european journal of paediatric neurology 14 (2010) 197–205

Official Journal of the European Paediatric Neurology Society

Review article

The epidemiology of childhood stroke

Andrew A. Mallick, Finbar J.K. O’Callaghan*

Bristol Institute of Child Life and Health, Academic Unit of Child Health, Department of Paediatric Neurology, Level 6,
UHB Education Centre, Upper Maudlin Street, Bristol, BS2 8AE, UK

article info abstract

Article history: This paper reviews the epidemiology of childhood stroke. Stroke is an important condition
Received 24 June 2009 in children. It is one of the top ten causes of childhood death and there is a high risk of
Received in revised form serious morbidity for the survivors. Epidemiological data are an integral part of disease
14 September 2009 understanding and high quality studies are required to ensure that this data is robust.
Accepted 17 September 2009 Incidence rates from population-based studies vary from 1.3 per 100,000 to 13.0 per 100,000.
Factors found to influence incidence rates include age, gender, and ethnicity but there are
Keywords: also many inherent differences between studies. Temporal analysis of mortality rates from
Child childhood stroke shows falling rates but there has been little long-term study of changes in
Epidemiology incidence rates. Improved epidemiological data should be a goal of the national and
Incidence international collaborative networks that are studying childhood stroke.
Mortality ª 2009 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights
Stroke reserved.

Contents

1. Introduction . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
2. Incidence . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
3. Mortality . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 198
4. Age . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 200
5. Gender . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
6. Ethnicity and geography . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 201
7. Temporal trends . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 202
8. Summary . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
Acknowledgements . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203
References . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 203

