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Social competence following pediatric stroke:

Contributions of brain insult and family environment
abc ad ac a ab
Vicki Anderson , Alison Gomes , Mardee Greenham , Stephen Hearps , Anne Gordon ,
e bd fg f fg
Nicole Rinehart , Linda Gonzalez , Keith Owen Yeates , Christine A. Hajek , Warren Lo &
abc
Mark Mackay
a
Child Neuropsychology, Murdoch Childrens Research Institute, Melbourne, Australia
b
Royal Children’s Hospital, Melbourne, Australia
c
University of Melbourne, Melbourne, Australia
d
Monash University, Melbourne, Australia
e
Deakin University, Melbourne, Australia
Click for updates f
The Research Institute at Nationwide Children’s Hospital, Columbus, OH, USA
g
Department of Pediatrics, The Ohio State University College of Medicine, Columbus, OH,
USA
Published online: 21 Jul 2014.

To cite this article: Vicki Anderson, Alison Gomes, Mardee Greenham, Stephen Hearps, Anne Gordon, Nicole Rinehart,
Linda Gonzalez, Keith Owen Yeates, Christine A. Hajek, Warren Lo & Mark Mackay (2014) Social competence following
pediatric stroke: Contributions of brain insult and family environment, Social Neuroscience, 9:5, 471-483, DOI:
10.1080/17470919.2014.932308

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 SOCIAL NEUROSCIENCE, 2014
Vol. 9, No. 5, 471–483, http://dx.doi.org/10.1080/17470919.2014.932308

Social competence following pediatric stroke:

Contributions of brain insult and family environment

Vicki Anderson1,2,3, Alison Gomes1,4, Mardee Greenham1,3, Stephen Hearps1,

Anne Gordon1,2, Nicole Rinehart5, Linda Gonzalez2,4, Keith Owen Yeates6,7,
Christine A. Hajek6, Warren Lo6,7, and Mark Mackay1,2,3
Downloaded by [Archives & Bibliothèques de l'ULB] at 22:14 02 February 2015

1
Child Neuropsychology, Murdoch Childrens Research Institute, Melbourne, Australia
2
Royal Children’s Hospital, Melbourne, Australia
3
University of Melbourne, Melbourne, Australia
4
Monash University, Melbourne, Australia
5
Deakin University, Melbourne, Australia
6
The Research Institute at Nationwide Children’s Hospital, Columbus, OH, USA
7
Department of Pediatrics, The Ohio State University College of Medicine, Columbus, OH, USA

Limited information is available regarding predictors of psychosocial difficulties in children following stroke. This
study aimed to (i) compare social competence of children with arterial ischemic stroke (AIS) to those with chronic
illness and healthy controls and (ii) investigate the contribution of stroke pathology, neurological outcome and
environment. Thirty-six children with AIS > 12 months prior to recruitment were compared with children with
chronic illness (asthma) (n = 15) and healthy controls (n = 43). Children underwent intellectual assessment, and
children and parents completed questionnaires to assess social competence. Children with AIS underwent MRI
scan and neurological evaluation. Child AIS was associated with poorer social adjustment and participation, and
children with AIS were rated as having more social problems than controls. Lesion volume was not associated
with social outcome, but subcortical stroke was linked to reduced social participation and younger stroke onset
predicted better social interaction and higher self-esteem. Family function was the sole predictor of social
adjustment. Findings highlight the risk of social impairment following pediatric stroke, with both stroke and
environmental factors influencing children's social competence in the chronic stages of recovery. They indicate the
potential for intervention targeting support at the family level.

Keywords: Child stroke; Pediatric stroke; Social function; Recovery; Brain; Family.

Pediatric stroke is an acute cerebrovascular event that
can occur during any stage of development. Due to
variations in comorbidities, lesion location and volume
(Deveber, 2003; Ganesan, Prengler, Mcshane, Wade, &
Kirkham, 2003; Kirton, Westmacott, & Deveber,
2007), the pediatric stroke population is heterogeneous
and is characterized by diverse functional and cognitive
deficits. Only a handful of studies have considered the
impact of stroke on children’s social competence,
despite social impairment being closely linked to poor
self-esteem, academic failure and reduced quality of
life (Anderson, Rosema, Gomes, & Catroppa, 2012;
Gomes, Rinehart, Greenham, & Anderson, 2014).
Even fewer studies have examined the contributions

Correspondence should be addressed to: Vicki Anderson, Murdoch Childrens Research Institute, Flemington Road, Parkville, Victoria,
3052. Australia. E-mail: vicki.anderson@rch.org.au
This study was supported by grants from the Australian National Health and Medical Research Council (Practitioner Fellowship, Anderson),
the Research Institute at Nationwide Children’s Hospital [# 231308], the Murdoch Childrens Research Institute, and the Victorian Governmental
Operational Infrastructure Scheme. Image analysis was supported by Elizabeth Perkins.

