Abstract #1456

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 Ziegler^3,4, John Ashburner⁵, Karl Friston⁵, Nikolaus Weiskopf⁶, Armin Curt¹, and Patrick Freund^1,5,6,7

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

Synopsis

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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