TY - JOUR
T1 - Contribution of white matter lesions to gray matter atrophy in multiple sclerosis evidence from voxel-based analysis of T1 lesions in the visual pathway
AU - Sepulcre, Jorge
AU - Goñi, Joaquín
AU - Masdeu, Joseph C.
AU - Bejarano, Bartolome
AU - De Mendizábal, Nieves Vélez
AU - Toledo, Juan B.
AU - Villoslada, Pablo
N1 - Copyright:
Copyright 2009 Elsevier B.V., All rights reserved.
PY - 2009/2
Y1 - 2009/2
N2 - Background: The biological basis of gray matter (GM) atrophy in multiple sclerosis is not well understood, but GM damage seems to be the most critical factor leading to permanent disability. Objective: To assess to what extent white matter (WM) lesions contribute to regional GM atrophy in multiple sclerosis. Design: Because optic pathway GM atrophy and optic radiation lesions, rather than being related to each other, could be independent results of the disease, we applied a nonaprioristic WM method to analyze the interrelationships of both phenomena. On a voxel-by-voxel basis, we correlated T1 magnetic resonance imaging-derived lesion probability maps of the entire brain with atrophy of the lateral geniculate nuclei and calcarine/pericalcarine cortices. Setting: Multiple sclerosis center, University of Navarra, Pamplona, Spain. Patients: Sixty-one patients with multiple sclerosis. Main Outcome Measure: Mapping of WM regions contributing to GM atrophy in the optic pathway. Results: Patients with multiple sclerosis had lateral ge-niculate nucleus atrophy, which correlated with the presence of lesions specifically in the optic radiations but not in the rest of the brain. Optic pathway lesions explained up to 28% of the change of variance in lateral geniculate nucleus atrophy. Patients also had occipital cortex atrophy, which did not correlate with lesions in the optic radiations or any other WM region. Conclusions: Focal WM damage is associated with upstream GM atrophy, suggesting that retrograde damage of the perikarya from axonal injury in multiple sclerosis plaques is one of the significant factors in the genesis of GM atrophy, although other neurodegenerative processes are probably at work as well.
AB - Background: The biological basis of gray matter (GM) atrophy in multiple sclerosis is not well understood, but GM damage seems to be the most critical factor leading to permanent disability. Objective: To assess to what extent white matter (WM) lesions contribute to regional GM atrophy in multiple sclerosis. Design: Because optic pathway GM atrophy and optic radiation lesions, rather than being related to each other, could be independent results of the disease, we applied a nonaprioristic WM method to analyze the interrelationships of both phenomena. On a voxel-by-voxel basis, we correlated T1 magnetic resonance imaging-derived lesion probability maps of the entire brain with atrophy of the lateral geniculate nuclei and calcarine/pericalcarine cortices. Setting: Multiple sclerosis center, University of Navarra, Pamplona, Spain. Patients: Sixty-one patients with multiple sclerosis. Main Outcome Measure: Mapping of WM regions contributing to GM atrophy in the optic pathway. Results: Patients with multiple sclerosis had lateral ge-niculate nucleus atrophy, which correlated with the presence of lesions specifically in the optic radiations but not in the rest of the brain. Optic pathway lesions explained up to 28% of the change of variance in lateral geniculate nucleus atrophy. Patients also had occipital cortex atrophy, which did not correlate with lesions in the optic radiations or any other WM region. Conclusions: Focal WM damage is associated with upstream GM atrophy, suggesting that retrograde damage of the perikarya from axonal injury in multiple sclerosis plaques is one of the significant factors in the genesis of GM atrophy, although other neurodegenerative processes are probably at work as well.
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U2 - 10.1001/archneurol.2008.562
DO - 10.1001/archneurol.2008.562
M3 - Article
C2 - 19204153
AN - SCOPUS:60549091927
SN - 0003-9942
VL - 66
SP - 173
EP - 179
JO - Archives of neurology
JF - Archives of neurology
IS - 2
ER -