Clinical Neurology and Neurosurgery 106 (2004) 305–308

Occipital stroke shortly after cannabis consumption
Josef Finsterer a,∗ , Prainer Christian a , Kopsa Wolfgang b
a Department of Neurology, Krankenanstalt Rudolfstiftung, Juchg, 25, 1130 Vienna, Austria
b Department of Radiology, Krankenanstalt Rudolfstiftung, Juchg, 25, 1130 Vienna, Austria

Received 10 September 2003; received in revised form 23 January 2004; accepted 3 February 2004

Abstract
There are several indications that imply cannabis consumption triggers cerebrovascular events. A right occipital ischemic stroke occurred
in a 37-year-old Albanese man with a previously uneventful medical history, 15 min after having smoked a cigarette with approximately
250 mg of marijuana. Clinical manifestations of the stroke were left-sided hemiparesis, hemi-hypesthesia and blurred vision, which vanished
spontaneously and almost completely after 3 days. He has been smoking joints regularly from the age of 27, with a frequency of 2–3 joints
per week during the 6 months that preceded his stroke. Except for cigarette smoking and slight dyslipidaemia, classical risk factors for
stroke/embolism were absent. Therefore, as the family history for cerebrovascular events, blood pressure, clotting tests, examinations for
thrombophilia, vasculitis, extracranial and intracranial arteries and cardiac investigations were normal or respectively negative, the stroke was
attributed to the chronic cannabis consumption.
© 2004 Elsevier B.V. All rights reserved.
Keywords: Drug abuse; Cerebral ischaemia; Vascular event; Stroke; Marijuana; Side effect

1. Introduction
Several reports have suggested a causal role of cannabis
in the development of cerebro-vascular disease [1–9]. In
the majority of these cases, patients experience a cerebral
ischaemia during cannabis smoking. This report refers to a
patient, who suffered from an ischemic stroke in the posterior circulation 15 min after having smoked a marijuana
cigarette (joint).

2. Case report
The patient is a 37-year-old, HIV-negative Albanese man
with a previously uneventful medical history. Except for
smoking up to 20 cigarettes per day, classical risk factors for
stroke/embolism were absent. He did not require any regular medication and there was no significant family history
for cerebro-vascular disease. He drank regularly 2–2.5 l of
non-alcoholic liquids per day. He has been smoking joints
regularly from the age of 27, initially with a frequency of
∗ Corresponding author. Tel.: +43-1-71165-92085;
fax: +43-1-4781711.
E-mail address: duarte@aonmail.at (J. Finsterer).

0303-8467/$ – see front matter © 2004 Elsevier B.V. All rights reserved.
doi:10.1016/j.clineuro.2004.02.001

1–2 per month. During the 6 months prior to his admission
he had increased the frequency to 2–3 joints per week. He
denied taking any amphetamines, ecstasy or any other illicit
drugs. He was not screened for opiates, cocaine, cannabinoids, amphetamines, or bezodiazepines, but his relatives
convincingly confirmed that he was taking cannabinoids
exclusively. In May 2003 the patient was admitted as an
emergency because of a sudden onset of left-sided hemiparesis, left-sided hemihypesthesia and recurrent double
vision. These symptoms and signs developed acutely 15 min
after having smoked a joint, containing approximately
250 mg marijuana, 2 h before his hospitalisation. Most of
the symptoms disappeared within one hour after their onset.
Clinical neurologic examination on admission revealed
blurred vision when looking to the upper and lower left,
discrete left-sided dysdiadochokinesia, and a discrete weakness of the left upper limb (MRC grade 5-). There was
no double vision and no visual field defect on confrontational perimetry. Blood pressure was 130/70 mmHg. The
ECG showed sinustachycardia of 112 per min. Blood
chemical investigations revealed a creatine-kinase of
229 U/l (normal: <170 U/l), which decreased to 179 U/l
2 days later, a cholesterol level of 208 mg/dl (normal:
<200 mg/dl), a HDL-cholesterol level of 37 mg/dl (normal: >55 mg/dl), a LDL-cholesterol level of 160 mg/dl

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J. Finsterer et al. / Clinical Neurology and Neurosurgery 106 (2004) 305–308
Fig. 1. Coronary MRI of the brain shows a slightly hyperintense lesion on the base of the occipital lobe (left). On diffusion-weighted MRI (B = 1000 T) this area is hyperintense (middle) and hypointense
on the corresponding ADC sequences (right).

