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

Department of Neurology, Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, University at Buffalo, State University of New York, Buffalo, NY, USA, rzivadinov{at}thejni.org

L. Locatelli

Department of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy

D. Cookfair

Department of Neurology, Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, University at Buffalo, State University of New York, Buffalo, NY, USA

B. Srinivasaraghavan

Department of Neurology, Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, University at Buffalo, State University of New York, Buffalo, NY, USA

A. Bertolotto

Centro Riferimento Regionale Sclerosi Multipla (CReSM) and Laboratori di Neurobiologia Clinica, Ospedale Universitario San Luigi, Orbassano, Italy

M. Ukmar

Department of Clinical, Morphological and Technological Sciences, University of Trieste, Trieste, Italy

A. Bratina

Department of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy

C. Maggiore

Department of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy

A. Bosco

Department of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy

A. Grop

Department of Neurology, Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, University at Buffalo, State University of New York, Buffalo, NY, USA

M. Catalan

Department of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy

M. Zorzon

Department of Clinical Medicine and Neurology, University of Trieste, Trieste, Italy

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 ß-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 ß-1a treatment group (IFN ß-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 ß-1a treatment group, and P<0.001 for the control group), a significant within-patient decrease in WMF for the IFN ß-1a treatment group (P=0.01), and a significant decrease in GMF for the control group (P=0.013) when compared with baseline.

Conclusion Over a three-year period, treatment with IFN ß-1a significantly slowed the progression of whole-brain and GM atrophy, and of T1-hypointense LV accumulation, when compared with the control group. Multiple Sclerosis 2007; 13: 490-501. http://msj.sagepub.com

Key Words: atrophy • brain atrophy • gray matter atrophy • interferon beta-1a • magnetic resonance imaging • multiple sclerosis • white matter atrophy

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