Melissa Cambron1,2, Tatjana Reynders3,4, Jan Debruyne5, Harmen Reyngoudt6, Annemie Ribbens7, Erik Achten6, Guy Laureys5. 1. Department of Neurology, Universitair Ziekenhuis Brussel, Jette, Belgium. melissa.cambron@gmail.com. 2. Department of Neurology, AZ Sint-Jan Hospital, Ruddershove 10, 8000, Brugge, Belgium. melissa.cambron@gmail.com. 3. Department of Neurology, Universitair Ziekenhuis Brussel, Jette, Belgium. 4. Department of Neurology, University Hospital Antwerp, Antwerp, Belgium. 5. Department of Neurology, University Hospital Ghent, Ghent, Belgium. 6. Department of Radiology and Nuclear Medicine, Ghent University, Ghent, Belgium. 7. Icometrix, Leuven, Belgium.
Abstract
BACKGROUND/ OBJECTIVES:Fluoxetine and prucalopride might change phosphocreatine (PCr) levels via the cAMP-PKA pathway, an interesting target in the neurodegenerative mechanisms of MS. METHODS: We conducted a two-center double-blind, placebo-controlled, randomized trial including 48 relapsing-remitting MS patients. Patients were randomized to receive placebo (n = 13), fluoxetine (n = 15), or prucalopride (n = 14) for 6 weeks. Proton (1H) and phosphorus (31P) magnetic resonance spectroscopy (MRS) as well as volumetric and perfusion MR imaging were performed at weeks 0, 2, and 6. Clinical and cognitive testing were evaluated at weeks 0 and 6. RESULTS: No significant changes were observed for both 31P and 1H MRS indices. We found a significant effect on white matter volume and a trend towards an increase in grey matter and whole brain volume in the fluoxetine group at week 2; however, these effects were not sustained at week 6 for white matter and whole brain volume. Fluoxetine and prucalopride showed a positive effect on 9-HPT, depression, and fatigue scores. CONCLUSION: Both fluoxetine and prucalopride had a symptomatic effect on upper limb function, fatigue, and depression, but this should be interpreted with caution. No effect of treatment was found on 31P and 1H MRS parameters, suggesting that these molecules do not influence the PCr metabolism.
RCT Entities:
BACKGROUND/ OBJECTIVES:Fluoxetine and prucalopride might change phosphocreatine (PCr) levels via the cAMP-PKA pathway, an interesting target in the neurodegenerative mechanisms of MS. METHODS: We conducted a two-center double-blind, placebo-controlled, randomized trial including 48 relapsing-remitting MSpatients. Patients were randomized to receive placebo (n = 13), fluoxetine (n = 15), or prucalopride (n = 14) for 6 weeks. Proton (1H) and phosphorus (31P) magnetic resonance spectroscopy (MRS) as well as volumetric and perfusion MR imaging were performed at weeks 0, 2, and 6. Clinical and cognitive testing were evaluated at weeks 0 and 6. RESULTS: No significant changes were observed for both 31P and 1HMRS indices. We found a significant effect on white matter volume and a trend towards an increase in grey matter and whole brain volume in the fluoxetine group at week 2; however, these effects were not sustained at week 6 for white matter and whole brain volume. Fluoxetine and prucalopride showed a positive effect on 9-HPT, depression, and fatigue scores. CONCLUSION: Both fluoxetine and prucalopride had a symptomatic effect on upper limb function, fatigue, and depression, but this should be interpreted with caution. No effect of treatment was found on 31P and 1HMRS parameters, suggesting that these molecules do not influence the PCr metabolism.
Entities:
Keywords:
Fluoxetine; Magnetic resonance spectroscopy; Multiple sclerosis; Phosphocreatine; Prucalopride
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