Please use this identifier to cite or link to this item: http://hdl.handle.net/10609/152314
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dc.contributor.authorCortese, Rosa-
dc.contributor.authorBattaglini, Marco-
dc.contributor.authorPrados Carrasco, Ferran-
dc.contributor.authorGentile, Giordano-
dc.contributor.authorLuchetti, Ludovico-
dc.contributor.authorBianchi, Alessia-
dc.contributor.authorHaider, Lukas-
dc.contributor.authorJacob, Anu-
dc.contributor.authorPalace, Jacqueline-
dc.contributor.authorMessina, Silvia-
dc.contributor.authorpaul, friedemann-
dc.contributor.authorMARIGNIER, Romain-
dc.contributor.authorDurand-Dubief, Françoise-
dc.contributor.authorde Medeiros Rimkus, Carolina-
dc.contributor.authorApostolos Pereira, Samira Luisa-
dc.contributor.authorSato, Douglas Kazutoshi-
dc.contributor.authorFilippi, Massimo-
dc.contributor.authorRocca, Maria A-
dc.contributor.authorCacciaguerra, Laura-
dc.contributor.authorRovira, Alex-
dc.contributor.authorSastre Garriga, Jaume-
dc.contributor.authorArrambide, Georgina-
dc.contributor.author刘, 亚欧-
dc.contributor.authorDuan, Yunyun-
dc.contributor.authorgasperini, claudio-
dc.contributor.authorTortorella, Carla-
dc.contributor.authorRuggieri, Serena-
dc.contributor.authorPia Amato, Maria-
dc.contributor.authorUlivelli, Monica-
dc.contributor.authorGroppa, Sergiu-
dc.contributor.authorGrothe, Matthias-
dc.contributor.authorLlufriu, Sara-
dc.contributor.authorSepulveda, Maria-
dc.contributor.authorLukas, Carsten-
dc.contributor.authorBellenberg, Barbara-
dc.contributor.authorSchneider, Ruth-
dc.contributor.authorSowa, Piotr-
dc.contributor.authorCelius, Elisabeth G.-
dc.contributor.authorPröbstel, Anne-Katrin-
dc.contributor.authorGranziera, Cristina-
dc.contributor.authorYaldizli, Özgür-
dc.contributor.authorMüller, Jannis-
dc.contributor.authorStankoff, Bruno-
dc.contributor.authorBodini, Benedetta-
dc.contributor.authorBarkhof, Frederik-
dc.contributor.authorCiccarelli, Olga-
dc.contributor.authorDe Stefano, Nicola-
dc.contributor.authorMAGNIMS Study Group-
dc.date.accessioned2025-03-12T14:27:12Z-
dc.date.available2025-03-12T14:27:12Z-
dc.date.issued2024-05-23-
dc.identifier.citationCortese, R. [Rosa], Battaglini, M. [Marco], Prados, F. [Ferran], Gentile, G. [Giordano], Luchetti, L. [Ludovico], Bianchi, A. [Alessia], ... & De Stefano, N. [Nicola]. (2024). Grey matter atrophy and its relationship with white matter lesions in patients with myelin oligodendrocyte glycoprotein antibody-associated disease, aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder, and multiple sclerosis. Annals of Neurology, 96(2), 276-88. doi: 10.1002/ana.26951-
dc.identifier.issn0364-5134MIAR
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dc.identifier.urihttp://hdl.handle.net/10609/152314-
dc.description.abstractObjective. To evaluate: (1) the distribution of gray matter (GM) atrophy in myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder (AQP4+NMOSD), and relapsing–remitting multiple sclerosis (RRMS); and (2) the relationship between GM volumes and white matter lesions in various brain regions within each disease. Methods. A retrospective, multicenter analysis of magnetic resonance imaging data included patients with MOGAD/AQP4+NMOSD/RRMS in non-acute disease stage. Voxel-wise analyses and general linear models were used to evaluate the relevance of regional GM atrophy. For significant results (p < 0.05), volumes of atrophic areas are reported. Results- We studied 135 MOGAD patients, 135 AQP4+NMOSD, 175 RRMS, and 144 healthy controls (HC). Compared with HC, MOGAD showed lower GM volumes in the temporal lobes, deep GM, insula, and cingulate cortex (75.79 cm3); AQP4+NMOSD in the occipital cortex (32.83 cm3); and RRMS diffusely in the GM (260.61 cm3). MOGAD showed more pronounced temporal cortex atrophy than RRMS (6.71 cm3), whereas AQP4+NMOSD displayed greater occipital cortex atrophy than RRMS (19.82 cm3). RRMS demonstrated more pronounced deep GM atrophy in comparison with MOGAD (27.90 cm3) and AQP4+NMOSD (47.04 cm3). In MOGAD, higher periventricular and cortical/juxtacortical lesions were linked to reduced temporal cortex, deep GM, and insula volumes. In RRMS, the diffuse GM atrophy was associated with lesions in all locations. AQP4+NMOSD showed no lesion/GM volume correlation. Interpretation. GM atrophy is more widespread in RRMS compared with the other two conditions. MOGAD primarily affects the temporal cortex, whereas AQP4+NMOSD mainly involves the occipital cortex. In MOGAD and RRMS, lesion-related tract degeneration is associated with atrophy, but this link is absent in AQP4+NMOSD. ANN NEUROL 2024;96:276–288en
dc.format.mimetypeapplication/pdfca
dc.language.isoengca
dc.publisherJohn Wiley & Sons, Inc.ca
dc.relation.ispartofAnnals of Neurology, 2024, 96(2)ca
dc.relation.urihttps://onlinelibrary.wiley.com/doi/10.1002/ana.26951-
dc.rightsCC BY-NC-
dc.rights.urihttp://creativecommons.org/licenses/by-nc/3.0/es/-
dc.titleGrey matter atrophy and its relationship with white matter lesions in patients with myelin oligodendrocyte glycoprotein antibody-associated disease, aquaporin-4 antibody-positive neuromyelitis optica spectrum disorder, and multiple sclerosisen
dc.typeinfo:eu-repo/semantics/articleca
dc.rights.accessRightsinfo:eu-repo/semantics/openAccess-
dc.identifier.doihttps://doi.org/10.1002/ana.26951-
dc.gir.idAR/0000011759-
dc.type.versioninfo:eu-repo/semantics/publishedVersion-
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