Steal is a pathophysiological process in which increased blood flow through a low-resistance vascular bed is sufficient to divert flow away from a region of the central nervous system. Three disease states in which steal may cause neurological deficits due to central nervous system ischemia are reviewed. Subclavian steal occurs when stenosis of the subclavian artery proximal to the vertebral origin causes retrograde flow in the left vertebral artery. Patients with anatomic subclavian steal usually do not develop neurological symptoms but may rarely present with posterior circulation ischemia. Arteriovenous malformations alter cerebral blood flow patterns and regional perfusion pressure. It has been hypothesized that cerebral arteriovenous malformations may cause neurological deficits due to steal and that these deficits may be cured with arteriovenous malformation treatment. Intra-arterial pressure measurements and transcranial velocity studies show regional hemodynamic alterations. However, these changes have not been correlated with presenting symptoms. Evidence from single-photon emission computed tomography does suggest a relationship between regional hypoperfusion and neurological deficits. Coarctation of the aorta may divert flow from the spinal cord circulation through intercostal arteries distal to the stenosis. This is a possible but unproven mechanism of myelopathology. Steal syndromes may be amenable to treatment by open surgical or endovascular approaches. Experimental studies of the pathophysiology of steal are strengthened by precise definitions of the measured parameters and innovative applications of technology.