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Accepted Manuscript
Title: Developmental Sequelae and Neurophysiologic
Substrates of Sensory Seeking in Infant Siblings of Children
with Autism Spectrum Disorder
Authors: Cara R. Damiano-Goodwin, Tiffany G. Woynaroski,
David M. Simon, Lisa V. Iba˜
nez, Michael Murias, Anne
Kirby, Cassandra R. Newsom, Mark T. Wallace, Wendy L.
Stone, Carissa J. Cascio
PII: S1878-9293(16)30147-5
DOI: http://dx.doi.org/doi:10.1016/j.dcn.2017.08.005
Reference: DCN 480
To appear in:
Received date: 9-8-2016
Revised date: 6-7-2017
Accepted date: 9-8-2017
Please cite this article as: Damiano-Goodwin, Cara R., Woynaroski, Tiffany G.,
Simon, David M., Iba˜
nez, Lisa V., Murias, Michael, Kirby, Anne, Newsom,
Cassandra R., Wallace, Mark T., Stone, Wendy L., Cascio, Carissa J., Developmental
Sequelae and Neurophysiologic Substrates of Sensory Seeking in Infant Siblings
of Children with Autism Spectrum Disorder.Developmental Cognitive Neuroscience
http://dx.doi.org/10.1016/j.dcn.2017.08.005
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SENSORY SEEKING IN INFANT SIBLINGS 1
Developmental Sequelae and Neurophysiologic Substrates of
Sensory Seeking in Infant Siblings of Children with Autism Spectrum Disorder
Cara R. Damiano-Goodwin1*, Tiffany G. Woynaroski2 3*, David M. Simon4 5, Lisa V. Ibañez6,
Michael Murias7, Anne Kirby8, Cassandra R. Newsom3 9, Mark T. Wallace 2 3 5 10 11, Wendy L.
Stone6, Carissa J. Cascio3 5 11
1 Duke Center for Autism and Brain Development, Duke University, Durham, NC, USA
2 Department of Hearing and Speech Sciences, Vanderbilt University Medical Center, Nashville,
TN, USA
3 Vanderbilt Kennedy Center, Vanderbilt University Medical Center, Nashville, TN, USA
4 Neuroscience Graduate Program, Vanderbilt University Medical Center, Vanderbilt University,
Nashville, TN, USA
5 Vanderbilt Brain Institute, Vanderbilt University Medical Center, Vanderbilt University,
Nashville, TN, USA
6 Department of Psychology, University of Washington, Seattle, WA, USA
7 Duke Institute for Brain Sciences, Duke University, Durham, NC, USA
8 Department of Occupational Therapy, University of Utah, Salt Lake City, UT, USA
9 Department of Pediatrics, Vanderbilt University Medical Center, Nashville, TN, USA
10 Department of Psychological Sciences, Vanderbilt University, Nashville, TN, USA
11 Department of Psychiatry and Behavioral Sciences, Vanderbilt University Medical Center,
Nashville, TN, USA
*Drs. Damiano-Goodwin and Woynaroski made equal contributions to this work.
SENSORY SEEKING IN INFANT SIBLINGS 3
Graphical Abstract
SENSORY SEEKING IN INFANT SIBLINGS 4
Highlights
Infant siblings of children with autism (Sibs-ASD) display elevated sensory seeking.
Sibs-ASD who will be diagnosed with ASD show the highest levels of sensory seeking.
Sensory seeking at 18 months predicts future social symptomatology in Sibs-ASD.
The effect of seeking on social symptomatology is explained by reduced social orienting.
Atypical frontal asymmetry may underlie early differences in sensory seeking.
Abstract
It has been proposed that early differences in sensory responsiveness arise from atypical neural
function and produce cascading effects on development across domains. This longitudinal study
prospectively followed infants at heightened risk for autism spectrum disorder (ASD) based on
their status as younger siblings of children diagnosed with ASD (Sibs-ASD) and infants at
relatively lower risk for ASD (siblings of typically developing children; Sibs-TD) to examine the
developmental sequelae and possible neurophysiological substrates of a specific sensory
response pattern: unusually intense interest in nonsocial sensory stimuli or “sensory seeking.”
At 18 months, sensory seeking and social orienting were measured with the Sensory
Processing Assessment, and a potential neural signature for sensory seeking (i.e., frontal alpha
asymmetry) was measured via resting state electroencephalography. At 36 months, infants’
social symptomatology was assessed in a comprehensive diagnostic evaluation. Sibs-ASD
showed elevated sensory seeking relative to Sibs-TD, and increased sensory seeking was
concurrently associated with reduced social orienting across groups and resting frontal
asymmetry in Sibs-ASD. Sensory seeking also predicted later social symptomatology. Findings
suggest that sensory seeking may produce cascading effects on social development in infants
at risk for ASD and that atypical frontal asymmetry may underlie this atypical pattern of sensory
responsiveness.
