Glatiramer acetate recovers microscopic tissue damage in patients with multiple sclerosis. A case-control diffusion imaging study

R Zivadinov; Sara Hussein; Milena Stosic; Jacqueline Durfee; Jennifer L Cox; Komal Hashmi; Nadir Abdelrahman; Neeta Garg; Michael G Dwyer; B Weinstock-Guttman

doi:10.1016/j.pathophys.2010.04.007

Glatiramer acetate recovers microscopic tissue damage in patients with multiple sclerosis. A case-control diffusion imaging study

Pathophysiology. 2011 Feb;18(1):61-8. doi: 10.1016/j.pathophys.2010.04.007. Epub 2010 May 26.

Authors

R Zivadinov¹, Sara Hussein, Milena Stosic, Jacqueline Durfee, Jennifer L Cox, Komal Hashmi, Nadir Abdelrahman, Neeta Garg, Michael G Dwyer, B Weinstock-Guttman

Affiliation

¹ Buffalo Neuroimaging Analysis Center, Department of Neurology, University of Buffalo, Buffalo, NY, United States; The Jacobs Neurological Institute, Department of Neurology, University of Buffalo, Buffalo, NY, United States.

PMID: 20510590
DOI: 10.1016/j.pathophys.2010.04.007

Abstract

Traditional magnetic resonance imaging (MRI) techniques have contributed to the management of multiple sclerosis (MS) but are limited in their ability to detect neuronal damage. Advanced MRI metrics provide assessment of microscopic neuronal changes; however, few studies have examined the effects of MS therapies on these measures. This prospective, open-label, observational study evaluated the effect of subcutaneous glatiramer acetate (GA) 20mg/day on the 1- and 2-year changes in diffusion-weighted imaging (DWI) measures in patients with relapsing-remitting (RR) MS and in age- and sex-matched healthy controls (HC). Inclusion criteria were age 18-65, RR disease course, expanded disability status scale (EDSS) score ≤5.5 and disease duration<20 years. MS patients and HC underwent 1.5T MRI scans and clinical examinations at baseline and at 1- and 2-year follow-up. Nineteen RRMS patients and 16 HC completed the 1-year follow-up and 16 MS patients and 13 HC the 2-year follow-up of the study. In MS patients, treatment with GA promoted recovery of DWI mean parenchymal diffusivity (MPD) at year 1 (-7.1%, p=0.007) and at year 2 (-10.1%, p=0.028). The recovery of DWI MPD was significantly higher in MS patients compared to HC at year 1 (p=0.01) and year 2 (p<0.001). GA promoted recovery of DWI entropy at 2 years (-1.2%, p=0.018). No significant DWI MPD and entropy changes were observed in HC over the follow-up. No significant deterioration in magnetization transfer ratio occurred over the follow-up in MS patients and HC. Patients on GA and HC did not develop significant global or regional atrophy over 2 years. GA significantly improved microscopic tissue damage in the brain, as measured by DWI over the 1- and 2-year follow-up.