© 2014 Taylor & Francis

 472 ANDERSON ET AL.
of clinical features of pediatric stroke, such as lesion
characteristics and functional neurological outcome, or
environmental influences as predictors of social com-
petence (Anderson et al., 2012). A better understanding
of the frequency and nature of social impairments post-
stroke, and their relationship to clinical and environ-
mental factors will provide information for clinicians
and families to prevent or minimize such difficulties.
SOCIAL COMPETENCE FOLLOWING
PEDIATRIC STROKE
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The bulk of research examining social competence
after pediatric stroke has taken a global view, report-
ing poor “socialization” and emphasizing children’s
difficulties in implementing social skills in real-life
situations (Friefeld, Westmacott, Macgregor, &
Deveber, 2011; Mosch, Max, & Tranel, 2005;
Neuner et al., 2011; O'Keeffe, Ganesan, King, &
Murphy, 2012; Trauner, Panyard-Davis, &
Ballantyne, 1996). Recent advances in theoretical
models in the social domain challenge researchers to
take a more fine-grained approach to examining social
competence. These models divide social competence
into several domains: (i) social participation: involve-
ment in social situations is critical for health and
quality of life (World Health Organization, 2002);
(ii) social interaction: social actions and reactions
between individuals or groups modified to their inter-
action partner(s) (Beauchamp & Anderson, 2010);
(iii) social adjustment: the individual’s capacity to
adapt to the demands of the social environment
(Beauchamp & Anderson, 2010), or to engage in
adaptive, competent social and communicative beha-
vior; and the extent to which they inhibit aversive,
incompetent behavior (Crick & Dodge, 1994); and
(iv) social cognition: aspects of higher cognitive func-
tion, including the processing of social cues, empathy,
perspective taking and moral reasoning (Beauchamp
& Anderson, 2010).
Very few studies have examined specific social
domains following pediatric stroke. A handful of stu-
dies describe significant reduction in family and school
participation compared to normative data (Blom et al.,
2003; De Schryver, Kappelle, Jennekens-Schinkel, &
Boudewyn Peters, 2000). Hurvitz, Warschausky, Berg,
and Tsai (2004) describe socialization difficulties in
adult survivors of pediatric stroke despite high levels
of high school completion and employment. For social
interaction, findings indicate reduced social acceptance
and decreased social support from peers (Everts et al.,
2008), as well as changes in companionship and peer
interactions (De Schryver et al., 2000; Steinlin, Roellin,
& Schroth, 2004).
BRAIN CORRELATES OF SOCIAL
COMPETENCE
Stroke can impact a range of brain regions, many of
which have been linked to social competence
(Adolphs, 2001; Adolphs, Baron-Cohen, & Tranel,
2002; Beauchamp & Anderson, 2010), including the
basal ganglia, putamen, pre-frontal, temporal and par-
ietal cortices, and the rostral midbrain structures
(Ganesan et al., 2000; Gordon, Ganesan, Towell, &
Kirkham, 2002; Max et al., 2002). The multiple reci-
procal connections in the brain suggest that damage to
any of these regions could cause disruptions to the
entire social brain network, resulting in a variety of
social deficits (Yeates et al., 2007). This may be
especially relevant for pediatric stroke, where lesions
occur during critical stages of brain development,
when functional brain networks are immature.
Notably, studies of pediatric stroke indicate that chil-
dren sustaining perinatal stroke (i.e., before 1 month
of age) have more global and severe deficits (Nass &
Trauner, 2004) and higher rates of psychopathology
(Max, Bruce, Keatley, & Delis, 2010). However, cur-
rent evidence suggests that age at stroke onset is
unrelated to social outcomes (Hurvitz et al., 2004).
Rather, the risk of social deficits appears to be ele-
vated following stroke at any age during childhood
(Anderson et al., 2010, 2009; Greenham, Spencer-
Smith, Anderson, Coleman, & Anderson, 2010;
Trauner et al., 1996).
Little is known regarding the impact of focal brain
insult on social competence and, of interest, studies
attempting to identify brain–behavior links for other
cognitive and functional outcomes following pediatric
stroke have been disappointing (Ganesan, Ng, Chong,
Kirkham, & Connelly, 1999; Westmacott, Askalan,
Macgregor, Anderson, & Deveber, 2010). Trauner
et al. (1996) describe elevated risk of social impair-
ment with pediatric stroke involving extra-frontal
structures, while Long, Anderson, et al. (2011) report
that children with stroke involving subcortical brain
regions may be vulnerable, particularly with respect to
emotional regulation. Studies conducted by Max et al.
(2002, 2010) also link lesion location, particularly
frontal pathology, to elevated risk of attention deficit

