Association of Cerebrospinal Fluid–Restricted Oligoclonal Bands With Relapsing Pediatric Myelin Oligodendrocyte Glycoprotein Antibody–Associated Disease

Background: Cerebrospinal fluid (CSF)-restricted oligoclonal bands (OCBs) are observed in a minority of patients with pediatric myelin oligodendrocyte glycoprotein antibody–associated disease (MOGAD). They indicate chronic intrathecal immune activation and thus may be associated with relapsing disease. We aimed to assess the association of CSF-restricted OCBs with relapsing versus monophasic disease in children with MOGAD. Methods: A retrospective single-center cohort study of children diagnosed between 2017 and 2023 meeting the 2023 international consensus criteria for MOGAD was performed. All patients had at least one CSF and paired serum OCB evaluation. Clinical characteristics, laboratory data, disease course (monophasic vs relapsing), and treatments were collected by chart review. Patients were considered OCB-positive if ≥ 2 CSF-restricted OCBs were detected on one or more testing time points. Multivariable logistic regression assessed the association of OCB-positivity with relapsing disease, controlling for female sex, age at disease onset, and optic neuritis as a presenting phenotype. Results: We evaluated 83 children (52/83 [63%] female) with median age 10 (interquartile range [IQR]: 5-13) years at first attack. Median follow-up duration from disease onset was 25 (IQR: 10-54) months. Fourteen (17%) were OCB-positive, with a median of 2.5 (IQR: 2-5) bands. Twenty-nine (35%) individuals had relapsing MOGAD. OCB-positivity was associated with relapsing disease in univariate logistic regression (odds ratio 4.41, 95%-confidence interval 1.31-14.8, P = 0.016), and in multivariate logistic regression (odds ratio 3.85, 95%-confidence interval 1.09-13.6, P = 0.036). Conclusions: The presence of CSF-restricted OCBs in children with MOGAD was associated with increased risk of relapsing disease, independent of sex, age at disease onset, and optic neuritis as a presenting phenotype.