The natural history and pathogenesis of ischemic spinal cord infarction remain largely unknown because most clinical studies have included mostly patients with ischemic lesions associated with aortic surgery or prolonged arterial hypotension. To assess the pathogenetic mechanisms and outcomes of these cord infarctions based on clinical findings and spinal vascular anatomy. Retrospective review. We analyzed the clinical, laboratory, imaging, and outcome data for 27 patients with acute spinal cord infarction admitted between 1990 and 2003. There were 11 men and 16 women (age range, 19-80 years [mean age, 56 years]). Ten patients had anterior spinal artery patterns, 4 each had anterior and posterior unilateral patterns, 3 had central patterns, and 2 each had posterior spinal artery patterns, transverse syndromes, and unclassifiable clinical pictures. Twenty patients had no identifiable etiology. Patients with a central or transverse infarct showed a high frequency of peripheral vascular disease, and all transverse infarcts occurred following prolonged arterial hypotension. The onset of all other infarcts was associated with mechanical triggering movements (P = .02), and these patients frequently had diseases of the spine (P = .003) at the level of the spinal lesion, with the clinical data suggesting root involvement at the level of the spinal cord lesion and pointing to mechanical injury of a radicular artery. The outcomes were favorable, with only 13 patients showing significant gait impairment on leaving the hospital. There are 2 main types of spinal cord ischemia: (1) radicular artery territory infarct (bilateral anterior or posterior spinal artery infarcts and unilateral infarcts) and (2) extensive spinal cord hypoperfusion (central and transverse infarcts). Each type has characteristic clinical, imaging, pathogenetic, and prognostic features.