Abstract

<p indent="0mm">Spinal cord injury causes necrosis of nerve tissue, disruption of conduction pathways, loss of movement and sensation below the injury level, resulting in paralysis and even death. The pathological changes of spinal cord injury are extremely complex. At the early stage, the changes were mainly at the molecular/gene level, while the changes at the cell/tissue level were mainly in the subacute stage. These changes cause secondary damage, resulting in tissue necrosis, neuron death, axon rupture, the formation of cystic cavities wrapped by scar tissue and the subsequent inhibition of axon regeneration. At present, the function of the damaged nerve cannot be fundamentally improved by surgical decompression alone, or by symptomatic intervention with drugs. There are several reasons for the difficulty in functional recovery after spinal cord injury: inflammatory reactions take place through the whole process of spinal cord injury, and the inflammatory mediators lead to degeneration and necrosis of neurons and glial cells in the injured area, and axon atrophy due to valerosis. Regeneration of neurons and axons are both weak, and scar tissues prevent axons from crossing the damaged area to form connection with the contralateral axons. This article reviews the pathological changes after spinal cord injury and discusses the repair strategies.

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