From: MOG encephalomyelitis: international recommendations on diagnosis and antibody testing
Disease course Chronic progressive disease (very rare in MOG-IgG-positive patients [3]), including SPMS (especially SPMS without relapses) and PPMSa Sudden onset of symptoms, e.g., < 4 h from onset to maximum (consider ischemic cause), or continuous worsening of symptoms over weeks (consider tumor, sarcoidosis, etc.) MRI Lesion adjacent to a lateral ventricle that is ovoid/round or associated with an inferior temporal lobe lesion, or Dawson’s finger-type lesion Active brain MRI over time with silent increase in lesion burden between relapses (limited evidence) CSF Bi- or trispecific MRZ reactionb (consider MS) Serology MOG-IgG levels at or just barely above the assay-specific cut-offc, especially (but not exclusively) if clinical picture is atypical Positive MOG-IgM and/or MOG-IgA result with negative MOG-IgG (clinical significance unknown) MOG-IgG positivity in the CSF but not in the serumd (MOG-IgG is typically produced extrathecally) AQP4-IgG/MOG-IgG “double-positive” test results (extremely rare; should prompt retesting for both antibodies)e Others Clinical or paraclinical findings suggesting diagnoses other than MOG-EM, NMOSD or MS (e.g., neurotuberculosis, neuroborreliosis, neurosyphilis, neurosarcoidosis, Behçet syndrome, subacute combined degeneration of the spinal cord, Leber’s hereditary optic neuropathy, vasculitis, CNS lymphoma, gliomatosis cerebri, paraneoplastic neurological disordersf, PRES, PML, and evidence for CNS infectiong) Combined central and peripheral demyelination [69] (MOG is not expressed in the peripheral nervous system)h |