http://link.springer.de/link/service/journals/00415/bibs/1248011/12480979.htm
Online publication: October 29, 2001
Journal of Neurology
Volume 248 Issue 11 (2001) pp 979-986
Sridar Narayanan (1), Nicola De
Stefano (1)(2), Gordon S. Francis (1), Rozie Arnaoutelis (1), Zografos
Caramanos (1), D. Louis Collins (1), Daniel Pelletier (1), Barry G. W.
Arnason (3), Jack P. Antel (1), Douglas L. Arnold (1)
(1) Montreal Neurological Institute,
3801 University Street, Montreal, Quebec H3A 2B4, Canada, Tel.: (514) 398-8185,
Fax: (514) 398-2975, E-mail: doug@mrs.mni.mcgill.ca
(2) Institute of Neurological Sciences,
Neurometabolic Unit, University of Siena, Italy
(3) Department of Neurology, Pritzker
School of Medicine, and the Brain Research Institute, University of Chicago,
Chicago Illinois, USA
Abstract
Patients with multiple sclerosis (MS) can benefit from treatment with interferon beta-1b. However, the mechanisms of action of this drug are incompletely understood and effects of interferon beta-1b on axonal injury are not known.
A measure of axonal injury can be obtained in vivo using magnetic resonance spectroscopy to quantify the resonance intensity of the neuronal marker, N-acetylaspartate (NAA).
In a small pilot study, we performed combined magnetic resonance imaging and magnetic resonance spectroscopic imaging on 10 patients with relapsing-remitting MS before and 1 year after starting treatment with subcutaneous interferon beta-1b.
Resonance intensities of NAA relative to creatine (Cr) were measured in a large, central brain volume.
These measurements were compared with those made in a group of 6 untreated patients selected to have a similar range of scores on the Expanded Disability Status Scale and mean NAA/Cr at baseline.
NAA/Cr in the treated group [2.74 (0.16), mean (SD)] showed an increase of 5.5 % 12 months after the start of therapy [2.89 (0.24), p = 0.05], while NAA/Cr in the untreated group decreased, but not significantly [2.76 (0.1) at baseline, 2.65 (0.14) at 12 months, p > 0.1].
NAA/Cr had become significantly higher in the treated group at 12 months than in the untreated group (p = 0.03).
Our data suggest that, in addition
to losing axons, patients with chronic multiple sclerosis suffer from chronic,
sublethal axonal injury that is at least partially reversible with interferon
beta-1b therapy.
© Steinkopff Verlag 2001