What is spinal cord injury (SCI)?

A spinal cord injury (SCI) refers to damage to the spinal cord that results in loss of function, sensation, or mobility. The spinal cord is a bundle of nerves that runs from the base of the brain down the vertebral column (backbone) and is responsible for transmitting signals between the brain and the rest of the body. SCI can lead to various degrees of paralysis and loss of sensation below the level of injury.


Spinal cord injuries can occur due to trauma, such as a sudden blow or impact to the spine, which may result from motor vehicle accidents, falls, sports injuries, or acts of violence. They can also result from non-traumatic causes, such as infections, tumors, or degenerative diseases affecting the spinal cord.


The severity and symptoms of a spinal cord injury depend on the location and extent of damage to the spinal cord. In general, SCI is classified as either complete or incomplete:


  • Complete SCI: In a complete spinal cord injury, there is a total loss of sensation and motor function below the level of injury. This means that the individual has no voluntary movement or sensation in the affected areas.


  • Incomplete SCI: In an incomplete spinal cord injury, there is some degree of preservation of sensation or motor function below the level of injury. The extent of impairment can vary widely, with some individuals experiencing partial paralysis or sensory loss while retaining some function.


What is the relationship between SCI and oxidative stress?

Spinal cord injury (SCI) can lead to oxidative stress, which is an imbalance between the production of reactive oxygen species (ROS) and the body’s ability to detoxify them or repair the resulting damage. Here’s how SCI contributes to oxidative stress:


  • Acute Inflammatory Response: Following SCI, there is an acute inflammatory response characterized by the activation of immune cells and the release of pro-inflammatory cytokines. This inflammatory cascade can trigger the production of ROS by immune cells, exacerbating oxidative stress in the injured spinal cord tissue.


  • Ischemia-Reperfusion Injury: SCI can disrupt blood flow to the spinal cord, leading to ischemia (reduced blood supply) followed by reperfusion (restoration of blood flow). The reperfusion phase is associated with the generation of ROS due to the sudden reintroduction of oxygen to ischemic tissues. This ischemia-reperfusion injury contributes to oxidative stress and further damage to the spinal cord.


  • Mitochondrial Dysfunction: SCI can impair mitochondrial function in spinal cord cells. Mitochondria are the primary producers of ROS within cells, and dysfunction of these organelles can lead to excessive ROS production. Mitochondrial dysfunction following SCI contributes to oxidative stress and cellular damage in the injured spinal cord tissue.


  • Activation of Oxidative Enzymes: SCI can activate oxidative enzymes, such as NADPH oxidase and xanthine oxidase, which are involved in the generation of ROS. These enzymes can become upregulated in response to inflammation and tissue damage, leading to increased ROS production and oxidative stress in the spinal cord.


  • Loss of Antioxidant Defenses: SCI can disrupt the body’s antioxidant defense systems, which normally help neutralize ROS and protect cells from oxidative damage. This may involve a decrease in the activity of antioxidant enzymes such as superoxide dismutase, catalase, and glutathione peroxidase, leaving cells more vulnerable to oxidative stress.


Overall, the relationship between spinal cord injury and oxidative stress is bidirectional, with oxidative stress contributing to the secondary damage and pathology observed following SCI, and SCI itself exacerbating oxidative stress.