Rate of Leptomeningeal Enhancement in Pediatric Myelin Oligodendrocyte Glycoprotein Antibody-Associated Encephalomyelitis

• Type of Material: Article
• Authors: Judith Gadde, Emory University; David Wolf, Emory University; Stephanie Keller, Emory University; Grace Gombolay, Emory University
• Language: English
• Date: 2021-10-01
• Publisher: SAGE PUBLICATIONS INC
• Publication Version: Author Accepted Manuscript (After Peer Review)
• Copyright Statement: © The Author(s) 2021.
• Final Published Version (URL): http://dx.doi.org/10.1177/08830738211025867
• Title of Journal or Parent Work: JOURNAL OF CHILD NEUROLOGY
• Volume: 36
• Issue: 11
• Start Page: 1042
• End Page: 1046
• Grant/Funding Information: The authors received no financial support for the research, authorship, and/or publication of this article.
• Keywords: CNS; MOG antibody associated disorder; Clinical Neurology; demyelinating disease; multiple sclerosis; myelin oligodendrocyte glycoprotein; leptomeningeal enhancement; Science & Technology; MOG; aseptic meningitis; pediatric; Neurosciences & Neurology; Pediatrics; Life Sciences & Biomedicine

Abstract

Introduction: Myelin oligodendrocyte glycoprotein antibodies (MOG-abs) are associated with demyelinating diseases. Leptomeningeal enhancement occurs in 6% of adult MOG-abs patients but rates in pediatric MOG-abs patients are unknown. Methods: Retrospective review of pediatric MOG-abs patients was performed. Results: Twenty-one patients (7 boys, 14 girls) were included with an average age of 8.6 years (range 2-15 years). Seven of 21 (33%) pediatric MOG-abs patients had leptomeningeal enhancement. Two patients’ relapses were manifested by leptomeningeal enhancement alone and another patient presented with seizures, encephalopathy, and aseptic meningitis without demyelinating lesions. Cerebrospinal fluid pleocytosis was seen in both leptomeningeal (4/7 patients) and nonleptomeningeal enhancement (10/14 patients). Interestingly, 3 patients with leptomeningeal enhancement had normal cerebrospinal fluid white blood cell count. Cortical edema was more likely in patients with leptomeningeal enhancement (P =.0263). Conclusion: We expand the clinical spectrum of anti-MOG antibody–associated disorder. Patients with recurrent leptomeningeal enhancement without demyelinating lesions should be tested for MOG antibodies.