SENSORY SEEKING IN INFANT SIBLINGS 5
Keywords: sensory, autism, infant siblings, longitudinal, frontal asymmetry, EEG
1. Introduction
Autism spectrum disorder (ASD) is characterized by social and communication deficits
accompanied by a pattern of repetitive behaviors, restricted interests, and unusual responses to
sensory stimuli. Atypical sensory responsiveness has been observed or reported in many
individuals with ASD from infancy to adulthood (Baranek, David, Poe, Stone, & Watson, 2006;
Crane, Goddard, & Pring, 2009; Dawson & Watling, 2000). Previous research indicates that
atypical sensory responsiveness emerges early in life (i.e., as early as 2-6 months of age;
Bryson et al., 2007; Dawson, Osterling, Meltzoff, & Kuhl, 2000), possibly before some of the
social and communicative impairments typically associated with ASD (Baranek, 1999; Dawson
et al., 2000; Mulligan & White, 2012). This evidence is consistent with the developmental
primacy of basic sensory neural pathways, many of which are in place prenatally (Anderson &
Thomason, 2013). Recent work also suggests that sensory responsiveness is related to other
core symptoms of ASD (Foss-Feig, Heacock, & Cascio, 2012; Gabriels et al., 2008; Kern et al.,
2007; Stevenson, Segers, Ferber, Barense, & Wallace, 2015). Together, this evidence suggests
that atypical sensory behaviors may serve as early markers of ASD risk. Furthermore, since the
early sensory environment likely influences the development of social and communicative skills
associated with ASD, a better understanding of the cascading effects of basic sensory
disturbances may elucidate the developmental trajectory of later-developing social and
communication deficits in ASD. However, to better understand this process, prospective
longitudinal studies are needed to examine the predictive value of sensory behaviors on social
and communicative development (Cascio, Woynaroski, Baranek, & Wallace, 2016).
SENSORY SEEKING IN INFANT SIBLINGS 6
Given the early development of atypical sensory responsiveness, it is possible that
behavioral response patterns to sensory stimuli may serve as an early biomarker or
endophenotype of ASD. An endophenotype is a heritable intermediate phenotype that is
expressed in both affected and non-affected family members. The identification of
endophenotypes provides clues into the biological underpinnings of a disorder (Gottesman &
Gould, 2003), and may ultimately help to discriminate between inherited behavioral features of
the disorder and features that are secondary or epiphenomenal. Infant siblings of individuals
with ASD are an ideal population in which to study candidate endophenotypes. This line of
research compares infant siblings of children diagnosed with ASD (Sibs-ASD) to infant siblings
of typically developing children (Sibs-TD), in order to better understand the characteristics
associated with a genetic risk for ASD. Sibs-ASD are at heightened risk for ASD and, even
when they are not later diagnosed with ASD, often show subclinical symptoms associated with
the disorder (Georgiades et al., 2013; Messinger et al., 2013; Ozonoff et al., 2014; Stone,
McMahon, Yoder, & Walden, 2007). Despite some preliminary studies suggesting that atypical
sensory responsiveness may be an early characteristic of the broader ASD phenotype (Brian et
al., 2008; Loh et al., 2007; Ozonoff et al., 2008), the developmental trajectory of atypical
sensory responsiveness in Sibs-ASD and the neural mechanisms driving these atypicalities
remain poorly understood.
Previous research suggests that atypical sensory responsiveness in ASD can be
characterized as three separate empirically-derived constructs: hyper-responsivity, hypo-
responsivity, and sensory seeking (Ben‐Sasson et al., 2008; Boyd et al., 2010). Most previous
research has focused on hypo- or hyper-responsivity (i.e., reduced or exaggerated behavioral
responses to sensory stimuli, respectively) in ASD. There is little research focusing specifically
on sensory seeking (Ben-Sasson et al., 2009), defined here as behaviors with the goal of
enhancing or prolonging a nonsocial sensory experience (e.g., visual examination, repetitive
touching, banging, or licking an object). In understanding the developmental trajectory of ASD
SENSORY SEEKING IN INFANT SIBLINGS 7
symptoms, sensory seeking is particularly of interest because these behaviors are likely to
divert attention away from social learning opportunities. In addition, though sensory seeking
may be directed towards other individuals (e.g., hair stroking), the odd nature of these behaviors
may actually obstruct the development of typical social relationships. Supporting this, sensory
seeking has been linked to increased severity of concurrent social and communication deficits in
children with ASD (Hilton, Graver, & LaVesser, 2007; Liss, Saulnier, Fein, & Kinsbourne, 2006;
Watson et al., 2011).
The extent to which early sensory seeking behaviors and early sensory experiences
more broadly relate to later ASD symptomatology remains unclear, however. In addition,
because sensory atypicalities are present so early in infancy and emerge before many of the
social and communicative impairments associated with ASD, the neural networks that support
these atypical sensory behaviors may also be critically involved in the emergence of the core
diagnostic features of ASD. Yet, very little is currently known about the neural correlates of
sensory responsiveness in typically developing infants, and virtually nothing is known about
these processes in Sibs-ASD. To address these questions, the present study examines sensory
seeking behaviors in Sibs-ASD and the neural mechanisms that may be driving these
behaviors. The present study also investigates the extent to which sensory seeking behaviors
might be related to later ASD symptomatology, and thus their potential utility as early markers or
endophenotypes for ASD.
