Cannabis is the most used illicit drug worldwide. About 2.5% of the world population consumes cannabis; and its use has grown more rapidly in developed regions like North America, Western Europe and Australia. The major psychoactive constituent tetrahydrocannabinol has been shown to have temporal associations to serious adverse events as acute myocardial infarction [1], cardiomyopathy, sudden cardiac death [2-4] effects on brain development, various acute neurological deficits [5-8] and stroke.

Most of these cases of stroke or acute neurological dysfunction were described in male who smoked marijuana heavily (14 cigars/day or about 5 - 7 g of marijuana) for more than a decade. Some cases occurred while the drug was actually being smoked and some reports illustrated recurrence of stroke in patients who didn’t comply with cessation. Potential mechanism behind many of these effects is attributable to marijuana-induced hypertension, dyslipidemia, higher caloric intake [9] and increased platelet coagulability [10].

About 2-39% of cases of ischemic stroke in young adults are suspected to be associated with recreational drug use. Cases of stroke after marijuana smoking have been reported in many prior studies where its use was found to be a prominent risk factor [11-13]. Most of the cases described were acute neurological dysfunction during actual marijuana inhalation suggesting a reversible effect of cannabis inhalation on cranial circulation likely due to spasm or, increase in blood pressure [14, 15]. Later studies showed that misuse of marijuana was more frequently associated with stroke in young population with no other traditional risk factors. A prospective cohort on 48 young patients also revealed significant association between multifocal intracranial stenosis and marijuana consumption with odds ratio of 113 (9 - 5,047) and P value < 0.001 [16]. Similarly, a case series by Singh et al [13] described a causal role of cannabis in cases of ischemic stroke by showing recurrence of symptoms in a few patients with re-exposure. Majority of the patients in mentioned studies had posterior circulation strokes. Recently a France-based cohort study found that majority strokes in marijuana abusers were caused by intracranial arterial stenosis [17]. However, none of the studies described above would explain our case of ischemic stroke secondary to bilateral thrombotic athero-occlusive disease of ICA. Relation between marijuana smoking and atherosclerotic coronary heart disease has been studied before. Animal model studies showed that cannabinoids can potentially lead toward progression of atherosclerosis by its proatherogenic effect on endothelial cells, vascular smooth muscle cells and lipid metabolism precipitating acute coronary syndrome and decreasing angina threshold [18]. Same process could explain thrombosis of ICA in our case leading to ischemic stroke. Such case of bilateral occlusion secondary to chronic marijuana smoking has been never mentioned in literatures. Although in this case a direct correlation between marijuana and carotid occlusion cannot be established due to presence of confounding factors, we can argue that it might have contributed to the progression of atherosclerosis. However, definitive conclusions as to the underlying pathophysiology and hence exact mechanism is still not well established and hence further research in this arena should be sought. Fighting stroke must remain a priority in young patients and hence potential occurrence of stroke associated with cannabis should be reported more for better awareness in the society. Also community should focus to intensify research regarding the safety of marijuana use as cannabis is not as harmless as was thought, and cerebrovascular risk is probably underestimated.