Traumatic spinal cord injury – transition from a focal lesion to widespread neurodegeneration: Lessons from 60-month observational data
Tim Max Emmenegger1, Dario Pfyffer1, Simon Schading1, Alan Thompson2, Gabriel Ziegler3,4, John Ashburner5, Karl Friston5, Nikolaus Weiskopf6, Armin Curt1, and Patrick Freund1,5,6,7
1Spinal Cord Injury Center, Balgrist University Hospital Zurich, University of Zurich, Zurich, Switzerland, 2Queen Square Multiple Sclerosis Centre, Institute of Neurology, University College London, London, United Kingdom, 3Institute of Cognitive Neurology and Dementia Research, Otto-von-Guericke-University Magdeburg, Magdeburg, Germany, 4German Center for Neurodegenerative Diseases (DZNE), Bonn, Germany, 5Wellcome Centre for Human Neuroimaging, Queen Square Institute of Neurology, University College London, London, United Kingdom, 6Department of Neurophysics, Max Planck Institute for Human Cognitive and Brain Sciences, Leipzig, Germany, 7Department of Brain Repair and Rehabilitation,, Queen Square Institute of Neurology, University College London, London, United Kingdom
Traumatic spinal cord injury (SCI) triggers a cascade of neurodegenerative events across the neuroaxis. The trajectories of lesion characteristics and brain and spinal cord macro-and microstructural changes were analysed over five years in 23 SCI patients and 21 healthy controls. Initially, SCI patients showed higher volume and iron content in the spinal cord which decreased over time. They showed lower myelin-sensitive MTsat values in the dorsal column and cortex which also decreased over time and were associated with acute lesion characteristics. These observations illustrate the widespread and progressive neuroplastic processes after SCI, its magnitude being predicted by acute lesion characteristics.
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