Epidemiology and Etiology of Ischemic

Stroke in Young Adults Aged 18 to 44

Years in Northern Sweden
+ Author Affiliations

1. From the Departments of Neurology (B.K., J.M.), Medicine (B.C., B.S.,

T.O.), Clinical Physiology (C.B.), and Neuroradiology (M.F.), University
Hospital, Ume, Sweden.

1. Correspondence to Bo Kristensen, MD, Department of Neurology,

University Hospital, S-901 85 Ume, Sweden. E-mail
Bo.Kristensen@neuro.umu.se

Abstract
Background and Purpose The aim of this study was to conduct a population-
based epidemiological survey among young adults aged 18 to 44 years in
Northern Sweden and furthermore to gain further insight into the etiology of
ischemic stroke in this age group.

Methods Two studies were done. In the first part, epidemiological data were
collected to calculate incidence and mortality from 1991 through 1994. This was
based on the World Health Organization Northern Sweden MONICA register of
acute stroke events. Eighty-eight first-ever ischemic stroke patients were
identified during that period. In the second part, 107 consecutive patients aged
18 to 44 years with ischemic stroke referred to a university hospital were
studied prospectively during a 5-year period and were extensively evaluated
according to a standardized protocol. On the basis of modified Trial of ORG
10172 in Acute Stroke Treatment (TOAST) criteria, the patients were classified
into eight subtypes of ischemic stroke.

Results The average population-based annual incidence rate for ischemic stroke
(cases per 100 000 per year) was 11.3 (95% confidence interval, 6.7 to 16.1).
The case-fatality rate was 5.7%. According to the modified TOAST criteria, a
probable cause of ischemic stroke was identified in 36% and remained
unexplained in 21% of cases. Spontaneous cervical arterial dissection was the
leading probable etiology (13%). Patent foramen ovale or atrial septal aneurysm
was a possible cause of stroke in 28% of cases. The percentages of ischemic
stroke attributed to IgG anticardiolipin antibodies (4.7%), atherothrombotic
vasculopathy (3.7%), oral contraceptive use (7%), and migraine (1%) were lower
than reported in recent clinical series.
Conclusions The incidence rate for ischemic stroke was higher than previously
reported from most countries in Western Europe. The higher incidence was not
explained by a higher prevalence of premature atherosclerotic vasculopathy.
Without the additional diagnostic information derived from advanced cardiac
imaging, the proportion of indeterminate cases would have constituted 37% of
the patients.

Introduction
Ischemic stroke in young adults has been considered a relatively rare event,
with fewer than 5%1 of all cerebral ischemic infarctions occurring below the age
of 45 years, although more than 10% has been reported.2 The age-specific
incidence of stroke among individuals in this young age group has been
reported by community and hospital surveys from various geographic areas.
However, hardly any population-based data have been reported.3

The causes of stroke among young adults are more diverse than in the elderly
and require a thorough diagnostic workup. A major problem has thus been that
previous studies addressing the etiology of ischemic cerebral infarction in the
young have often been retrospective and nonstandardized, with highly variable
investigational techniques and sets of diagnostic criteria being applied.4 In
addition, advances in technology, including transesophageal investigation and
new biochemical assays, have introduced new potential causes of ischemic
stroke that still need to be substantiated. Finally, without the acknowledgment of
cases not referred for investigation, a biased pattern of the causes of the
disease may be present in hospital-based studies from third-level facility
hospitals.

The objectives of the present study were to evaluate a true age-specific

incidence and furthermore to delineate the causes of ischemic stroke in young
adults. The study was thus undertaken in two parts. First, a prospective
population-based epidemiological survey was conducted to provide data on the
incidence and mortality rates of ischemic stroke in young adults from northern
Sweden. Second, in a series of patients admitted to our university hospital, an
accurate hierarchy of causes of ischemic stroke was established on the basis of
the TOAST classification modified for ischemic stroke in young adults.5

Subjects and Methods

Epidemiological Study

Acute stroke events in the two northernmost counties of our catchment area
(Fig 1) have been monitored since 1985 by the WHO Northern Sweden MONICA
project.6 The case finding and validation of data quality have been described in
detail earlier.7
View larger version:

Map of Sweden displaying the MONICA surveillance area for Northern Sweden
(dark gray color) and the catchment area of Ume University Hospital. Eighty-
eight patients were included during 1991 to 1994 from the MONICA register for
the epidemiological part of the study. One hundred seven patients were
recruited and evaluated from the catchment area of Ume University Hospital
during 1991 to 1996 for the etiological part of the study. This includes the 71
patients from the MONICA surveillance area evaluated between 1991 and 1994.