hyperactivity disorder (ADHD) symptoms. As yet
other authors have failed to replicate these relation-
ships, reporting no clear evidence of links between
lesion site and social or behavioral outcomes (Everts
et al., 2008).
While few studies of child brain injury have docu-
mented a relationship between lesion location and
recovery, lesion volume appears to play a role in out-
come, with larger lesions associated with poorer out-
come in IQ and executive function (Anderson et al.,
2009; Hajek et al., 2014). This relationship has been
examined only rarely in pediatric stroke. Ganesan and
colleagues (Ganesan et al., 2000, 1999; Gordon et al.,
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2002) report that larger stroke infarcts (>10% supra-
tentorial intracranial volume) are associated with
poorer functional outcomes (language, self-care, phy-
sical mobility), which persist over time. A similar
result has been reported by Long, Spencer-Smith,
et al. (2011), who found an association between larger
lesions and impaired executive skills.
ENVIRONMENTAL INFLUENCES ON
SOCIAL OUTCOME
It is not only “brain” that plays a role in outcome from
early brain insult. Research examining outcomes from
acquired brain insult (e.g., traumatic brain injury)
demonstrates that, as the time since insult increases,
and the consequences of brain insult become more
chronic, the child’s capacity to adapt to persisting def-
icits grows in significance, especially within the social
domain (Anderson et al., 2006; Yeates et al., 2007). Of
note, similar findings have been reported for chronic
illnesses with no direct brain involvement, for example,
asthma or cancer (Barrera, Shaw, Speechley, Maunsell,
& Pogany, 2005; Beauchamp & Anderson, 2010; Eiser,
1997; Wolman, Resnick, Harris, & Blum, 1994).
Adapting to chronic medical conditions and their func-
tional limitations can reduce a child’s confidence in
their social abilities and their exposure to social inter-
actions (Lazarus & Folkman, 1984; Mood & Schaefer,
1984; Wallander & Varni, 1998). Few studies to date
have explored the relative contributions of brain insult
and chronic illness factors in the context of pediatric
stroke. In addition to child-based chronic illness fac-
tors, home environment has been linked to social out-
comes following acquired brain injury (Anderson et al.,
2009; Beauchamp & Anderson, 2010; Gerring &
Wade, 2012; Yeates et al., 2007). In particular, more
proximal factors, such as parent mental health and
family function, have been found to predict social out-
comes in both healthy and brain-injured groups
(Beauchamp & Anderson, 2010; Gerring & Wade,
SOCIAL OUTCOME AFTER PEDIATRIC STROKE 473
2012; Rubin, Chen, Mcdougall, Bowker, &
Mckinnon, 1995).
This study aimed to compare the social compe-
tence of children with a history of pediatric stroke,
children with a chronic illness (asthma) and healthy
controls, in order to explore the relative contribution
of stroke-specific factors and chronic illness within
this domain. Within the pediatric stroke group, we
also explored the contribution of key clinical markers
to social outcome: insult-specific factors (lesion loca-
tion and volume, neurological function); age at stroke
onset (perinatal <1 month versus child >1 month); and
environmental influences (parent mental health,
family function).
We hypothesized that (1) social competence fol-
lowing pediatric stroke would be poorer than for
chronic illness and healthy control groups, reflecting
the unique impact of brain insult on social function;
(2) within the stroke group, lesion location (i.e., cor-
tical versus subcortical, frontal versus extra-frontal,
lesion laterality) would not be related to social com-
petence. In contrast, there would be associations
between social competence and lesion volume, neuro-
logical status and age at stroke onset and (3) within
the stroke group, we predicted that proximal environ-
mental factors (caregiver mental health, family func-
tion) would contribute to social competence.
MATERIALS AND METHODS
Participants
Participants were part of a two-site study exploring
social competence following pediatric stroke (chronic
illness + brain insult) as compared with children with
asthma (chronic illness—brain insult) and healthy
controls. For the stroke group, children with arterial
ischemic stroke (AIS) were selected for participation.
The asthma group was recruited as the chronic illness
control “condition” because it is a chronic illness not
impacting the central nervous system (CNS) and so
could account for generic effects of chronic illness
(e.g., acute episode requiring hospitalization, ongoing
medical contact/medication, limitations to normal par-
ticipation), similar to that experienced by children
with AIS. Children were recruited retrospectively,
based on medical and radiological records, at The
Royal Children’s Hospital (RCH), Melbourne,
Australia and Nationwide Children’s Hospital
(NCH), Columbus, Ohio, USA. Healthy controls
were recruited from local schools in the Melbourne
metropolitan area.
 474 ANDERSON ET AL.

In total, 94 children were recruited: 36 with AIS,
15 with asthma and 43 healthy controls. Two partici-
pants with AIS were later excluded due to excessive
missing data. Children were aged 6 to 15 years at the
time of recruitment. Both the child and their family
were required to have sufficient English to complete
the study protocol. Children with AIS or asthma were
recruited at least 1 year post-diagnosis.
Children were selected for the AIS group if their
acute presentation included a clinical deficit and radi-
ological evidence of an ischemic stroke consistent with
the clinical deficit. Children with AIS occurring during
the perinatal period or during childhood were recruited.
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Exclusion criteria for the asthma control group
were as for the AIS group. Further, children with
asthma were excluded if they had been admitted to
intensive care for acute asthma (to minimize chance of
CNS insult), organ failure or a significant hypoxic
event. In addition, children in both the asthma and
healthy control groups were excluded if they had a
history of any condition affecting the CNS, diagnosed
developmental delay or psychiatric condition, chronic
use of oral steroids; current use of psychotropic med-
ication or history of a significant hypoxic event.

Those with prenatal stroke were excluded. Age at stroke

onset was dichotomized into perinatal <1 month;
n = 10) or childhood (>1 month; n = 26). Excluded
stroke etiologies were hemoglobinopathies, including
sickle cell disease; progressive neurometabolic disor-
ders; malignancy; stroke during neurosurgery; moya-
moya syndrome; brain trauma-induced hemorrhage
and autoimmune vasculitis. Other exclusionary condi-
tions with CNS involvement were congenital hydroce-
phalus; intracerebral shunts; CNS infections; pre-
existing mental retardation; prenatal exposure to alco-
hol/drugs; premorbid neurological or psychiatric disor-
der; genetic disorders with CNS involvement and use of
antipsychotic medications. Other exclusionary condi-
tions were previous organ or bone marrow transplant;
nonaccidental brain injury; severe psychiatric diagnosis
requiring hospitalization and sensory or motor impair-
ment preventing valid administration of the measures
(e.g., severe cerebral palsy). Children with epilepsy
were not excluded, except for cases in which the epi-
lepsy predated the stroke.
Measures
Demographic, descriptive and clinical measures
Demographic, neurological and medical character-
istics were obtained via parent interview and medical
file review (Table 1). Intelligence was assessed using
the two-subtest version of the Wechsler Abbreviated
Scale of Intelligence (Wechsler, 1999), from which
the Full Scale Intelligence Quotient (FSIQ)
(M = 100, SD = 15) was derived. Behavioral charac-
teristics were documented via parent ratings on the
Child Behavior Checklist (CBCL; Achenbach, 1991),
which assesses problem behaviors, using a three-point
scale from “not true” to “very true or often true”.
Externalizing, Internalizing and Social Problems sub-
scales were analyzed (M = 50, SD = 10).
Socioeconomic status (SES) was derived based on
the primary caregiver’s level of education and income.
Low scores indicate higher social risk.