As a potential neural basis for sensory seeking in infants at risk for ASD, the current
study measured asymmetry in resting state alpha band oscillations (approximately 6-9 Hz in
infants) at frontal electrode sites using EEG. Frontal asymmetry as measured by resting state
EEG (i.e., the relative difference in power between hemispheres in the alpha band) is a reliable
and stable measure that has been used to index risk for psychopathology across the lifespan
(Coan & Allen, 2004). Frontal asymmetry is believed to reflect individual differences in the
SENSORY SEEKING IN INFANT SIBLINGS 8
lateralization of brain activity which may be attributable to differences in thalamic inhibition of
cortical processing across hemispheres (Jensen & Mazaheri, 2010). It is partly heritable
(Anokhin, Heath, & Myers, 2006) and has been studied as a potential endophenotype in other
clinical conditions, such as depression (Allen & Cohen, 2010). Frontal asymmetry may also
serve as a marker of cortical development, as hemispheric differences in alpha power tend to
change over the course of the first two years of life, and may contribute to changes in
exploratory behavior over this developmental period (Fox, Calkins, & Bell, 1994; Fox,
Henderson, Rubin, Calkins, & Schmidt, 2001).
Patterns of resting frontal asymmetry may be particularly useful for understanding
sensory seeking in Sibs-ASD, as frontal asymmetry has already been correlated with ASD
symptomatology. More specifically, more severe ASD symptoms and social inhibition have been
observed in children with ASD with relatively greater right frontal asymmetry (Burnette et al.,
2011; Sutton et al., 2005), whereas fewer parent-reported social deficits have been observed in
children with relatively greater left frontal asymmetry. Most relevant to the present study, by the
age of 18 months Sibs-ASD on average demonstrate relatively greater right frontal asymmetry,
whereas Sibs-TD on average display relatively greater left frontal asymmetry (Gabard-Durnam,
Tierney, Vogel-Farley, Tager-Flusberg, & Nelson, 2015).
Frontal asymmetry has also been associated with sensory responsiveness in Sibs-ASD.
Specifically, the atypical pattern of greater right frontal asymmetry has already been observed to
co-occur with higher sensory hyporesponsivity in this high risk group (Simon et al., under
review). This finding is of interest because hyporesponsivity has been theoretically and
empirically linked to sensory seeking. Dunn's (1997) Model of Sensory Processing postulates
that sensory seeking and hyporesponsivity are both associated with a high neurological
threshold, but represent different behavioral response patterns (i.e., active versus passive).
Consistent with this theoretical framework, past studies have demonstrated behavioral
SENSORY SEEKING IN INFANT SIBLINGS 9
associations between hyporesponsivity and sensory seeking in children diagnosed with ASD
(Ausderau et al., 2014; Dunn, 1997; Freuler, Baranek, Watson, Boyd, & Bulluck, 2012).
Together, these results suggest that frontal asymmetry may reflect differences in neural
organization and processing that relate to sensory atypicalities in a population at risk for ASD.
The specific aims of the present study are as follows: (a) to determine whether high-risk
Sibs-ASD differ from low-risk Sibs-TD in sensory seeking behaviors at 18 months, (b) to
evaluate whether resting frontal asymmetry may reflect a potential neural mechanism underlying
sensory seeking differences, and (c) to examine whether early sensory seeking is related to
concurrent social orienting and later social deficits associated with ASD at 36 months. We
hypothesized that increased sensory seeking at 18 months diverts attention from important
social cues and thus reduces social orienting, which ultimately has cascading effects on social
development and results in more social deficits at 36 months. We also anticipated that Sibs-
ASD would exhibit more atypical frontal asymmetry patterns (i.e., greater right frontal
asymmetry) as previously observed in Sibs-ASD at 18 months (Gabard-Durnam et al., 2015).
Further, we predicted that right frontal asymmetry would serve as a potential neural correlate of
increased sensory seeking, as right frontal asymmetry has been linked with ASD
symptomatology in children who are diagnosed with or at risk for ASD (Burnette et al., 2011;
Simon et al., under review; Sutton et al., 2005).
2. Materials and Methods
2.1. Overview of Study Design
To test our hypotheses, we drew upon data from a multisite, longitudinal study of Sibs-
ASD and Sibs-TD (Edmunds, Ibañez, Warren, Messinger, & Stone, 2016; Key et al., 2015). For
a subset of participants in the aforementioned study, sensory seeking and social orienting
behavior were measured when infants were 18 months old. Frontal asymmetry was measured
SENSORY SEEKING IN INFANT SIBLINGS 10
via resting state EEG at this same time point. Social symptomatology was measured when
participants were 36 months old, in the context of a comprehensive diagnostic assessment.
