From the Neuroimaging Research Unit (M.A.R., P.V., A.M., P.P., M.F.), Division of Neuroscience, Neurology Unit (M.A.R., P.P., M.F.), Neurorehabilitation Unit, and Neurophysiology Service (M.F.), IRCCS San Raffaele Scientific Institute, Milan, Italy; Vita-Salute San Raffaele University (M.A.R., M.F.), Milan, Italy; Multiple Sclerosis Center (C.G., C.Z.), Department of Neurology, Neurocenter of Southern Switzerland, Civic Hospital; Faculty of Biomedical Sciences Università della Svizzera Italiana (C.G., C.Z.), Lugano, Switzerland; Section of Neuroradiology (A.R.), Department of Radiology, and Department of Neurology/Neuroimmunology (J.S.-G.), Multiple Sclerosis Center of Catalonia, Hospital Universitari Vall d'Hebron, Barcelona, Spain; NMR Research Unit (H.K., O.C.), Queen Square MS Centre, Department of Neuroinflammation, UCL Institute of Neurology, London; Nuffield Department of Clinical Neurosciences (L.M., J.P.), University of Oxford, UK; Department of Advanced Medical and Surgical Sciences (A.G., A.B.) and 3T MRI-Center (A.G., A.B.), University of Campania Luigi Vanvitelli, Naples, Italy; Institute of Neuroradiology at the Department of Radiology and Nuclear Medicine (C.L., B.B.), St. Josef Hospital, Ruhr University Bochum, Germany; Department of Radiology and Nuclear Medicine (F.B., H.V.), MS Center Amsterdam, Amsterdam Neuroscience Amsterdam UMC, location VUmc, the Netherlands; and Institutes of Neurology and Healthcare Engineering (F.B.), University College London, UK.
Neurology. 2021 Mar 16;96(11):e1561-e1573. doi: 10.1212/WNL.0000000000011494. Epub 2021 Jan 13.
Gay matter (GM) involvement is clinically relevant in multiple sclerosis (MS). Using source-based morphometry (SBM), we characterized GM atrophy and its 1-year evolution across different MS phenotypes.
Clinical and MRI data were obtained at 8 European sites from 170 healthy controls (HCs) and 398 patients with MS (34 with clinically isolated syndrome [CIS], 226 with relapsing-remitting MS [RRMS], 95 with secondary progressive MS [SPMS], and 43 with primary progressive MS [PPMS]). Fifty-seven HCs and 144 with MS underwent 1-year follow-up. Baseline GM loss, atrophy progression, and correlations with disability and 1-year clinical worsening were assessed.
SBM identified 26 cerebellar, subcortical, sensory, motor, and cognitive GM components. GM atrophy was found in patients with MS vs HCs in almost all components ( range <0.001-0.04). Compared to HCs, patients with CIS showed circumscribed subcortical, cerebellar, temporal, and salience GM atrophy, while patients with RRMS exhibited widespread GM atrophy. Cerebellar, subcortical, sensorimotor, salience, and frontoparietal GM atrophy was found in patients with PPMS vs HCs and in patients with SPMS vs those with RRMS. At 1 year, 21 (15%) patients had clinically worsened. GM atrophy progressed in MS in subcortical, cerebellar, sensorimotor, and fronto-temporo-parietal components. Baseline higher disability was associated ( = 0.65) with baseline lower normalized brain volume (β = -0.13, = 0.001), greater sensorimotor GM atrophy (β = -0.12, = 0.002), and longer disease duration (β = 0.09, = 0.04). Baseline normalized GM volume (odds ratio 0.98, = 0.008) and cerebellar GM atrophy (odds ratio 0.40, = 0.01) independently predicted clinical worsening (area under the curve 0.83).
GM atrophy differed across disease phenotypes and progressed at 1 year in MS. In addition to global atrophy measures, sensorimotor and cerebellar GM atrophy explained baseline disability and clinical worsening.
同性恋问题(GM)在多发性硬化症(MS)中具有临床相关性。我们使用基于源的形态测量学(SBM),描述了不同 MS 表型的 GM 萎缩及其 1 年的演变。
从 8 个欧洲站点获得了 170 名健康对照者(HCs)和 398 名 MS 患者(34 名患有临床孤立综合征 [CIS],226 名患有复发缓解型 MS [RRMS],95 名患有继发进展型 MS [SPMS],43 名患有原发进展型 MS [PPMS])的临床和 MRI 数据。57 名 HCs 和 144 名 MS 患者接受了 1 年的随访。评估了基线 GM 损失、萎缩进展以及与残疾和 1 年临床恶化的相关性。
SBM 确定了 26 个小脑、皮质下、感觉、运动和认知 GM 成分。与 HCs 相比,MS 患者的 GM 萎缩几乎存在于所有成分中(范围<0.001-0.04)。与 HCs 相比,CIS 患者表现为局限性皮质下、小脑、颞叶和突显 GM 萎缩,而 RRMS 患者则表现为广泛的 GM 萎缩。与 HCs 相比,PPMS 患者和 SPMS 患者均存在小脑、皮质下、感觉运动、突显和额顶颞叶 GM 萎缩。1 年后,21 名(15%)患者出现临床恶化。MS 患者的 GM 萎缩在皮质下、小脑、感觉运动和额颞顶叶成分中进展。基线时较高的残疾与基线时较低的正常化脑容量(β=-0.13, =0.001)、更大的感觉运动 GM 萎缩(β=-0.12, =0.002)和更长的疾病持续时间(β=0.09, =0.04)相关。基线时的正常化 GM 体积(比值比 0.98, =0.008)和小脑 GM 萎缩(比值比 0.40, =0.01)独立预测了临床恶化(曲线下面积 0.83)。
GM 萎缩在不同的疾病表型中存在差异,并在 MS 中 1 年内进展。除了整体萎缩测量外,感觉运动和小脑 GM 萎缩还解释了基线残疾和临床恶化。