TABLE 1
Sample demographics
Stroke Asthma Healthy controls p

N 36 15 43
Male (%) 16 (44.4) 9 (60.0) 24 (55.8) .482
Age at presentation (years) M (SD) 4.2 (4.3) 3.1 (4.0) — .407
Age at assessment (years) M (SD) 9.1 (3.0) 9.8 (2.6) 10.3 (3.0) .262
Time since stroke (years) M (SD) 5.0 (3.3) 6.8 (3.2) — .075
Caregiver education (%)
High school or less 17 (47.2) 7 (46.7) 6 (14.0) <.001
More than high school 17 (47.2) 8 (53.3) 37 (86.7)
FSIQ M (SD) 94.7 (13.6) 99.5 (11.8) 106.8 (15.2) .0011
Environment
FAD M (SD) 1.6 (0.4) 1.6 (0.4) 1.5 (0.3) .126
GHQ M (SD) 2.2 (3.8) 2.1 (4.3) 2.3 (3.3) .964
Child behavior
CBCL: Internalizing M (SD) 53.3 (11.4) 54.9 (10.5) 47.2 (8.3) .0072
CBCL: Externalizing M (SD) 49.4 (11.4) 50.5 (12.1) 46.6 (7.0) .293

Notes: 1Significant post hoc, stroke vs healthy controls.

2
Significant post hoc, stroke vs healthy controls, asthma vs healthy controls.

Predictors
Neuroimaging
MRI was conducted as part of routine clinical
practice for the AIS sample. Scans were conducted
on a 1.5 Tesla scanner using a standard stroke proto-
col. Two of the authors (WL, MM) determined stroke
location through review of radiological reports and
inspection of neuroimaging using the coding protocol
described by Leventer et al. (2010, 1999). Lesion
location was qualitatively coded for hemisphere
(right, left, bilateral or brainstem/cerebellum) and cer-
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ebral location (cortical, subcortical, combined cortical
and subcortical).
Brain and infarct volumes were measured by man-
ual segmentation using ITK-SNAP 1.8 (Yushkevich
et al., 2006). Infarct borders were defined on T2-
weighted sections, infarct areas were delineated on
each section and volumes summed for all sections
through the infarct. Volumes for cerebral hemispheres,
cerebellum, brainstem and ventricles were determined
similarly. In preliminary analyses, inter-rater reliabil-
ity was greater than 90%. Other investigators have
shown that manual segmentation has a similarly high
level of inter-rater reliability (Beslow et al., 2010;
Haller et al., 1997). Because of variations in total
brain volume across ages, lesion volume was
expressed as a percentage of total brain volume.
Due to small sample size, lesion locations were
collapsed into two groups: (i) frontal pathology,
defined as lesions involving brain structures within
the frontal lobe, and (ii) extra-frontal pathology,
defined as lesions involving brain structures outside
the frontal lobe. Further, cortical pathology included
lesions that affected regions of the cerebral cortex,
while subcortical pathology included brain regions
below the cerebral cortex, as well as the brain stem
and cerebellum.
Neurological examination
Neurological status was assessed in the AIS group
only using the Pediatric Stroke Outcome Measure
(PSOM: Deveber, Macgregor, Curtis, & Mayank,
2000). This provides objective rating of deficit severity
(0–2) in five domains: sensorimotor left, sensorimotor
right, language expression, language reception and cog-
nitive/behavioral. Scores for each domain are combined
to form a composite score, ranging from “0” (no defi-
cits) to a maximum of 10. The PSOM was completed
by trained clinicians (WL, AG), blinded to results of
psychological testing.
SOCIAL OUTCOME AFTER PEDIATRIC STROKE 475
Environment
These measures were completed for all partici-
pants. The General Family Functioning Scale from
the McMaster Family Assessment Device (FAD:
Epstein, Baldwin, & Bishop, 1983) provided a mea-
sure of family functioning. This 12-item scale
is based on 6 domains of problem-solving, commu-
nication, roles, affective responsiveness, affective
involvement and behavior control. Low scores indi-
cate better family functioning. The General Health
Questionnaire (GHQ: Jackson, 2006) is a self-admi-
nistered screening tool that assesses caregiver men-
tal health. It focuses on two major areas: inability to
carry out normal functions and appearance of new
and distressing phenomena. The maximum score is
28, with scores >4 suggesting probable distress.
Social competence measures
Social competence was assessed across three domains:
social adjustment, social interaction and social parti-
cipation. For nonstandardized measures, psychometric
properties are reported.
Social participation
This domain was assessed with the Child and
Adolescent Scale of Participation (CASP: Bedell,
2009), a 20-item, a parent-rated measure of child
participation in home, school and community life
situations and activities as reported by family care-
givers. It is divided into four sections: home participa-
tion; community participation; school participation;
home and community living activities, and an overall
summary score, with the latter employed in analyses.
Higher scores indicate greater extent of age-expected
participation. The CASP has demonstrated good inter-
nal consistency (alpha = 0.96) and test–retest reliabil-
ity (intraclass correlation coefficient = 0.94) and
correlates with scores from other social participation
scales (Bedell, 2009).
Social interaction
This domain was assessed through child ratings
on three questionnaires: (i) Friendship Quality
Questionnaire (FQQ: Parker & Asher, 1993) is a
40-item questionnaire designed to assess the quality
of children’s friendships with their best friend,
using a five-point scale. The FQQ generates a
Total Positive Relationships score, which was used
in the present study. The FQQ has shown adequate
 476 ANDERSON ET AL.
internal consistency (alpha = .73–.90) and scores
are significantly correlated with other measures of
loneliness and acceptance (Parker & Asher, 1993);
(ii) Network of Relationships Inventory (NRI:
Furman, 1996; Furman & Buhrmester, 1985, 1992)
is a 36-item measure of children’s perceptions of
their relationship characteristics, categorized into
four scales—support, conflict, punishment and rela-
tive power. Participants rate how much each feature
occurs in their relationships, using a five-point
Likert scale. Higher scores represent better relation-
ships. For this study, mother (NRI: mother), father
(NRI: father) and friend (NRI: friend) relationships
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were considered. The internal consistency coeffi-
cients for the scales have been calculated for
each relationship and found to be satisfactory
(M alpha = .81) and (iii) Relational Provisions
Questionnaire (RPQ: Rubin et al., 1995; Terrell-
Deutsch, 1999) consists of 28 items rated on a
five-point scale assessing children’s perceptions of
their social and emotional relatedness with peers
(RPQ:PG) and family (RPQ:F). Higher scores
reflect greater disability. The RPQ has adequate
reliability (alpha = .82–.93, test–retest r = .67–.85)
and is correlated with measures of peer acceptance
and withdrawal (Rubin et al., 1995).
Social adjustment
Participants completed the following: (i) Adaptive
Behavior Assessment System–II: Social Subscale
(ABAS-Social: Harrison & Oakland, 2003): parent
ratings of interpersonal and social competence skills
(M = 10, SD = 3); (ii) Harter Self-Perception Profile
for Children: Social Competence subscale (HARTER:
SC: Harter, 1985): children decide which descriptions
best fits them and whether the statement is “sort of
true” or “really true” for him or her. Higher scores on
these measures reflect better social adjustment; and
(iii) the CBCL social problems subscale (Achenbach,
1991, see above for details): parents report on their
child’s social problems, with higher scores reflecting
greater social problems.
Procedure
The study was approved by the human research
ethics committees of the participating institutions.
Participants with AIS were identified from a child
stroke registry or medical record audit. Those meeting
eligibility criteria were sent information packs
describing the study. For consenting families, a visit
was arranged to complete the neurological measures
and to obtain parent and child ratings of social com-
petence. Children were recruited over a period of
approximately 24 months. The test protocol was per-
formed in a set order for all participants.
Statistical analysis
For sample demographics, clinical and descriptive
measures and for hypothesis 1, analysis of variance
(ANOVA, with Bonferroni-adjusted post hoc compar-
isons) was utilized to compare groups on continuous
variables, and χ2 tests for categorical variables.
For hypothesis 2, within the AIS group, t-tests were
conducted to examine the impact of lesion location
(subcortical versus cortical, frontal versus extra-frontal)
and age at stroke onset (perinatal versus child) on
social measures, with Cohen’s d measuring size of
effect. Only effect sizes of >0.65 (i.e., 2/3 SD) were
considered (Cohen, 1988; Tabachnick & Fidell, 2001).
Note, analyses investigating laterality of lesion found
no significant relationships and are not reported. For
hypothesis 3, multiple regressions were conducted to
determine the contribution of overall lesion volume,
functional neurological outcome (PSOM), caregiver
mental health and family function to social measures.
RESULTS
Demographic, descriptive and clinical
measures
The groups did not differ in age at testing, gender,
family function or caregiver mental health. There was
a significant group difference for caregiver education,
with parents in the healthy control group more highly
educated, p = .002 (Table 1). For child descriptors,
healthy controls demonstrated higher FSIQ scores,
p = .001, than AIS children, but all group means fell
within the average range. For child behavior, while all
group means fell within the average range, the AIS
and asthma groups were rated significantly higher for
internalizing problems than healthy controls. AIS and
asthma groups were similar with respect to age at
onset and time since presentation (Table 2).
Social outcomes: Group differences
Children in the AIS group scored poorest for social
participation (CASP: p = .002). In contrast, no group
 SOCIAL OUTCOME AFTER PEDIATRIC STROKE 477

