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

被引：1

作者：

Cortese, Rosa ^{[1
,2
]}

Battaglini, Marco ^{[1
,3
]}

Prados, Ferran ^{[2
,4
,5
]}

Gentile, Giordano ^{[1
,3
]}

Luchetti, Ludovico ^{[1
,3
]}

Bianchi, Alessia ^{[2
]}

Haider, Lukas ^{[2
]}

Jacob, Anu ^{[6
,7
]}

Palace, Jacqueline ^{[8
]}

Messina, Silvia ^{[8
]}

Paul, Friedemann ^{[9
,10
]}

Marignier, Romain ^{[11
]}

Durand-Dubief, Francoise ^{[11
]}

Rimkus, Carolina de Medeiros ^{[12
]}

Pereira, Samira Luisa Apostolos ^{[13
]}

Sato, Douglas Kazutoshi ^{[14
]}

Filippi, Massimo ^{[15
,16
,17
,18
,19
]}

Rocca, Maria Assunta ^{[15
,16
,19
]}

Cacciaguerra, Laura ^{[15
,16
]}

Rovira, Alex ^{[20
]}

Sastre-Garriga, Jaume ^{[21
]}

Arrambide, Georgina ^{[21
]}

Liu, Yaou ^{[22
]}

Duan, Yunyun ^{[22
]}

Gasperini, Claudio ^{[23
]}

Tortorella, Carla ^{[23
]}

Ruggieri, Serena ^{[24
,25
]}

Amato, Maria Pia ^{[26
,27
]}

Ulivelli, Monica ^{[1
]}

Groppa, Sergiu ^{[28
]}

Grothe, Matthias ^{[29
]}

Llufriu, Sara ^{[30
,31
]}

Sepulveda, Maria ^{[30
,31
]}

Lukas, Carsten ^{[2
,32
,33
]}

Bellenberg, Barbara ^{[32
]}

Schneider, Ruth ^{[32
,33
]}

Sowa, Piotr ^{[34
]}

Celius, Elisabeth G. ^{[35
,36
]}

Probstel, Anne-Katrin ^{[37
,38
,39
]}

Granziera, Cristina ^{[37
,38
,39
,40
]}

Yaldizli, Ozgur ^{[37
,38
,39
]}

Muller, Jannis ^{[37
,38
,39
,40
]}

Stankoff, Bruno ^{[41
]}

Bodini, Benedetta ^{[41
]}

Barkhof, Frederik ^{[4
,42
]}

Ciccarelli, Olga ^{[2
,43
]}

De Stefano, Nicola ^{[1
]}

机构：

[1] Univ Siena, Dept Med Surg & Neurosci, Siena, Italy

[2] UCL, UCL Queen Sq Inst Neurol, Fac Brain Sci, Queen Sq MS Ctr,Dept Neuroinflammat, London, England

[3] SIENA imaging SRL, Siena, Italy

[4] UCL, Ctr Med Imaging Comp Med Phys & Biomed Engn, London, England

[5] Univ Oberta Catalunya, Ehlth Ctr, Barcelona, Spain

[6] Walton Ctr, NMO Clin Serv, Liverpool, England

[7] Cleveland Clin, Dept Neurol, Abu Dhabi, U Arab Emirates

[8] John Radcliffe Hosp, Dept Clin Neurol, Oxford, England

[9] Max Delbrueck Ctr Mol Med, Expt & Clin Res Ctr, Berlin, Germany

[10] Charite Univ med Berlin, Berlin, Germany

[11] Hosp Civils Lyon, Pierre Wertheimer Neurol Hosp, Dept Neurol Multiple Sclerosis Myelin Disorders &, Lyon, France

[12] Univ Sao Paulo FMUSP, Fac Med, Dept Radiol & Oncol, Sao Paulo, Brazil

[13] Univ Sao Paulo FMUSP, Fac Med, Dept Neurol, Sao Paulo, Brazil

[14] Pontifical Catholic Univ Rio Grande Do Sul PUCRS, Sch Med, Porto Alegre, Brazil

