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Abstract Details

COVID-19 Infection Linked to MOG Antibody-Associated Disease (MOGAD): Case Report
Autoimmune Neurology
P10 - Poster Session 10 (8:00 AM-9:00 AM)
6-023
Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an inflammatory disorder of the central nervous system characterized by attacks of immune-mediated demyelination predominantly targeting the optic nerves, brain, and spinal cord. In some cases of MOG associated Acute Transverse Myelitis (ATM), there is an antecedent history of infection or vaccination. 
To describe a case of MOG associated Transverse Myelitis after COVID-19 infection in a young adult.

We report the case of a patient with different neurological manifestations of CNS demyelination presenting within six weeks of moderate COVID-19 illness.

A 28-year-old man with hypertension presented with a three-week history of rapidly progressive paraparesis, sensory disturbances, saddle anesthesia, constipation and urinary retention, starting six weeks after moderate COVID-19 illness. MRI revealed non-enhancing T2 and FLAIR hyperintensities in the periventricular and subcortical white matter of both cerebral hemispheres, corpus callosum, inferior aspect of medulla, and a long segment, non-enhancing T2 signal intensity involving the cervical and thoracic spinal cord. Laboratory testing was remarkable for normal CSF analysis, positive serum COVID-19 IGG/IGM antibodies, and MOG antibodies titer at >1:160. Multiple courses of systemic glucocorticoids provided mild to moderate improvement, so subsequent plasma exchange therapy was started with significant resolution of patient's symptoms. Follow-up MRIs at 2 and 8 months showed interval resolution of cervical spinal cord edema and near-complete resolution of focal hyperintense T2/STIR cord lesions.

MOGAD is typically steroid-responsive with favorable long-term recovery. Although the present case involved a rare condition of MOGAD associated ATM after COVID-19 infection, detailed studies of additional clinical cases are necessary to determine the causation and the risk of developing this condition. We hypothesized the possibility of an immune mediated reaction triggered by COVID-19, inducing demyelination and autoimmune encephalomyelitis mediated by MOG-antibodies.

Authors/Disclosures
Gira Ileana Graciano, MD
PRESENTER
Dr. Graciano has nothing to disclose.
Mohammad Ghatali, MD (Texas Tech Health Science Center) Dr. Ghatali has nothing to disclose.