Axonal metabolic recovery in multiple sclerosis patients treated with interferon beta-1b

Citation
S. Narayanan et al., Axonal metabolic recovery in multiple sclerosis patients treated with interferon beta-1b, J NEUROL, 248(11), 2001, pp. 979-986
Citations number
62
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF NEUROLOGY
ISSN journal
03405354 → ACNP
Volume
248
Issue
11
Year of publication
2001
Pages
979 - 986
Database
ISI
SICI code
0340-5354(200111)248:11<979:AMRIMS>2.0.ZU;2-Y
Abstract
Patients with multiple sclerosis (MS) can benefit from treatment with inter feron beta -1b. However, the mechanisms of action of this drug are incomple tely 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 r esonance spectroscopy to quantify the resonance intensity of the neuronal m arker, N-acetylas-partate (NAA). In a small pilot study, we performed combi ned magnetic resonance imaging and magnetic resonance spectroscopic imaging on 10 patients with relapsing-remitting MS before and 1 year after startin g treatment with subcutaneous interferon beta -1b. Resonance intensities of NAA relative to creatine (Cr) were measured in a large, central brain volu me. These measurements were compared with those made in a group of 6 untrea ted patients selected to have a similar range of scores on the Expanded Dis ability Status Scale and mean NAA/Cr at baseline. NAA/Cr in the treated gro up [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 gr oup decreased, but not significantly [2.76 (0.1) at baseline, 2.65 (0.14) a t 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 sugges t that, in addition to losing axons, patients with chronic multiple scleros is suffer from chronic, sublethal axonal injury that is at least partially reversible with interferon beta -1b therapy.