Clinical and MRI phenotype of children with MOG antibodies

Author:

Fernandez-Carbonell Cristina1,Vargas-Lowy David1,Musallam Alexander2,Healy Brian3,McLaughlin Katherine4,Wucherpfennig Kai W4,Chitnis Tanuja5

Affiliation:

1. Center for Neurologic Diseases, Brigham and Women’s Hospital, Boston, MA, USA

2. Partners MS Center, Brigham and Women’s Hospital, Boston, MA, USA

3. Partners MS Center, Brigham and Women’s Hospital, Boston, MA, USA/Biostatistics Center, Massachusetts General Hospital, Boston, MA, USA

4. Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Boston, MA, USA

5. Center for Neurologic Diseases, Brigham and Women’s Hospital, Boston, MA, USA/Partners MS Center, Brigham and Women’s Hospital, Boston, MA, USA/Partners Pediatric MS Center, Massachusetts General Hospital, Boston, MA, USA

Abstract

Objective: To investigate the clinical and magnetic resonance imaging (MRI) features of anti-myelin oligodendrocyte glycoprotein (MOG) antibody-seropositive pediatric demyelinating syndromes. Methods: Serum samples collected from 74 children with suspected demyelinating disorders whom were being followed at Massachusetts General Hospital were incubated with control green fluorescent protein (GFP)- and MOG-GFP-transfected Jurkat cell clones. The binding ratios were calculated using flow cytometry. Using statistical analyses, we compared the demographic, clinical and radiological features in our seropositive and seronegative patients. Results: We found that 13 out of 74 (17.5%) patients were seropositive for MOG. The MOG-seropositive patients were younger than the seronegative patients ( p = 0.049). No single disease category predominated among the seropositive patients, nor was one group more likely to have a polyphasic course. There were two out of four neuromyelitis optica (NMO) patients who had MOG antibodies; both were seronegative for aquaporin −4 (AQP4) antibodies. One had monophasic disease and the other had frequent relapses. There was a bimodal distribution of the MOG-seropositive patients by age at onset, with a distinct younger group (4–8 years) having a high prevalence of encephalopathy and an older group (13–18 years), whom presented almost exclusively with optic neuritis. MRI analysis demonstrated the absence of corpus callosum lesions in the seropositive patients ( p = 0.012). The annualized relapse rate (ARR) and the Expanded Disability Status Scale (EDSS) results at 2 years did not differ between the seropositive and seronegative patients. Conclusion: MOG antibodies are found across a variety of pediatric demyelinating syndromes having some distinct clinical and MRI features.

Publisher

SAGE Publications

Subject

Clinical Neurology,Neurology

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