Neurologic complications of cocaine, amphetamine, and their derivatives

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By Douglas J Lanska MD MS MSPH

Abuse of certain illicit drugs can be complicated by ischemic stroke, intracerebral or subarachnoid hemorrhage, and other neurologic complications (Mathew and Wilson 1991; Baquero and Alfaro 1994; Auer et al 2002). Such agents include the sympathomimetic drugs cocaine and amphetamine, and their derivatives, including "crack," methamphetamine ("meth" or "crystal" or "speed"), "ecstasy," and "eve."

Cocaine and amphetamine are strong risk factors for stroke in adolescents and young adults in most (Kaku and Lowenstein 1990; Petitti et al 1998), but not all (Qureshi et al 1997; 2001) epidemiological studies. There are multiple pathophysiological mechanisms for the cerebrovascular diseases related to use of these drugs, including vasospasm, altered platelet function, excitotoxicity, hyperthermia, and acute severe hypertension, which can cause endothelial disruption, loss of cerebral autoregulation, and hemorrhage. In many cases with abuse of such drugs, intracerebral hemorrhage is associated with an underlying vascular malformation (Klonoff et al 1989; Levine et al 1991; Daras et al 1994; Konzen et al 1995; Fessler et al 1997; McEvoy et al 2000; Auer et al 2002). In addition, individuals who abuse such drugs are also potentially susceptible to particulate embolization (from contaminants injected with intravenous drug abuse), cardiac arrhythmias, mycotic aneurysms, and endocarditis.

Synergistic vasoconstrictive effects may occur with combined use of sympathomimetic agents in both human reports (Lambrecht et al 1993; Vallee et al 1993) and animal models (Wang et al 1990). Interestingly, basilar artery vasospasm has been produced in animal models by combined administration of cocaine and amphetamine (Wang et al 1990) and basilar artery thrombosis has been reported with combined abuse of cocaine and "ecstasy," an amphetamine derivative (Vallee et al 1993).