Trends in Substance Abuse Preceding Stroke
Among Young Adults
A Population-Based Study
Felipe de los Ríos, MD; Dawn O. Kleindorfer, MD; Jane Khoury, PhD;
Joseph P. Broderick, MD; Charles J. Moomaw, PhD; Opeolu Adeoye, MD;
Matthew L. Flaherty, MD; Pooja Khatri, MD; Daniel Woo, MD; Kathleen Alwell, BSN;
Jane Eilerman, RN; Simona Ferioli, MD; Brett M. Kissela, MD
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Background and Purpose—Approximately 5% of strokes occur in adults aged 18 to 44 years. Substance abuse is a prevalent
risk factor for stroke in young adults. We sought to identify trends in substance abuse detection among stroke patients.
Methods—Using a population-based design, we sought to identify all patients aged 18 to 54 years experiencing a stroke
(ischemic or hemorrhagic) in the Greater Cincinnati and Northern Kentucky Study region during 1993 to 1994, 1999, and
2005. Demographic and clinical characteristics and substance use data were obtained retrospectively from chart review
and adjudicated by physicians.
Results—The number of young patients identified with a stroke increased from 1993 to 1994 (297) to 2005 (501). Blacks
(61% vs 51%; P<0.02) and men (61% vs 47%; P<0.002) reported substance abuse (current smoking, alcohol, or illegal
drug use) more frequently than did whites and women. Overall use of substances increased across study periods, 45% in
1993 versus 62% in 2005 (P=0.003). The trend was significant for illegal drug use (3.8% in 1993 vs 19.8% in 2005) and
ever smoking (49% in 1993 vs 66% in 2005). Documentation of both cocaine and marijuana use increased over time. In
2005, half of young adults with a stroke were current smokers, and 1 in 5 abused illegal drugs.
Conclusions—Substance abuse is common in young adults experiencing a stroke. The observed increase in substance abuse
is contributing to the increased incidence of stroke in young adults. Patients aged younger than 55 years who experience
a stroke should be routinely screened and counseled regarding substance abuse. (Stroke. 2012;43:3179–3183.)
Key Words: acute stroke ■ alcohol ■ cocaine ■ epidemiology ■ marijuana ■ smoking
■ stroke ■ substance abuse ■ young adults
I
illicit drugs was found to be the fifth most common etiology
for ischemic stroke (9% of the study population).4 However,
this study included only ischemic strokes and likely underestimates the contribution of substance abuse as an etiology for
all strokes in this population, because hemorrhagic stroke also
is associated with substance abuse. Smoking,5 cocaine,6 and
alcohol7 are associated with both ischemic and hemorrhagic
strokes, whereas amphetamines are associated mostly with
hemorrhagic events.2 The relationship between marijuana and
stroke is less clear.8
In the present study, we sought to identify trends in substance
abuse detection among persons aged 18 to 54 years who had a
diagnosis of stroke during the periods of July 1, 1993 to June
30, 1994, 1999, and 2005, who live in the Greater Cincinnati
and Northern Kentucky areas.
n 2007, national estimates from the Nationwide Inpatient
Sample reported that 4.9% of all strokes in the United States
were in adults aged between 18 and 44 years.1 Stroke in this
young age group is associated with higher societal costs compared with older age groups.1 More worrisome, stroke in this
age group appears to be increasing.2 In our population-based
stroke study of Northern Kentucky and Southern Ohio, the
stroke incidence in those aged 20 to 54 years significantly
increased from 1993 to 2005.3 The reasons for this increase
are unclear but may involve earlier age of onset and increasing
prevalence of traditional risk factors, such as diabetes mellitus, hypertension, and obesity. It also may be secondary, in
part, to increased use of illicit drugs,2 a more common cause
of stroke among the young.
In the Baltimore–Washington Cooperative Young Stroke
Study that included patients 18 to 44 years old, the use of
Received June 12, 2012; final revision received September 7, 2012; accepted October 1, 2012.
From the Department of Neurology, University of Cincinnati College of Medicine, Cincinnati, OH, (F.R.R., D.O.K., J.P.B., O.A., M.L.F., P.K., D.W.,
J.E., S.F., B.M.K.); Division of Biostatistics and Epidemiology, Cincinnati Children’s Hospital, Cincinnati, OH (J.K.); and University of Cincinnati,
Cincinnati, OH (C.J.M., K.A.).
