Albulena Bajrami1, Marco Pitteri1, Marco Castellaro1,2, Francesca Pizzini3, Chiara Romualdi4, Stefania Montemezzi3, Salvatore Monaco1, Massimiliano Calabrese5. 1. Neurology B, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Policlinico "G.B. Rossi" Borgo Roma, Piazzale L.A. Scuro, 10, 37134, Verona, Italy. 2. Department of Information Engineering, University of Padova, Padua, Italy. 3. Neuroradiology and Radiology Units, Department of Diagnostic and Pathology, University Hospital of Verona, Verona, Italy. 4. Department of Biology, University of Padova, Padua, Italy. 5. Neurology B, Department of Neurosciences, Biomedicine and Movement Sciences, University of Verona, Policlinico "G.B. Rossi" Borgo Roma, Piazzale L.A. Scuro, 10, 37134, Verona, Italy. massimiliano.calabrese@univr.it.
Abstract
INTRODUCTION: The mechanism of action of fingolimod within the central nervous system and its efficacy in reducing/preventing both focal and diffuse grey matter (GM) damage in active multiple sclerosis (MS) are not completely understood. METHODS: In this longitudinal, 2-year prospective, phase IV, single-blind study, 40 MS patients treated with fingolimod and 39 untreated age, gender, and disability-matched MS patients were enrolled. Each patient underwent a neurological examination every 6 months and a 3T MRI at the beginning of the treatment and after 24 months. The accumulation of new cortical lesions (CLs) and the progression of regional GM atrophy were compared between the two groups. RESULTS: At the end of the study (T24), the percentage of patients with new CLs (13.5 vs. 89%, p < 0.001) and the percentage of GM volume change was lower in the treated group (p < 0.001). The regional analysis revealed that the treated group had also less volume loss in thalamus, caudatus, globus pallidus, cingulate cortex, and hippocampus (p < 0.001), as well as in, cerebellum, superior frontal gyrus, and insular-long gyrus (p < 0.05). Patients with no evidence of disease activity were 60% in the treated group and 10% in the untreated group (p < 0.001). CONCLUSIONS: These results suggest a possible protective effect of fingolimod on focal and diffuse GM damage.
INTRODUCTION: The mechanism of action of fingolimod within the central nervous system and its efficacy in reducing/preventing both focal and diffuse grey matter (GM) damage in active multiple sclerosis (MS) are not completely understood. METHODS: In this longitudinal, 2-year prospective, phase IV, single-blind study, 40 MSpatients treated with fingolimod and 39 untreated age, gender, and disability-matched MSpatients were enrolled. Each patient underwent a neurological examination every 6 months and a 3T MRI at the beginning of the treatment and after 24 months. The accumulation of new cortical lesions (CLs) and the progression of regional GM atrophy were compared between the two groups. RESULTS: At the end of the study (T24), the percentage of patients with new CLs (13.5 vs. 89%, p < 0.001) and the percentage of GM volume change was lower in the treated group (p < 0.001). The regional analysis revealed that the treated group had also less volume loss in thalamus, caudatus, globus pallidus, cingulate cortex, and hippocampus (p < 0.001), as well as in, cerebellum, superior frontal gyrus, and insular-long gyrus (p < 0.05). Patients with no evidence of disease activity were 60% in the treated group and 10% in the untreated group (p < 0.001). CONCLUSIONS: These results suggest a possible protective effect of fingolimod on focal and diffuse GM damage.
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