Myelin oligodendrocyte glycoprotein antibody disease (MOGAD) is a discrete autoimmune, neuroinflammatory demyelinating disease with a broad clinical spectrum caused by antibodies against MOG proteins on myelin and oligodendrocytes. It is now recognized as a separate disease from multiple sclerosis and neuromyelitis optica spectrum disorder (AQP4-IgG + NMOSD). A 40-year-old female presented with a history of fever, acute onset visual impairment and painful extra ocular movements of left eye, ataxia, giddiness, bitemporal headache, and urinary retention. Cerebrospinal fluid evaluation showed lymphocytic pleiocytosis, serum anti-MOG antibodies were positive (1:100), and magnetic resonance imaging (MRI) showed multiple lesions involving the diencephalon, brainstem and periventricular white matter and conus medullaris. The patient was started on a 5 day pulse dose of injection METHYLPREDNISOLONE 1 g followed by a gradually tapering dose of oral prednisolone for 1 month. Patient recovered completely with no residual disease and was followed up for 1 year. Repeat serum MOG antibodies were negative and MRI showed complete resolution of both brain and spinal lesions. MOGAD is an emerging autoimmune neuroinflammatory disease that is not only distinct in its presentation, but also in response to disease modifying therapies with a better prognosis and lower morbidity than the other demyelinating diseases. A high suspicion for its clinical phenotypes and radiological peculiarities must be held for avoiding misdiagnosis and for early management.
Malik et al. (Mon,) studied this question.