Recurrent stroke associated with cannabis use
I Mateo, A Pinedo, M Gomez-Beldarrain, J M Basterretxea, J C Garcia-Monco
J Neurol Neurosurg Psychiatry 2005;76:435–437. doi: 10.1136/jnnp.2004.042382
Drug misuse represents a risk factor for cerebrovascular
disease, especially among young people. Despite the fact
that cannabis is the most widely used illicit drug, there are
only a few reports associating its use with cerebrovascular
disease. We describe a patient who suffered three ischaemic
strokes immediately after cannabis consumption. Other
stroke aetiologies were ruled out, and neuroimaging
revealed infarcts in different arterial areas as well as
evidence of non-atherosclerotic arterial disease, which
suggests an underlying vasculopathy of uncertain (toxic or
inflammatory) origin. Cannabis use may be associated with
ischaemic stroke in young patients, but its mechanism is
other sympathomimetic agents.1
cannabis is the most widely consumed illicit drug worldwide,
it has only exceptionally been associated with cerebrovas-
cular disease. We describe a patient with three recurrent
strokes temporally related to hashish smoking.
rug misuse is a risk factor for stroke, especially among
young people, and the substances most frequently
implicated are cocaine, heroin, amphetamines, and
Despite the fact that
A 36 year old primary school teacher, right handed, male,
with no known vascular risk factors or migraine history, who
had consumed hashish sporadically in the past, developed,
after an unusually heavy hashish consumption and 3–4
alcoholic drinks at a party, an acute episode of isolated
aphasia followed a few hours later by a convulsive seizure. He
did not consume any other illicit drugs or medication, and
only sporadically consumed alcohol (2–3 drinks on occasional
The patient’s blood pressure was 120/80 mmHg on admis-
sion. Cranial MRI revealed two acute ischaemic infarcts, one
over the left temporal lobe, consistent with his neurological
deficit, and another area of silent ischaemia in the right
parietal lobe. Magnetic resonance angiography (MRA) of the
intracranial vasculature revealed a diminished calibre of the
distal temporal branches of the left middle cerebral artery
(MCA) without involvement of its proximal segment (fig 1a).
MRA of the extracranial neck vasculature was normal, and
no evidence of diffuse atherosclerotic disease was present.
Urine toxicological screening on admission was positive for
cannabis and negative for amphetamines, cocaine, metha-
done, opiates, benzodiazepines, and barbiturates. Serum
glucose, creatinine, sodium, potassium, liver enzymes, blood
count and differential, coagulation times, anticardiolipin
antibodies, lupus anticoagulant, C and S proteins, anti-
thrombin III levels, erythrocyte sedimentation rate, C reactive
protein, venereal disease research laboratory slide test, HIV
serology, and biochemical and microbiological cerebrospinal
Transoesophageal echocardiogram, including agitated saline
administration and provocative manoeuvres, was normal.
Seizures did not recur and repeated electroencephalograms
were normal; antiepileptic therapy was not initiated.
The patient was treated with ticlopidine. Despite therapy,
and advice against drug consumption, he suffered another
episode of aphasia and right hemiparesis a year later,
immediately after hashish smoking at another party. His
blood pressure at the emergency room was 140/80. Between
the two episodes, he denied having consumed cannabis and
he had been normotensive. MRI disclosed an acute left
frontal cortical infarction, responsible for his symptoms, as
well as another area of silent acute ischaemia over the
contralateral frontal lobe. Repeated head and neck MRA
studies did not reveal any additional abnormalities compared
with the first study; the known diminished calibre of the
distal temporal branches of the left MCA was still present.
Again, a repeated diagnostic investigation gave only positive
results for the presence of cannabis in urine.
The patient abstained from drug use for another 1K years,
then, after another heavy intake of hashish and 3–4 drinks of
alcohol, he suffered from auditory agnosia. His blood
pressure was 110/75 mmHg on admission. MRI disclosed
the presence of an acute infarct involving the right posterior
temporal and lower parietal lobes and evidenced previous
infarcts (fig 1b–d). It disclosed no new changes compared
with the first study. The patient recovered and has since
(2 years after the last stroke) remained stable, on therapy
with clopidogrel and denies further drug consumption.
Cannabis ingestion can result in a variety of side effects. The
most frequent are psychiatric reactions, including beha-
vioural abnormalities and an increased risk of schizophre-
nia.2 3Less known but no less important are its cardiovascular
effects, which include tachycardia,4hypertension, especially
in decubitus,5and postural hypotension.6Carboxy-haemo-
globin levels are also increased, thus decreasing the oxygen
transportation capacity.7Furthermore, cannabis increases the
risk of myocardial infarction 4.8-fold during the hour
following its intake8and has been associated with parox-
ysmal atrial fibrillation,9and there are reports of sudden
death of cardiovascular origin following its consumption.10
Despite the fact that cannabis is the most consumed illicit
drug, only 15 patients have so far been described with strokes
associated to cannabis consumption.11–21In our patient the
most relevant data were the presence of three repeated
strokes in close temporal relationship with cannabis and
alcohol intake, involving different arterial territories in the
absence of an embolic source or atherosclerotic disease, and
the favourable outcome after cessation of drug consumption.
