Cortese, Rosa; Battaglini, Marco; Prados, Ferran; Gentile, Giordano; Luchetti, Ludovico; Bianchi, Alessia; Haider, Lukas; ... De Stefano, Nicola; + view all Cortese, Rosa; Battaglini, Marco; Prados, Ferran; Gentile, Giordano; Luchetti, Ludovico; Bianchi, Alessia; Haider, Lukas; Jacob, Anu; Palace, Jacqueline; Messina, Silvia; Paul, Friedemann; Marignier, Romain; Durand-Dubief, Francoise; Rimkus, Carolina de Medeiros; Pereira, Samira Luisa Apostolos; Sato, Douglas Kazutoshi; Filippi, Massimo; Rocca, Maria Assunta; Cacciaguerra, Laura; Rovira, Alex; Sastre-Garriga, Jaume; Arrambide, Georgina; Liu, Yaou; Duan, Yunyun; Gasperini, Claudio; Tortorella, Carla; Ruggieri, Serena; Amato, Maria Pia; Ulivelli, Monica; Groppa, Sergiu; Grothe, Matthias; Llufriu, Sara; Sepulveda, Maria; Lukas, Carsten; Bellenberg, Barbara; Schneider, Ruth; Sowa, Piotr; Celius, Elisabeth G; Probstel, Anne-Katrin; Granziera, Cristina; Yaldizli, Ozgur; Muller, Jannis; Stankoff, Bruno; Bodini, Benedetta; Barkhof, Frederik; Ciccarelli, Olga; De Stefano, Nicola; - view fewer (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) pp. 276-288. 10.1002/ana.26951.

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Abstract

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

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