Evaluation of the predictive value of CSF-restricted oligoclonal bands on residual disability and risk of relapse in adult patients with MOGAD: MOGADOC study.

Background: The clinical course of myelin oligodendrocyte glycoprotein (MOG) antibody-associated disease (MOGAD) is variable. However, robust markers of poor outcome and/or relapse risk are still missing.
Objective: To evaluate the frequency of cerebrospinal fluid-restricted oligoclonal bands (CSF-OCB) in a national cohort of adult MOGAD patients and to assess their prognostic value for the risk of relapse and severity.
Methods: We included MOGAD adult patients fulfilling the MOGAD 2023 criteria who underwent CSF analysis at maximum 3 months from onset.
Results: Data from 190 patients were collected. We found the presence of CSF-OCB in 32 patients (16.8%). Positive and negative CSF-OCB patients were similar for median age at onset, sex, clinical presentation, severity at onset, and residual disability. Relapses were more frequent in the CSF-OCB+ group ( p = 0.049), particularly within the first year of follow-up ( p = 0.007). Although CSF-OCB+ was more frequently associated with imaging features suggestive of multiple sclerosis (MS) ( p = 0.014), 78% of these patients fulfilled the 2023 supportive features and 65% experienced lesion vanishing at follow-up magnetic resonance imaging (MRI).
Conclusion: We found a higher risk of relapse in MOGAD with CSF-OCB particularly during the first year. Close attention is recommended regarding the risk of misdiagnosis with MS.
Competing Interests: Declaration of Conflicting InterestsThe author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: R.D. has received personal compensation for serving on a scientific advisory board or travel grants from Biogen, Alexion, and Novartis. J.C. has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen, Novartis, Merck, Sanofi, Roche, Alexion, and Horizon Therapeutics-Amgen, none related to this study. M.C. has received personal compensation for consulting, serving on a scientific advisory board, speaking, or other activities with Biogen, Merck, Sanofi, Roche, Celgene-BMS, Janssen, Alexion, Horizon Therapeutics, and Ad Scientiam. Professor N.C. has received honoraria for consulting or presentation from Biogen Idec, Alexion, Novartis, Merck Serono, Bristol-Myers Squibb, Sanofi-Genzyme, and Roche and is a member of the Editorial Board of the Journal de la Ligue Française contre la Sclérose en plaques. A.R. has received grant research for the institution from Biogen, BMS, Merck, Roche, and Sanofi-Genzyme and non-financial support and honoraria from Biogen, Novartis, Alexion, and Horizon Th. B.B. serves on scientific advisory board and has received funding for travel and honoraria from Alexion, Biogen, BMS, Horizon, Janssen, Merck, Novartis, Sanofi, and Roche. C.P. reports personal fees for lectures and advisory boards or travel grants from Alexion, Horizon-Amgen, and Novartis outside the submitted work. All other authors have declared no conflict of interest.