Regional brain atrophy in children with multiple sclerosis

被引:71
作者
Aubert-Broche, B. [1 ]
Fonov, V. [1 ]
Ghassemi, R. [1 ]
Narayanan, S. [1 ]
Arnold, D. L. [1 ]
Banwell, B. [2 ]
Sled, J. G. [3 ]
Collins, D. L. [1 ]
机构
[1] McGill Univ, Montreal Neurol Inst, McConnell Brain Imaging Ctr, Montreal, PQ, Canada
[2] Univ Toronto, Hosp Sick Children, Div Neurol, Toronto, ON M5G 1X8, Canada
[3] Univ Toronto, Hosp Sick Children, Ctr Phenogenom, Toronto, ON M5G 1X8, Canada
基金
加拿大健康研究院;
关键词
GRAY-MATTER ATROPHY; VOXEL-BASED MORPHOMETRY; GREY; MRI; MS; DISABILITY; VOLUME;
D O I
10.1016/j.neuroimage.2011.03.025
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
We used cross-sectional tensor-based morphometry to visualize reduced volume in the whole brains of pediatric patients with multiple sclerosis, relative to healthy controls. As a marker of local volume difference, we used the Jacobian determinant of the deformation field that maps each subject to a standard space. To properly assess abnormal differences in volume in this age group, it is necessary to account for the normal, age-related differences in brain volume. This was accomplished by computing normalized z-score Jacobian determinant values at each voxel to represent the local volume difference (in standard deviations) between an individual subject and an age- and sex-matched healthy normal population. Compared with healthy controls, pediatric patients with multiple sclerosis exhibited significantly reduced volumes within the thalamus and the splenium of the corpus callosum and significant expansions in the ventricles. While T2-weighted lesion volume was correlated with reduced splenium volume, no correlation was found between T2-weighted lesion volume and reduced thalamic volume. Reduced volumes of the optic pathways, including that of the optic tracts and optic radiations, correlated with disease duration. Our results suggest that focal inflammatory lesions may play an important role in tract degeneration, including transsynaptic degeneration. Crown Copyright (C) 2011 Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:409 / 415
页数:7
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