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.
Physiologically speaking, spinal cord trauma differs from other types of central nervous system injuries. Instead of cell bodies (as in the brain), the spine is predominantly composed of long axon tracts. As such, spinal cord damage results in loss of sensory, motor, or autonomies function. More specifically, damage to the spinal cord prevents transmission of sensory information to the brain, as well as transmission of motor and autonomies commands from the brain to the body. Effectively, areas below the level of injury lose sensation and control, which manifests as numbness and paralysis. Full loss of sensation and control is considered a “complete” spinal cord injury, whereas partial loss of function is “incomplete.” Characteristic of the central nervous system, neurons of the spinal cord have limited regenerative abilities, rendering most injuries permanent.
The advantage of damaging an axon is that it does not necessarily imply the death of its corresponding neuron. Rather, via a process known as Wallerian degeneration, only the severed portion of an axon is lost; the remaining, nucleus—containing segment remains viable, with the potential for regrowth. However, a cocktail of inhibitory biochemical signals produced by the microenvironment of the spine seems to be partially responsible for its limited regenerative properties. An associated process of Wallerian degeneration is the demyelization of damaged axons. This important component of neurons normally surrounds the axon tract to effectively serve as an electrical insulator. Through this mechanism, speeds of signal propagation through the axon can increase up to 70-fold. Without myelination, axons in the spine transmit information too slowly to support a functional human being.
Lest one believe that the full extent of spinal cord injuries arises only from the primary event, it should be noted that a secondary insult comes about from physiologic causes. Local invasion of inflammatory components and changes in vascular integrity results in fluid and cellular accumulation, which exacerbates cord ...