2.2. Participants
The current sample included 20 Sibs-ASD and 20 Sibs-TD from the larger longitudinal
study for whom sensory seeking, social orienting, and/or resting frontal asymmetry was
measured at 18 months (+/- 30 days) and for whom diagnostic outcomes were ascertained.
Infants were excluded from participation in the study if they had (a) severe motor, hearing or
vision impairment according to parent report, (b) identified metabolic, genetic or progressive
neurological disorders, (c) birth weight under 2500 grams, and/or (d) a gestational age of less
than 37 weeks. Sibs-TD were also required to have no history or present concern of
developmental delay and no family history of ASD in first-degree relatives. Proband diagnoses
for older siblings of Sibs-ASD and 36 month outcome diagnoses for Sibs-ASD and Sibs-TD
were confirmed by the Autism Diagnostic Observation Schedule (ADOS; Lord et al., 2000),
Autism Diagnostic Interview-Revised (Lord, Rutter, & Le Couteur, 1994) and clinical judgment of
a licensed psychologist according to criteria from the Diagnostic and Statistical Manual of
Mental Disorders – 4th Edition (DSM-IV; American Psychiatric Association, 2000). The Mullen
Scales of Early Learning (Mullen, 1995) was administered at 12 months to characterize the
sample. Table 1 further details participant characteristics.
2.3. Measurement of Early Sensory Seeking
Infants’ sensory seeking was measured using the Sensory Processing Assessment
(SPA; Baranek, 1999), a behavioral sampling procedure developed to assess patterns of
sensory responsiveness in young children (with chronological ages approximately 9 months – 6
years). During this 15- to 20-minute observational sample, children are presented with a series
of novel toys (e.g., musical dome, bubble blower, vibrating toy) that afford sensory experiences
across a number of modalities (e.g., visual, auditory, tactile). For each novel toy, two aspects of
sensory seeking were coded from video records of SPA administrations (Kirby, Little, Schultz, &
SENSORY SEEKING IN INFANT SIBLINGS 11
Baranek, 2015). An overall rating of sensory seeking behavior from 0-2, wherein 0 = no unusual
sensory seeking behavior, 1 = occasional clearly unusual and/or intense seeking interests, and
2 = frequent, intense and/or unusual sensory seeking, was assigned. Additionally, the presence
or absence (Y/N) of discrete sensory seeking behaviors in 12 categories (flap, posture, lick, bite,
smell, sight, touch, proprioceptive, spin, auditory, other repetitive, other) was recorded. From
these codes, we derived two variables for sensory seeking. Seeking intensity was quantified as
the sum of overall ratings of sensory seeking behavior (0-2) across all novel toys. Seeking
inventory was quantified as the total number of discrete sensory seeking behaviors endorsed for
the 12 aforementioned categories across the SPA sample. The z-scores for these two
component variables were averaged to create one aggregate variable that reflected both the
intensity and inventory of sensory seeking behavior. We aggregated these two component
variables because they were conceptually linked and empirically related, and because doing so
increases the stability and thus the potential validity, of the predictor (Rushton, Brainerd, &
Pressley, 1983). Evidence of the empirical relation amongst component variables will be
presented in the Preliminary Analyses section of the Results.
2.4. Measurement of Concurrent Social Orienting and Future Social Symptomatology
Within the context of the SPA, infants are also presented with a number of “presses” for
social orienting. When the infant is engaged with a novel toy, social stimuli (e.g., name call,
shoulder tap, wave) are presented until the child shows a definite behavioral orienting response
or for a maximum of three trials, whichever comes first. No prompting or scaffolding, aside from
the prescribed repetitions (max of three per bid), is provided in response to a failure of the infant
to orient. The infant is simply permitted to continue his or her ongoing activity. Infants’
responses are assigned a score from 1-4, wherein 1 = child orients on the 1st trial, 2 = child
does not orient until the 2nd trial, 3 = child does not orient until the 3rd trial, or 4 = child does not
orient across the three trials for that stimulus. Social orienting was operationalized as the sum
of scores (1-4) assigned across all social orienting items. Thus, a higher score for social
SENSORY SEEKING IN INFANT SIBLINGS 12
orienting reflects reduced orienting/the need for increased cueing in order to elicit an orienting
response.
The ADOS Module 2 (Lord et al., 2000) was utilized to measure social symptomatology
at 36 months. This assessment was administered as part of comprehensive diagnostic
evaluation by a licensed psychologist who was research-reliable in ADOS administration and
experienced in evaluating young children with ASD. The Social Interaction domain score was
utilized as the metric of social symptomatology in analyses.
2.5. Measurement of Resting Frontal Asymmetry
Eyes open resting EEG was recorded while infants sat quietly on their parents’ laps in a
sound- and light-attenuated psychophysiology laboratory. Parents were instructed to help their
child sit as still as possible and watch a muted video that involved simple moving shapes (‘Baby
Einstein’, Kids II, Inc.). EEG data were collected from 124 (four eye channels excluded) or 128
electrodes using a NetAmp 200 or 400 amplifier and Geodesic Sensor Net (Electrical Geodesics
Inc.). Data were acquired at a sampling rate of 250 or 500 Hz, referenced to the vertex (Cz),
and online filtered from 0.1 to 100 Hz. Data were then exported and further processed using
EEGLAB (Delorme & Makeig, 2004), down sampled to 250 Hz and band-pass filtered with a
zero phase finite impulse response filter between 1-50 Hz.