* Corresponding author. Tel.: þ44 117 3420202; fax: þ44 117 3420186.
E-mail address: finbar.ocallaghan@bristol.ac.uk (F.J.K. O’Callaghan).
1090-3798/$ – see front matter ª 2009 European Paediatric Neurology Society. Published by Elsevier Ltd. All rights reserved.
doi:10.1016/j.ejpn.2009.09.006
198 european journal of paediatric neurology 14 (2010) 197–205
1. Introduction
Stroke is defined by the World Health Organisation as ‘‘rapidly
developing clinical signs of focal (or global) disturbance of
cerebral function, with symptoms lasting 24 h or longer, or
leading to death, with no apparent cause other than of
vascular origin’’.1 This definition includes both ischaemic
stroke and haemorrhagic stroke. Arterial ischaemic stroke
(AIS) and cerebral venous thrombosis (CVT) are both subtypes
of ischaemic stroke. Strictly, the WHO definition excludes
cases of subarachnoid haemorrhage (SAH) without distur-
bance of cerebral function but most investigators include SAH
as a subtype of haemorrhagic stroke.2
Stroke is the second most frequent cause of death in adults
worldwide, responsible for over 5 million deaths per year.3 As
befits the importance of stroke, its epidemiology in adults has
been extensively studied.4–6 However, stroke is also an
important disease in children. Childhood stroke is one of the
top ten causes of death in US children,7 has a high risk of
serious morbidity for survivors8 and has high financial cost
implications for healthcare services.9 Epidemiological data are
important as they quantify the scale of a disease, provide
aetiological insights and provide data to inform other studies
such as clinical trials. This paper reviews the epidemiology of
childhood stroke and considers whether the quality of the
epidemiological data currently available corresponds to the
importance of this condition.
2. Incidence
There have been various population-based studies of the
incidence of childhood stroke published over the last 30 years
(Table 1). Some studies have only estimated the incidence of
ischaemic stroke whereas others also included haemorrhagic
stroke. Studies also vary regarding the inclusion of cases of CVT
and SAH, although for a number of studies it was not possible to
ascertain whether CVT and SAH were included. There is
considerable variation in the reported incidence rates (for
clarity always referred to in this paper as the rate per 100,000
population at risk per year). Reported incidence rates for
overall (ischaemic and haemorrhagic) childhood stroke range
from 1.310 to 13.0.11 Rates for ischaemic stroke range from 0.212
to 7.9.11 Few studies report an incidence rate for CVT but the
large majority of ischaemic strokes are due to AIS, with CVT
only responsible for a small proportion of ischaemic strokes.13
The largest study of childhood CVT reports an incidence rate of
0.67 per 100,000.14 Haemorrhagic stroke rates range from 0.710
to 5.1.11 Most of the population-based incidence studies have
included SAH within the haemorrhagic stroke cases and have
not reported a separate incidence rate for SAH although Full-
erton et al. report that the incidence of SAH alone is 0.4 per
100,000.13 In contrast to adult stroke where ischaemic stroke
predominates, the rates of ischaemic stroke and haemorrhagic
stroke are approximately equal in childhood.
The two main methodologies used to ascertain cases were
retrospective analyses of hospital databases (for example,
Fullerton et al.13 and Chung and Wong15) or prospective
reporting and recording of cases (for example, Kirkham et al.16
and Steinlin et al.17). Retrospective analyses typically used
International Classification of Diseases (ICD) codes to search
for cases although some prospective registries also checked
case ascertainment by ICD code searches as well.18 Various
other strategies to improve ascertainment were also
employed such as checking of death certificates and autopsy
reports.19,20 However, it is likely that case ascertainment
remained incomplete and that consequently the incidence of
stroke in children has been underestimated. The possibility of
low ascertainment is reflected by evidence that there is often
considerable time delay from onset of symptoms until diag-
nosis21–23 and a high frequency of incorrect initial
diagnoses.24,25
There are various reasons that may explain the large
differences in reported childhood stroke incidence rates.
Firstly, there are differences in methodology and case defini-
tion between studies. The completeness of case ascertain-
ment is also likely to vary between studies. Other factors that
may influence the incidence rate are the age range of the
study population, geographical region or ethnicity of the
population, and time period of the study.
One of the most striking differences between the various
studies reporting incidence rates is the study sizes. The
precision of the estimate of incidence is dependent on the size
of the population under investigation.26 Not only are small
studies likely to have less robust estimates of disease occur-
rence but they are also less likely to be representative of the
population beyond that examined by the study.26 Many of the
studies only included the population of single cities or small
regions11,27,28 whereas the largest studied the entire pop-
ulation of countries or large states of the USA.13,16,17 There is
an over 600-fold difference between the smallest number of
person years studied (160,000)28 and the largest (99 million).13
Only four studies analysed greater than 10 million person
years and 10 studies estimated incidence by analysing less
than 1 million person years. Differences in the study sizes are
reflected in the large differences in the sizes of the 95%
confidence intervals for stroke incidence (Fig. 1).
3. Mortality
The US National Centre for Health Statistics reports mortality
rates from cerebrovascular diseases as 3.1 per 100,000 for
children aged under 1 year, 0.4 per 100,000 for children aged 1–
4 years and 0.2 per 100,000 for children aged 5–14 years.29
There have been two studies that have specifically inves-
tigated mortality from childhood stroke30,31 although
a number of other studies have reported case fatality rates of
patient series.18,20,32 Both of the mortality studies used
national death certificate data to analyse temporal trends in
mortality rates. The first studied mortality rates between 1979
and 1998 in the USA30 and the second studied rates between
1921 and 2000 in England and Wales.31 In the US study
mortality rates from childhood stroke were found to have
declined throughout the entire period studied30 whereas in
England and Wales a decline was seen from the 1960s to the
early 1980s before reaching a plateau.31 Both studies found
Table 1 – Population-based studies of the incidence of childhood stroke.
Study Location Age range Mean annual Person years Number of M:F ratio Mean incidence per 100,000 Included
population at risk studied cases
Ischaemic Haemorrhagic Overall stroke CVT SAH
19 a
Gudmundsson Iceland 0 to <15 yr 65,184 720,000 22 – – – 3.1 Yes
1977
a
15 to <20 yr 16,826 190,000 15 – – – 8.1 Yes
Schoenberg28 Rochester, 0 to <15 yr 15,834 160,000 4 – 0.6 1.9 2.5 a a