The total population in the MONICA surveillance area was 518 669 on January 1,
1991, and 527 423 on December 31, 1994. The target population considered to
be at risk included all residents aged 18 to 44 years in this area. They
represented 37% (194 194 and 193 113, respectively) of the total population at
the beginning and at the end of the epidemiological survey period.

Clinical information from discharge records on all subjects in the age range 25
to 45 years with ICD-9 codes 430 to 438 was screened and validated for acute
stroke events that met the definition of ischemic stroke. Data from the group
aged 18 to 25 years not originally computed in the MONICA register were
obtained, adhering to the same guidelines. This part of the study thus contains
patients referred to our university hospital (included in the etiological study; see
below) as well as patients investigated only at local acute-care hospitals in
Northern Sweden. The same inclusion and exclusion criteria as in the etiological
study were used.

Etiological Study

Northern Sweden is served by 13 local hospitals and a third-level university

hospital (Fig 1). The population in the present study consists of patients aged
18 to 44 years who were admitted to Ume University Hospital between January
1991 and May 1996 as a result of ischemic stroke. The inclusion criteria were as
follows: (1) first-ever completed ischemic stroke, defined as a rapidly
developing focal neurological deficit with no apparent cause other than a
vascular origin, that persisted beyond 24 hours in surviving patients; (2) age
from 18 through 44 years; and (3) evaluation possible within 3 months after
stroke onset. Patients were scheduled for follow-up at 4 and 12 months after
admission. Exclusion criteria were as follows: ischemic stroke due to
complications of subarachnoid hemorrhage, cardiac surgery, and malignancy in
a terminal stage or occurring as an immediate consequence of trauma.

Clinical and Laboratory Evaluation

Medical history and information regarding cerebrovascular risk factors such as

arterial hypertension, diabetes mellitus, smoking, alcohol use, illicit drug use,
hyperlipidemia, oral contraceptive use, history of migraine, and occurrence of
venous or arterial thrombosis in the family were obtained according to a
standardized protocol. Hypertension was defined as systolic blood pressure
>160 mm Hg and/or diastolic pressure >95 mm Hg on two different occasions
measured outside of the acute phase of stroke or treatment with
antihypertensive drugs during the last 2 weeks before recruitment; diagnosis of
diabetes mellitus was documented by medical records or at recruitment
according to the WHO criteria8 ; hypercholesterolemia was considered present
if fasting blood level was 6.5 mmol/L at recruitment; and hypertriglyceridemia
was present if fasting triglyceride levels were >2.2 mmol/L at recruitment.
Current smoking was defined as smoking one or more cigarettes per day.
Migraine was defined according to the criteria of the International Headache
Society.9

Neuroimaging included CT and MRI of the brain, assessment of cerebral blood

flow (single-photon emission CT with Tchexamethylpropyleneamine oxime), and
cerebral angiography including posterior circulation angiography. Furthermore,
duplex ultrasonography of the cervical arteries, chest roentgenography,
electrocardiography, and 24-hour Holter electrocardiography recording was
performed.

In reference to echocardiographic studies, the TTE studies were performed with

the use of standard techniques. Views were obtained in the parasternal, apical,
and subcostal windows. The TEE images were obtained with a 5-MHz monoplane
transducer in 69 patients and with a multiplane transducer in 28 patients. All
examinations were recorded on videotape and analyzed in a blinded manner off-
line in a random order. ASA was diagnosed when the atrial septum appeared
abnormally redundant and mobile and exhibited an excursion into the left or
right atrium, or both, of >10 mm and a base of 10 mm. For PFO, the
echocardiographic detection of interatrial right-to-left shunting was identified by
color-flow Doppler or by the administration of 5 mL agitated saline in an
antecubital vein. Two to four contrast injections were systematically performed
in each patient, in the resting state and during provocative maneuvers (Valsalva
and cough test) to transiently reverse the interatrial pressure gradient. The
echocardiographic diagnosis of PFO was based on the appearance of at least
three microcavitations, either spontaneously or after provocation maneuvers,
into the left atrium, not later than four cycles after the appearance of the
microcavitations in the right atrium. The presence of atheroma of any severity
was noted when detected on echocardiography, occurring between the aortic
valve and the origin of the left subclavian artery. Mitral valve prolapse was
defined on TTE as mitral leaflet thickening and displacement beyond the plane of
the mitral annulus and into the left atrium in the parasternal long-axis view
during systole.

