More MS news articles for Jan 2002

The effect of IFNß-1b on the evolution of enhancing lesions in secondary progressive MS

http://www.neurology.org/cgi/content/abstract/57/12/2185

Neurology 2001;57:2185-2190
P. A. Brex, MRCP, P. D. Molyneux, MD, P. Smiddy, FRCR, F. Barkhof, MD, M. Filippi, MD, T. A. Yousry, MD, D. Hahn, MD, Y. Rolland, MD, O. Salonen, MD, C. Pozzilli, PhD, C. H. Polman, MD, A. J. Thompson, FRCP, L. Kappos, MD and D. H. Miller
NMR Research Unit, Institute of Neurology, Queen Square, London, UK;
MR-MS centre, VU Medical Centre, Amsterdam, the Netherlands;
Neuroimaging Research Unit, Scientific Institute San Raffaele, University of Milan, Italy;
Department of Neuroradiology, Klinikum Gosshadern, Munich, Germany;
Institut for Röntgendiagnostik, Universitat Würzberg, Germany;
Department of Neurology, Centre Hospitalier, Universitaire, Rennes, France;
Department of Neurology, University of Helsinki, Finland;
Department of Neurology, La Sapienza, Rome, Italy;
Department of Neurology, University Hospitals, Kantonsspittal, Basal, Switzerland.

Background:

After the resolution of contrast enhancement, the majority of new MS lesions become isointense with surrounding white matter on T1-weighted MRI. Less commonly, a hypointense T1 lesion develops, representing the development of more severe focal tissue damage. Interferon beta (IFNß) reduces both the number of new enhancing lesions and the duration of contrast enhancement.

Objective:

To determine if IFNß affects the degree of tissue damage within new lesions and if its effects are related to lesion size.

Methods:

One hundred twenty-five patients with secondary progressive MS from seven European sites were randomized to receive either IFNß-1b or placebo. Monthly, contrast-enhanced T1-weighted MR images were acquired at baseline, at months 1 to 6, and at months 19 to 24. The size of all new enhancing lesions developing between months 1 and 6 was recorded and their appearance at follow-up documented.

Results:

In the first 6 months, fewer new enhancing lesions occurred in the IFNß-1b arm. This difference was greater for small (70% decrease) than for large (46% decrease) lesions. Hypointense T1 lesions were more likely to form from large (25%) than from small (9%) enhancing lesions in both treatment arms. Patients taking IFNß-1b developed fewer hypointense T1 lesions; however, the proportion of enhancing lesions developing into hypointense T1 lesions was similar in both arms.

Conclusion:

IFNß-1b reduced the number of new enhancing lesions, with a greater effect on small lesions. However, when a new enhancing lesion did become established, treatment with IFNß-1b did not alter its subsequent course.
 

© 2001 American Academy of Neurology