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-Kingshott^7,8,9, 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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