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Cannabis and stroke
Cannabis is currently the most widely used illicit drug in Western populations.1 The question of whether or not it should remain prohibited is under debate in many European countries. Possible adverse health effects play an important role in this debate. The classical anxiolytic, sedative, analgesic, and psychedelic properties of cannabis are well known,1 but it has recently been suggested that it may also induce cerebrovascular disease.2 Now for the first time, Mateo et al have shown (this issue, see page 435) that a causal relation with cerebrovascular events is highly plausible. The major argument in favour of this is that the events only occurred during periods when the patient was consuming cannabis, and this is a major criterion of adverse drug reaction monitoring.3
Several possible mechanisms are discussed by the authors, the most likely being a drug induced vasculopathy. Others include postural hypotension with secondary impairment of the autoregulation of cerebral blood flow, atrial fibrillation, other arrhythmias, and vasospasm.2,4 Though concomitant alcohol consumption may be a confounder, the absence of any proven cause, particularly the absence of haemodynamic or cardiac abnormalities, and the presence of multiple infarcts associated with narrowing of the intracranial arteries strongly suggest a toxic vasculopathy. The long duration of these alterations argues in favour of a drug induced vasculitis rather than vasospasm. Such a vasculitis has already been described in peripheral vessels as a result of chronic cannabis consumption, with many similarities to Buerger’s disease.5 In the present case, the patient was not a regular user and both the arterial abnormalities and the time course of the disease suggest an immuno-allergic vasculitis.
The systemic effects of natural cannabis compounds (Δ9-tetrahydrocannabinol, Δ8-tetrahydrocannabinol, canna binol, and cannabidiol) are primarily mediated by the activation of cannabinoid receptors (CB1 and CB2), which are present in various tissues including the brain, cells of the immune system, blood vessels, and heart.1 Apart from the vasoactive properties of cannabinoids, it is also possible that a central nervous system vasculitis could result from a dysfunction of the immune system.6 It remains to be determined whether the immunomodulatory effects of cannabinoids could be involved as a mechanism of cannabis induced vasculitis through their action on CB2 receptors.1 The very low frequency of such complications2 may reflect a genetic predisposition in a few individuals.6 Better identification of patients with cannabis related strokes may lead to epidemiological case–control studies that include genomic investigations. In that recreational cannabis use appears not to be as harmless as was thought, there is a need to improve public information. The therapeutic potential of cannabis and its derivatives should be rigorously evaluated and the benefit to risk ratio taken into account before authorising their medical use.
Cannabis and stroke
Competing interests: none declared