Correspondence to Brett M. Kissela, MD, University of Cincinnati, Department of Neurology, 260 Stetson St, Suite 2300, Cincinnati, OH 45267. E-mail
[email protected]
© 2012 American Heart Association, Inc.
Stroke is available at http://stroke.ahajournals.org
DOI: 10.1161/STROKEAHA.112.667808
3179
3180 Stroke December 2012
Methods
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The Greater Cincinnati and Northern Kentucky regions include 2
southern Ohio counties and 3 Northern Kentucky counties that abut
the Ohio River. This represents a large, 1.3-million, biracial, metropolitan population, with similar proportions of blacks and similar demographic and socioeconomic status indicators to the US population
in general, except that the Hispanic population is relatively underrepresented. Although residents of nearby counties seek care at the 17 to
19 acute care hospitals in the study region, dependent on study year,
only residents of the 5 study area counties and aged 18 to 54 years
are included in this analysis (identified as being from the study area
based on their zip code). Study periods are July 1, 1993 to June 30,
1994; January 1, 1999 to December 31, 1999; and January 1, 2005
to December 31, 2005. The screening of cases has been described
elsewhere.9
Briefly, study nurses reviewed the medical records of all patients
with International Classification of Diseases, 9th revision, codes 430
to 436 as primary or secondary discharge diagnoses from the acute
care hospitals in the study region. Strokes not found by the latter
screening were ascertained by monitoring all stroke-related visits to
all local public health clinics, hospital-based outpatient clinics, and
the 5 county coroners’ offices. Further monitoring was performed by
examining the records of potential stroke cases in a random sample
of primary care physicians’ offices and nursing homes in the Greater
Cincinnati and Northern Kentucky ­regions. Sampling was necessary
given the large number of physician offices and nursing homes in
the region. Nonhospital sites were s­ elected randomly for each study
period by the study statistician from a list generated from a combination of the local yellow pages and the American Medical Association
listing of physicians in the region. All events were cross-checked
within and between sources to prevent double counting. Institutional
Review Board approval was obtained at each participating study site
during all study periods. Abstracted information and all available
neuroimages were then reviewed by a study physician who decided
whether the patient met the case definition of stroke. The events were
classified as ischemic stroke, transient ischemic attack, intracerebral
hemorrhage, or subarachnoid hemorrhage according to definitions
adapted from the Classification of Cerebrovascular Diseases III.10
All ischemic strokes, hemorrhagic strokes, and strokes of unknown
subtype during the study period were included in this analysis. Events
classified as transient ischemic attacks were not included. Results of
serum or urine drug testing were noted when performed, but because
this study is based on retrospective medical record review, drug testing was not mandated.
Race was identified by the patient’s self-assessment in the medical record. Traditional risk factors were assigned based on historical
diagnosis. Patient who did not report previous diagnosis of hypertension but were using blood pressure medications were considered
hypertensive. Alcohol abuse was considered present if subjects consumed more than 3 servings per day (where 1 serving equals 1 oz of
hard liquor, 4 oz of wine, or 12 oz of beer); this threshold level has
been identified to be the minimum intake required to increase the risk
of ischemic stroke.11 Alcohol abuse also was considered present if
documented as heavy in the chart. Smoking was defined as current if
present within the last 3 months. Illicit drugs (marijuana, cocaine or
crack, others) were recorded as present if found on routine urine or
blood drug tests, or if self-reported in the medical chart. Information
regarding illicit drug use within 24 hours of stroke onset also was
abstracted if noted in the medical chart.
Statistical Methods
Data management and descriptive and comparative analyses were performed using SAS versions 8.02 and 9.3, respectively (SAS Institute).
Proportions are reported using the weighted estimates that were obtained by including the sampling weights in all analyses as dictated
by the study design. A detailed description of the sample weights has
been described elsewhere.12 Generalized estimating equations methods13 were used to examine the differences over time. This methodology also accounted for those patients with >1 event within a study
time period. The working correlation structure giving the best model
fit was obtained. A binary or multinomial distribution was specified
for categorical variables, as appropriate.