J. Finsterer et al. / Clinical Neurology and Neurosurgery 106 (2004) 305–308

(normal: <130 mg/dl), but normal clotting tests. Risk factors for thrombosis including: homocystein, antithrombin,
protein-S, protein-C, factor-VIII, factor-IX, APC-resistance,
lupus-antigen, ␤-glykoprotein-antibodies and the 20.210
G → A prothrombin-mutation were normal or negative.
Parameters indicating vasculitis were negative. Ultrasound
investigations of the extracranial and intracranial arteries were normal. Transthoracic echocardiography did not
reveal intracardial thrombi or any other cardiac abnormality. A cerebral CT scan on admission was normal, but
a diffusion-weighted MRI revealed an area of impaired
diffusion, 2 cm in diameter, in the right occipital area subcortically (Fig. 1). Acetylsalicylic acid with dipyridamol
and atorvastatin were begun. On dismissal 3 days after the
stroke, blurred vision when looking to the left had remained
the only neurological deficit.

3. Discussion
Although strokes in the posterior circulation during
marijuana smoking have been reported earlier [5,8], the
presented patient is noteworthy for right-sided occipital ischaemia, occurring less than 15 min after having smoked
a marijuana cigarette. Except for nicotine smoking and
slight dyslipidaemia, risk factors for stroke/embolism were
absent. ECG and transthoracic echocardiography excluded
a cardiac source of embolism. Extracranial and intracranial
cerebral arteries were morphologically and functionally
normal. The examination for thrombophilia and vasculitis
was negative and there was no known family history of cardiovascular disease. Consequently, the stroke was attributed
to the cannabis consumption rather than nicotine cigarette
smoking or the slight dyslipidaemia.
Previous reports, showing an association or even causal
relationship between strokes and drug abuse [1,3,6,9] and
the documented vasogenic effect of marijuana [10–17] support the arguments for cannabis as the cause of the stroke
in this case. Marijuana increases catecholamine levels,
carboxy-haemoglobin, supine blood pressure, heart rate,
cardiac output, and impairs peripheral vasomotor reflex,
occasionally producing marked orthostatic hypotension
[8,17,18]. With repeated exposure, supine blood pressure decreases slightly, orthostatic hypotension disappears,
blood volume increases, and the reaction to the Valsalva
manoeuvre diminishes [19], consistent with centrally mediated reduced sympathetic and increased parasympathomimetic drive. Concerning the cerebral perfusion, marijuana increases the pulsatility index, a measure of the
cerebrovascular resistance, increases systolic velocity [20]
and reduces cerebral blood flow [21]. In chronic marijuana
abusers the cerebral blood flow is reduced during abstinence
[10–12,22]. However, acute administration of marijuana,
increases the cerebral blood flow [13–17]. Additionally,
marijuana diminishes the cerebral autoregulatory capacity.
It could be possible that, marijuana had increased the

307

systolic blood pressure in the presented patient, which has
been previously reported as a pathogenetic mechanism of
strokes in these patients [9]. Another speculation suggests
drug-induced reversible vasospasms due to marijuana consumption [9]. This assumption is supported by the fact that
most of the previously reported strokes associated with
cannabis abuse occurred whilst the drug was actually being
smoked. However, there are also single cases, in which
strokes have occurred up to half an hour after the last
joint has been smoked [9]. A further assumption suggests
strokes due to an immune-complex vasculitis [23]. Sinustachycardia in the presented patient was also interpreted
as cannabis-induced. Usually the cardiovascular effects of
cannabis are not associated with serious health problems
for young, healthy volunteers. Nevertheless, occasionally,
myocardial infarction, stroke and other cardiovascular adverse events occur in chronic cannabis users [19]. The
reasons for the rarity of strokes in cannabis users, remain
speculative. Contrary to the negative effects, marijuana
has also a therapeutic potential in disorders resulting from
cerebral ischaemia [24]. Whether the patient suffered from
drug-induced arteriopathy or arteriitis, causing the infarct,
remains speculative as no intra-arterial angiography had
been carried out.
In conclusion, this case shows that marijuana smoking
may cause stroke and that there may be a latency between
resorbtion of the drug and the occurrence of the cerebrovascular event. Deficits caused by the stroke may be short-lived
and may be followed by complete recovery after a few days.