A detailed laboratory study was performed, including complete blood cell count;
electrolytes; serum creatinine; amino-transferases; creatine kinase; urinary
analysis; erythrocyte sedimentation rate; serum protein electrophoresis;
concentrations of blood glucose and glycosylated hemoglobin; antinuclear
antibodies and IgG aCLs; rheumatoid factor; complement factors (C3/C4);
serological testing for syphilis, borreliosis, and viral infections, including HIV;
serum cholesterol and triglyceride levels; LDL and HDL levels; lipoprotein(a);
and prothrombin and activated partial thromboplastin times. Activated partial
thromboplastin time was also used as a screening test for the presence of lupus
anticoagulants. Levels of protein C, protein S, and antithrombin III were
analyzed both in the acute phase and at least 4 months after first admission.

Classification of Subtypes

We used a modified stroke subtype classification for the etiology of ischemic

stroke with the definitions based on the TOAST classification, accommodated
and validated for stroke in the young.5 The patients were classified
independently by two groups of paired investigators. A consensus approach
was applied when necessary. The main diagnostic criteria are presented in Fig
2.

View larger version:

Causes of ischemic stroke in young patients evaluated at Ume University

Hospital in the etiologic (*, n=71) and the epidemiological (**, n=107) parts of the
study. The lower-priority diagnoses were not to be coded as probable when a
higher-priority probable or possible diagnosis was present, but there could be
two probable diagnoses if criteria for two conditions of equal priority were met.
IHS indicates International Headache Society; APLA, antiphospholipid
antibodies.

Statistical Analyses

Incidence rate was derived from the number of first episodes of ischemic stroke
among the residents in the two counties during the study period. The average of
the populations living in the area between January 1, 1991, and December 31,
1994, was the denominator of the equations for the incidence rates. Case-
fatality rate was defined as the number of subjects who died within 28 days from
the onset of stroke during the same period. Ninety-five percent confidence
intervals were computed according to the Poisson variation for the number of
events within the age groups. Fishers exact and 2 tests were used when
appropriate for statistical analysis. Probability was two tailed, and P<.05 was
considered significant.

The study was approved by the Research Ethics Committee of Ume University;
data handling procedures were approved by the National Computer Data
Inspection Board.

Results
A total of 88 first-ever ischemic strokes in the age range 18 through 44 years
from the MONICA surveillance area were recognized during the time period of
January 1, 1991, to December 31, 1994. Seventy-one cases (81%) were primarily
evaluated or referred from secondary-level care settings for further
investigations at the university hospital. These patients are thus included in the
etiologic study part. The additional 17 cases, all admitted to local acute-care
hospitals, were identified from the MONICA project register. These additional
cases had all undergone CT scan or necropsy. No further cases were
recognized from death certificates only or from medical discharge records in
the group aged 18 to 24 years.

The average annual incidence rate of first-ever ischemic stroke in the group
aged 18 to 44 years was 11.3/100 000. The age- and sex-specific incidence rates
and the 95% confidence intervals are shown in Table 1. In both sexes the risk of
stroke increased with age, but there was no statistically significant difference
between men and women (2=3.03, P=.08).

Five patients died within 28 days, resulting in a case-fatality rate of 5.7%. Deaths
resulted from ischemic cerebral edema and herniation in 3 patients and from the
effects of severe brain stem cerebellar infarction in 1 patient. One patient died
as a result of a myocardial infarction and subsequent congestive heart failure.
Data pertaining to the yearly average of ischemic stroke events in men and
women in the group aged 25 to 74 years during the time period 1991 to 1993
were available from the MONICA register.7 On average, 562 first-ever ischemic
stroke events occurred yearly during 1991 to 1993. Ischemic stroke in young
adults thus represented 3.9% of all ischemic strokes in the group aged 18 to 74
years.

The distribution of the main diagnostic categories for the 71 patients evaluated
at the university hospital during the epidemiological survey period is shown in
Fig 2. The mean age of the 17 patients (10 men, 7 women) not evaluated at our
university hospital was 40.22.3 years (range, 27 to 44 years). Based on
information from local hospital records on admission and on discharge, an
apparent probable diagnosis could be assigned to 3 patients. Because of
incomplete evaluation at the local- level hospitals, it was not possible to allocate
the remaining 14 patients to a particular etiologic subtype.