1978 Minnesota, USA

Eeg-Olofsson27 Linköping, Sweden 0 to <15 yr 23,400 230,000 5 – – – 2.1 a a

european journal of paediatric neurology 14 (2010) 197–205

1983
Satoh12 1991 Tohoku, Japan 0 to <16 yr 2,400,000 24,000,000 48 1.0 0.2 – – a
No
Broderick78 1993 Greater Cincinnati, 0 to <15 yr 295,577 590,000 16 1.29 1.2 1.5 2.7 Yes Yes
USA
Giroud11 1995 Dijon, France 0 to <16 yr 23,877 210,000 28 1.15 7.9 5.1 13.0 No Yes
Earley10 1998 Baltimore and 1 to <15 yr 773,016 1,500,000 20 – 0.6 0.7 1.3 Yes No
Washington DC,
USA
Al-Rajeh90 1998 Eastern Province 0 to <24 yr 334,000 1,000,000 15 4 – – 1.5 a
Yes
of Saudi Arabia
Beran-Koehn91 Rochester, 28 d to <15 yr 14,000 560,000 13 – 1.3 1.1 2.3 a
Yes
1999d Minnesota, USA
DeVeber18 2000d Canada 0 to <18 yr 3,970,000 24,000,000 620 1.38 2.6 – – No No
Fullerton13 2003 California, USA 30 d to <20 yr 9,907,432 99,000,000 2278 1.28 1.2 0.8 (ICH), 2.3 Yes Yes
0.4 (SAH)
Kirkham16 2003d UK and Eire 0 to <16 yr 11,370,000 12,000,000 239 1.39 – – 1.94 Yes Yes
Chung and Wong15 2004 Hong Kong >1 month 1,136,325 4,500,000 94 NR – – 2.1 Yes Yes
to <15 yr
Barnes et al.32 Melbourne, 0 to <20 yr 681,000 5,400,000 98 1.71 1.8 – – No No
2004d Australia
Steinlin17 2005d Switzerland 0 to <17 yr 1,270,000 3,800,000 80 2.08 2.1 – – Yes No
Zahuranec Nueces County, >1 month 92,418 180,000 8 1.0 1.1 2.7 (ICH), 4.3 Yes Yes
et al.49 2005 Texas, USA to <20 yr 0.5 (SAH)
Kleindorfer Greater Cincinnati 0 to <15 yr (1988–1989) 286,000 570,000 16 – – – 2.8 Yes Yes
et al.20 2006d metropolitan
area, USA
0 to <15 yr (1993–1994) 306,000 310,000 11b – – – 3.6 Yes Yes
0 to <15 yr (1999) 277,000 280,000 15b – – 5.4 Yes Yes
54 0.8
Ghandehari92 Southern Khorasan, 0 to <15 yr 196,000 980,000 18 1.43c 1.83 – – No No
2007 Iran

CVT ¼ cerebral venous thrombosis; SAH ¼ subarachnoid haemorrhage; NR ¼ not reported on cases used for calculation of incidence.
a Unable to be determined from published paper.
b Data in addition to that published in the paper provided by Dr Kleindorfer.
c Male to female ratio of underlying <15 yr old population was 1.44.
d Mean annual population at risk was not available in published paper but was calculated by AAM.

199
200 european journal of paediatric neurology 14 (2010) 197–205

that haemorrhagic stroke was responsible for over 70% of the
deaths during the study periods.
Neither mortality study investigated whether the declining
mortality rates reflected changes in the incidence of child-
hood stroke or changes in case fatality rates. However, both
emphasised that such declines could not be explained by
changes in factors such as blood pressure, smoking and serum
cholesterol levels that are linked to declines in adult stroke
mortality rates.33 Risk factors for childhood stroke mortality
that are yet to be identified may have an important influence
on declining mortality rates,30 including the possibility of very
early life factors exerting influence in the pre or perinatal
period.31
4. Age
There is considerable variation in the risk of childhood stroke
according to age. Five of the 6 studies with the largest number
of cases published the age distribution of cases.13,16–18,32,34 In
all of these studies the greatest risk of childhood stroke is for
children aged less than 1 year. In studies that analysed
neonates (aged under 1 month) separately, this group was
found to be at particularly high risk, responsible for between
8%32 and 35%17 of all cases of childhood stroke. The incidence
of perinatal stroke is estimated to be between 20 and 60 per
100,000 live births.35,36
Both studies of mortality also found that the greatest risk of
death from childhood stroke was for children aged less than 1
year.30,31 The US mortality data did not allow separate anal-
ysis of neonates but the last 15 years of data from England and
Wales did so and suggested that this youngest age group was
only a minor component to the overall mortality in the under 1
year age group.31 A low mortality rate from neonatal stroke
appears to be incongruous with a very high incidence rate.
One explanation is that although the highest risk of stroke
occurrence is in the neonatal period there may be a lag
between stroke and death that results in most deaths occur-
ring after 1 month of age. Alternatively, stroke in the neonatal
period may have a lower case fatality rate than later stroke.
Both Fullerton et al.13 and Kirkham et al.16 found that after
the age of 1 year the risk of overall stroke fell to a nadir between
the ages of 5 and 9 years before rising again in adolescence.
Fullerton reported this age distribution pattern in the incidence
of both ischaemic and haemorrhagic stroke.13 The same pattern
was also seen in the mortality studies in both the US30 and
England and Wales.31 A high incidence or mortality rate in
infancy, a lower rate in mid-childhood and then a rise in