References
[1] Alvaro LC, Iriondo I, Villaverde FJ. Sexual headache and stroke in
a heavy cannabis smoker. Headache 2002;42:224–6.
[2] Barnes D, Palace J, O’Brien MD. Stroke following marijuana smoking. Stroke 1992;23:1381.
[3] Cooles P, Michaud R. Stroke after heavy cannabis smoking. Postgrad
Med J 1987;63:511.
[4] Lawson TM, Rees A. Stroke and transient ischaemic attacks in
association with substance abuse in a young man. Postgrad Med J
1996;72:692–3.
[5] Marinella MA. Stroke after marijuana smoking in a teenager with
factor V Leiden mutation. South Med J 2001;94:1217–8.
[6] McCarron MO, Thomas AM. Cannabis and alcohol in stroke. Postgrad Med J 1997;73:448.
[7] Mesec A, Rot U, Grad A. Cerebrovascular disease associated with
marijuana abuse: a case report. Cerebrovasc Dis 2001;11:284–5.
[8] White D, Martin D, Geller T, Pittman T. Stroke associated with
marijuana abuse. Pediatr Neurosurg 2000;32:92–4.
[9] Zachariah SB. Stroke after heavy marijuana smoking. Stroke
1991;22:406–9.
[10] Amen DG, Waugh M. High resolution brain SPECT imaging of
marijuana smokers with AD/HD. J Psychoactive Drugs 1998;30:209–
14.
[11] Block RI, O’Leary DS, Hichwa RD, Augustiniak JC, Ponto LL,
Ghonein MM, et al. Cerebellar hypoactivity in frequent marijuana
users. Neuroreport 2000;11:749–53.
[12] Lundqvist T, Jonsson S, Warkentin S. Frontal lobe dysfunction in
long-term cannabis users. Neurotoxicol Teratol 2001;23:437–43.

308

J. Finsterer et al. / Clinical Neurology and Neurosurgery 106 (2004) 305–308

[13] Mathew RJ, Wilson WH, Turkington TG, Hawk TC, Coleman RE,
DeGrado TR, et al. Time course of tetrahydrocannabinol-induced
changes in regional cerebral blood flow measured with positron
emission tomography. Psychiat Res 2002;116:173–85.
[14] Mathew RJ, Wilson WH, Chiu NY, Turkington TG, Degrado TR,
Coleman RE. Regional cerebral blood flow and depersonalization after tetrahydrocannabinol administration. Acta Psychiat Scand
1999;100:67–75.
[15] Mathew RJ, Wilson WH, Coleman RE, Turkington TG, DeGrado TR.
Marijuana intoxication and brain activation in marijuana smokers.
Life Sci 1997;60:2075–89.
[16] Mathew RJ, Wilson WH, Humphreys DF, Lowe JV, Wiethe KE.
Regional cerebral blood flow after marijuana smoking. J Cereb Blood
Flow Metab 1992;12:750–8.
[17] O’Leary DS, Block RI, Koeppel JA, Flaum M, Schultz SK, Andreasen
NC, et al. Effects of smoking marijuana on brain perfusion and
cognition. Neuropsychopharmacol 2002;26:802–16.
[18] Sidney S. Cardiovascular consequences of marijuana use. J Clin
Pharmacol 2002;42(Suppl):S64–70.

[19] Jones RT. Cardiovascular system effects of marijuana. J Clin Pharmacol 2002;42(Suppl):58S–63S.
[20] Herning RI, Better WE, Tate K, Cadet JL. Marijuana abusers are at
increased risk for stroke. Preliminary evidence from cerebrovascular
perfusion data. Ann NY Acad Sci 2001;939:413–5.
[21] Mathew RJ, Wilson WH. Substance abuse and cerebral blood flow.
Am J Psychiat 1991;148:292–305.
[22] Tunving K, Thulin SO, Risberg J, Warkentin S. Regional cerebral blood flow in long-term heavy cannabis use. Psychiat Res
1986;17:15–21.
[23] Krendel DA, Ditter SM, Frankel MR, Ross WK. Biopsy proven
cerebral vasculitis associated with cocaine abuse. Neurology
1990;40:1092–4.
[24] Nagayama T, Sinor AD, Simon RP, Chen J, Graham SH, Jin
K, et al. Cannabinoids and neuroprotection in global and focal
cerebral ischemia and in neuronal cultures. J Neurosci 1999;19:
2987–95.