TABLE 2 Predictors of social outcomes

Medical characteristics of stroke sample
N 36 Lesion location
Seizures at presentation, n (%) 10 (29.4)
Stroke age <1 month, n (%) 10 (29.4) Examination of lesion location data found only two
Brain insult characteristics cases with “cortical only” lesions and thus, for analysis,
Cortical involvement, n (%) 2 (5.6)
Subcortical involvement, n (%) 13 (36.1)
strokes involving discrete subcortical (n = 16) areas
Cortical + subcortical, n (%) 18 (50.0) were compared with those involving both cortical and
Frontal, n (%) 14 (38.9) cortical + subcortical areas (n = 20) for social outcomes.
Extrafrontal, n (%) 22 (61.1)
Laterality No significant differences were found between groups
Left, n (%) 16 (44.4) in age at testing, PSOM or FSIQ, suggesting that differ-
Right, n (%) 13 (36.1) ences in scores cannot be attributed to these factors
Bilateral, n (%) 5 (14.5)
(Table 4). Lesions in the discrete subcortical group
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Volume
Focal, n (%) 32 (88.9)
Multifocal, n (%) 4 (11.1)
Antiepileptic medication, n (%) 3 (8.8)
PSOM total, M (SD) 1.7 (1.7)
differences were identified on child-rated measures of
social interaction, either with family or peers (FFQ:
p = .735; NRI: mother: p = .270; NRI: father:
p = .061; NRI: friend: p = .255; RPQ: family:
p = .284; RPQ: peer: p = .556). Results indicate
significant group differences for all measures of social
adjustment. The AIS group performed significantly
poorer than healthy controls for parent ratings of
social adjustment (ABAS-Social: p = .039) and self-
confidence (Harter: SC: p = .035). For parent ratings
of overall social problems, the AIS group also
recorded significantly poorer results than both healthy
controls and asthma groups (CBCL: SP: p = .001) (see
Table 3).
were significantly larger in volume compared with
those in the cortical/cortical plus subcortical lesion
group, p = .018, d = 1.17. Despite this, significant
differences were not consistently observed between
groups for any social measure, with the exception of
the CASP, on which children with discrete subcortical
lesions participated less in social activities, p = .040,
d = 0.80. This effect was larger when adjusted for lesion
volume, p = .018. Children with discrete subcortical
lesions also reported a trend to better self-esteem
(Harter: SC: Adj p = .029, d = 0.66).
There were no significant differences between fron-
tal (n = 14) and extrafrontal (n = 22) pathology groups
for age at testing or FSIQ (Table 5), but the frontal
group demonstrated significantly greater lesion
volume compared with the extrafrontal group,
p = .009. While the frontal group tended to score
more poorly on all social outcomes, group differences
did not reach significance, and this remained true after
adjusting for lesion volume.