Fig. 1 – Mean incidence of childhood stroke and 95% confidence intervals. If figures were available in the published papers
for 95% confidence intervals they were used for this figure. If not available they were calculated by AAM using the Poisson
distribution for studies with less than 100 cases and the normal approximation for studies with 100 or more cases.89
 european journal of paediatric neurology 14 (2010) 197–205
adolescence is a pattern seen in other conditions in childhood
such as bacterial meningitis, epilepsy and diabetes.37–40 There is
evidence that suggests a link between preceding varicella
infection and ischaemic stroke in children.41,42 Varicella infec-
tion is particularly linked to arteriopathy which is one of the
commonest causes of ischaemic stroke.43 It is, therefore, inter-
esting to note that the age-specific incidence rates of varicella
infection in temperate countries are highest between the ages of
1 year and 10 years and the rates are low in infancy and
adolescence.44–46 Hence, different varicella infection rates at
different ages would not explain the patterns seen in childhood
stroke reported by Fullerton et al.13 and Kirkham et al.16
In a study of ischaemic stroke only, deVeber reported that
the highest risk of stroke was for children aged less than 1 year
and then progressively lower risk with increasing age so that
those aged 12–18 years were at lowest risk.34 Neither Barnes
et al.32 nor Steinlin et al.17 found a rise in stroke risk in
adolescence but arguably the numbers of cases were too small
to robustly allow this degree of stratification.
The different risk of stroke at different ages is likely to have
implications for the incidence rates reported by the various
studies in Table 1 and Fig. 1. Studies not including neonates
are likely to find a lower incidence rate than if neonates had
been included. Also, if there is a rise in stroke risk in adoles-
cence then those studies with an upper age limit of 15 or 16
years may find a lower incidence than if people up to the age
of 18 or 19 years were included as was the case in some
studies. Of particular note, the largest study by Fullerton
et al.13 did not include children under the age of 30 days. The
study with the lowest reported incidence for overall stroke not
only excluded neonates and those over the age of 15 years but
also excluded all children under the age of 1 year.10
5. Gender
It is well known that age-specific stroke rates are higher in
adult men than women.47,48 Most of the population-based
studies of childhood stroke have reported the male to female
ratio. Kleindorfer et al.20 reported a male to female ratio of 0.8.
Satoh et al.12 and Zahuranec et al.49 both reported equal
numbers of males and females. The other 9 studies all found
an increased risk for males with a male to female ratio of
between 1.15 and 4.0 (see Table 1). The International Pediatric
Stroke Study (IPSS) found a male to female ratio of 1.49
amongst the first 1187 patients enrolled.50 Although the IPSS is
not population based there is no reason to suspect a gender
bias in the patients enrolled into the study.
Studies of mortality from childhood stroke have also
shown a preponderance of males. In the USA males were at
increased risk of death from ICH (relative risk [RR] ¼ 1.21) and
SAH (RR ¼ 1.30) but not ischaemic stroke (RR ¼ 1.02)30 whereas
in England and Wales males were at increased risk of death
from both ischaemic (RR ¼ 1.28) and haemorrhagic stroke
(RR ¼ 1.28).31
Increased levels of risk factors in men such as smoking and
alcohol overuse are associated with an increased adult male
risk of stroke.51 However, such factors cannot explain the
increased risk of stroke for male children. A number of
intrinsic factors have been postulated to explain the gender
201
difference. Oestrogen has vasodilatory and anti-inflammatory
effects that may offer relative protection from stroke to
females.52 Oestrogen levels are higher in girls than boys
throughout childhood, even in the pre-pubertal period
(particularly during the ‘‘mini-puberty’’ of infancy).53,54 In
addition to hormonal factors there may be inherent differ-
ences between male and female cells of the central nervous
system in response to hypoxic/ischaemic insults. For
example, neuronal cells derived from female animals cultured
in steroid-free media have been shown to be more resistant
than male derived cells to a range of stimuli simulating
hypoxic, ischaemic, and toxic insults.55,56
Behavioural differences may also play a role in explaining
the male predominance. Arterial dissection is implicated in
a significant proportion of ischaemic strokes in children57,58
and follows physical activity or trauma (minor or major) in
over two-thirds of patients.59 A systematic review of pub-
lished cases of childhood cerebral arterial dissection found
over 75% of cases were male.59 Differences in sports and other
physical activities may partially explain gender differences in
childhood stroke.
6. Ethnicity and geography
The epidemiology of childhood stroke has not been exten-
sively studied outside of highly developed nations with only
two of the studies listed in Table 1 being within less
economically developed countries. The studies in developed
