ABSTRACT
The pathophysiology of spinal cord injury (SCI) is a two-step process involving primary and secondary mechanisms. Clinical scenarios where impact alone occurs without ongoing compression may include severe ligamentous injuries in which the spinal column dislocates and then spontaneously reduces. Large vessels of the cord such as the anterior spinal artery and the anterior sulcal arteries, however, almost always remain patent even after severe cord injury. The molecular basis of spinal cord inflammation draws from a vast arsenal of known immunologic molecules, including cytokines and chemokines, as well as growth factors, trophic factors, and other agents. Upper motor neuron type of SCI initially leads to a phase of spinal shock, which is followed by a recovery phase during which neurologic changes emerge. During the period of spinal shock immediately after SCI, there is a flaccid paralysis and absence of reflex activity below the level of lesion; thus the urinary bladder becomes areflexic.
