Sleep-disordered breathing (SDB) is more probably the cause rather than the consequence of stroke because: apneas are essentially obstructive rather than central, the frequency of SDB is not different between transient ischemic attack and cerebral infarction; and previous excessive daytime sleepiness is significantly more frequent among stroke patients with SDB than those without. The presence of SDB in stroke patients could lead to a poor outcome. Pathophysiological relationships between strokes and SDB are multiple. Experimental and clinical studies have shown that both short- and long-term factors may play a role in increasing the susceptibility to stroke in patients with obstructive sleep apnea syndrome. The former include changes in cerebral hemodynamics, hematologic alterations, and cardiocirculatory dysfunctions that typically and repeatedly occur during apnea episodes and also may persist during wakefulness. Regarding long-term factors, some changes in the anatomical characteristics of carotid arteries wall have been recognized in SDB patients. This finding seems to suggest that the link between SDB and cerebrovascular disease might be explained, at least in part, by an increase in the progression of the atherosclerosis process involving cerebral vessels. There are several practical implications from the demonstrated significant role of sleep apnea in increasing the predisposition to developing stroke. Specific investigation is fundamental in the presence of a clinical suspect of SDB, especially in patients with history of transient ischemic attacks and stroke. Specific treatment of SDB may reduce the possibility of further cerebrovascular disturbances.