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SPINAL CORD INJURY is defined as damage to the spinal cord that results in partial or complete loss of function, whether temporary or permanent. In the United States, approximately 10,000 new spinal cord injury cases arise every year, bringing the prevalence to anywhere between 180,000 and 230,000 injuries. The three most common causes of spinal cord injury are direct trauma, compression by disk herniation, and damage caused by occluded spinal arteries. Although the range of symptoms that result from a spinal cord injury is largely determined by the size and location of the lesion, most patients will at least experience chronic pain accompanied by lifelong heart and lung complications. Current therapies focus on physical rehabilitation and counseling to deal with the emotional frustration of disability, but nothing can be done to regenerate the spinal cord. As such, research for treatments targets four main concepts: limiting the damage, neuroreconstruction, stimulating regrowth of neurons, and retraining neural circuits to restore body functions. Stem cells have shown great promise and potential for restoration of the damaged spine.

Mechanism of Injury

Most spinal cord injuries arise from a direct traumatic blow to the spine. Motor vehicle accidents, violent encounters, falls, and sports accidents cause the majority of these injuries. The destructive process, however, occurs in two steps. First, the initiating event dislocates or fragments the vertebrae, sending shards of bone into spinal cord tissue. This causes the obvious lesion. Following that, a slew of biochemical and cellular events alter the blood flow to and integrity of the surrounding vasculature. Leakage from the compromised blood vessels exacerbates compression of the spinal cord, and inflammatory agents trigger a huge invasion of immune system cells, causing even more cellular and fluid accumulation. The release of inflammatory signaling molecules, or cytokines, induces morphologic and functional changes in the supporting cells in the region. These, in turn, secrete their own signals to recruit more cells, bringing about additional fluid influx and cord compression. Aside from mechanically induced cell death, noninvolved neurons can also deteriorate because of overex—citement from an inappropriate release of neu—rotransmitters and improper cell—to-cell signaling. This ensuing cascade of inflammatory reactions causes a second wave of damage, which increases the area of the original injury, both horizontally and vertically, throughout the spinal cord. Damaged axons become dysfunctional, and inflammation results in scarring of the cord, which creates a barrier against future repairs. At this stage, spinal shock—a temporary but complete loss of sensory and motor functions—can occur.

Classification of Spinal Cord Injuries

After the injury has been stabilized, a complete neurological exam is performed to determine the true degree of damage. Injuries may be classified as either paraplegic (affecting only the lower extremities) or tétraplégie (affecting all four limbs, also known as quadriplegic). Approximately 40 percent of those with spinal cord injuries are tétraplégie, and the other 60 percent suffer from paraplegia. Within this breakdown, the American Spinal Injury Association has developed a more specific classification system to help predict the likelihood and extent of recovery. The categories range from an A level, at which no motor or sensory functions are retained below the level of injury (also referred to as a complete injury) to E—level injuries, in which motor and sensory functions are normal. Categories B through D are incomplete injuries, in which varying degrees of sensation and motor function are preserved.

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