The causes of spinal cord ischemia (SCI) are as multiple as those of cerebral infarction. In the fetal stage, the spinal cord is provided with an extensive arterial network guaranteeing arterial blood supply. This extensive network gradually regresses during maturation. True spinal arterial transient ischemic attacks (TIAs), for example, due to cardiac embolism, from extensive aortic atheromatous lesions, or intermittent radicular artery mechanical compression, are rare events (6% of ischemic events in the spinal cord). The differential diagnosis includes other acute myelopathies, of traumatic, compressive, infectious, and inflammatory origin. SCI shares with cerebral infarction a common range of vascular disorders that includes general hypoxia and ischemia, cardiogenic embolism, disorders of the vessel wall (atherosclerosis, vasculitis, collagen and elastin disorders), blood dyscrasias (polycythemia, hypercoagulability), arteriovenous malformations (AVM), paradoxical embolism via patent foramen ovale, and cocaine use.