[15] IRCCS San Raffaele Sci Inst, Div Neurosci, Neuroimaging Res Unit, Milan, Italy

[16] IRCCS San Raffaele Sci Inst, Neurol Unit, Milan, Italy

[17] IRCCS San Raffaele Sci Inst, Neurorehabil Unit, Milan, Italy

[18] IRCCS San Raffaele Sci Inst, Neurophysiol Serv, Milan, Italy

[19] Univ Vita Salute San Raffaele, Milan, Italy

[20] Univ Autonoma Barcelona, Hosp Univ Vall dHebron, Dept Radiol, Sect Neuroradiol, Barcelona, Spain

[21] Univ Autonoma Barcelona, Hosp Univ Vall dHebron, Multiple Sclerosis Ctr Catalonia Cemcat, Dept Neurol, Barcelona, Spain

[22] Capital Med Univ, Beijing Tiantan Hosp, Dept Radiol, Beijing, Peoples R China

[23] S Camillo Forlanini Hosp, Dept Neurosci, Rome, Italy

[24] Sapienza Univ Rome, Dept Human Neurosci, Rome, Italy

[25] IRCSS Fdn St Lucia, Neuroimmunol Unit, Rome, Italy

[26] Univ Florence, Dept Neurofarba, Florence, Italy

[27] IRCCS Don Carlo Gnocchi Fdn, Florence, Italy

[28] Johannes Gutenberg Univ Mainz, Univ Med Ctr, Dept Neurol, Mainz, Germany

[29] Univ Med Greifswald, Dept Neurol, Greifswald, Germany

[30] Hosp Clin Barcelona, Inst Invest Biomed August Pi i Sunyer IDIBAPS, Ctr Neuroimmunol, Serv Neurol,Lab Adv Imaging Neuroimmunol Dis, Barcelona, Spain

[31] Univ Barcelona, Barcelona, Spain

[32] Ruhr Univ Bochum, St Josef Hosp, Inst Neuroradiol, Bochum, Germany

[33] Ruhr Univ Bochum, St Josef Hosp, Dept Neurol, Bochum, Germany

[34] Oslo Univ Hosp, Div Radiol & Nucl Med, Oslo, Norway

[35] Univ Oslo, Oslo Univ Hosp, Dept Neurol, Oslo, Norway

[36] Univ Oslo, Fac Med, Oslo, Norway

[37] Univ Hosp, Dept Neurol Biomed & Clin Res, Basel, Switzerland

[38] Univ Hosp, Res Ctr Clin Neuroimmunol & Neurosci Basel, Basel, Switzerland

[39] Univ Basel, Basel, Switzerland

[40] Univ Hosp Basel, Dept Biomed Engn, Translat Imaging Neurol ThINk Basel, Basel, Switzerland

[41] Sorbonne Univ, Pitie Salpetriere Hosp, Paris Brain Inst, ICM, Paris, France

[42] Vrije Univ Amsterdam, Radiol & Nucl Med, Med Ctr, Amsterdam, Netherlands

[43] Univ Coll London Hosp UCLH, Natl Inst Hlth Res NIHR, Biomed Res Ctr, London, England

来源：

ANNALS OF NEUROLOGY | 2024年 / 96卷 / 02期

关键词：

NEURODEGENERATION; DEMYELINATION; MECHANISMS; CRITERIA; DAMAGE;

D O I：

10.1002/ana.26951

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

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 cm(3)); AQP4+NMOSD in the occipital cortex (32.83 cm(3)); and RRMS diffusely in the GM (260.61 cm(3)). MOGAD showed more pronounced temporal cortex atrophy than RRMS (6.71 cm(3)), whereas AQP4+NMOSD displayed greater occipital cortex atrophy than RRMS (19.82 cm(3)). RRMS demonstrated more pronounced deep GM atrophy in comparison with MOGAD (27.90 cm(3)) and AQP4+NMOSD (47.04 cm(3)). 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

引用

页码：276 / 288

页数：13

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