Results
In 1993 to 1994, 1999, and 2005, there were totals of 2735,
2875, and 2697 patients aged 18 years or older who experienced a stroke (ischemic or hemorrhagic). The number
of patients aged 18 to 54 years who experienced a stroke
increased from 1993 to 1994 to 2005; there were 297, 376,
and 501 strokes for each of the periods (1993–1994, 1999,
and 2005, respectively). Baseline patient and stroke characteristics and an overview of the percentage of substance
abuse across study periods are given in Table 1. There was a
decrease in the percentage of ischemic strokes over time, but
this did not achieve statistical significance. Blacks reported
Table 1. Patient Characteristics Across Study Periods
Patients
1993–1994
N=297
1999
N=376
2005
N=501
White
189 (69%)
239 (66%)
321 (63%)
Black
103 (30%)
134(34%)
176 (37%)
Other
5 (1.4%)
3 (0.7%)
138 (45%)
206 (52%)
5 (1.4%)
25 (6.3%)
Race
4 (0.7%)
*Substance abuse†
Present
Alcohol or drugs within 24 h of stroke*
286 (62%)
72 (12.8%)
Stroke type
Ischemic
Hemorrhagic
Unknown
219 (78%)
260 (71%)
374 (69%)
78 (22%)
114 (29%)
121 (22%)
0 (0%)
Data presented as raw n (weighted %).
*Change over time, P<0.05.
†Substance abuse combined (current smoking, alcohol, and illicit drug use).
2 (0.5%)
6 (9.2%)
de los Rios et al Substance Abuse Trends in Young Stroke Patients 3181
Table 2. Trends in Substance Use Over Time Among Stroke Patients
Strokes Only
1993–1994 (n=297)
1999 (n=376)
2005 (n=501)
129 (42%)
187 (47%)
245 (52%)
24 (7%)
29 (7%)
61 (14%)
144 (51%)
160 (46%)
195 (35%)
28 (8%)
48 (12%)
52 (15%)
13 (3.8%)
39 (9.8%)
96 (19.8%)
Smoking
Current*
Past
†Never
Heavy alcohol use
Yes
‡Illicit drug use
Yes
Data presented as raw n (weighted %).
*Current if present within the last 3 mo.
†Change over time, P=0.01.
‡Change over time, P<0.001.
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substance abuse (current smoking, alcohol, or illicit drug
use) more frequently than whites (61% vs 51%; P<0.02),
and men reported substance abuse more frequently than
women (61% vs 47%; P<0.002).
We showed an increase in the overall use of substances
(current smoking, alcohol, and illicit drug use combined) from
1993 (45%) and 1999 (52%) to 2005 (62%) (P=0.003). This
paralleled an increase in the documented use of substances
within 24 hours of stroke (1.4% in 1993–1994; 6.3% in 1999
and 12.8% in 2005; P<0.0001). Across all study periods, 28
patients had laboratory evidence of abusing illicit drugs; the
percentage was lower in 1993 to 1994 (8%), increasing in 1999
(15%) and 2005 (19%); this was not statistically significant.
The absolute number of patients detected only by self-report
on the medical chart increased across study periods (9 in 1993–
1994 to 22 in 1999 and 34 in 2005); however, the percentage of
patients detected by the combination of self-report and testing,
although increasing, showed no statistically significant change
over time (23% for 1993; 28% for 1999, and 37% for 2005).
When each substance is analyzed separately, the trend is statistically significant for both illicit drug use and ever smoking (Table 2), with illicit drug use showing the most marked
increase over time (3.8%, 9.8%, and 19.8% for 1993–1994,
1999; and 2005, respectively; P=0.001). Documented cocaine
use increased from 2.0% in 1993 to 4.5% in 1999 and to 6.6%
in 2005 (P<0.01), and documented marijuana increased from
0.6% in 1993 to 5.5% in 1999 and to 11.4% in 2005 (P<0.01).
Across study periods, the highest percentage of patients who
had documented abuse of illicit drugs were aged younger than
35 years, 19% compared with 12% for those aged 35 to 54 years
(P=0.06). Statistically significant increase in documented use
over time was only evident for those aged 35 to 54 years (P<0.01).
In contrast to Illicit drug use, there was a trend toward smoking
being more common in those aged 35 to 54 years (49%) vs those
aged 20 to 34 years (39%) (P=0.06). Current smoking did not
significantly change over time (Table 3). Substance abuse was
found in both ischemic and hemorrhagic events. Compared with
intracerebral hemorrhage patients with subarachnoid hemorrhage
and ischemic stroke had higher rates of documented current
tobacco use (33% vs 52% and 49%, respectively; P<0.01), and
subarachnoid hemorrhage patients reported less alcohol abuse
than intracerebral hemorrhage patients (13% vs 6% and 10%
for intracerebral hemorrhage, subarachnoid hemorrhage, and
ischemic stroke, respectively; P=0.02). There was no significant
difference between type of event and illicit drugs use.
