encephalitis with later detected MOG-IgG-Positive cortical encephalitis: a case report
- 1Department of Neurology, Tianjin Huanhu Hospital, Tianjin Key Laboratory of Cerebral Vascular and Neurodegenerative Diseases, Tianjin, China
Abstract
Background: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most common autoimmune encephalitis. Neuroimaging findings are frequently normal or nonspecific, and predominant cortical involvement at disease onset is uncommon in anti-NMDAR encephalitis. Overlap with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has been increasingly recognized; therefore, the value of individual reports lies in defining their longitudinal phenotypic evolution and diagnostic limitations.
Case presentation: We report a 28-year-old woman with relapsing anti-NMDAR encephalitis followed for nearly seven years across three episodes (the index attack and two relapses). The initial presentation in 2018 was typical anti-NMDAR encephalitis, with positive cerebrospinal fluid (CSF) anti-NMDAR antibodies and complete clinical remission after the first episode. The 2022 relapse manifested as focal cortical encephalitis with progressive unilateral cortical swelling, sulcal enhancement, and seizures; MOG-IgG was not tested. In 2025, she developed recurrent headache, intracranial hypertension, and extensive unilateral cortical involvement, with later detected serum MOG-IgG at 1:32. CSF anti-NMDAR and MOG-IgG were not tested at this admission. The episode was therefore adjudicated as MOG-IgG-positive cortical encephalitis within a longitudinal anti-NMDAR/MOGAD overlap course rather than a proven simultaneous dual-antibody relapse. Oral methylprednisolone was followed by clinical and radiological improvement.
Conclusions: Across nearly seven years, this case documents phenotypic evolution from CSF-confirmed anti-NMDAR encephalitis to recurrent unilateral cortical encephalitis and later serum MOG-IgG detection. A changing cortical phenotype should prompt renewed antibody assessment at each recurrence rather than reliance on the index antibody profile. Because MOG-IgG was not tested in earlier episodes and CSF anti-NMDAR was not tested in 2025, the timing and mechanistic contribution of each antibody cannot be determined.
Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12883-026-05217-5.
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BibTeX
@article{lu2026relapsing,
title = {{Relapsing Anti-NMDAR encephalitis with later detected MOG-IgG-Positive cortical encephalitis: a case report}},
author = {Yixiu Lu and Zhihong Zhao and Ziwei Song and Zikai Xin and Baiwei Liu and Zilong Zhu},
journal = {BMC Neurology},
year = {2026},
month = aug,
doi = {10.1186/s12883-026-05217-5},
url = {https://doi.org/10.1186/s12883-026-05217-5},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - JOUR
TI - Relapsing Anti-NMDAR encephalitis with later detected MOG-IgG-Positive cortical encephalitis: a case report
AU - Yixiu Lu
AU - Zhihong Zhao
AU - Ziwei Song
AU - Zikai Xin
AU - Baiwei Liu
AU - Zilong Zhu
PY - 2026
DA - 2026/08/11
JO - BMC Neurology
DO - 10.1186/s12883-026-05217-5
UR - https://doi.org/10.1186/s12883-026-05217-5
AB - Background: Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is the most common autoimmune encephalitis. Neuroimaging findings are frequently normal or nonspecific, and predominant cortical involvement at disease onset is uncommon in anti-NMDAR encephalitis. Overlap with myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) has been increasingly recognized; therefore, the value of individual reports lies in defining their longitudinal phenotypic evolution and diagnostic limitations. Case presentation: We report a 28-year-old woman with relapsing anti-NMDAR encephalitis followed for nearly seven years across three episodes (the index attack and two relapses). The initial presentation in 2018 was typical anti-NMDAR encephalitis, with positive cerebrospinal fluid (CSF) anti-NMDAR antibodies and complete clinical remission after the first episode. The 2022 relapse manifested as focal cortical encephalitis with progressive unilateral cortical swelling, sulcal enhancement, and seizures; MOG-IgG was not tested. In 2025, she developed recurrent headache, intracranial hypertension, and extensive unilateral cortical involvement, with later detected serum MOG-IgG at 1:32. CSF anti-NMDAR and MOG-IgG were not tested at this admission. The episode was therefore adjudicated as MOG-IgG-positive cortical encephalitis within a longitudinal anti-NMDAR/MOGAD overlap course rather than a proven simultaneous dual-antibody relapse. Oral methylprednisolone was followed by clinical and radiological improvement. Conclusions: Across nearly seven years, this case documents phenotypic evolution from CSF-confirmed anti-NMDAR encephalitis to recurrent unilateral cortical encephalitis and later serum MOG-IgG detection. A changing cortical phenotype should prompt renewed antibody assessment at each recurrence rather than reliance on the index antibody profile. Because MOG-IgG was not tested in earlier episodes and CSF anti-NMDAR was not tested in 2025, the timing and mechanistic contribution of each antibody cannot be determined. Supplementary Information: The online version contains supplementary material available at https://doi.org/10.1186/s12883-026-05217-5.
SN - 1471-2377
ER -