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