nations are almost all of relatively homogenous, predomi-
nantly white Caucasian populations. The notable exceptions
are the studies by Satoh et al.12 and Chung and Wong15 which
studied populations that are almost exclusively (>98%) Japa-
nese and Chinese respectively. The US studies have less
homogenous populations with variable proportions of chil-
dren of mainly white, Hispanic, African-American, or Asian
ethnicity. For example, the baseline population in Kleindorf-
er’s study20 was 82% white and 15% African-America, whereas
it was 43% white, 39% Hispanic, 10% Asian and 7% African-
American in Fullerton’s study.13 Although there have been
studies of childhood stroke in other population groups they
have typically been small and not population based and,
therefore, have not been able to rigorously estimate the inci-
dence of stroke.60–62
The range of aetiological factors associated with childhood
stroke is very wide.63,64 It is very likely that the rates of many
of these factors are very different in different parts of the
world and hence, the epidemiology is also likely to be
different. For example various hospital based series of child-
hood stroke have found higher rates of associated infection in
Saudi Arabia,65 moyamoya in Taiwan,66 and sickle cell disease
in Brazil67 than is typically seen in Western Europe58 or North
America.13 It should be noted that, due to moyamoya being
relatively common in Japan, Satoh considered it as a special
entity of cerebrovascular disease and excluded cases from the
study of stroke incidence in Japan.12 Reported rates of risk
factors are likely to be heavily influenced by the type and
range of investigations that are performed in order to eluci-
date aetiology. As there is no universally agreed protocol for
the investigation of childhood stroke, large variations in the
202 european journal of paediatric neurology 14 (2010) 197–205
laboratory and neuroimaging investigations used in different
studies and different countries are likely to be present.
Investigations may greatly depend on the ‘‘focus of interest’’
of the research group or referral centre. Such differences may
partly explain wide differences in reported rates of risk
factors. For example the rates of abnormal vascular imaging
or arteriopathy found in different studies vary from 18% to
over 60% and is at least partially explained by variations in the
comprehensiveness of the vascular imaging performed.43,68–70
Of the population-based studies, only that of Fullerton was
sufficiently ethnically heterogeneous and large enough to
make direct comparisons between different ethnic groups
living within the same country.13 This study found that the
risk of stroke for black children was twice that for white
children. The relative risk for Hispanics compared to whites
was 0.76 but Asians and whites had equal risk. Blacks were at
increased risk compared to whites even when cases of sickle
cell disease were excluded. An increased risk of mortality
from childhood stroke for blacks compared to whites was also
found in the USA.30
As with gender disparities in stroke risk, the increased risk
for black adults compared to whites is well known.71 This
increased risk is typically attributed to higher rates of risk
factors such as smoking, diabetes, and hypertension.72,73
Again, these adult risk factors are not found to play a role in
childhood stroke and the finding of ethnic differences in
stroke risk for children suggests the role of other aetiological
influences such as genetic factors. For example, promoter
polymorphisms in the nitric oxidase synthase 3 gene have
been found to be associated with increased stroke risk in
young (15–44 years old) black women.74
7. Temporal trends
It has been suggested that the incidence of childhood stroke is
increasing with time.75–77 In support of this suggestion it is
noted34,76 that the reported incidence of childhood stroke
increases from the study by Schoenberg et al.28 (1965–1974), to
that of Broderick et al.78 (1988–1989) and finally to that of
Giroud et al.11 (1985–1993) or deVeber18 (1992–1998). However,
this progression does not robustly support the hypothesis that
childhood stroke incidence is rising. As discussed, there is
great variability in factors such as methodology, case defini-
tion, and baseline population characteristics between
different studies. Hence, drawing any conclusions about the
temporal trends in childhood stroke incidence by making
comparisons between different studies is fraught with
difficulties.
As discussed, mortality rates from childhood stroke in the
USA and England and Wales have been shown to be
declining.30,31 If incidence rates are indeed increasing and
mortality rates are falling then case fatality rates must also be
falling. The most plausible explanation for declining case
fatality rates is improved care post-stroke.
To examine temporal trends of incidence and case
mortality rates in a satisfactory manner requires the long-
term study of the population of a fixed region using the same
methodology throughout. Kleindorfer’s study of the Greater
Cincinnati metropolitan area over 3 periods between 1988 and
1999 showed a non-significant trend towards increasing inci-
dence over time.20 There was a non-significant decrease in