Epochs 2 seconds long with 50% overlap were extracted, baseline corrected to the
mean, and rigorously visually inspected for artifacts and bad channels. We manually inspected
all channels for EOG, EMG, and movement artifacts and rejected epochs and channels
containing artifacts. Residual artifacts were corrected with independent component analysis.
Data were then re-referenced to the average, and removed channels were interpolated.
Peripheral electrodes (26 total) were excluded from all analyses due to high levels of artifact
contamination and interpolation. A total of 602 (± 118) seconds of data were recorded per
subject (range 232 – 803 seconds) and 279 (± 106) epochs were retained per subject (range 85
SENSORY SEEKING IN INFANT SIBLINGS 13
– 475). An average of 9.46 (± 3.23) channels were interpolated per subject, and an average of
2.96 (± 1.06) artifact related independent components were removed.
EEG epochs were transformed using a zero padded fast Fourier transform (0.061 Hz
resolution) after application of a Hann window. We selected two electrode groupings (six
electrodes each) centered on the F3/F4 selections used in previous studies of frontal alpha
power in children diagnosed with and infants at risk for ASD (Gabard-Durnam et al., 2015;
Sutton et al., 2005). The left frontal grouping consisted of electrode 25 (F3) and its five
neighbors (20, 21, 24, 28, and 29). The right frontal grouping consisted of electrode 124 (F4)
and its five neighbors (3, 4, 118, 119, and 123). Amplitude values were averaged across these
electrodes, squared to power, and natural log transformed. Frontal asymmetry was calculated
by subtracting log left power from log right power (log R – log L). The alpha band was defined
as 6-9 Hz based on previous literature in children this age and confirmed by a notable peak in
this range in the average power spectrum.
2.6. Analytic Plan
An independent-samples t-test was utilized to test between-group differences in sensory
seeking and resting frontal asymmetry at 18 months. A series of multiple regression analyses
was then utilized to test (a) whether early sensory seeking was related to concurrent social
orienting and future social symptomatology and (b) whether early sensory seeking was related
to resting frontal asymmetry. For each of these models, variables were added in step-wise
fashion. The predictor of interest (sensory seeking or frontal asymmetry, respectively) was
entered first to examine whether it accounted for a significant amount of variance in the
dependent variable of interest (social indices and sensory seeking, respectively) across groups.
Risk group (Sibs-ASD versus Sibs-TD) and the relevant product (risk group × predictor of
interest) terms were then added to determine if risk group moderated the effects of the predictor
of interest on the dependent variable. Throughout regression analyses, Cook’s D was used to
determine whether any individual data points were unduly influencing regression coefficients
SENSORY SEEKING IN INFANT SIBLINGS 14
(Cook’s D greater than 1 was the criterion value applied for determining undue influence on the
regression line across all analyses).
2.7. Preparation of Data for Analysis
The chosen analysis method assumed multivariate normality, and multivariate normality
is more likely when univariate distributions do not grossly depart from the normal distribution
(Tabachnick & Fidell, 2001). Thus, all variables were evaluated for normality. Variables showing
univariate skewness > |1.0| or kurtosis > |3.0| were transformed prior to imputation and analysis.
Missing data points (ranging from 5 - 32.5% across variables) were then imputed using
stochastic regression imputation, which generates plausible values for missing scores according
to the association of variables with missing data to variables with observed scores. This method
is preferable to traditional methods for dealing with missing data (e.g., listwise deletion, mean
imputation, last observation carried forward) in longitudinal data sets because it prevents loss of
information related to missing data, reduces bias, improves parameter estimates, and preserves
statistical power to detect effects of interest (Enders, 2010). This is particularly true when
auxiliary variables (which are not utilized in the primary analyses but provide extra information
about missing values) are considered in the imputation process (Enders, 2010), as was afforded
by the rich dataset from the multisite, longitudinal study of Sibs-ASD and Sibs-TD on which we
drew (Edmunds et al., 2016; Key et al., 2015). The data used in the present imputation model
included all variables involved in primary analyses as well as auxiliary variables from the
aforementioned larger dataset (e.g., Vineland Socialization scores) that were theoretically and
empirically (r values > .40 per Enders, 2010) related to, and thus possible of informing the
imputation of, one or more of the variables involved in primary analyses. Note that all analyses
reported in the results, by virtue of the stochastic regression imputation, are based on the
complete sample of 20 Sibs-ASD and 20 Sibs-TD, unless otherwise indicated (i.e., with the
exception of instances wherein undue influence was detected). Further information regarding
missing data, as well as effect sizes in observed versus imputed data for group differences and
SENSORY SEEKING IN INFANT SIBLINGS 15
associations contributing to the results we report here, are provided in accompanying
Supplemental Material (Tables S.1-S.3).
