Literature DB >> 20108225

Spatiotemporal distribution pattern of white matter lesion volumes and their association with regional grey matter volume reductions in relapsing-remitting multiple sclerosis.

Kerstin Bendfeldt1, Jan Ole Blumhagen, Hanspeter Egger, Patrick Loetscher, Niklaus Denier, Pascal Kuster, Stefan Traud, Nicole Mueller-Lenke, Yvonne Naegelin, Achim Gass, Jochen Hirsch, Ludwig Kappos, Thomas E Nichols, Ernst-Wilhelm Radue, Stefan J Borgwardt.   

Abstract

The association of white matter (WM) lesions and grey matter (GM) atrophy is a feature in relapsing-remitting multiple sclerosis (RRMS). The spatiotemporal distribution pattern of WM lesions, their relations to regional GM changes and the underlying dynamics are unclear. Here we combined parametric and non-parametric voxel-based morphometry (VBM) to clarify these issues. MRI data from RRMS patients with progressive (PLV, n = 45) and non-progressive WM lesion volumes (NPLV, n = 44) followed up for 12 months were analysed. Cross-sectionally, the spatial WM lesion distribution was compared using lesion probability maps (LPMs). Longitudinally, WM lesions and GM volumes were studied using FSL-VBM and SPM5-VBM, respectively. WM lesions clustered around the lateral ventricles and in the centrum semiovale with a more widespread pattern in the PLV than in the NPLV group. The maximum local probabilities were similar in both groups and higher for T2 lesions (PLV: 27%, NPLV: 25%) than for T1 lesions (PLV: 15%, NPLV 14%). Significant WM lesion changes accompanied by cortical GM volume reductions occurred in the corpus callosum and optic radiations (P = 0.01 corrected), and more liberally tested (uncorrected P < 0.01) in the inferior fronto-occipital and longitudinal fasciculi, and corona radiata in the PLV group. Not any WM or GM changes were found in the NPLV group. In the PLV group, WM lesion distribution and development in fibres, was associated with regional GM volume loss. The different spatiotemporal distribution patterns of patients with progressive compared to patients with non-progressive WM lesions suggest differences in the dynamics of pathogenesis.
© 2010 Wiley-Liss, Inc.

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Year:  2010        PMID: 20108225      PMCID: PMC6870732          DOI: 10.1002/hbm.20951

Source DB:  PubMed          Journal:  Hum Brain Mapp        ISSN: 1065-9471            Impact factor:   5.038


  77 in total

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4.  Neocortical volume decrease in relapsing-remitting MS patients with mild cognitive impairment.

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7.  Progression of gray matter atrophy and its association with white matter lesions in relapsing-remitting multiple sclerosis.

Authors:  K Bendfeldt; L Kappos; E W Radue; S J Borgwardt
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8.  Structural brain abnormalities in individuals with an at-risk mental state who later develop psychosis.

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9.  Regional gray matter atrophy in early primary progressive multiple sclerosis: a voxel-based morphometry study.

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2.  Longitudinal gray matter changes in multiple sclerosis--differential scanner and overall disease-related effects.

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Journal:  Hum Brain Mapp       Date:  2011-04-29       Impact factor: 5.038

Review 3.  Neuroimaging in multiple sclerosis: neurotherapeutic implications.

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4.  Longitudinal spatiotemporal distribution of gray and white matter pathology in multiple sclerosis.

Authors:  K Bendfeldt; L Kappos; E W Radue; S Borgwardt
Journal:  AJNR Am J Neuroradiol       Date:  2010-03-11       Impact factor: 3.825

5.  Impact of Lesion Location on Longitudinal Myelin Water Fraction Change in Chronic Multiple Sclerosis Lesions.

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6.  Corpus callosum atrophy correlates with gray matter atrophy in patients with multiple sclerosis.

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7.  Cognitive impairment in multiple sclerosis is associated to different patterns of gray matter atrophy according to clinical phenotype.

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8.  Disability-Specific Atlases of Gray Matter Loss in Relapsing-Remitting Multiple Sclerosis.

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9.  The effect of hypointense white matter lesions on automated gray matter segmentation in multiple sclerosis.

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Journal:  Hum Brain Mapp       Date:  2011-10-05       Impact factor: 5.038

10.  Lesion load may predict long-term cognitive dysfunction in multiple sclerosis patients.

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