Etiology

In this part of the study, 63 men and 44 women referred to our hospital from
January 1, 1991, through May 31, 1996, fulfilled the inclusion criteria. The mean
age of the patients was 36.56.2 years (range, 19 to 44 years); age and sex
distribution is shown in Table 2. Unwillingness to participate in certain
procedures, technical problems, pregnancy, and early death explained why
scheduled investigations were not accomplished in all cases. Selective
angiography of both carotids and at least one vertebral artery was performed in
95 patients (89%), and abnormalities related to clinical symptoms were found in
58 patients (61%). In addition, 3 patients underwent MRI angiography. All
patients were investigated by CT, and 80 patients (75%) were investigated by
MRI of the brain. The carotid territory was involved in 56%, the posterior
circulation was affected in 41%, and multiple territories were involved in 3%. Six
patients did not display any visible ischemic lesions on neuroimaging. One
hundred five patients (98%) underwent either a TTE or TEE investigation.

After completion of the etiologic workup, assessment of a probable or possible

etiology led to classification of the patients into one or more of eight diagnostic
groups subdivided into higher-priority (I to IV) and lower-priority (V to VIII)
diagnoses (Fig 2). The distribution of diagnoses relating to the specific age
groups of 18 to 34 years and 35 to 44 years is shown in Table 3. The main
finding was an increased occurrence of nonatherosclerotic vasculopathy in the
older age group.

Risk factors were distributed as reported in Table 4. There were no statistically

significant differences between sexes with regard to atherosclerotic risk
factors, whereas migraine history was more frequently associated with female
sex (P=.041).
Higher-Priority Diagnoses

Ninety higher-priority diagnoses were identified in 76 patients. In 14 patients

two higher-priority diagnoses coexisted. Atherosclerotic vasculopathy was
diagnosed as the cause of cerebral infarction in 13 patients (11%). Atherogenic
risk factors were present in all of these patients except 1. All patients with a
possible diagnosis of atherothrombotic vasculopathy demonstrated only
discrete plaque formation in the carotid arteries without any signs of flow
abnormalities. In addition, TEE revealed a simple aortic arch atheroma in 3
patients.

The main cause for nonatherosclerotic vasculopathy was nontraumatic

cervicocerebral arterial dissection. The carotid arteries were affected in 9
patients and the vertebral arteries in 10 patients. One patient with fibromuscular
dysplasia as an underlying cause had bilateral carotid dissections. Isolated
intracranial arteritis was diagnosed in 1 patient. Coexistent higher-priority
diagnosis was found in 7 patients with probable or possible arterial dissection, 5
with a PFO/ASA, 1 with low positive IgG aCL titer, and 1 patient with a simple
aortic arch atheroma, in which case priority in the final classification was given
to the diagnosis of arterial dissection.

A cardioembolic etiology was presumed in 35 patients (33%). The most frequent

abnormality was right to left cardiac shunts consistent with PFO, which became
evident in 32 of 97 patients (33%) investigated with TEE. In one patient PFO was
associated with pulmonary arteriovenous fistulas. Atrial septum aneurysm was
detected in 9 patients (9%), isolated in 5 patients, and associated with PFO in 4
patients. Angiographic lesions compatible with intracranial embolic occlusion
were detected in 16 of 30 patients (53%) with PFO/ASA as the possible cause of
stroke. Coexistent higher-priority diagnoses was found in 6 patients with
PFO/ASA, 1 with a low positive IgG aCL titer and 5 with a possible
atherothrombotic vasculopathy, including 1 patient with a simple aortic arch
atheroma, but in the final classification priority was given to the cardioembolic
diagnosis. Additionally, 6 patients with PFO/ASA had coexisting lower-priority
diagnoses (lacunar infarction [n=2], migraine-induced infarction [n=2], and oral
contraceptive use [n=2]). Mitral valve prolapse was observed in 1 patient. In 4
patients a probable source of cardiac embolism was present (congenital heart
disease [n=2], ischemic dilated cardiomyopthy with left ventricular thrombus
and PFO [n=1], and atrial septum defect with left atrial thrombus [n=1]). There
was no evidence of potential emboligenic arrhythmias from electrocardiography
or Holter monitoring.

