The body responds to a spinal
cord injury in two phases, the primary injury and the secondary
injury: The primary injury includes the initial impact,
compression, and contusion of the spinal cord (10,
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,
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
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.