Cocaine abuse remains a devastating medical problem for our society. Current concepts suggest that both hemorrhagic
and ischemic stroke, particularly in young people, can result as a consequence of cocaine exposure. We provide
an analysis of mechanisms of injury and a discussion of the pharmacological management of stroke following cocaine
use. Preclinical research suggests that the cause of cocaine-mediated stroke is multifactorial and involves vasospasm,
changes in cerebral vasculature, and platelet aggregation. We suggest that drugs able to induce vasospastic, thrombogenic,
or neurotoxic effects of cocaine could be suitable as therapeutic agents. In contrast caution should be exerted when using
anti-platelet and thrombolytic agents in cocaine users with stroke.