When a person experiences a spinal cord injury (SCI), the nerve fibers at the immediate point of damage are destroyed and experience necrosis. This is when the cells split open, leaking contents in the areas surrounding them, and provoke an inflammatory response. However, this is not the sole damage which occurs, as secondary degeneration can come into play and prove further impairment concerns.
The damage from the point of the injury itself does not remain in the immediate area but initiates a series of secondary events, delayed reactions, which spread outwards and cause destruction at further sites. This destructive response in the following hours after the trauma can lead to further functional impairment and permanent neurological deficit through the destruction of cells and circuits.
By disrupting the barrier between the blood and spinal cord, an inflammatory response is triggered. At the time, this inflammation is often indistinguishable as whether it is secondary degeneration damage after the spinal cord injury, or the body’s attempt at self-repair.
Unfortunately, the causes of secondary degeneration have not been identified conclusively, although some research has concentrated on diving into its occurrence at a cellular level in order to determine methods of effectively preventing, or treating, its onset. The discovery of a method of preventing secondary degeneration would greatly improve the prospects of spinal cord injury patients in regards to minimizing functional impairment.