Spinal cord injury (SCI) is a severe traumatic injury affecting the central nervous system, significantly impacting health and quality of life. The most common type of spinal cord injury in humans is a spinal cord contusion, which typically results from traumatic events causing a dislocation or fracture of the spine.

Spinal cord injury accounts for a significant portion of the global injury burden, primarily caused by falls and road traffic accidents, with prevalence varying by geographic region. Traumatic spinal cord injuries result in cell death and axonal degeneration, leading to loss of sensory and motor function. The disease progresses through primary and secondary

stages after the injury. Primary injury includes axonal damage, tissue necrosis, and death of neurons and glial cells resulting from stretching or tearing of the spinal cord. Secondary injury, initiated by molecular cascades and signaling pathways, leads to further axonal damage and cell membrane disintegration. The death of neurons and glial cells results in the production of free radicals and oxidative stress, both consequences of secondary damage. This secondary injury can also lead to myelin breakdown and demyelination. In response to this damage, astrocytes proliferate and replace injured neurons, forming a dense glial scar. This scar acts as a physical and chemical barrier, preventing axonal growth.

In addition, after a spinal cord puncture, neurons and glial cells gradually decrease and die. In addition to glial scarring, the inflammatory response impedes nerve healing. The role of inflammation in the spinal cord is a double-edged sword. While microglia and macrophages, the primary agents of the inflammatory response, help clear inflammatory components and dispose of waste, excessive accumulation of inflammatory cytokines and neurotoxins can negate these benefits and impede nerve repair.