Progressive myelopathy in myelin oligodendrocyte glycoprotein antibody-associated disease: A new mimicker of progressive multiple sclerosis?

Background MOG-IgG-associated disease (MOGAD) in adults typically presents as a monophasic or relapsing optic, spinal, or opticospinal neuroinflammatory syndrome. Current recommendations discourage testing for MOG-IgG in patients with clinical or paraclinical findings more typical of MS, or in patients with a progressive clinical course. However, this approach may impede identification of the full phenotypic spectrum of this recently described disorder. Methods We retrospectively reviewed charts of 39 MOG-IgG-seropositive patients from two Ohio-based neuroimmunology centers to identify unusual disease patterns. Those with a progressive course were included in this case series. Results We describe five cases of progressive myelopathy associated with MOG-IgG. Most patients had features suggestive of MS, including typical MRI and cerebrospinal fluid findings. However, MOG-IgG positive patients with progressive myelopathy showed poor response to MS disease modifying therapy and better response to intravenous immunoglobulins similar to previous reports on MOGAD patients. Conclusion MOG-IgG-seropositive patients may present with progressive myelopathy and may have a clinical and radiologic phenotype suggestive of primary progressive or secondary progressive MS, or progressive solitary sclerosis. MOG-IgG testing should be considered in patients with progressive myelopathy, especially if clinically worsening on MS therapy.

EBNA1, EBNA2, and EBNA3 link Epstein-Barr virus and hypovitaminosis D in multiple sclerosis pathogenesis.

A strong north-to-south gradient is observed in the distribution of multiple sclerosis (MS), hinting toward an environmental etiology. Vitamin D has been associated with a decreased incidence of MS and may explain, in part, the lower prevalence in tropical climates. However, the existence of MS epidemics implies the possibility of an infectious etiology. Epstein-Barr virus (EBV) infection precedes MS presentation in nearly all affected individuals. While the individual contribution of EBV, vitamin D deficiency, and specific risk genes to MS etiology is possible, their potential interaction is of great interest and may have a synergistic effect on the development of MS.