TABLE 3
Social skills for stroke and asthma groups
Healthy controls
Stroke (n = 36) Asthma (n = 15) (n = 43)

M (SD) M (SD) M (SD) p

Social participation
CASP: total 92.5 (11.3) 97.3 (4.1) 98.4 (2.9) 0.0021
Social interaction
FFQ total 3.8 (0.8) 3.9 (1.1) 3.7 (0.6) 0.735
NRI: mother 98.7 (11.4) 93.7 (13.8) 100.1 (14.0) 0.270
NRI: father 87.9 (20.3) 89.2 (11.3) 96.9 (15.1) 0.061
NRI: friend 88.0 (20.6) 86.1 (21.6) 93.6 (14.2) 0.255
RPQ: family 20.9 (7.3) 24.4 (11.0) 21.3 (5.7) 0.284
RPQ: peers 27.1 (10.3) 29.1 (11.5) 26.1 (7.4) 0.556
Social adjustment
Harter: SC 2.8 (0.7) 3.1 (0.6) 3.1 (0.6) 0.0351
ABAS social scale 8.5 (3.9) 9.4 (3.4) 10.4 (2.7) 0.0391
CBCL: social problems 56.8 (8.3) 56.3 (6.7) 51.8 (3.3) 0.0012

Notes: 1Significant post hoc, stroke vs healthy controls.

2
Significant post hoc, stroke vs healthy controls, asthma vs healthy controls.
For CBCL and RPQ, higher scores represent poorer social competence. For all other measures, higher scores reflect better social outcomes.
 478 ANDERSON ET AL.

TABLE 4
Mean comparison of outcomes between cortical/cortical + subcortical and discrete subcortical
Discrete subcortical Cortical/ cortical +
(n = 16) subcortical (n = 20)

Variable M SD M SD p Adj. p* ES#

Demographics and lesion characteristics

FSIQ 92.9 (14.7) 96.7 (13.0) 0.430 — 0.27
Age (at assessment) 9.0 (3.4) 9.3 (2.6) 0.811 — 0.08
Lesion volume (% of total volume) 4.2 (4.5) 0.4 (0.8) 0.002 — 1.17
PSOM total 2.2 (2.0) 1.1 (0.9) 0.057 0.265 0.69
CBCL: internalizing problems 54.9 (12.1) 51.1 (10.3) 0.349 0.180 0.34
CBCL: externalizing problems 51.4 (12.9) 46.6 (8.5) 0.235 0.177 0.44
Social participation
CASP: total 89.2 (13.4) 97.2 (4.6) 0.040 0.018 0.80
Social interaction
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FQQ: total 3.8 (0.5) 3.9 (1.0) 0.739 0.729 0.12

NRI: mother 99.1 (10.9) 98.4 (12.2) 0.868 0.520 0.06
NRI: father 85.7 (19.4) 90.2 (21.7) 0.536 0.995 0.22
NRI: friend 93.6 (17.4) 82.3 (22.5) 0.122 0.131 0.56
RPQ: peer 14.4 (7.0) 15.3 (5.7) 0.711 0.607 0.13
RPQ: family 9.9 (2.7) 10.8 (4.5) 0.504 0.281 0.23
Social adjustment
Harter Social Competence 3.0 (0.8) 2.6 (0.5) 0.068 0.029 0.66
ABAS: social 94.8 (18.4) 99.8 (14.9) 0.419 0.278 0.30
CBCL: social problems 58.5 (9.9) 54.5 (4.8) 0.176 0.352 0.51

Notes: *Adjusted for lesion volume.

#Effect size: Cohen’s d.

Age at stroke onset
Perinatal and child onset groups did not differ in
age at testing, FSIQ or lesion volume. The
perinatal onset group demonstrated significantly
better peer group integration (RPQ: peer) than the
child onset group, p = .044; d = 0.89, with a trend
for higher self-esteem (Harter: SC: p = .079,
d = .70). No other differences were identified (see
Table 6).

TABLE 5
Mean comparison of outcomes between extrafrontal and frontal.
Frontal (n = 14) Extrafrontal (n = 22)

M SD M SD p Adj. p* ES#

Demographics and lesion characteristics

FSIQ 91.8 (14.6) 96.3 (13.6) 0.371 — 0.31
Age (at assessment) 9.1 (3.2) 9.2 (3.0) 0.957 — 0.02
Lesion volume (% total volume) 4.7 (5.2) 1.2 (2.0) 0.009 — 0.87
PSOM total 2.1 (2.1) 1.4 (1.4) 0.264 0.690 0.370
CBCL: internalizing problems 55.9 (12.8) 51.5 (10.2) 0.266 0.096 0.39
CBCL: externalizing problems 53.1 (14.6) 46.8 (7.9) 0.109 0.072 0.55
Social participation
CASP: total 89.2 (12.6) 94.8 (10.0) 0.164 0.103 0.49
Social interaction
FQQ: total 3.9 (0.7) 3.8 (0.8) 0.567 0.559 0.22
NRI: mother 100.5 (13.8) 97.8 (10.2) 0.541 0.920 0.22
NRI: father 84.1 (22.4) 90.0 (19.3) 0.427 0.678 0.29
NRI: friend 93.5 (16.3) 85.1 (22.4) 0.283 0.358 0.43
RPQ: peer 15.5 (7.8) 14.5 (5.7) 0.690 0.642 0.14
RPQ: family 10.5 (2.9) 10.3 (4.1) 0.922 0.971 0.04
Social adjustment
Harter Social Competence 2.9 (0.8) 2.7 (0.6) 0.509 0.557 0.23
ABAS: social 92.2 (17.6) 100.3 (16.0) 0.183 0.070 0.49
CBCL: social problems 59.7 (11.1) 54.8 (5.0) 0.090 0.154 0.57