With respect to hematological causes of stroke, natural anticoagulant levels

were determined for 102 patients at admission and for 97 patients at follow-up.
One patient had an inherited protein S deficiency. Seven patients (7%) had low
positive readings for IgG aCL. Other laboratory features such as ANA titers,
VDRL tests, complement C4, thrombocytes, and aPPT were negative or within
normal range in all IgG aCLpositive patients, and no valve abnormalities were
detected by echocardiographic investigation. A history of heavy alcohol
ingestion within the preceding 24 hours was elicited in 1 patient. Ischemic
stroke occurred in the postpartum state in 1 patient.

Lower-Priority Diagnoses

Thirteen patients met the criteria for lacunar infarct, ie, a lacunar syndrome and
small deep infarction compatible with small-artery disease. In 8 patients a
coexistent higher-order diagnosis was present (possible cardiac embolism
[n=2], possible atherothrombotic vasculopathy [n=5], and IgG aCL low-positive
reading [n=1]).

Eighteen percent of men and 35% of women had a history of migraine, but only 1
woman fulfilled the criteria of the International Headache Society for a probable
migraine-induced stroke.9 Migraine-induced stroke was possible in an additional
3 patients with higher-priority diagnosis (possible cardiac embolism [n=2] and
probable arterial dissection [n=1]).

Oral contraceptive use was the likely cause of stroke in 3 female patients with
additional risk factors (smoking and migraine [n=1], smoking [n=1], and
hypertension [n=1]). Five women qualified for another diagnosis (possible
cardiac embolism [n=2], probable arterial dissection [n=2], and possible
atherothrombotic vasculopathy [n=1]).

The etiology of cerebral infarction was indeterminate in 22 patients (21%). The

evaluation was truly negative except for 1 patient who did not have an
angiography and 1 patient who was unable to endure TEE but had a normal TTE
investigation. In this subgroup of patients, angiographic investigations were
abnormal in 12 patients (52%) with unexplained intracranial occlusion of a major
artery or a branch cortical artery. Overall, there was a preponderance of
ischemic lesions in the vertebrobasilar system (57%). Fourteen patients (61%)
with an indeterminate diagnosis had at least one risk factor for atherosclerosis
(6 with one and 8 with two or more atherogenic risk factors).

Discussion
The present study is one of the largest reported series of young adults with
ischemic stroke investigated by a group of physicians at a single medical center
and the first study of stroke in young individuals in which a clear population-
based strategy for case finding has been combined with a very extensive
diagnostic workup.

By international standards, the crude incidence rates for ischemic stroke in the
present study are higher than those reported earlier from most countries in
Western Europe3 10 11 12 (Table 5) and similar to those among whites in
Baltimore, Md.13 One study from Israel has provided information from this
decade with an estimated incidence for ischemic stroke of 5/100 000 in the
group aged 17 to 44 years.14 Our rates are only lower than the unusually high
rates of stroke among males and females aged 15 to 40 years of age in
Benghazi, Libya,15 and among blacks in Baltimore, Md.13 The reported 50%
higher incidence rates for ischemic stroke in the elderly population of the
Northern Sweden MONICA study compared with available data from the
MONICA study of Gothenburg, Sweden,10 together with older limited data from
the Stockholm region11 may suggest a south to north stroke gradient in
Sweden. The explanation for such a possible geographic variation is currently
unclear.

Similar to reports from other countries, incidence rates for both men and women
were found to rise steeply after the age of 35 years.16 In our study this increase
was mainly explained by an increase in the number of arterial dissections and
cardioembolic cases, but it was influenced to only a minor degree by an
increase in premature atherosclerosis (Table 3).

A case-fatality rate of 5.7% in the present study is considerably lower, as

expected, in comparison with elderly stroke patients but corresponds to case-
fatality rates reported for similar age groups in epidemiological studies3 10 and
case series.17 18

The topography of cerebral infarctions in young adults with ischemic stroke has
rarely been detailed in previous studies. The proportion of patients with
involvement of the vertebrobasilar territory has varied from 25% to 34%.2 19 The
relatively high proportion of involvement of the vertebrobasilar territory in our
study (41%) may at least partially be due to the extensive use of MRI
investigations. Thus, quite a few cases with ischemic lesions in this territory,
including cerebellar strokes, may have gone undetected in studies mainly
relying on CT scanning.

