Background and Purpose-Our objective was to evaluate the relationship between cannabis use and ischemic stroke in a young adult population. Methods-Forty-eight consecutive young patients admitted for acute ischemic stroke participated in the study. First-line screening was performed, including blood tests, cardiovascular investigations, and urine analysis for cannabinoids. If no etiology was found, 3D rotational angiography and cerebrospinal fluid analysis were performed. A control was planned through neurovascular imaging within 3 to 6 months. Results-In this series, there was multifocal intracranial stenosis associated with cannabis use in 21% (nϭ10). Conclusions-Multifocal MethodsFrom October 2005 to September 2007, 48 consecutive patients younger than 45 years of age who were admitted to our stroke unit for IS were included in this study. Patients were informed that they were included in a prospective study and agreed to participate. Standard T1, T2, FLAIR sequences, diffusion weighted-imaging magnetic resonance imaging scans were acquired for all patients. Vascular imaging comprised 3D-time of flight magnetic resonance angiography (nϭ43) or cerebral computed tomography angiography (nϭ5). Cardiac explorations included electrocardiogram (nϭ48), transthoracic echocardiography (nϭ48), and transoesophageal echocardiography (nϭ29). Exhaustive laboratory analyses were performed for all patients. If first-line investigations were inconclusive, 3D rotational angiography (nϭ30) and cerebrospinal fluid analysis (nϭ29) were performed. A questionnaire was used to determine cardiovascular risk factors, history of medication, and illicit drug or alcohol use. Urines were systematically screened for cannabinoids, cocaine, amphetamine, and methylenedioxymethamphetamine. Follow-up clinical visits (nϭ44) and control of vascular imaging (nϭ20) were planned within 3 to 6 months after discharge from hospital.One study neurologist and 1 study radiologist separately reviewed all 3D-time of flight or computed tomography angiography images. A single operator performed all 3D rotational angiography, and 2 study radiologists, who were unaware of magnetic resonance angiography results, reviewed the 3D rotational angiography images. Involvement of single or several vessel segments were respectively classified as monoarterial stenosis or as multifocal intracranial stenosis (MIS). Statistical AnalysisData are summarized using descriptive statistics. Because of sparseness of data, computations of odds ratio and 95% CI, as well as multivariate logistic regression, were obtained using exact methods (StatXact and LogXact). The logistic regression was designed using the group of MIS as the dependent variable and the other variables as potential predictors. A probability value Յ5% was considered statistically significant. ResultsTable displays the relationship between stroke etiology, classical risk factors, and cannabis use in the 48 patients. There were no patients undergoing serotonergic medical treatment, and there were no amphetamine, meth...

Cannabis has potential therapeutic use but tetrahydrocannabinol (THC), its main psychoactive component, appears as a risk factor for ischemic stroke in young adults. We therefore evaluate the effects of THC on brain mitochondrial function and oxidative stress, key factors involved in stroke. Maximal oxidative capacities V max (complexes I, III, and IV activities), V succ (complexes II, III, and IV activities), V tmpd (complex IV activity), together with mitochondrial coupling (V max/V 0), were determined in control conditions and after exposure to THC in isolated mitochondria extracted from rat brain, using differential centrifugations. Oxidative stress was also assessed through hydrogen peroxide (H2O2) production, measured with Amplex Red. THC significantly decreased V max (−71%; P < 0.0001), V succ (−65%; P < 0.0001), and V tmpd (−3.5%; P < 0.001). Mitochondrial coupling (V max/V 0) was also significantly decreased after THC exposure (1.8±0.2 versus 6.3±0.7; P < 0.001). Furthermore, THC significantly enhanced H2O2 production by cerebral mitochondria (+171%; P < 0.05) and mitochondrial free radical leak was increased from 0.01±0.01 to 0.10±0.01% (P < 0.001). Thus, THC increases oxidative stress and induces cerebral mitochondrial dysfunction. This mechanism may be involved in young cannabis users who develop ischemic stroke since THC might increase patient's vulnerability to stroke.

Ischemic preconditioning counteracted ischemia-induced impairments of mitochondrial complexes I and II. These data support that ischemic preconditioning might be an interesting approach to reduce muscular injuries in the setting of ischemic vascular diseases.

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