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Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
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Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
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Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis

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Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis
Journal Article

Spatiotemporal distribution of white matter lesions in relapsing–remitting and secondary progressive multiple sclerosis

2012
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Overview
Background: Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system. MS lesions show a typical distribution pattern and primarily affect the white matter (WM) in the periventricular zone and in the centrum semiovale. Objective: To track lesion development during disease progression, we compared the spatiotemporal distribution patterns of lesions in relapsing–remitting MS (RRMS) and secondary progressive MS (SPMS). Methods: We used T1 and T2 weighted MR images of 209 RRMS and 62 SPMS patients acquired on two different 1.5 Tesla MR scanners in two clinical centers followed up for 25 (± 1.7) months. Both cross-sectional and longitudinal differences in lesion distribution between RRMS and SPMS patients were analyzed with lesion probability maps (LPMs) and permutation-based inference. Results: MS lesions clustered around the lateral ventricles and in the centrum semiovale. Cross-sectionally, compared to RRMS patients, the SPMS patients showed a significantly higher regional probability of T1 hypointense lesions (p≤0.03) in the callosal body, the corticospinal tract, and other tracts adjacent to the lateral ventricles, but not of T2 lesions (peak probabilities were RRMS: T1 9%, T2 18%; SPMS: T1 21%, T2 27%). No longitudinal changes of regional T1 and T2 lesion volumes between baseline and follow-up scan were found. Conclusion: The results suggest a particular vulnerability to neurodegeneration during disease progression in a number of WM tracts.