Acute flaccid myelitis is an acquired spinal cord disorder that presents after a febrile or respiratory illness, usually viral in nature, with rapid onset flaccid limb weakness¹. Myelin oligodendrocyte glycoprotein associated antibody disease (MOGAD) is an immune-mediated demyelinating disease of the central nervous system presenting with acute limb weakness as transverse myelitis². Distinguishing between the two entities on initial clinical presentation can be challenging. We present a case of MOGAD masquerading as acute para-infectious flaccid myelitis.

Case report: 

32 year old woman with history of linear scleroderma (off methotrexate since 2019) presented for acute onset urinary retention and bilateral leg numbness and weakness. Patient endorsed worsening posterior occipital pounding headaches, low grade fevers, and generalized weakness two weeks prior to this acute change. MRI of the total spine showed T2 hyperintense signal abnormality spanning from C3 to T9-10 consistent with longitudinally extensive transverse myelitis (LETM). Lumbar puncture was performed, showing marked lymphocytic pleocytosis (WBC 770, 68% lymph) and elevated protein (166mg/dL). She was empirically treated with vancomycin, ceftriaxone, and acyclovir. Nasal swab revealed Parainfluenza 3 virus. CSF viral studies were negative. She was then started on IV Solumedrol, with addition of plasmapheresis given worsening of limb weakness. MOG antibody titers in serum resulted at 1:160. She was discharged to acute rehab with improvement of leg weakness and urinary retention following a 10 day course of antibiotics, 7 days of IV solumedrol and 7 sessions of plasmapheresis. 

This case illustrates that CSF findings in patients with transverse myelitis due to MOGAD can demonstrate marked pleocytosis and elevated protein in the acute phase - similar to findings expected in infectious flaccid myelitis. The possibility that infections trigger MOGAD remains under investigation, though some case series demonstrate EBV, HSV and Influenza as possible triggers of MOGAD encephalomyelitis ^3,4.