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. 2022 Dec 1;13:1014013. doi: 10.3389/fimmu.2022.1014013

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Copyright © 2022 Fu, Chen, Pang, Zhang, Wu, Wan, Wan, Ao and Zhang

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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This figure shows the combination of pathophysiological events that occur post-SCI. This includes hemorrhage, oedema, inflammation, apoptosis, necrosis, oxidative damage, ischemia and vasospasm. Following primary injury, resident cells (astrocytes, microglia) are immediately activated and migrate to the site of injury. Subsequently, peripheral inflammatory cells, including neutrophils, macrophages and lymphocytes, infiltrate into the center of the damaged spinal cord. These activated immune cells can exacerbate the injury, causing neuronal death, which leads to axonal demyelination and disruption of synaptic transmission. In the subacute phase, fluid-filled cavities form in the center of the spinal cord. Astrocytes form a glial scar to isolate the damaged area. These sustained pathophysiological changes eventually lead to severe dysfunction below the damaged segment.