3. Results
3.1. Preliminary Analyses
3.1.1. Interobserver reliability for coded variables. Interobserver reliability of the
sensory seeking component variables, and the social orienting variable from the SPA, was
estimated for a randomly selected 20% of samples using absolute agreement intra-class
correlation coefficients (ICCs). The ICCs for seeking inventory and intensity were .78 and .80,
respectively. The ICC for social orienting was .99. Thus, inter-rater reliability was good-excellent
for coded variables.
3.1.2. Justification for aggregation of sensory seeking component variables. The
intercorrelation among the sensory seeking inventory and intensity component variables
exceeded our criterion (r ≥ .4) for aggregation (r = .86, p < .001).
3.1.3. Transformation of variables. ADOS Social Interaction domain scores at 36
months were positively skewed, but were corrected with a square-root transformation.
3.2. Primary Analyses
3.2.1. Group differences in sensory seeking and frontal asymmetry. Analyses
confirmed that Sibs-ASD and Sibs-TD groups significantly differed in early sensory seeking, t(38)
= -2.26, p = .029. Sibs-ASD (M = .24, SD = 1.09) showed significantly higher seeking relative to
Sibs-TD (M = -.44, SD = .79). This effect was moderate in magnitude (d = .72). Figure A.1
illustrates this result. Sibs-ASD also differed from Sibs-TD in frontal asymmetry at 18 months,
t(38) = 2.311, p = .026. Sibs-ASD (M = -.19, SD = .31) showed significantly greater right
asymmetry relative to Sibs-TD (M = .13, SD = .53). This effect was also moderate in magnitude
(d = .73). Figure A.2 depicts this result. Levene’s tests indicated Sibs-ASD and Sibs-TD were
non-significantly different in variance for early sensory seeking and/or resting frontal asymmetry,
SENSORY SEEKING IN INFANT SIBLINGS 16
and thus that the assumption of equal variance inherent to the t-test was not violated in either of
the aforementioned analyses.
3.2.2. Associations between frontal asymmetry and sensory seeking. The relation
between frontal asymmetry and sensory seeking at 18 months varied according to risk group (p
value for the frontal asymmetry x risk group product term in the moderation model < .001). One
participant unduly influenced the regression line within the Sibs-TD group (Cook’s D = 4.43).
Even with this participant removed from analyses, however, this moderated effect remained
significant (p value for the frontal asymmetry x risk group product term in the moderation model
= .002). The frontal asymmetry score was negatively correlated with sensory seeking (zero-
order correlation = -.528, p = .017) within the Sibs-ASD group, but positively correlated with
sensory seeking (zero-order correlation = .486, p = .035) within the Sibs-TD group. Thus,
increased sensory seeking was associated with relatively greater right asymmetry (reflected by
more negative scores for frontal asymmetry) in Sibs-ASD. Conversely, sensory seeking was
associated with relatively greater left asymmetry (reflected by more positive scores for frontal
asymmetry) in Sibs-TD. See Table A.2 for the results of regression analyses and Figure A.3 for
a depiction of this result. Note that the relation between frontal asymmetry and social orienting
at 18 months also varied according to risk group. Further information on this moderated relation
is provided in accompanying Supplemental Material (Result S.1).
3.2.3. Associations between sensory seeking and concurrent social orienting and
later social symptomatology. Sensory seeking at 18 months was related to concurrent social
orienting across groups (p value for the effect of seeking on social orienting, not controlling for
any additional factors < .001), and this effect did not significantly vary according to risk group (p
value for the sensory seeking x risk group product term in the moderation model = .24). One
infant was found to unduly influence the regression line within the Sibs-TD group (Cook’s D =
1.76). Yet, even with this participant removed from the analyses, this association remained
significant (p value for the effect of seeking on social orienting, not controlling for any additional
SENSORY SEEKING IN INFANT SIBLINGS 17
factors < .001), and the moderated effect did not reach statistical significance (p value for the
sensory seeking x risk group product term in the moderation model = .11). Within group
analyses excluding this participant, however, suggested that this effect was driven by the Sibs-
ASD group, who showed an extended range of seeking relative to the Sibs-TD group
(magnitude of the relation between sensory seeking and concurrent social orienting, excluding
the statistical outlier within the Sibs-TD group = .76 and .10 for Sibs-ASD and Sibs-TD,
respectively). Thus, increased sensory seeking was associated with reduced social orienting (as
a higher social orienting score reflects delayed or absent social orienting), but this effect is
largely limited to Sibs-ASD. See Table A.3 for the results of regression analyses and Figure A.4
for a depiction of this result.
