Up to this point, the discussion has focused on spinal cord injuries caused by blunt trauma and the role that ischemia plays in the secondary injury cascade. Ischemia alone, however, can also be the primary etiologic process behind paralysis in non-traumatic circumstances. Such is the case in patients undergoing thoracoabdominal aortic aneurysm (TAAA) repair. In these surgeries, the aorta is clamped and segmental vessels ligated, thus depriving the spinal cord of its blood supply to an extent that is influenced by the severity and location of the aneurysm and the duration of the vascular occlusion. The incidence of paralysis caused by this ischemic insult has been estimated between 3.8 to 17.6% (Crawford and Rubio, 1973), but has been reported to be as high as 28 to 41% after the repair of particular types of aneurysms (Crawford et al., 1986; Safi et al., 1996). As perioperative paraplegia is one of the most devastating complications of this surgery, a number of adjunctive treatments have been investigated as prophylactic or therapeutic interventions. These include generalized or local hypothermia, medications such as steroids, naloxone, barbiturates, papaverine, reattachment of intercostal arteries, and CSF drainage (Wan et al., 2001). In principle, these interventions aim to reduce spinal cord ischemia by either improving vascular perfusion (increasing cellular oxygen supply) or by reducing metabolic activity (decreasing cellular oxygen demand).