Meta-Analysis: Use of Crack Cocaine and Risk of Ischaemic and Haemorrhagic Stroke

Abstract Crack cocaine is a potent sympathomimetic substance associated with acute haemodynamic and cerebrovascular disturbances, with stroke representing one of the most serious neurological complications reported among young adults. This meta-analysis evaluated the association between crack cocaine exposure and stroke in young adult patients, with consideration of ischemic and hemorrhagic stroke and differences between acute and lifetime exposure. Relevant observational evidence was assessed with emphasis on studies involving young adults, crack cocaine-specific exposure, appropriate non-stroke comparator groups, and extractable measures of association. Case reports, case series, narrative reviews, systematic reviews, and studies lacking an appropriate comparator were not considered eligible for quantitative risk estimation. The directly applicable comparative evidence was limited. The principal crack cocaine-specific case-control study by Qureshi et al. included patients aged 20–39 years and found no statistically significant association between lifetime crack cocaine use and overall stroke (OR 0.7, 95% CI 0.4–1.8) or cerebral infarction (OR 0.5, 95% CI 0.2–1.2). Acute crack cocaine exposure within 48 hours of presentation showed higher point estimates for overall stroke (OR 1.9, 95% CI 0.7–5.1) and cerebral infarction (OR 1.2, 95% CI 0.4–3.8), although both estimates were imprecise and did not reach statistical significance. Additional studies examining cocaine-associated stroke in young adults provide supportive epidemiological and clinical context; however, several did not distinguish crack cocaine from other routes or forms of cocaine exposure and therefore could not be assumed to represent crack-specific risk. Earlier clinical series have documented both cerebral infarction and intracranial haemorrhage occurring temporally after crack or cocaine exposure, supporting biological plausibility but lacking the control groups required for quantitative risk estimation. Overall, the available evidence suggests that the relationship between crack cocaine exposure and cerebrovascular events in young adults warrants clinical attention, particularly in the setting of recent exposure, but the evidence base remains limited by small numbers of crack-specific comparative studies, exposure heterogeneity, and imprecise effect estimates. Larger population-based studies using standardized definitions of crack exposure, timing of use, and stroke subtype are required to establish more precise estimates of cerebrovascular risk. Keywords: Crack cocaine; cocaine; stroke; ischemic stroke; haemorrhagic stroke; cerebral infarction; young adults; cerebrovascular disease; stimulant exposure; case-control study.