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I nterferon beta-1a slows progression of brain atrophy in relapsing-remitting multiple sclerosis predominantly by reducing gray matter atrophy

Background Brain atrophy, as assessed by magnetic resonance imaging (MRI), has been correlated with disability in patients with multiple sclerosis (MS). Recent evidence indicates that both white matter (WM) and gray matter (GM) are subject to atrophy in patients with MS. Although neurological defici...

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Bibliographic Details
Published in:Multiple sclerosis 2007-05, Vol.13 (4), p.490-501
Main Authors: Zivadinov, R., Locatelli, L., Cookfair, D., Srinivasaraghavan, B., Bertolotto, A., Ukmar, M., Bratina, A., Maggiore, C., Bosco, A., Grop, A., Catalan, M., Zorzon, M.
Format: Article
Language:English
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Summary:Background Brain atrophy, as assessed by magnetic resonance imaging (MRI), has been correlated with disability in patients with multiple sclerosis (MS). Recent evidence indicates that both white matter (WM) and gray matter (GM) are subject to atrophy in patients with MS. Although neurological deficiencies in MS are primarily due to loss of WM, the clinical significance of GM atrophy has not been fully explored in MS. Methods We have undertaken a three-year, open-label study, comparing 26 patients who elected to receive intramuscular interferon beta-1a (IFN β-1a) therapy, with 28 patients who elected not to receive therapy. Both groups had quantitative cranial MRI scans at study entry and after three years, and standardized clinical assessments every six months. Brain parenchymal fraction (BPF), GM fraction (GMF), and WM fraction (WMF) percent changes were calculated, and T2- and T1-lesion volumes (LVs) assessed. Results After three years, mean percent (%) change in BPF favored the IFN β-1a treatment group (IFN β-1a —1.3% versus the control group —2.5%, P=0.009), as did the mean percent change in GMF (+0.2 versus —1.4%, P=0.014), and the mean percent change in T1-LV (—9.3 versus +91.6%, P=0.011). At the end of the study, there was a significant within-patient decrease in BPF for both groups (P=0.02 for the IFN β-1a treatment group, and P
ISSN:1352-4585
1477-0970
DOI:10.1177/1352458506070446