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Dear Sir: Drug misuse is a known risk factor for cerebrovascular disease, especially among young people.1,2 Cannabis is the most widely-consumed illicit drug worldwide, but it has only occasionally been associated with ischemic vascular events.13 Vasospasm, hypotension, arrhythmias, and vasculitis have been proposed as potential mechanisms.14 We report on a case of recurrent stroke in a young cannabis user.
A 27-year-old man, a heavy cannabis user, was admitted in a Stroke Unit in August 2006, with acute right hemiparesis. He did not consume other illicit drugs or medication, and only sporadically consumed alcohol. Computed tomographic (CT) scan showed a recent left basal ganglia infarct. Urine toxicological screening was positive for cannabis and negative for amphetamines, cocaine, and benzodiazepines. Laboratory studies (including biochemistry, infectious serology, prothrombotic, and immunologic studies), carotid and vertebral ultrasound, trans-esophageal echocardiogram (TEE), and Holter were normal. Cerebrospinal fluid (CSF) examination showed 14 cells (75% lymphocytes). Angiography revealed a left middle cerebral artery (MCA) occlusion. Vasculitis was suspected, and prednisone was started. In February 2007 (prednisone had been suspended in December 2006), he presented with acute-onset of left hemichorea. CT scan revealed a right lenticulostriate infarct. His urine tested positive for cannabinoid. Laboratory studies (including CSF and now MELAS, Fabry and CADASIL genetic testing) did not reveal any abnormalities. TEE suggested the hypothesis of a small patent foramen ovale (PFO). Brain magnetic resonance imaging (MRI) revealed multiple infarcts. Facing the possibility of an embolic source, hypocoagulation was started. Despite therapeutic INR, he suffered another abrupt onset of left hemiparesis, in August 2008. His urine tested positive for cannabinoid. Repeated laboratory studies, CSF, echocardiogram, and Holter were normal. Brain MRI revealed multiple recent ischemic lesions in the right carotid territory and old lesions bilaterally, and MRI angiography showed diffuse irregularities of the anterior and posterior circulation (Figure 1). No evidence of diffuse atherosclerotic disease was present. At this point, aspirin and prednisolone were restarted, with no repetition of cerebrovascular events.
FIGURE 1. [A]: Axial diffusion-weighted imaging shows right frontal and parietal cortical and subcortical acute ischemic lesions, corresponding to the anterior cerebral artery (ACA) and middle cerebral artery (MCA) regions; [B]: Axial T2-weighted image demonstrates old vascular lesions in the basal ganglia bilaterally; [C]: MR angiography, 3D-TOF imaging, reveals proximal occlusion of the left MCA and distal occlusion of the right M1 MCA segment. Diffuse ectasia and irregularities of both carotids, left ACA and right M-1 segment, are seen. Increased visualization of external carotid branches suggests collateralization.
Effects of cannabis include psychiatric reactions,24 cognitive dysfunction,4 memory and time-assessment alterations,4 motor incoordination,4 poor executive functioning,4 sedative effects,4 and cardiovascular changes.14 Ischemic strokes related to cannabis have been reported in the literature;14 however, because of the widespread use of the drug, it is difficult to establish a causal relationship. We believe that the recurrent strokes in this case were associated with the chronic use of cannabis, with vasculopathy being the most likely mechanism. There was no evidence of postural hypotension, and repeated blood pressure measurements on admission were normal. Electrocardiograms and Holter monitoring did not show abnormalities on the three different occasions. Facing the possibility of a PFO, hypocoagulation was started after the second event, and, despite this therapy, the patient suffered another stroke. The involvement of multiple arterial territories and the diffuse irregularities revealed in the MRI angiography suggest the existence of an underlying vasculopathy, toxic or immune-inflammatory. This case report supports a potential risk of stroke associated with cannabis use and suggests that toxicological screening for cannabinoid metabolites should be done in young stroke patients with no known vascular risk factors or evidence of dissection.

References

1.
Singh NN, Pan Y, Muengtaweeponsa S, et al.: Cannabis-related stroke: case series and review of literature. J Stroke Cerebrovasc Dis 2012; 21:555–560
2.
Mateo I, Pinedo A, Gomez-Beldarrain M, et al.: Recurrent stroke associated with cannabis use. J Neurol Neurosurg Psychiatry 2005; 76:435–437
3.
Wolff V, Armspach JP, Lauer V, et al.: Cannabis-related stroke: myth or reality? Stroke 2013; 44:558–563
4.
Geibprasert S, Gallucci M, Krings T: Addictive illegal drugs: structural neuroimaging. AJNR Am J Neuroradiol 2010; 31:803–808

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Go to The Journal of Neuropsychiatry and Clinical Neurosciences
Go to The Journal of Neuropsychiatry and Clinical Neurosciences
The Journal of Neuropsychiatry and Clinical Neurosciences
Pages: E41 - E42
PubMed: 24515708

History

Published online: 1 January 2014
Published in print: Winter 2014

Authors

Details

Ana Filipa Santos, M.D.
Neurology Department, Hospital de Braga, Braga, Portugal
Margarida Rodrigues, M.D.
Neurology Department, Hospital de Braga, Braga, Portugal
Ricardo Maré, M.D.
Neurology Department, Hospital de Braga, Braga, Portugal
Carla Ferreira, M.D.
Neurology Department, Hospital de Braga, Braga, Portugal
João Soares-Fernandes, M.D.
Neuroradiology Department, Hospital de Braga, Braga, Portugal
Jaime Rocha, M.D.
Neuroradiology Department, Hospital de Braga, Braga, Portugal

Notes

Correspondence: Dr. Santos; e-mail: [email protected]

Funding Information

Disclosure: the authors do not have any conflict of interest.

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