Discussion
Illicit drug use and ever smoking among young adults with a
diagnosis of acute stroke is common and is being more frequently detected within our study population across study
periods. It is worrisome that in 2005, half of young adults
with stroke were current smokers and 1 out of 5 abused illicit
drugs. Tobacco is a well-known risk factor for stroke; the relative risk of stroke associated with cigarette smoking has been
calculated at 2.9 for ischemic events (in those aged <55 years
old)5 and 1.31 for intracerebral hemorrhage.14 In the period
of 2000 to 2004, cigarette smoking resulted in an estimated
yearly 443 000 premature deaths.15 Smoking increases cardiovascular risk by inducing a proinflammatory state, arterial
endothelial dysfunction, oxidative stress, increased platelet aggregability, blood viscocity, and coagulability, as well
as impaired insulin and lipid metabolism.16 Similarly, many
illicit drugs have been linked to increased stroke risk (cocaine,
amphetamines, opiates, phencyclidine, and marijuana). In our
Table 3. Substance Use by Age in Stroke Patients Across Study Periods
Current Smoker
Age
1993–1994
1999
Illicit Drug Abuse
2005
1993–1994
1999
2005
18–35 y
15 (38%)
17 (44%)
17 (36%)
5 (12%)
6 (15%)
13 (28%)
35–44 y
26 (41%)
45 (48%)
66 (55%)
2 (3%)
15 (16%)
24 (20%)*
45–54 y
88 (43%)
125 (47%)
162 (53%)
6 (2%)
18 (7%)
59 (19%)†
Data presented as raw n (weighted %).
*Change from 1993–1994 to 2005, P<0.01.
†Change from 1993 to 1994 and 1999 to 2005, P<0.01.
3182 Stroke December 2012
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study, marijuana was the most commonly detected illicit drug,
followed by cocaine. Marijuana may increase stroke risk,8,17
but the evidence is more robust for cocaine.18–22 Petitti et al23
reported an odds ratio of 13.9 for cocaine use associated with
stroke in a case control study of women aged 15 to 44 years
in the Kaiser Permanente Medical Care Program. Postulated
stroke mechanisms include cocaine-induced vasospasm, cerebral vasculitis, enhanced platelet aggregation, hypertensive
crisis associated with altered cerebral autoregulation, and cardioembolism.24 Amphetamines also have been associated with
acute intracranial hypertension and possibly vasculitis.2,23
Our findings build on those reported by George et al.25 Using
data from 1995 to 2008, from the Nationwide Inpatient Sample
of the Healthcare Cost and Utilization Project, they found
increasing use of substances, alcohol, and tobacco, as well as
other traditional stroke risk factors, in adolescents and young
adults hospitalized with acute ischemic stroke. We, however,
found a high prevalence, but no increasing trends, for current
tobacco and heavy alcohol use. This likely reflects state-specific
trends, because our findings are similar to what has been
reported for the states of Ohio and Kentucky. From 1995 to
2005, the Behavioral Risk Factor Surveillance System did not
report an increase in adult current smokers or heavy drinkers.26
Even though illicit drug use was more commonly found in
those aged 18 to 35 years, increased documentation (and thus
detection) across study periods was evident only in the group
of those 35 to 54 years old. In our study, both blacks and men
had increased association with overall use of substances (current smoking, alcohol, and illicit drug use combined). Alcohol
intake in small amounts appears to be protective against cardiovascular events, whereas consumption at higher amounts is
associated with increased risk of atrial fibrillation, ventricular
fibrillation, dilated cardiomyopathy, hypertension, dyslipidemia,
and a systemic anticoagulant effect,27,28 all of which increase
the risk of stroke. An analysis of a national survey reported
an increased use of cocaine among men and blacks,29 and the
Baltimore–Washington Young Stroke Study found more illicit
drug use among blacks (but no sex differences).30 Our analysis
incorporated a retrospective design and cannot correct for testing or diagnosis bias. During all study periods, only 28 patients
were identified solely on the basis of illicit drug test results. It is
impossible to tell from our data if there were truly higher rates of
use, or higher rates of testing, or higher rates of documentation
over time. It is possible that black men were singled out in particular for questioning and drug testing, leading to a higher rate of
documented use. We are not aware of any guideline or national
recommendation that advocated for more aggressive drug questioning and testing in the setting of acute stroke in young adults.
Another finding of our study was the significant increased
detection of cocaine and marijuana from 1993 to 2005.