Notes: *Adjusted for lesion volume.

#Effect size: Cohen’s d.
 SOCIAL OUTCOME AFTER PEDIATRIC STROKE 479

TABLE 6
Mean comparison of outcomes between early (perinatal) and later (1 month or older) age at stroke
Perinatal stroke 1 month or older stroke
(n = 10) (n = 26)

M SD M SD p ES#

Demographics and lesion characteristics

FSIQ 98.8 (14.4) 93.0 (13.7) 0.268 0.42
Age (at assessment) 8.3 (3.5) 9.5 (2.8) 0.323 0.36
Lesion volume (% total volume) 4.3 (4.5) 1.8 (3.4) 0.086 0.62
PSOM total 4.3 (4.5) 1.8 (3.4) 0.252 0.380
CBCL: internalizing problems 53.8 (10.3) 53.1 (12.0) 0.870 0.06
CBCL: externalizing problems 46.9 (8.2) 50.4 (12.5) 0.421 0.33
Social participation
CASP: total 95.8 (4.3) 91.1 (13.0) 0.282 0.48
Social interaction
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FQQ: total 3.6 (0.6) 3.9 (0.8) 0.338 0.41

NRI: mother 93.4 (3.2) 100.8 (12.8) 0.102 0.79
NRI: father 89.2 (7.1) 87.4 (23.6) 0.821 0.11
NRI: friend 81.8 (19.4) 90.0 (21.0) 0.332 0.41
RPQ: peer 11.2 (4.4) 16.2 (6.5) 0.044 0.89
RPQ: family 9.4 (2.9) 10.7 (3.9) 0.387 0.37
Social adjustment
Harter Social Competence 3.1 (0.6) 2.7 (0.7) 0.079 0.70
ABAS: social 99.4 (12.8) 96.0 (18.4) 0.616 0.21
CBCL: social problems 54.3 (4.4) 57.9 (9.4) 0.259 0.49

Note: #Effect size: Cohen’s d.

Lesion volume, neurological status and
environmental influences
To explore the impact of lesion volume, neurolo-
gical status (PSOM) and environmental influences on
social outcomes multiple regressions were conducted
within the AIS group. Lesion volume did not predict
any social measure, but the overall model for the
CASP was significant, with higher scores on the
PSOM (p = .004) predictive of reduced social partici-
pation (Table 7). Family function (FAD) predicted the
Harter: SC (p = .048), ABAS: social (p = .010) and
CBCL: social problems (p < .001), with poorer family
functioning predicting poorer child social outcomes in
all cases.
DISCUSSION
This study investigated the impact of AIS on social
competence, including social participation, social
interaction and social adjustment. In keeping with

TABLE 7
Social outcome multiple linear regressions
Harter: SC ABAS: Social CBCL: SP FQQ total CASP total

B p B p B p B p B p

Lesion volume (%) 0.00 .891 0.39 .626 0.17 .607 −0.02 .546 0.50 .335
PSOM total −0.10 .190 −3.05 .096 1.47 .056 −0.05 .676 −3.67 .004
FAD −0.64 .048 −20.91 .010 13.32 <.001 −0.06 .862 −8.31 .097
Parent education (>12 years) 0.00 .986 −3.79 .536 4.52 .079 0.18 .528 −0.04 .992

