This patient had monophasic and subacute encephalopathy that could not be explained by fever. Spinal MRI showed multiple short-segment T2-weighted hyperintense lesions with partial enhancement in the cervical cord ( Fig. Gadolinium (Gd)-enhanced T1-weighted images showed multiple open-ring enhancement patterns ( Fig. Brain magnetic resonance imaging (MRI) fluid-attenuated inversion recovery (FLAIR) images showed multifocal hyperintense subcortical and periventricular white-matter and brainstem lesions ( Fig. CSF cytology, anti-AQP4 antibody, and CSF oligoclonal band tests were negative. The results of a cerebrospinal fluid (CSF) examination were unremarkable, with a total nucleated cell count of 3/μL, protein level of 45 mg/dL, and glucose level of 73 mg/dL. Her score on the Expanded Disability Status Scale (EDSS) was 9.5. Ankle clonus and Babinski's sign were observed bilaterally. Bilateral upper and lower extremity deep tendon reflexes were brisk. A neurologic examination revealed paresis of all extremities, which was more severe on the right side (grades 2, 3, 4, and 4 on the Medical Research Council scale in the right arm, right leg, left arm, and left leg, respectively). On admission she was alert, but she exhibited severe dysarthria and cognitive impairment with decreased orientation to time and place. Preceding vaccinations, systemic infections, and other neurologic symptoms were not reported. One month later she experienced dysarthria and reduced verbal output, followed by decreased mentality, confusion, and dysphagia. She initially experienced recurrent falls and progressive bilateral lower limb weakness. Here we report a case of late-onset MOG-immunoglobulin G (IgG)-positive encephalomyelitis with an ADEM-like phenotype.Ī 57-year-old female developed gait disturbance with recurrent falls, dysarthria, and cognitive decline 3 months prior to admission to our hospital. When MOGAD involves the brain, an acute disseminated encephalomyelitis (ADEM)-like phenotype is most commonly observed however, this is more common in pediatric or young adult patients. 1 The clinical manifestations of adult MOGAD resemble those of neuromyelitis optica spectrum disorder (NMOSD), which usually involve the optic nerve and spinal cord. Myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) has recently been classified as a distinct inflammatory demyelinating disease of the central nervous system.
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