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A 62-year-old unimmunized man with HIV well-controlled on anti-retroviral therapy presented with abrupt onset burning sensation below the T4 dermatomal level followed by ascending numbness in his lower extremities. He had experienced an antecedent upper respiratory infection and bilateral parotid gland swelling.  Within weeks he developed bowel incontinence, urinary retention, gait instability and dysarthria. MRI brain, cervical and thoracic spine with and without contrast demonstrated multiple patchy contrast-enhancing lesions in the cervical and thoracic cord spanning 2-4 vertebrae, as well as a non-enhancing T2 hyperintense right cerebellopontine junction lesion. CSF evaluation revealed 5 nucleated cells, mildly elevated protein, no unique oligoclonal bands, and infectious studies were negative. Serum aquaporin-4 antibody testing was negative. Serum mumps IgM was negative and IgG was positive. He was treated with 3 days of IV methylprednisolone with gradual neurological improvement. Two months later, serum anti-MOG antibody was positive at a titer of 1:100. Repeat imaging demonstrated persistence of the right cerebellopontine lesion and resolution or improvement of cord signal abnormalities. Repeat anti-MOG antibody testing 8 months after initial titer was negative.

While anti-MOG antibody associated inflammatory disorders and encephalopathy have been reported following other viral infections, this is the first case of anti-MOG associated encephalomyelitis preceded by presumed acute mumps infection. Post-infectious anti-MOG antibody titers often become negative within months of the acute illness supporting a favorable prognosis; these cases are not typically treated with long-term immunosuppression. Transverse myelitis is a known sequela of primary HIV infection, however our patient had been well controlled on anti-retroviral therapy suggesting alternative explanation for his CNS inflammatory pathology.