NRI mother NRI father NRI friend RPQ: peers RPQ: family

B p B p B P B p B p

Lesion volume (%) 0.82 .196 −1.20 .312 0.01 .993 0.20 .658 0.16 .654
PSOM total −1.95 .149 −3.46 .156 −1.74 .600 2.14 .122 0.92 .400
FAD 2.51 .638 −9.17 .355 0.47 .965 3.46 .426 0.14 .967
Parent education (>12 years) 2.53 .561 9.04 .271 7.60 .376 −4.84 .170 −2.12 .449
 480 ANDERSON ET AL.
study expectations, children with AIS demonstrated
lower levels of social participation than both healthy
and chronic illness controls and poorer social adjust-
ment compared with healthy controls and children
with chronic illness. The hypothesis that social com-
petence would not be dependent on lesion location
was generally supported, in that lesion location (cor-
tical/subcortical, frontal/extrafrontal, laterality) was
not consistently associated with social outcomes,
with the exception that discrete subcortical lesions
were found to be associated with reduced social parti-
cipation and better self-reported social competence.
Contrary to expectations based on previous literature,
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social competence did not generally differ signifi-
cantly as a function of age at stroke onset. In fact,
children with perinatal onset demonstrated a trend for
better social participation, peer interactions and self-
esteem than did those with childhood onset, despite
having lesions that were somewhat larger than those
of participants with childhood onset. Neurological
status predicted social participation, while family
function was the sole contributor to social adjustment.
Lesion volume did not contribute to any social out-
comes examined in this study.
Parent ratings of children with AIS suggested that
they exhibited poorer social competence than healthy
controls but were similar to children with a history of
chronic illness on measures of social adjustment and
participation. Further, parents identified more social
problems in children with AIS than did parents of
either asthma or healthy controls. Our results suggest
that poor social competence is not simply a reflection
of brain insult characteristics, but also of the overall
experience of the child. For example, response to
hospitalization, ongoing need for medical care, inter-
ruptions to friendships, reduced confidence and ability
to cope with day-to-day limitations associated with a
chronic illness may all impact on a child’s ability to
cope with their social world.
Using multiple regression and considering both
stroke and environmental predictors concurrently,
neither lesion volume nor frontal lobe involvement
was associated with any social outcome measure.
Our findings did suggest a relationship between dis-
crete subcortical lesions and poorer parent-rated social
participation, and self-reported self-confidence, but
not for social interaction. This is in contrast to the
study of Westmacott et al. (2010), which reported on
one of the largest cohorts of pediatric stroke survivors
to date. However, it is largely consistent with other
stroke research (Long, Spencer-Smith, et al., 2011;
Roach, 2000), reporting that stroke localization is
not predictive of neurobehavioral outcome. Further
corroboration of this finding comes from recent
studies examining children with other forms of early
focal brain insult (Everts et al., 2008; Gordon et al.,
2002; Greenham et al., 2010), where no association
was detected between social/emotional outcomes and
lesion characteristics. Within the context of a multi-
plicity of other noninjury factors, lesion characteristics
may not be a strong predictor of social outcomes,
particularly as time poststroke increases (Middleton,
2001; Yeates et al., 2007).
Younger age at stroke onset led to better developed
self-esteem and social interactions, with children sur-
viving perinatal stroke reporting significantly less pro-
blems in peer interactions than did those sustaining
stroke in later childhood. This finding is somewhat at
odds with previous findings, which have found no
such relationship. For example, Gordon et al. (2002)
and Everts et al. (2008) found no association between
social outcomes and age at stroke onset, with similar
findings in other instances of early focal insult
(Greenham et al., 2010). Of note, each of these studies
reported only on global social outcomes, and more
importantly used only parent report measures, which
may not be as valid as self-report with regard to social
interactions.
Neurological outcome was related to children’s
social participation, highlighting that children with
AIS who demonstrate physical, language and cogni-
tive and behavioral impairment are at elevated risk of
reduced social participation, consistent with
Beauchamp and Anderson’s “SOCIAL” model
(2010). We found a strong relationship between
family function and all measures of children’s social
adjustment. While we had predicted this association,
such a strong link is a relatively novel finding within
the child brain insult literature (Gerring & Wade,
2012) and emphasizes the critical importance of the
child–family relationship in the development of social
competence in the context of early brain insult. Given
that family function is a potentially modifiable risk
factor, this finding indicates that attention to family
stress and burden may enhance the quality of the
child’s environment with secondary benefits to the
child. Indeed, growing evidence suggests that, follow-
ing child brain insult, family and parent-based beha-
vioral interventions are able to reduce parent stress
and psychopathology, and improve children’s beha-
vior and social competence (Wade, Carey, & Wolfe,
2006; Woods, Catroppa, & Anderson, 2012; Woods,
Catroppa, Barnett, & Anderson, 2011).
The small sample size, although larger than most
other child stroke outcome studies, is a shortcoming
because it limited analyses and reduced statistical
power to detect group differences, most notably in
subanalyses (lesion location, age at stroke onset).

Larger, multisite studies are critical to extend our
understanding of child stroke. We included only chil-
dren who could complete our study protocol, thus
excluding those with very severe stroke. This
approach means that our findings likely underestimate
the social consequences for those with more severe
strokes. Additionally, lack of comparison data across
groups for brain structure restricted our ability to
explore the relative contributions of brain and envir-
onment to social outcomes. In particular, given group
differences in distal factors (i.e., career education), we
may not have captured key environmental influences
with our study design. Of note, no such group differ-
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ences were identified on more proximal environmental
factors, such as caregiver mental health and family
function, more often linked to social outcomes
(Gerring & Wade, 2012).
Our results suggested that, while group differences
were present across the range of parent-rated mea-
sures, children with AIS did not rate themselves as
socially impaired. This informant discrepancy may
suggest a lack of self-awareness as a consequence of
brain insult, although it has also been argued that
child perceptions are particularly valuable in the social
domain, as parents have limited opportunity to
observe their children in social situations. Further
research incorporating objective measures of social
competence (see Yeates et al., 2007) is needed to
explore these discrepancies.
Lastly, while we believe we have conducted a
comprehensive evaluation of social competence post-
stroke, results may reflect a lack of sensitivity of out-
come measures, which were not designed specifically
for brain-injured populations and may not detect
subtle deficits.
CONCLUSIONS
Children with AIS displayed greater risk of impair-
ments in social adjustment and social participation
than healthy controls, and more parent-reported social
problems compared with both healthy controls and
those with chronic illness. Exploration of potential
predictors of these problems shows little impact of
lesion characteristics. Lesion volume was not predic-
tive of social outcomes. Discrete subcortical lesions
and poorer neurological outcomes were associated
with less social participation, likely reflecting the
effect of neurological impairment on a child’s capacity
to participate in day-to-day social situations. Self-
reports by children with perinatal stroke indicated
that they saw themselves as having higher self-esteem
and better social interactions than did children with
SOCIAL OUTCOME AFTER PEDIATRIC STROKE 481
later stroke onset, highlighting the importance of child
report in studies of social outcome. Finally and of
clinical relevance, family function was found to con-
tribute significantly to social competence, suggesting
a possible avenue for intervention in the social
domain.
Original manuscript received 23 September 2013
Revised manuscript accepted 3 June 2014
First published online 18 July 2014
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