The criteria for atherosclerotic disease have varied considerably in previous

studies, and several studies included cases defined only by the coexistence of
risk factors for atherosclerosis, which may explain why atherosclerosis has
been considered to be the cause of stroke in 5% to 50% of patients younger than
50 years.17 20 Using the TOAST classification, we detected 3.7% of patients with a
probable atherosclerotic vasculopathy; when similar criteria for probable
atherosclerotic vasculopathy were used, the rate of atherosclerotic etiology in
recent studies has varied from 5% to 23%.17 18 21 22 23

Several recent studies have demonstrated that the presence of plaques 4 mm

in the aortic arch is an important new source of emboli to the brain in patients
older than 60 years.24 However, this does not seem to be the case in a young
stroke population. This is consistent with the results reported from a few
previous studies including young as well as old stroke patients.25 26
The use of duplex ultrasonographic and arteriographic evaluation of
precerebral and intracerebral vessels resulted in a diagnosis of cervicocerebral
arterial dissection in approximately 20% of patients, a proportion considerably
higher than reported in most earlier studies.17 20 27 Our routine use of posterior
circulation angiography revealed that vertebrobasilar dissection was a common
cause of stroke in this age group. This emphasizes that a diagnosis of arterial
dissection should be considered in all cases of stroke in young adults and that a
thorough angiographic evaluation, including the vertebrobasilar territory, is
warranted in most cases.

The prevalence of PFO and ASA is increased in younger adults with stroke, 28 29
particularly in patients with otherwise unexplained stroke.21 30 In those younger
than 45 years, a prevalence of PFO within the same range as in our study (24%
to 50%) has been reported from three previous studies.26 30 31 The mechanism
underlying thromboembolic events in patients with interatrial septum
abnormalities is not well known.21 32 Angiographic evidence of embolic
intracranial arterial occlusions was present in 53% of our patients and gave
some evidence of a nidus for thrombus formation. It is of interest to note that
50% of our patients with vertebral dissection had a PFO, an ASA, or both. It is
thus important to emphasize that significant vascular pathology must be
excluded before these cardiac abnormalities are accepted as the cause of
stroke in each individual case.

In our stroke population, hereditary deficiency of natural anticoagulants (protein

S, protein C, and antithrombin III deficiency) was very rarely encountered, which
is in agreement with results reported by Adams et al33 but at variance with the
findings reported from small or selected case series.34 35 Furthermore, the low
frequency and low titers of IgG aCL in the present study imply that these
antibodies do not account for a significant proportion of strokes in young
people, at least not in all young stroke populations. These findings are in
agreement with two recent larger prospective studies in which the relevance of
aCL for ischemic stroke in unselected stroke populations has been questioned. 36
37
However, in respect to other hematologic causes of stroke, it is possible that
factor V Leiden gene point mutation could be of interest, although whether
activat ed protein C resistance secondary to this mutation causes arterial
vascular disorder is still controversial.38 39

The definition of migraine-induced stroke applied in studies conducted thus far

has been inconsistent and probably explains why cerebral infarctions in the
young attributed to migrainous infarction have varied between 1.2% and
25%.18 40 41 In the present study only 1% of the patients (one patient), based on
the criteria of the International Headache Society,9 fulfilled the criteria for
migrainous infarction, although the prevalence of migraine with or without aura
was higher than might be expected from the background.42 43 Based on data
from our epidemiological survey, the incidence of migraine-induced infarction
meeting the criteria of the International Headache Society can be estimated at
0.14/100 000 per year and including possible migraine-induced infarction can be
estimated at 0.7/100 000 per year in the group aged 18 to 44 years.

The risk increment for cardiovascular disease, including stroke, among users of
oral contraceptives is currently a matter of controversy.44 45 46 By ruling out
coexistent and more convincing etiologies such as cardioembolism and arterial
dissection, we could attribute a probable pathogenetic role to oral
contraceptive use in 7% of women.

Conclusions

We report a high incidence of stroke among young adults in Northern Sweden.

This finding is not explained by conventional causes of stroke, particularly not
by a high prevalence of premature atherosclerotic disease. Without the
additional diagnostic information derived from TEE contrast investigation, the
proportion of indeterminate cases would have constituted 37% of the patients.
Nontraumatic arterial dissection was a leading cause of ischemic stroke in our
study. New exciting data pointing toward the possibility that spontaneous
cervical artery dissections may be due to an underlying connective tissue
disorder warrant further investigations of this specific subgroup of patients.47