Cortical atrophy patterns in myelin oligodendrocyte glycoprotein antibody-associated disease
- PMID: 39054631
- PMCID: PMC11330211
- DOI: 10.1002/acn3.52137
Cortical atrophy patterns in myelin oligodendrocyte glycoprotein antibody-associated disease
Abstract
Objectives: Global brain volume changes in patients with myelin oligodendrocyte glycoprotein antibody-associated disease compared with healthy controls (HC) could be revealed by magnetic resonance imaging, but specific atrophy patterns of cortical structures and relation to cognitive impairment are not yet comprehensively known. Thus, we aimed to investigate cortical thickness differences in patients with myelin oligodendrocyte glycoprotein antibody-associated disease compared with HC.
Methods: 3-Tesla brain magnetic resonance imaging was performed in 23 patients with myelin oligodendrocyte glycoprotein antibody-associated disease and 49 HC for voxel-wise group comparisons and neuropsychological testing in patients. Surface-based morphometry with region of interest-based surface analysis and region of interest-based extraction of cortical thickness was performed in patients compared with HC and in patient subgroups with and without cognitive impairment.
Results: Comparing patients with myelin oligodendrocyte glycoprotein antibody-associated disease with HC, exploratory surface-based morphometry demonstrated cortical volume reduction in pericalcarine and lingual cortical regions. Region of interest-based surface analysis specified reduced cortical thickness in the adjacent pericalcarine and orbitofrontal regions in myelin oligodendrocyte glycoprotein antibody-associated disease, as well as reduced temporal cortical thickness in patients with cognitive impairment (n = 10). Patients without cognitive impairment (n = 13) showed only circumscribed cortical brain volume loss compared with HC in the pericalcarine region.
Interpretation: In conclusion, cortical atrophy in myelin oligodendrocyte glycoprotein antibody-associated disease was characterized by cortical thickness reduction in the adjacent pericalcarine and orbitofrontal regions, with a tendency of temporal thickness reduction in cognitively impaired patients.
© 2024 The Author(s). Annals of Clinical and Translational Neurology published by Wiley Periodicals LLC on behalf of American Neurological Association.
Conflict of interest statement
The authors declare no conflict of interest with the present work. Irrespective of the present work the authors report following conflict s of interest: R.S. has received speaker's honoraria from Bayer HealthCare, Alexion Pharma, Novartis Pharma, and Roche Pharma AG, congress travel support from Merck, Biogen Idec GmbH and has received research scientific grant support from Novartis Pharma. T.L.: has received research scientific grant support from Novartis Pharma. A.K., N.S., B.K., B.B.: nothing to disclose. R.G.: has received compensation for serving as a consultant or speaker from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis, and Teva Neuroscience; he, or the institution he works for, has received research support from Bayer HealthCare, Biogen Idec, Merck Serono, Novartis, and Teva Neuroscience; he has also received honoraria as a Journal Editor from SAGE and Thieme Verlag. I.A.: has received travel grants from Alexion, BMS, Horizon, Roche, Biogen Idec, and Guthy‐Jackson Charitable Foundation, served on scientific advisory boards for Merck, Roche, Alexion, Horizon, and Sanofi and received research support from Diamed and Roche. C.L.: received a research grant by the German Federal Ministry for Education and Research, BMBF, German Competence Network Multiple Sclerosis (KKNMS), grant no.01GI1601I, has received consulting and 415 speaker's honoraria from Biogen Idec, Bayer Schering, Daiichi Sanykyo, Merck Serono, Novartis, 416 Sanofi, Genzyme, and TEVA.
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