Relapsing Anti-NMDAR encephalitis with later detected MOG-IgG-Positive cortical encephalitis: a case report

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. 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. 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.