case mortality rate from the 1988–1989 period to the 1993–1994
period and no change between the 1993–1994 and 1999
periods. Data from the Canadian Pediatric Ischemic Stroke
Registry may also show increasing stroke incidence since the
establishment of the registry in 1992.79 However, a decade is
a short time period within which to examine such temporal
trends and there is a risk that apparent rising incidence may
be due to an ascertainment bias on account of improving case
ascertainment with time.
An interpretation of a rising incidence rate may be that
children are ‘‘truly’’ more likely to suffer a stroke than in the
past. Alternatively, increasing use of sophisticated diagnostic
tools may be increasing the recognition and diagnosis of
childhood stroke.80 For example, Kleindorfer found that the
use of CT increased between the 1993–1994 period and the
1999 period in the Cincinnati study.20 A number of the studies
that have estimated the incidence of childhood stroke19,28
collected cases prior to the ready availability of CT neuro-
imaging in the late 1970s to early 1980s. Perhaps more
importantly, MRI and newer MRI modalities such as perfusion,
gradient echo, and fluid attenuated inversion recovery
imaging are being used with increased frequency in childhood
stroke.81 Of particular note is diffusion weighted MRI which
has very high sensitivity for cerebral infarction, even within
a few minutes of the insult.82 The incidence of conditions that
mimic the presentation of stroke is unknown but it is likely to
be high.25 Although one study found that less than a quarter of
children who are referred with suspected stroke to a well
established stroke team were ultimately given another diag-
nosis, MRI was frequently required to differentiate stroke
from stroke mimics even in cases with an abnormal CT scan.83
Hence, increased use of MRI and associated neuroimaging
techniques may have the effect of increasing the apparent
incidence of childhood stroke by facilitating more frequent
diagnosis.75
Another factor that may facilitate recognition and diag-
nosis of childhood stroke is heightened awareness,81 amongst
both the general population and medical professionals.
Intensive stroke awareness programmes in a number of
countries have probably increased the awareness of stroke
and its symptoms in the general population.84,85 There are
now a number of national and international collaborative
groups studying childhood stroke79,86 and the number of
published articles on the subject of childhood stroke has been
steadily rising which is likely to lead to greater awareness
amongst medical professionals. Papers found on PubMed
using the search terms ‘‘stroke AND children’’ make up
a rising proportion of the total number of indexed papers. The
proportion in the 1970s was 9 per 100,000 papers, 32 per
100,000 in the 1980s, 43 per 100,000 in the 1990s and 55 per
100,000 from 2000 to 2008.87
Increasing survival of children with conditions known to
predispose to stroke such as complex congenital heart
disease, meningitis and malignancy may be a factor that
contributes to a ‘‘true’’ rise in the incidence of childhood
stroke.75 However, increased awareness of these risk factors
and improved management of conditions such as sickle cell
disease may ameliorate any such rise in incidence.88
 european journal of paediatric neurology 14 (2010) 197–205
8. Summary
Robust and comprehensive epidemiological data are an
important aspect of the understanding of a disease. Stroke is
a significant cause of childhood mortality and morbidity.8,29
The mortality rate of childhood stroke is falling although there
are suggestions that the incidence may be rising. Epidemio-
logical studies of childhood stroke have shown that the
greatest risk is in infancy, that males are at increased risk
compared to females and that there are ethnic and
geographical differences in stroke risk such as the increased
risk for black children compared to white. Many of the
differences in stroke risk between different groups of children
cannot be explained by differences in the risk factors that
influence adult stroke and so these data provide clues to
different aetiological factors. However, many of the epidemi-
ological studies of childhood stroke have been of small pop-
ulations and there has been little study of the epidemiology
outside of North America and Western Europe. There have
been insufficient long-term studies to be able to analyse
temporal trends satisfactorily. To improve the epidemiolog-
ical data available for this important condition requires
collaborative efforts to study large defined populations.49
National and international co-operative networks can help in
these efforts and these can form the basis of the large
collaborations that will be required to eventually perform
clinical trials of interventions aimed at improving the
outcomes from childhood stroke.
Acknowledgements
Both of the authors are contributors to a prospective study of
childhood stroke funded by the Stroke Association (UK). The
funding source had no involvement in study design; in the
collection, analysis, or interpretation of data; in the writing of
the report; or in the decision to submit the paper for publication.
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