Format

Send to

Choose Destination
Mult Scler. 2016 Feb;22(2):174-84. doi: 10.1177/1352458515587751. Epub 2015 Jun 3.

Clinical and MRI phenotype of children with MOG antibodies.

Author information

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 tchitnis@partners.org.

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.

KEYWORDS:

Acute disseminated encephalomyelitis; demyelinating syndromes; encephalopathy; glycoprotein; magnetic resonance imaging; multiple sclerosis; myelin; myelin oligodendrocyte glycoprotein; neuromyelitis optica; optic neuritis; pediatric multiple sclerosis; serology

PMID:
26041801
PMCID:
PMC4669239
DOI:
10.1177/1352458515587751
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Atypon Icon for PubMed Central
Loading ...
Support Center