ArticleMedicine2026
Myelin oligodendrocyte glycoprotein antibody-related autoimmune encephalitis misdiagnosed as acute cerebral infarction: A case report.
Article in Medicine, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
rationaleMyelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory demyelinating autoimmune disorder of the central nervous system that exhibits a broad spectrum of known clinical phenotypes, including optic neuritis, myelitis, acute disseminated encephalomyelitis, encephalitis, meningoencephalitis, and brainstem encephalitis. However, new evidence indicates that a small subset of patients may present with cortical cerebral encephalitis (CCE). When CCE manifests as acute unilateral limb weakness, it may closely mimic acute cerebral infarction (ACI), resulting in misdiagnosis and delayed initiation of immunotherapy. Here, we report a case initially diagnosed as ACI and highlight key diagnostic clues and therapeutic considerations that may help to facilitate earlier recognition and appropriate management. PATIENT CONCERNS: A young woman was admitted with left-sided limb weakness and was initially diagnosed with ACI. DIAGNOSES: The final diagnosis was myelin oligodendrocyte glycoprotein (MOG) antibody-related autoimmune encephalitis, which was established by integrating the clinical presentation, contrast-enhanced brain magnetic resonance imaging (MRI) findings, cerebrospinal fluid (CSF) antibody testing, and systematic exclusion of alternative etiologies.
interventionsAfter an initial misdiagnosis, the patient received neuroprotective agents without meaningful improvement. Subsequent lumbar puncture and CSF testing supported the diagnosis of MOG antibody-related autoimmune encephalitis. Treatment was then adjusted to include both high-dose intravenous corticosteroid pulse therapy and immunotherapy, which resulted in marked clinical improvement. OUTCOMES: The patient's condition remained stable at 2-month follow-up, with no disease progression. Contrast-enhanced MRI showed no abnormalities in the unilateral cerebral cortex. LESSONS: CCE associated with MOGAD may be misdiagnosed as ACI, particularly when focal motor deficits are the predominant presenting feature. Early recognition, prompt diagnostic evaluation, and timely initiation of immunotherapy are crucial for improving clinical outcomes. Greater clinician awareness and improved neuroimaging-based differentiation between ACI and CCE are therefore needed. In patients with stroke-mimicking presentations but atypical imaging findings, contrast-enhanced MRI and cerebrospinal fluid testing for MOG immunoglobulin G should be prioritized. High-dose steroid pulse therapy combined with immunotherapy remains the recommended first-line treatment for suspected MOG antibody-related autoimmune encephalitis.
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