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Títol: 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
Autoria: Cortese, Rosa  
Battaglini, Marco
Prados Carrasco, Ferran  
Gentile, Giordano
Luchetti, Ludovico
Bianchi, Alessia  
Haider, Lukas  
Jacob, Anu
Palace, Jacqueline
Messina, Silvia  
paul, friedemann  
MARIGNIER, Romain  
Durand-Dubief, Françoise
de Medeiros Rimkus, Carolina
Apostolos Pereira, Samira Luisa
Sato, Douglas Kazutoshi  
Filippi, Massimo  
Rocca, Maria A  
Cacciaguerra, Laura
Rovira, Alex  
Sastre Garriga, Jaume  
Arrambide, Georgina  
刘, 亚欧  
Duan, Yunyun
gasperini, claudio  
Tortorella, Carla
Ruggieri, Serena
Pia Amato, Maria
Ulivelli, Monica
Groppa, Sergiu
Grothe, Matthias  
Llufriu, Sara  
Sepulveda, Maria  
Lukas, Carsten  
Bellenberg, Barbara
Schneider, Ruth
Sowa, Piotr
Celius, Elisabeth G.
Pröbstel, Anne-Katrin  
Granziera, Cristina
Yaldizli, Özgür
Müller, Jannis  
Stankoff, Bruno  
Bodini, Benedetta
Barkhof, Frederik
Ciccarelli, Olga
De Stefano, Nicola
MAGNIMS Study Group
Citació: Cortese, 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
Resum: Objective. 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;96:276–288
DOI: https://doi.org/10.1002/ana.26951
Tipus de document: info:eu-repo/semantics/article
Versió del document: info:eu-repo/semantics/publishedVersion
Data de publicació: 23-mai-2024
Llicència de publicació: http://creativecommons.org/licenses/by-nc/3.0/es/  
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