Irene M Vavasour1, Roger Tam2, David Kb Li3, Cornelia Laule4, Carolyn Taylor5, Shannon H Kolind6, Alex L MacKay7, Adil Javed8, Anthony Traboulsee9. 1. Department of Radiology and UBC MRI Research Centre, The University of British Columbia, Vancouver, BC, Canada. 2. Department of Radiology, The University of British Columbia, Vancouver, BC, Canada/School of Biomedical Engineering, The University of British Columbia, Vancouver, BC, Canada. 3. Department of Radiology, The University of British Columbia, Vancouver, BC, Canada/Division of Neurology, Department of Medicine, The University of British Columbia, Vancouver, BC, Canada. 4. Department of Radiology, The University of British Columbia, Vancouver, BC, Canada/Department of Pathology & Laboratory Medicine, The University of British Columbia, Vancouver, BC, Canada/Department of Physics & Astronomy, The University of British Columbia, Vancouver, BC, Canada/International Collaboration on Repair Discoveries, The University of British Columbia, Vancouver, BC, Canada. 5. Department of Statistics, The University of British Columbia, Vancouver, BC, Canada. 6. Department of Radiology, The University of British Columbia, Vancouver, BC, Canada/Division of Neurology, Department of Medicine, The University of British Columbia, Vancouver, BC, Canada/Department of Physics & Astronomy, The University of British Columbia, Vancouver, BC, Canada/International Collaboration on Repair Discoveries, The University of British Columbia, Vancouver, BC, Canada. 7. Department of Radiology, The University of British Columbia, Vancouver, BC, Canada/Department of Physics & Astronomy, The University of British Columbia, Vancouver, BC, Canada. 8. Department of Neurology, The University of Chicago, Chicago, IL, USA. 9. Division of Neurology, Department of Medicine, The University of British Columbia, Vancouver, BC, Canada.
Abstract
BACKGROUND: Tissue damage in both multiple sclerosis (MS) lesions and normal-appearing white matter (NAWM) are important contributors to disability and progression. Specific aspects of MS pathology can be measured using advanced imaging. Alemtuzumab is a humanised monoclonal antibody targeting CD52 developed for MS treatment. OBJECTIVE: To investigate changes over 2 years of advanced magnetic resonance (MR) metrics in lesions and NAWM of MS patients treated with alemtuzumab. METHODS: A total of 42 relapsing-remitting alemtuzumab-treated MS subjects were scanned for 2 years at 3 T. T1 relaxation, T2 relaxation, diffusion tensor, MR spectroscopy and volumetric sequences were performed. Mean T1 and myelin water fraction (MWF) were determined for stable lesions, new lesions and NAWM. Fractional anisotropy was calculated for the corpus callosum (CC) and N-acetylaspartate (NAA) concentration was determined from a large NAWM voxel. Brain parenchymal fraction (BPF), cortical thickness and CC area were also calculated. RESULTS: No change in any MR measurement was found in lesions or NAWM over 24 months. BPF, cortical thickness and CC area all showed decreases in the first year followed by stability in the second year. CONCLUSION: Advanced MR biomarkers of myelin (MWF) and neuron/axons (NAA) show no change in NAWM over 24 months in alemtuzumab-treated MS participants.
BACKGROUND: Tissue damage in both multiple sclerosis (MS) lesions and normal-appearing white matter (NAWM) are important contributors to disability and progression. Specific aspects of MS pathology can be measured using advanced imaging. Alemtuzumab is a humanised monoclonal antibody targeting CD52 developed for MS treatment. OBJECTIVE: To investigate changes over 2 years of advanced magnetic resonance (MR) metrics in lesions and NAWM of MS patients treated with alemtuzumab. METHODS: A total of 42 relapsing-remitting alemtuzumab-treated MS subjects were scanned for 2 years at 3 T. T1 relaxation, T2 relaxation, diffusion tensor, MR spectroscopy and volumetric sequences were performed. Mean T1 and myelin water fraction (MWF) were determined for stable lesions, new lesions and NAWM. Fractional anisotropy was calculated for the corpus callosum (CC) and N-acetylaspartate (NAA) concentration was determined from a large NAWM voxel. Brain parenchymal fraction (BPF), cortical thickness and CC area were also calculated. RESULTS: No change in any MR measurement was found in lesions or NAWM over 24 months. BPF, cortical thickness and CC area all showed decreases in the first year followed by stability in the second year. CONCLUSION: Advanced MR biomarkers of myelin (MWF) and neuron/axons (NAA) show no change in NAWM over 24 months in alemtuzumab-treated MS participants.
Entities:
Keywords:
MRI; Multiple sclerosis; alemtuzumab; longitudinal; multicentre; myelin water
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