Abstract #0998
Multi-channel 7 Tesla sodium MRI of the brain in children with epileptogenic SCN1A sodium channel mutations – a pilot study
Jon Orlando Cleary1, Samuel Rot2,3, Michael Ayre4,5,6, Philippa Bridgen6, Ayse Sila Dokumaci5,6, Yasmin Blunck7, Warda Syeda8, Bhavana S Solanky2,9, Shaihan J Malik5,6, Ming Lim4, Claudia A.M. Gandini Wheeler-Kingshott2,10,11, Shan-Shan Tang4, and David W Carmichael5,6
1Department of Radiology, Imperial College Healthcare NHS Trust, London, United Kingdom, 2MR Research Unit, Queen Square MS Centre, Faculty of Brain Sciences, UCL Queen Square Institute of Neurology, London, United Kingdom, 3Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom, 4Children's Neurosciences, Evelina London Children's Hospital at Guy's and St Thomas' NHS Foundation Trust, London, United Kingdom, 5Biomedical Engineering Department, School of Biomedical Engineering and Imaging Sciences, King's College London, London, United Kingdom, 6London Collaborative Ultra High Field System (LoCUS), London, United Kingdom, 7Melbourne Brain Centre Imaging Unit, The University of Melbourne, Parkville, Melbourne, Australia, 8Melbourne Neuropsychiatry Centre, The University of Melbourne, Parkville, Melbourne, Australia, 9Quantitative Imaging Group, Department of Medical Physics and Biomedical Engineering, University College London, London, United Kingdom, 10Department of Brain & Behavioural Sciences, University of Pavia, Pavia, Italy, 11Brain Connectivity Centre Research Department, IRCCS Mondino Foundation, Pavia, Italy
Synopsis
Keywords: Epilepsy, Non-Proton, brain, sodium MRI, high-field MRI, SCN1ASCN1A gene mutations disrupt sodium channel (NaV1.1) function, causing childhood epilepsy which can be severe. Predicting functional consequences in these children is challenging and new prognostic imaging biomarkers are needed. Sodium MRI directly assesses brain sodium and is a potential in vivo imaging biomarker. Using a multiecho sodium sequence, at 7T, we found children with SCN1A mutations had increased relative sodium concentrations across a large number of brain regions compared to controls. The cause of this change is likely complex, and may reflect an interplay between neuronal/axonal/glial dysfunction – with disruptions in microstructure and physiology – and possible medication effects.
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