Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is a rare autoimmune neurological condition characterized by clinical phenotypes that include acute disseminated encephalomyelitis, optic neuritis, and transverse myelitis. Neuroimaging features differ markedly between adults and children, and brain lesions are relatively uncommon in adult MOGAD patients. Atypical imaging patterns can complicate the differentiation of MOGAD from other diseases. We report a 21-year-old female presenting with dysarthria, gait deviation, blurred vision, and slow response. Brain MRI revealed multiple patchy, irregular T2-FLAIR hyperintense lesions involving the pons, midbrain, and strikingly symmetric bilateral thalami and basal ganglia. She had a history of chronic alcohol use and was initially misdiagnosed with Wernicke’s encephalopathy. No symptomatic improvement followed vitamin B1 supplementation. Serum and cerebrospinal fluid (CSF) analysis revealed low-positive myelin oligodendrocyte glycoprotein immunoglobulin G (MOG-IgG). After carefully excluding other differential diagnoses, a diagnosis of MOGAD was established. High-dose intravenous methylprednisolone followed by oral tapering resulted in significant clinical improvement, along with marked amelioration of MRI abnormalities. This case highlights an atypical adult MOGAD presentation with widespread brainstem to the basal ganglia and symmetric thalamic lesions. It underscores the importance of recognizing such imaging patterns to avoid misdiagnosis and prompt timely autoantibody testing and immunotherapy.
Atypical MRI presentation of symmetrical thalamic and basal ganglia lesions in adult-onset MOG-IgG-associated disease: a case report
Zilong Zhu

