406

Stroke After Heavy Marijuana Smoking

Sally B. Zachariah, MD

I examined two young men who developed cerebral infarction associated with heavy marijuana
smoking. Both were light tobacco smokers, but they did not drink alcohol or use other street
drugs. Diagnostic work-up for nonatherosclerotic causes of stroke was unremarkable. I
postulate that marijuana-associated alterations in systemic blood pressure resulted in vaso-
spasm, leading to strokes in these patients. (Stroke 1991;22:406-409)

S troke associated with drug abuse has been

reported frequently.1 Although the incidence
and prevalence of cerebral infarction and
intracranial hemorrhage associated with drug abuse
is uncertain, case series have provided extensive
documentation of stroke occurring with the use of
street drugs, especially cocaine, amphetamines, " T s
and blues," anabolic steroids, lysergic acid diethyl-
amide, barbiturates, alcohol, and heroin.2-8 How-
ever, an acute neurological deficit following heavy
marijuana smoking has been reported infrequent-
ly.1-9"13 I examined two young men who had cerebral
infarction during heavy marijuana smoking.
Case Reports
Case 1
A previously healthy 34-year-old right-handed
white man experienced the sudden onset of dizziness,
left arm and leg weakness, and slurred speech while
smoking a marijuana cigarette. There was no head-
ache, and he denied the use of other street drugs and
alcohol. He had smoked less than one pack of
tobacco cigarettes and up to seven marijuana ciga-
rettes per day for 15 years. Recently, he had in-
creased his marijuana smoking from seven to a 14
cigarettes per day. There was no family history of
stroke, heart disease, hypertension, diabetes mellitus,
migraine headache, lupus erythematosus, autoim-
mune disorders, or sickle cell disease.
This patient's blood pressure was 164/110 mm Hg
and his pulse was 104 beats/min on admission. Neu-
rological examination performed <,2 hours after the
onset of symptoms showed severe dysarthria, right-
left disorientation, and acalculia. Cranial nerve exam-
From the Stroke Division, Department of Neurology, University
of South Florida and Bay Pines Veterans Affairs Medical Center,
Bay Pines, Fla.
Presented in pan before the XTVth World Congress of Neurol-
ogy, New Delhi, India, October 22-27, 1989.
Address for correspondence: Sally B. Zachariah, MD, Depart-
ment of Neurology, Box 127, Bay Pines Veterans Affairs Hospital,
Bay Pines, FL 33504.
Received July 20, 1990; accepted November 20, 1990.
ination revealed left lower facial weakness. Strength of
the left leg was 0/5, strength of the left arm was 1/5,
and there was loss of pinprick and temperature sen-
sation on the left side.
Results of the following laboratory studies were
within normal ranges: complete blood count; platelet
count; fibrinogen level; prothrombin time; partial
thromboplastin time; concentrations of serum glu-
cose, electrolytes, cholesterol, high density lipopro-
tein, low density lipoprotein, and triglycerides; liver
and renal function tests; concentrations of meta-
nephrine and catecholamines; erythrocyte sedimen-
tation rate; presence of antinuclear antibodies and
rheumatoid factor; VDRL; concentrations of C3
and C4; platelet function tests; lupus anticoagulant,
anticardiolipin antibody, and protein C; human im-
munodeficiency virus titer; and concentration of
antithrombin-3. The results of 24-hour Holter
monitoring and echocardiography were normal. The
results of renal angiography, done because of the
patient's hypertension, were also normal. He did not
consent to cerebral angiography. The results of non-
invasive carotid Doppler and duplex studies were
normal. A computed tomogram (CT scan) of the
brain with and without contrast on the first hospital
day was normal. A repeat CT scan with contrast 3
days later showed right basal ganglia and periventric-
ular infarcts (Figure 1). On the sixth hospital day,
single-photon emission computed tomography with
delayed redistribution study revealed right frontopa-
rietal lobe and right basal ganglia infarcts. Analysis of
the marijuana cigarettes revealed pure Cannabis
without contaminants.
After hospital discharge the patient refused to stop
smoking marijuana in spite of being strongly advised
to do so because of its harmful effects; he consented
to an experiment testing the effect of marijuana on
his platelet function. He also agreed to have the case
written and published. The in vivo test involved the
collection of blood samples before and 0.5 and 2
hours after the patient smoked marijuana as wit-
nessed by his brother. Platelet function studies were

