MOG-AD, MOG-antibody-associated disease, is an autoimmune CNS demyelinating disease that commonly presents in childhood or young adulthood with optic neuritis, myelitis, acute disseminated encephalomyelitis or cortical encephalitis. We present an unusual case of an 89-year-old male with longitudinally extensive lower thoracic myelopathy and a positive MOG-IgG antibody titer.

The patient is an 89-year-old male with atrial fibrillation on Rivaroxaban who presented with a subacute onset of bilateral lower extremity weakness and numbness, new-onset bladder and fecal incontinence. He had a sensory level at T10 consistent with thoracic myelopathy.  MRI thoracic spine showed a T2 hyperintense signal extending from T8-T10. CSF analysis showed leukocytosis with a lymphocyte predominance and a high protein level. A repeat MRI of his thoracic spine showed interval progression of the T2 hyperintensity with new areas of T2 hypointensity concerning for hemorrhage within the lesion. Serum labs, including RPR, TB, HIV, B12, folate, Lyme, EBV, CMV, and HTLV were unremarkable. The CSF HSV2, cytology, and cytometry were also unremarkable. MOG-IgG antibody was detected in the serum through a cell-based assay at a titer of 1:40. The patient was diagnosed with MOGAD and started on IV Methylprednisolone followed by a Prednisone taper with improvement.

This is a unique case of MOGAD, given that the median age of onset is usually early to mid-thirties. Per a brief literature search on Pubmed, there have been no papers about MOGAD with an age range beyond the 70’s. The patient had intralesional bleeding, which was thought to be secondary to concomitant Rivaroxaban use. We found no papers describing bleeding in spinal cord lesions caused by MOG.

MOGAD should be considered on the differential for thoracic myelopathy, when the clinical features, imaging and CSF findings are suggestive of this diagnosis even in older patients outside the typical age range for this disease.