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April 10, 2018; 90 (15) Editorial

The value of including thalamic atrophy as a clinical trial endpoint in multiple sclerosis

Menno M. Schoonheim, Olga Ciccarelli
First published March 14, 2018, DOI: https://doi.org/10.1212/WNL.0000000000005279
Menno M. Schoonheim
From the Department of Anatomy and Neurosciences (M.M.S.), Amsterdam Neuroscience, MS Center Amsterdam, VU University Medical Center, the Netherlands; Department of Neuroinflammation (O.C.), UCL Institute of Neurology, University College London; and National Institute for Health Research (O.C.), University College London Hospitals Biomedical Research Centre, UK.
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Olga Ciccarelli
From the Department of Anatomy and Neurosciences (M.M.S.), Amsterdam Neuroscience, MS Center Amsterdam, VU University Medical Center, the Netherlands; Department of Neuroinflammation (O.C.), UCL Institute of Neurology, University College London; and National Institute for Health Research (O.C.), University College London Hospitals Biomedical Research Centre, UK.
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The value of including thalamic atrophy as a clinical trial endpoint in multiple sclerosis
Menno M. Schoonheim, Olga Ciccarelli
Neurology Apr 2018, 90 (15) 677-678; DOI: 10.1212/WNL.0000000000005279

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Multiple sclerosis (MS) features a substantial white matter (WM) pathology in the brain, which manifests as focal lesions and reduced volume (or atrophy) compared with healthy controls. In addition, extensive gray matter (GM) atrophy is strongly prevalent in MS and highly clinically relevant but can be difficult to measure, especially in a clinical setting.1 Recent work has shown clear patterns of GM atrophy in patients with MS2 that are focused on brain network hubs, i.e., regions that are strongly connected with the rest of the brain. These areas are important for cognitive decline and disability progression and include the thalamus3 and other regions belonging to the default-mode2,4 and motor networks.2 There has been a recent surge of interest in the thalamus, with some hope that thalamic atrophy and its associated dysfunction may be a treatment target of especially high potential3 because thalamic atrophy can be measured relatively easily. The value of including thalamic atrophy as a trial endpoint in clinical trials with disease-modifying treatment in MS is emerging.5

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  • Go to Neurology.org/N for full disclosures. Funding information and disclosures deemed relevant by the authors, if any, are provided at the end of the editorial.

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  • © 2018 American Academy of Neurology
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