Early sensory seeking additionally predicted future social symptomatology across groups
(p value for the effect of seeking on future social symptomatology, not controlling for other
factors = .008), but this effect significantly varied according to risk group (p value for the sensory
seeking x risk group product term in the moderation model = .008). Sensory seeking was
positively correlated with later social symptomatology in Sibs-ASD (r = .54, p = .014). Thus,
higher seeking at 18 months predicted increased social symptoms of ASD (i.e., reduced
reciprocal social interaction) at 36 months in Sibs-ASD. The relationship between sensory
seeking and social impairment trended in the opposite direction in Sibs-TD, but did not reach
statistical significance (r = -.34, p = .15). There was no evidence of undue influence within or
across groups in these analyses. See Table A.4 for the results of regression analyses and
Figure A.5 for a depiction of this result.
Early sensory seeking additionally predicted future social symptomatology across groups
(p value for the effect of seeking on future social symptomatology, not controlling for other
factors = .008), but this effect significantly varied according to risk group (p value for the sensory
seeking x risk group product term in the moderation model = .008). Sensory seeking was
positively correlated with later social symptomatology in Sibs-ASD (r = .54, p = .014). Thus,
SENSORY SEEKING IN INFANT SIBLINGS 18
higher seeking at 18 months predicted increased social symptoms of ASD (i.e., reduced
reciprocal social interaction) at 36 months in Sibs-ASD. The relationship between sensory
seeking and social impairment trended in the opposite direction in Sibs-TD, but did not reach
statistical significance (r = -.34, p = .15). There was no evidence of undue influence within or
across groups in these analyses. See Table A.4 for the results of regression analyses and
Figure A.5 for a depiction of this result.
3.3. Exploratory Analyses
Based on prior work, we anticipated that early social orienting would also be predictive of
future social symptomatology, at least in high risk infants (e.g., Baranek, 1999; Dawson et al.,
2004; Zwaigenbaum et al., 2005). Social orienting at 18 months did predict future social
symptomatology across risk groups (zero-order correlation for the effect of orienting on future
social symptomatology, not controlling for other factors = .38, p value = .017), but this effect
significantly varied according to risk group (p value for the social orienting x risk group product
term in the moderation model predicting future social symptomatology = .015). Social orienting
was positively correlated with later social symptomatology in Sibs-ASD (r = .68, p = .001), but
not in Sibs-TD (r = -.05, p = .84).
We subsequently examined whether the relation between early sensory seeking and
later social symptomatology could be explained, at least in part, by social orienting (i.e., whether
early sensory seeking indirectly impacted later reciprocal social interaction by reducing social
orienting in infancy). This possibility can be statistically tested using modern mediation analyses
that test the indirect effect of early sensory seeking on future social symptomatology through
social orienting (Hayes, 2009; See Figure A.6A). Two pathways comprise this indirect effect.
The first pathway, referred to as the “a path,” represents the relation between early sensory
seeking and social orienting. The second pathway, referred to as the “b path,” represents the
relation between social orienting and future social symptomatology, controlling for early sensory
seeking. An indirect effect is statistically significant when the confidence interval for the product
SENSORY SEEKING IN INFANT SIBLINGS 19
of the unstandardized coefficients for these two paths does not include zero. Because the
relations for early sensory seeking with social orienting and future social symptomatology were
only significant for Sibs-ASD in the analyses reported above, we suspected that this indirect
effect would only apply to the infants at heightened risk for ASD. That is, we thought that this
indirect effect would be conditional on risk group status. We therefore further evaluated whether
risk group moderated the mediation relation of interest.
The moderated mediation analysis depicted in Figure A.6A was tested using the
PROCESS macro in SPSS (Hayes, 2013). Bias-corrected confidence intervals for effects of
interest were generated using 1000 bootstrap samples with the confidence level set at 95%.
Results indicated that this proposed mediation relation was moderated by risk group, 95% CI for
the conditional indirect effect [.0001, .9148]. The indirect effect (a x b) was significant for the
Sibs-ASD group, 95% CI [.05, .84], but was not significant for the Sibs-TD group, 95% CI [-.10,
.30]. The significant indirect effect within the Sibs-ASD group confirms that social orienting
mediates the relation between early sensory seeking and later social symptomatology for the
high-risk group. This mediation is considered complete because the direct effect of early
sensory seeking on future social symptomatology, called the “c’ path,” becomes non-significant
when controlling for social orienting in Sibs-ASD, 95% CI [-.38, .45]. The indirect effect for the
Sibs-ASD group is depicted in Figure A.6B.
As sensory seeking and social orienting were measured concurrently, it is logical that
one may question whether the observed mediation relation would hold if the present predictor
(i.e., sensory seeking) and mediator (i.e., social orienting) were interchanged in the model. The
indirect effect of social orienting on future social symptomatology through sensory seeking was
not statistically significant, however, for either Sibs-ASD, 95% CI [-.33, .38] or Sibs-TD, 95% CI
[-.23, .33]. Thus, although this alternative explanation was an intriguing possibility, sensory
seeking does not appear to mediate the relation between social orienting and future social
symptomatology in either group.
