A common set of biological events take place following spinal cord injury:
Cells from the immune system migrate to the injury site, causing additional damage to some neurons and death to others that survived the initial trauma.
The death of oligodendrocytes causes axons to lose their myelination, which greatly impairs the conduction of action potential, messages, or renders the remaining connections useless. The neuronal information highway is further disrupted because many axons are severed, cutting off the lines of communication between the brain and muscles and between the body's sensory systems and the brain.
Within several weeks of the initial injury, the area of tissue damage has been cleared away by microglia, and a fluid-filled cavity surrounded by a glial scar is left behind. Molecules that inhibit regrowth of severed axons are now expressed at this site. The cavitation is called a syrinx, which acts as a barrier to the reconnection of the two sides of the damaged spinal cord.
Although spinal cord injury causes complex damage, a surprising amount of the basic circuitry to control movement and process information can remain intact. This is because the spinal cord is arranged in layers of circuitry. Many of the connections and neuronal cell bodies forming this circuitry above and below the site of injury survive the trauma. An important question to research scientists is, how much do these surviving neurons "know?" Can they regenerate and make new, correct connections?