Exploring the effect of glatiramer acetate on cerebral gray matter atrophy in multiple sclerosis

Background and purpose

Cerebral gray matter (GM) atrophy is a proposed measure of neuroprotection in multiple
sclerosis (MS). Glatiramer acetate (GA) limits clinical relapses, MRI lesions, and
whole brain atrophy in relapsing-remitting MS (RRMS). The effect of GA on GM atrophy
remains unclear. We assessed GM atrophy in patients with RRMS starting GA therapy
in comparison to a cohort of patients with clinically benign RRMS (BMS).


We studied 14 patients at GA start [age (mean ± SD) 44.2 ± 7.0 years, disease duration
(DD) 7.2 ± 6.4 years, Expanded Disability Status Scale score (EDSS) (median,IQR) 1.0,2.0]
and 6 patients with BMS [age 43.0 ± 6.1 years, DD 18.1 ± 8.4 years, EDSS 0.5,1.0].
Brain MRI was obtained at baseline and one year later (both groups) and two years
later in all patients in the GA group except one who was lost to follow-up. Semi-automated
algorithms assessed cerebral T2 hyperintense lesion volume (T2LV), white matter fraction
(WMF), GM fraction (GMF), and brain parenchymal fraction (BPF). The exact Wilcoxon-Mann-Whitney
test compared the groups. The Wilcoxon signed rank test assessed longitudinal changes
within groups.


During the first year, MRI changes did not differ significantly between groups (p > 0.15). Within the BMS group, WMF and BPF decreased during the first year (p = 0.03). Within the GA group, there was no significant change in MRI measures during
each annual period (p > 0.05). Over two years, the GA group had a significant increase in T2LV and decrease
in WMF (p < 0.05), while GMF and BPF remained stable (p > 0.05). MRI changes in brain volumes
(GMF or WMF) in the first year in the GA group were not significantly different from
those in the BMS group (p > 0.5).


In this pilot study with a small sample size, patients with RRMS started on GA did
not show significant GM or whole brain atrophy over 2 years, resembling MS patients
with a clinically benign disease course.

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