The body responds to a spinal cord injury in two phases, the primary injury and the secondary injury.

Primary injury: The primary injury includes the initial impact, compression, and contusion of the spinal cord (10, 13, 20). This phase damages nerve cells, axons, and blood vessels; bone fragments, injured vertebral material, and inflammation can maintain pressure on the spinal cord, compounding the damage. During this period, normal blood flow is disrupted resulting in oxygen deprivation to areas of the spinal cord (10, 13, 20). From the impact on the spine, the axonal membranes are disrupted causing an increase in electrolyte concentration at the injury site (13). This increases the amount of intracellular sodium, which then leads to activation of intracellular phospholipases, intracellular acidosis, and cell edema (13). Potassium concentrations also increase in extracellular spaces preventing axonal conduction, which may be the cause of the primary paralysis associated with a spinal cord injury (13). Calcium, which is responsible for the release of neurotransmitters at synaptic junctions and which maintains sodium and potassium concentrations during neural transmission, decreases after injury causing the release of phosphatase and phospholipase, which cause the injury to progress (13). In response to the injury, immune cells, which usually enter the central nervous system only as a result of injury (21), flow to the injured area, which begins the secondary injury. Primary injury leads to loss of nerve conduction, spinal neurogenic shock, bradycardia, as well as the problems associated with hemorrhaging in the gray matter as well as in the white matter if the injury is more severe. (13).