Oligoclonal Bands in Pediatric MOG Antibody-associated Disease: Prognostic Biomarker or Evidence of Distinctive Phenotype?
Sydney Talmi1, Shermila Pia1, Jonathan Santoro2, Vaishnavi Vaidyanathan1
1UC Davis School of Medicine, 2Department of Neurology, Children's Hospital Los Angeles
Objective:
Evaluate significance of cerebrospinal fluid (CSF) oligoclonal bands (OCBs) at symptom onset in pediatric MOG antibody-associated disease (MOGAD) to assess predictive value for relapsing disease or even a distinct phenotype. 
Background:
Up to 38% of pediatric MOGAD cases experience relapse, prompting the search for predictive markers such as CSF-OCBs and the possibility of a distinct MOGAD phenotype.
Design/Methods:
Children meeting 2023 MOGAD diagnostic criteria with confirmed MOG-IgG seropositivity, lumbar puncture at presentation, and ≥12 months follow-up were included. Clinical, laboratory, and radiographic data was collected on relapse frequency, presence of OCBS, initial phenotype, and MRI findings. Group comparisons used Fisher’s exact test for categorical and Kruskal-Wallis test for continuous variables (significance: p<0.05).
Results:
Fifty-nine patients (53% female, median age 11 years) were included, with eighteen patients (31%) who experienced relapsing disease. Thirteen (22%) had CSF-OCBs. OCB-positive patients experienced more relapses (p<0.001; H=9.83), were more likely to have persistent MOG-IgG >1 year after presentation (p=0.01; OR 0.18; RR 0.48), and remained on immunosuppressive therapy (p=0.01; OR 0.14; RR 0.24). Seven patients had severe relapsing MOGAD requiring additional long-term immunotherapy on final follow-up, three of which had positive OCBs (43%). Initial clinical phenotype and MRI lesion location did not differ, though OCB-positive patients had more frequent perineural enhancement (p=0.04; OR 0.14; RR 0.39). No significant differences were observed in EDSS at 12 months, CSF MOG-IgG (25 tested), CSF pleocytosis, or CSF white blood cell count.
Conclusions:
MOGAD with positive OCBs was associated with increased relapse risk, persistent MOG-IgG titers, and ongoing immunosuppressive therapy suggesting a more severe presentation requiring increased additional therapy. This may suggest OCBs as a prognostic marker for relapsing MOGAD or indicate heightened disease activity reflecting a distinct relapsing phenotype, however further investigation is needed. 
10.1212/WNL.0000000000217159
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