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Abstract #4639

Proton Spectroscopic Imaging of Secondary Progressive Multiple Sclerosis in the MS-SMART trial

Ian Marshall1, Michael J Thrippleton1, Mark E Bastin1, Daisy Mollison1, David A Dickie1, Francesca Chappell1, Scott IK Semple2, Annette Cooper3, David Miller4, Sue Pavitt5, Gavin Giovannoni6, Claudia AM Gandini Wheeler-Kingshott7,8,9, Bhavana S Solanky7, Christopher Weir10, Nigel Stallard11, Clive Hawkins12, Basil Sharrack13, Moira Ross10, Jeremy Chataway4, Peter Connick1, Siddharthan Chandran1, and the MS-SMART trialists

1Centre for Clinical Brain Sciences, University of Edinburgh, Edinburgh, United Kingdom, 2Centre for Cardiovascular Sciences, University of Edinburgh, Edinburgh, United Kingdom, 3Clinical Research Imaging Centre, University of Edinburgh, Edinburgh, United Kingdom, 4Queen Square Multiple Sclerosis Centre, Department of Neuroinflammation, UCL Institute of Neurology, University College London, London, United Kingdom, 5Dental Translational and Clinical Research Unit, School of Dentistry, Faculty of Medicine and Health, University of Leeds, Leeds, United Kingdom, 6Department of Neurology, Barts and the London NHS Trust, London, United Kingdom, 7UCL Institute of Neurology, Queen Square MS Centre, University College London, London, United Kingdom, 8Department of Brain and Behavioural Sciences, University of Pavia, Pavia, Italy, 9Brain MRI 3T Mondino Research Center, C. Mondino National Neurological Institute, Pavia, Italy, 10Edinburgh Clinical Trials Unit, Usher Institute of Population Health Sciences and Informatics, University of Edinburgh, Edinburgh, United Kingdom, 11Division of Health Sciences, University of Warwick, United Kingdom, 12Institute for Science and Technology in Medicine, Keele University, United Kingdom, 13Academic Department of Neuroscience, Royal Hallamshire Hospital, Sheffield, United Kingdom

1H MR Spectroscopy yields metabolic information and has proved to be a useful addition to structural imaging in neurological diseases. We applied short-TE Spectroscopic Imaging combined with linear modelling with respect to brain tissue type in a homogeneous cohort of 42 patients with Secondary Progressive Multiple Sclerosis. Metabolite levels were significantly different in lesions compared with normal appearing tissues, suggesting axonal damage (reduced NAA) and increased glial activity (increased myo-inositol) yet relatively stable lesions (reduced Glx).

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