Establishing a causal relationship between drug consump-
tion and stroke is not easy, and this relationship is usually
based on a temporal link between drug use and the
occurrence of stroke in young patients without any other
Abbreviations: MCA, middle cerebral artery; MRA, magnetic
See Editorial Commentary, p 306
vascular risk factors. Because cannabis use is so widespread,
this could represent a casual relationship; in fact, due to their
high liposolubility and persistence in fatty tissues, cannabis
metabolites persist in urine for weeks and therefore, their
presence in a patient with a stroke could merely represent
prior use. This patient’s case, however, is exceptional in that
there was a close and clearcut temporal relationship between
drug intake and stroke, which occurred on three separate
occasions. The repetition of events after exposure to cannabis,
previously undescribed, suggests a role for cannabis in this
patient’s strokes. Alcohol ingestion could also have con-
tributed. The relationship between alcohol and ischaemic
stroke is complex and whether binge drinking is associated
with stroke is controversial.22Nevertheless, the role of alcohol
in this patient’s strokes was probably secondary, as he did not
consume large amounts of the drug nor much higher levels
than he was used to consuming occasionally on weekends.
However, hashish is an illegal drug in Spain, not subject to
any regulation or control, and therefore other toxic sub-
stances could have been added during its manufacture.
The mechanisms most frequently postulated in cannabis
related stroke are vasospasm12–14and postural hypotension
with abnormal regulation of the brain blood flow.11 16 23In
our patient, there was no evidence of postural hypotension,
and blood pressure measurements in the emergency room
were repeatedly normal. MRI angiography revealed a
persistent mild decrease of the distal branches of the left
MCA, which, together with the involvement of multiple
arterial territories, simultaneously suggests the existence of
an underlying vasculopathy of some sort. Some of the
infarcts were not accompanied by arterial irregularities, but
it is possible that these abnormalities may be below the
sensitivity threshold of MRI angiography and therefore go
undetected. Conventional angiography might have revealed a
more diffuse damage or signs consistent with arteritis, but
the patient refused it. On the other hand, the narrowing of
the branches of the left MCA persisted over the years, which
argues against vasospasm in this patient.
Owing to the presence of multiple ischaemic infarcts, an
embolic source was insistently pursued, and was ruled out on
the three admissions. However, paroxysmal atrial fibrillation
can occur after cannabis consumption, and the simultaneous
intake of alcohol may predispose to weekend arrhythmias
and stroke. Furthermore, recent studies have shown a high
incidence of paroxysmal atrial fibrillation in patients with
stroke of idiopathic aetiology, mainly in patients with atrial
septal abnormalities.24 25Repeated electrocardiograms were
normal upon arrival at the emergency room on the three
different occasions; 24 hour Holter and invasive heart
electrophysiological studies to detect atrial vulnerability were
not performed. Although the possibility could not be ruled
out completely that this patient’s strokes were of cardio-
embolic origin due to a paroxysmal atrial fibrillation triggered
by alcohol and cannabis consumption, and that MRA
changes reflected a partial emboli recanalisation, the absence
of cardiac symptoms, the normality of the echocardiographic
studies, and the absence of systemic embolic events make
this possibility unlikely. As mentioned, we believe that the
most likely mechanism in this case was a vasculopathy,
either toxic or immune inflammatory, elicited by cannabis.
patient after his first stroke. Arterial
occlusion of the distal portions of the
middle cerebral artery can be seen
(black arrows). (b–d) Axial FLAIR MRI
sequences obtained after the last stroke.
An acute ischaemic infarct is observed
over the right temporal and parietal
lobes (b, open arrow). Old infarcts in
an atrophic stage are also evident
(a) MR angiography of this
436Mateo, Pinedo, Gomez-Beldarrain, et al
Although there are no descriptions of cerebral vasculitis in
cannabis users, the presence of arteritis involving peripheral
vessels has been described.26Cannabis arteritis resembles
Buerger’s disease, but in the first case patients are regular
cannabis users and only moderate tobacco smokers.26
Cannabis has a peripheral vasoconstrictor effect and its
prolonged use could be an additive risk factor for juvenile and
young adult arteritis.26
Cannabis is not as safe a drug as many believe; it can be
associated with ischaemic stroke in young people by unclear
mechanisms, and toxicological screening of patients with
stroke should be performed and should include the determi-
nation of cannabinoids. Future studies will be needed to
clarify the role of cannabis as a stroke risk factor, as it could
be underestimated. If this was the case, cerebrovascular risk
may increase in the future, due to an increased consumption
based on the potential therapeutic benefits of cannabis27and
its possible legalisation in some countries.
I Mateo, A Pinedo, M Gomez-Beldarrain, J M Basterretxea, J C Garcia-
Monco, Service of Neurology, Hospital de Galdacano, 48960
Galdacano, Vizcaya, Spain
Competing interests: none declared
Correspondence to: Dr J C Garcia-Monco, Service of Neurology,
Hospital de Galdacano, 48960 Galdacano, Vizcaya, Spain; hospit05@
Received 30 March 2004
In revised form 16 June 2004
Accepted 21 June 2004
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