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FIGURE 1. Case 1. Computed tomogram of brain with
contrast shows poorly defined focal area of low attenuation in
right periventricular white matter with mass effect on ventricle
consistent with acute ischemic infarct. Left side of body
appears on right side of figure.
performed using four concentrations of adenosine
diphosphate, collagen, epinephrine, arachidonic
acid, and ristocetin. There was no significant differ-
ence in platelet function among the different samples
of blood. The in vitro test involved collection of blood
samples 0.5 and 2 hours after the patient smoked
marijuana; A9-tetrahydrocannabinol (THC) in the
range of 0.1-10 Mg/ml was added to the samples.
There was no significant difference between platelet
function in these two different samples.
Physical therapy resolved this patient's dysarthria
and sensory deficit. Left-sided paresis remained and
worsened and was associated with palpitations and
dizziness whenever he smoked marijuana. He needed
antihypertensive medications to control his blood
pressure. One month after the stroke, the patient
discontinued his marijuana smoking. His blood pres-
sure then returned to normal without medical ther-
apy, and his hemiparesis improved to some extent.
Case 2
A previously healthy, 32-year-old right-handed
black man experienced the sudden onset of right arm
and leg weakness and slurred speech s0.5 hour after
smoking a marijuana cigarette. He denied the use of
alcohol or other street drugs. He had smoked one
half pack of tobacco cigarettes per day for 9 years and
marijuana heavily during the preceding 14 years. He
had increased his marijuana smoking during the 2
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Zachariah Stroke After Marijuana Smoking 407
FIGURE 2. Case 2. Computed tomogram of brain with
contrast shows enhancing lesion in left caudate nucleus and
left globus pallidus andputamen. Left side of body appears on
right side of figure.
weeks prior to the onset of symptoms. There was a
medical history of undifferentiated personality disor-
der. His family history was unremarkable.
This patient's blood pressure was 155/105 mm Hg
on admission. There was right hemiparesis, dysar-
thria, and lower facial weakness. Results of studies
identical to those performed for case 1 were also
within normal ranges. Results of magnetic resonance
imaging (MRI), angiography, and duplex studies of
his carotid system were normal. Toxicological evalu-
ation of the patient's urine and plasma showed only
cannabinoids. An initial CT scan of the brain was
normal. A contrast CT scan of the brain (Figure 2)
obtained ^1 week after the stroke demonstrated a
left basal ganglia infarct and a small left parietal lobe
infarct. Brain MRI revealed a left basal ganglia
infarct. Cerebral angiography was not performed due
to the patient's refusal. On a low-sodium diet the
patient's blood pressure returned to normal within 1
week, and after 3 months of physical and occupa-
tional therapy there was marked improvement of his
neurological deficits.
Discussion
Marijuana use became popular in the United
States in the 1960s and remains the most commonly
used illicit recreational drug. It is usually smoked in
cigarette form but may be consumed orally. Phanna-
cokinetic studies indicate that smoking is almost
equivalent to intravenous administration except that
408 Stroke Vol 22, No 3 March 1991
lower peak plasma concentrations of THC are at-
tained. In addition to its psychotropic effects, mari-
juana may induce hypotension, tachycardia, an in-
crease in the concentration of carboxyhemoglobin,
nausea, hunger, conjunctival congestion, and dryness
of the mouth and throat. 1011 Heavy smoking may be
associated with chronic bronchitis, airway obstruc-
tion, and squamous metaplasia of the respiratory
tract.14
Stroke symptoms have been described after mari-
juana smoking in only four prior cases.19"12 While the
neurological deficits were carefully documented, sup-
porting studies such as CT, MRI, toxicology, and
angiography were not carried out. Thus, the under-
lying pathophysiological mechanism of neurological
deficit in these cases is obscure.
Both of my patients had large, deep cerebral
infarcts associated with heavy marijuana use and a
recent increase in marijuana smoking. Although both
patients smoked tobacco cigarettes daily, since they
were light smokers (<10 cigarettes/day) the relative
risk of stroke from this factor may not be significant
according to the Framingham Study.15 There was no
concurrent use of alcohol or other drugs, and short of
cerebral angiography (though MRI angiography was
done) there was no evidence of an atherosclerotic
cause for stroke. Interestingly, in one patient repeat
marijuana smoking was associated with worsening of
the neurological deficit.
I postulate that marked swings in blood pres-
sure caused the strokes. Intravenous administration
of THC produces systemic and ocular hypoten-
sion.10-16'17 Fluctuations in blood pressure have been
well documented in healthy volunteers and mari-
juana users,10-12'18'19 and marijuana in particular can
produce inconstant changes in pulse rate and blood
pressure.15-2021 Both of my patients were hyperten-
sive without other risk factors for stroke22-23 at the
time of hospital admission, although their blood
pressure readings returned to normal in the weeks
following the stroke with no medical treatment and
abstinence from marijuana. I propose that the eleva-
tions of systemic blood pressure in my patients, who
had both recently increased their amount of mari-
juana smoking, could be a reaction to cerebral
vasospasm preceded by hypotension, which led to
cerebral infarction.24-25 It is also possible that to-
bacco smoking could have added to this problem.
Brain damage has not been confirmed in humans,
although some suggestions of ultrastructural dam-
age have been found in animals.26 Crawford and
Merrit 16 found that maximal decreases in systolic
pressure (15-22%) and diastolic pressure (13-
20%) were evident 60 minutes after THC inhala-
tion. Afterward, the systolic and diastolic pressures
increased simultaneously during 90-120 minutes to
control levels.15
Based on these cases, no definitive conclusions can
be drawn as to the etiology of the strokes. Similarly,
conflicting reports have been published relating the
effects of marijuana on adenylate cyclase activity,
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sympathetic nervous system stimulation, and para-
sympathetic nervous system blockage.27-28 More stud-
ies are needed to determine if marijuana is a risk
factor for stroke, especially in combination with
tobacco smoking.
Acknowledgments
I thank Philip Gorelick, MD, and David W. Schmidt
for their valuable comments and suggestions in the
preparation of this manuscript. I also wish to thank
Alfredo Giner Sorolla, PhD, for analyzing the mari-
juana cigarettes that were used in these cases, Thomas
Klein, PhD, for supplying the marijuana extract for the
in vitro test, Margie Morgan for typing the manuscript,
and Nancy Bernal, MA, for library assistance.
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Zachariah Stroke After Marijuana Smoking 409
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KEY WORDS marijuana smoking cerebrovascular disorders
risk factors
 Stroke after heavy marijuana smoking.
S B Zachariah

Stroke. 1991;22:406-409
doi: 10.1161/01.STR.22.3.406
Stroke is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231
Copyright 1991 American Heart Association, Inc. All rights reserved.
Print ISSN: 0039-2499. Online ISSN: 1524-4628

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