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Effect of glatiramer acetate on cerebral grey matter pathology in patients with relapsing-remitting multiple sclerosis
Author(s): ,
F. Crescenzo
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
,
D. Marastoni
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
,
C. Zuco
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
,
M. Pitteri
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
,
R. Magliozzi
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
,
S. Monaco
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
M. Calabrese
Affiliations:
Department of Neurosciences, Biomedicine and Movement Sciences, Verona University, Verona, Italy
ECTRIMS Online Library. Crescenzo F. Oct 12, 2018; 229063
Francesco Crescenzo
Francesco Crescenzo
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Abstract: P1223

Type: Poster Sessions

Abstract Category: Therapy - Neuroprotection and Repair

Introduction: Despite its use as first-line therapy in relapsing-remitting multiple sclerosis (RRMS), no conclusive data about the efficacy of glatiramer acetate (GA) in preventing grey matter (GM) damage are available.
Aim: In this two-years, prospective study we compared the progression of grey matter (GM) damage in a group of RRMS patients treated with GA with respect to untreated MS patients.
Methods: We studied 35 RRMS patients treated with GA and 35 untreated RRMS patients matched for age, gender, disease duration and EDSS. Each patient underwent a neurological examination with EDSS evaluation every 6 months and a 3 T-MRI scan at study entry (T0), after 1 year (T1) and at 2 years (T2). At each time point the number of new cortical lesions (CLs) was assessed on double inversion recovery (DIR) images by consensus of two independent observers following the recommendations for CLs scoring. The images were processed by the longitudinal stream of FreeSurfer to establish the evolution of regional volumes and thickness of several cortical areas over two years.
Results: The mean number of new CLs was significantly lower in GA group compared to untreated patients both at T1 (0.9±1.0, range 0-3 vs 1.7±1.0, range 0-4; p< 0.05) and at T2 (1.4±1.3, range 0-5 vs 2.9±1.8, range 0-7; p< 0.001). Volume loss of thalamus (-0.5%±0.2% vs. -1.1%±0.4%; p< 0.001), globus pallidus (-4.4%±3.1% vs. -8.2%±4.5%; p< 0.001), hippocampus (-0.7%±0.3% vs. -1.5%±0.5%; p< 0.001) and cerebellum (-0.5%±0.3% vs. -0.9%±0.4%; p< 0.001) was also lower in the GA group. A more pronounced cortical thinning was observed in the cingulate (p=0.04), cuneus (p=0.01) and frontomarginal gyrus (p=0.01) of the untreated patients
Conclusion: Our findings suggest that GA exerts its immunomodulatory action at the level of GM either reducing the accumulation of CLs or slowing down diffuse GM atrophy. Thus in turn, even if confirmation in a larger sample size is required, early GA treatment may reducing the cortical tissue damage.
Disclosure: "F. Crescenzo: nothing to disclose", "D. Marastoni: nothing to disclose","C. Zuco: nothing to disclose","M. Pitteri: nothing to disclose", "R. Magliozzi:nothing to disclose", "S. Monaco: nothing to disclose", "M. Calabrese received honoraria for reasearch or speaking from Sanofi-Genzyme, Merck-Serono, Biogen Idec, Bayer, Novartis Pharma and funds for travel from Sanofi-Genzyme, Merck-Serono, Biogen Idec, Teva, Novartis Pharma, Roche and Bayer"

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