Unfortunately, population data regarding trends of recreational
substance use, from the early 1990s to 2005, are lacking. The
National Survey on Drug Use and Health conducts periodical
surveys on the use of substances by those aged ≥12 years, but
because of changes in methodology starting in 2002, it is not
possible to compare reports older than this date with newer
ones. Nevertheless, at a national level, no significant increase
was reported by the National Survey on Drug Use and Health
in the use of substances (including alcohol, tobacco, and
marijuana) from 2002 to 2005, although a slight (not statistically significant) increase in the use of cocaine is mentioned.31
National trend analysis of the period from 1992 to 2002 showed
a national decrease in cocaine and an increase in marijuana substance abuse treatment admission rates, but data were incomplete for many states and no trends could be specified for the
states of Ohio and Kentucky.32 In a younger population, the
National Youth Risk Behavior Survey reported no change in
marijuana use and an increase in cocaine use between 1993
and 2005 for 9th through 12th grade students in public and private schools throughout the United States.33 Alternatively, an
increased intensity of substance use2 or adulterated drugs with
components that could pose further health hazards34 also could
explain our study findings without an overall change in the use
of recreational substances at a population level. Ultimately, the
design of our study does not allow us to draw conclusions on
substance abuse incidence rates given its observational nature
and retrospective design. We cannot correct for testing or diagnosis bias, because we did not uniformly record both negative
and positive drug test results across study periods, and the testing performed was not systematic. It is also possible that those
who experienced a stroke and abused substances in 1993 to
1994 were less inclined to seek medical care than their 1999
and 2005 counterparts.
It would have been useful to identify trends for the consumption of amphetamines or amphetamine-like substances
(mephedrone, pyrovalerone, methylenedioxypyrovalerone),
because consumption of these substances is presumed to be
on the rise and because amphetamines are associated with
hemorrhagic stroke.2 Another limitation of our study is that
we were unable to further classify smoking status by the number of cigarettes consumed, but it is known that the risks of
stroke and cardiovascular disease increase even with small
exposures.35 Strengths of our investigation include its population-based design that is comparable with that of the United
States, in general, in its proportion of blacks, demographics, and socioeconomic status, the large number of subjects
undergoing study, and the availability of data from 3 study
periods with consistent methodology allowing for testing
trends over time.
Substance abuse is 1 of many risk factors for stroke. It is
likely that no single factor, but rather a mixture of them, is
responsible for the increased incidence of stroke observed
among young adults in our population. As an example, unpublished analysis of our data shows an increasing prevalence
of dyslipidemia across study periods (13.1% in 1993–1994;
18.8% in 1999; and 24.2% in 2005; P=0.047), but no trend is
evident for hypertension, diabetes mellitus, or atrial fibrillation.
In summary, substance abuse is a common and important
risk factor for stroke in young adults. In our population, detection of both illicit drug use and ever smoking among young
adults with a diagnosis of stroke increased from 1993 to 2005,
preferentially in those aged 35 to 54 years. The observed
increase in substance abuse is contributing to the increased
incidence of stroke in young adults. All patients aged <55
years who experience a stroke should be routinely screened
and counseled regarding substance abuse.
de los Rios et al Substance Abuse Trends in Young Stroke Patients 3183
Sources of Funding
This work was funded by the National Institutes of Health
(NIH), National Institute of Neurological Disorders and Stroke
(NINDS). Division supported by NIH NINDS grants R01
NS30678 and P50 NS044283-09.
Disclosures
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Dr Woo, C.J. Moomaw (Grant No R01 NS30678; R01
NS36695; U01 NS069763), and J.C. Khoury (Grant No
R01 NS 30678) receive research support from the National
Institutes of Health (NIH). Dr Kissela receives research
support from the NIH (Grant No R01 NS30678) and honoraria
from Allergan and Reata pharmaceuticals. Dr Kleindorfer
receives research support (Grant No R01 NS30678) from
the NIH and the Centers for Disease Control and Prevention.
She is a member of the speaker’s bureau for Genentech, and
she has served as a legal expert. Dr Khatri receives research
support from the NIH, as well as research and travel support
as an unpaid consultant from Genentech. She also receives
research support from Penumbra as primary investigator
of THERAPY Trial (Assess the Penumbra System in the
Treatment of Acute Stroke). She is a consultant/advisor for
Jannsen Pharmaceuticals and has served as a legal expert. The
other authors have no conflicts to report.
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Stroke. 2012;43:3179-3183; originally published online November 15, 2012;
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