@article{8a392a4c37364cd8aa439383111957b9,
title = "Corpus callosum involvement in MOG antibody-associated disease in comparison to AQP4-IgG-seropositive neuromyelitis optica spectrum disorder and multiple sclerosis",
abstract = "Background: Data on corpus callosum involvement in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) are limited. Objective: The objective of the study was to compare callosal lesions in MOGAD, multiple sclerosis (MS), and aquaporin-4-IgG positive neuromyelitis optica spectrum disorder (AQP4+NMOSD). Results: Callosal lesion frequency was similar in MOGAD (38/171 (22%)), MS (24/72 (33%)), and AQP4+NMOSD (18/63 (29%)). Clinical phenotypes included encephalopathy (47%) and focal supratentorial (21%) or infratentorial (45%) deficits. None had callosal-disconnection syndromes. Maximal callosal-T2-lesion diameter (median (range)) in millimeter was similar in MOGAD (21 (4–77)) and AQP4+NMOSD (22 (5–49); p = 0.93) but greater than in MS (10.5 (2–64)). Extracallosal extension (21/38 (55%)) and T2-lesion resolution (19/34 (56%)) favored MOGAD. Conclusions: Despite similar frequency and imaging overlap, larger lesions, sagittal midline involvement, and lesion resolution favored MOGAD.",
keywords = "Myelin oligodendrocyte glycoprotein, aquaporin 4, corpus callosum, magnetic resonance imaging, multiple sclerosis, neuromyelitis optica",
author = "Chia, {Nicholas H.} and Vyanka Redenbaugh and Chen, {John J.} and Pittock, {Sean J.} and Flanagan, {Eoin P.}",
note = "Funding Information: The author(s) disclosed receipt of the following financial support for the research, authorship, and/or publication of this article: This study was supported with funding from the NIH (R01NS113828). Funding Information: The author(s) declared the following potential conflicts of interest with respect to the research, authorship, and/or publication of this article: N.H.C. has no conflicts of interest to report. V.R. has no conflicts of interest to report. J.J.C. is a consultant to UCB and Roche. S.J.P. reports grants, personal fees, and non-financial support from Alexion Pharmaceuticals, Inc.; grants, personal fees, non-financial support, and other support from MedImmune, Inc/Viela Bio.; personal fees for consulting from Genentech/Roche; has a patent, Patent# 8,889,102 (Application#12-678350, Neuromyelitis Optica Auto-antibodies as a Marker for Neoplasia)—issued; a patent, Patent# 9,891,219B2 (Application#12-573942, Methods for Treating Neuromyelitis Optica (NMO) by Administration of Eculizumab to an individual that is Aquaporin-4 (AQP4)-IgG Autoantibody positive)—issued. E.P.F. has served on advisory boards for Alexion, Genentech, and Horizon Therapeutics; has received research support from UCB; has received speaker honoraria from Pharmacy Times; has received royalties from UpToDate; was a site primary investigator in a randomized clinical trial on Inebilizumab in neuromyelitis optica spectrum disorder run by Medimmune/Viela-Bio/Horizon Therapeutics; has received funding from the NIH (R01NS113828); is a member of the medical advisory board of the MOG project; is an editorial board member of the Journal of the Neurological Sciences and Neuroimmunology Reports; and has a patent submitted on DACH1-IgG as a biomarker of paraneoplastic autoimmunity. Publisher Copyright: {\textcopyright} The Author(s), 2023.",
year = "2023",
month = may,
doi = "10.1177/13524585221150743",
language = "English (US)",
volume = "29",
pages = "748--752",
journal = "Multiple Sclerosis",
issn = "1352-4585",
publisher = "SAGE Publications Ltd",
number = "6",
}