Acute spinal cord injury: Pathophysiology and pharmacological intervention (Review)

Abstract

Spinal cord injury (SCI) is one of the most debilitating of all the traumatic conditions that afflict individuals. For a number of years, extensive studies have been conducted to clarify the molecular mechanisms of SCI. Experimental and clinical studies have indicated that two phases, primary damage and secondary damage, are involved in SCI. The initial mechanical damage is caused by local impairment of the spinal cord. In addition, the fundamental mechanisms are associated with hyperflexion, hyperextension, axial loading and rotation. By contrast, secondary injury mechanisms are led by systemic and cellular factors, which may also be initiated by the primary injury. Although significant advances in supportive care have improved clinical outcomes in recent years, a number of studies continue to explore specific pharmacological therapies to minimize SCI. The present review summarized some important pathophysiologic mechanisms that are involved in SCI and focused on several pharmacological and non-pharmacological therapies, which have either been previously investigated or have a potential in the management of this debilitating injury in the near future.

Multimodal therapy strategies based on hydrogels for the repair of spinal cord injury

“…Complex pathological change occurs in the central spinal cord after contusion, compression, or traumatic accident [ 1 ]. Spinal cord compression is the most common form of SCI and persists after injury [ 2 ]. It can lead to spinal canal hematomas.…”

“…It can lead to spinal canal hematomas. SCI is associated with bleeding in the early stages, followed by interruptions in the blood supply, which can lead to hypoxia and ischemic infarcts, both of which can damage gray matter with high metabolism and neurons and decrease the thickness of myelin, leading to a host of pathological changes [ 2 ].…”

“…Each model has slight differences in the degree of inflammatory infiltration, which hinders tissue regeneration. The functional loss caused by SCI is often lasting because of the limited regenerative ability of damaged neurons and the diffuse lesion site [ 2 , 25 ].…”

“…It leads to a gradual loss of motor and sensory function, which poses a threat to the patients’ health and seriously affects the life expectancy of patients. Long-term treatment, care costs and financial losses can affect patients and their families, causing social and physical problems [ 2 ]. However, effective treatments for SCI have not been developed to date.…”

Spinal Cord Injuries in Emergency Medicine

“…Excitotoxicity, oxidative damage, and ischemia can all be caused by high glutamate levels, whereas Ca2+dependent nitric oxide production can produce secondary spinal cord injury. Increased free radical damage and lipid peroxidation in the cell membrane, as well as additional injury signalling cascades in the wounded tissue locations, can eventually lead to neuronal death following secondary traumas [24][25][26][27][28][29][30][31].…”