• Jorge Sepulcre, Joaquín Goñi, Joseph C Masdeu, Bartolome Bejarano, Nieves Vélez de Mendizábal, Juan B Toledo, and Pablo Villoslada.
• Departamento de Neurología, Clínica Universitaria de Navarra, Universidad de Navarra, Pío XII 36, 31008 Pamplona, Navarra, Spain.
• Arch. Neurol. 2009 Feb 1;66(2):173-9.

BackgroundThe 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.ObjectiveTo assess to what extent white matter (WM) lesions contribute to regional GM atrophy in multiple sclerosis.DesignBecause 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.SettingMultiple sclerosis center, University of Navarra, Pamplona, Spain.PatientsSixty-one patients with multiple sclerosis.Main Outcome MeasureMapping of WM regions contributing to GM atrophy in the optic pathway.ResultsPatients with multiple sclerosis had lateral geniculate 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.ConclusionsFocal 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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