SENSORY SEEKING IN INFANT SIBLINGS 20
In post hoc analyses, we additionally examined whether sensory seeking varied not only
according to risk group, but also between the following outcome groups: (a) Sibs-TD, all of
whom had non-ASD outcomes (n = 20), (b) Sibs-ASD who did not receive a diagnosis (Sibs-
ASD-No ASD; n = 14), and (c) Sibs-ASD who did receive a diagnosis of ASD (Sibs-ASD-Dx
ASD; n = 6). To explore this possibility, we carried out a one-way ANOVA with Least Significant
Difference (LSD) comparisons. Results confirmed that outcome groups did differ in early
sensory seeking, F(2, 37) = 4.87, p = .013 (Figure A.7). Post hoc comparisons revealed that Sibs-
ASD-Dx ASD showed increased sensory seeking relative to both Sibs-ASD-No ASD (p = .048)
and Sibs-TD (p = .003). The between-group difference for Sibs-ASD-No ASD and Sibs-TD did
not reach statistical significance (p = .21).
4. Discussion
The present study examined the developmental sequelae and neurophysiological
substrates of an understudied pattern of atypical sensory responsiveness - sensory seeking - in
a group of infants who were at high risk for ASD based on their status as infant siblings of
children who are diagnosed with ASD relative to a control group of infants at relatively lower risk
for ASD. The overarching aim of this work was to investigate sensory seeking as a potential
early marker for ASD risk, or endophenotype, as well as the mechanisms by which sensory
seeking might impact later social development. Towards this aim, we examined how sensory
seeking relates to concurrent social orienting at 18 months, as well as social symptomatology at
36 months, in Sibs-ASD versus Sibs-TD. We also explored a potential neural signature for
sensory seeking – resting frontal asymmetry.
4.1. Sensory Seeking is Elevated and Related to Later Social Symptomatology in Sibs-
ASD
Past research has linked high levels of sensory seeking to social impairment in children
and adults who are diagnosed with ASD (Hilton et al., 2007; Liss et al., 2006; Watson et al.,
SENSORY SEEKING IN INFANT SIBLINGS 21
2011). We extend the aforementioned work to show that sensory seeking is elevated at 18
months and predictive of later social symptomatology in infants at high-risk for ASD, providing
further evidence that early differences in sensory function may produce cascading effects on
development across other domains, such as social skill (Cascio et al., 2016). Seeking appears
to be highest for those infant siblings who will go on to receive a diagnosis of ASD. These
findings suggest that sensory seeking behaviors at 18 months may serve as an endophenotype
of ASD or an early marker for social deficits in this high-risk population.
4.2. Social Orienting Mediates the Relation between Sensory Seeking and Social Deficits
Our findings indicate that high sensory seeking may impact social development via its
association with reduced social orienting. In our sample of Sibs-ASD, reduced social orienting
accounts for the significant association between sensory seeking and future social
symptomatology. This result suggests that infants at risk for ASD who engage in sensory
seeking behaviors may be too distracted or preoccupied with enhancing sensory experiences to
attend to social cues in their environment. By failing to orient to these social cues, these “high
seekers” are likely missing out on essential social learning opportunities, which may translate to
social deficits at 36 months. This finding has implications for clinical practice, as it suggests that
sensory seeking may be an important target of early intervention. Although, to our knowledge,
no treatment studies to date have attempted to target sensory seeking in infants at risk for ASD,
the current results suggest that social development might be facilitated by interventions that aim
to reduce the frequency of sensory seeking behaviors and/or to increase social orienting in
Sibs-ASD who are seeking out enhanced or prolonged non-social sensory experiences.
4.3. Atypical Resting Frontal Asymmetry May Underlie Sensory Seeking Behavior
As a potential neural marker for sensory seeking in this high-risk population, the present
study also examined whether frontal asymmetry, as indexed by the relative distribution of frontal
alpha oscillations, was (a) different in Sibs-ASD versus Sibs-TD and (b) associated with sensory
seeking. Alpha oscillations are believed to tap localized cortical inhibition from both cortical and
SENSORY SEEKING IN INFANT SIBLINGS 22
subcortical inputs, and this transient inhibition is believed to play a crucial role in the gating of
cortical processing (Jensen & Mazaheri, 2010). Although further research is warranted in order
to better understand the psychological constructs associated with frontal asymmetry, differences
in the relative balance of these inhibitory oscillations are believed to influence the degree to
which individual hemispheres contribute to top down regulatory functions critical for both ‘bottom
up’ processing of sensory inputs and regulation of complex behaviors such as attentional
orienting (e.g., Mazaheri, Nieuwenhuis, van Dijk, & Jensen, 2009).
Typically, infants gradually shift in the laterality of frontal asymmetry between 6 and 18
months of age, exhibiting relative left frontal asymmetry (i.e., relatively reduced alpha power in
the left versus right hemisphere) by 14 to 18 months of age (Fox et al., 1994; Fox et al., 2001;
Gabard-Durnam et al., 2015). Because alpha oscillations are inversely related to cortical
activation, this pattern can be interpreted as reflecting greater left hemisphere activation at rest
in typically developing infants by around 18 months. Recent research suggests that Sibs-ASD
show the opposite developmental trajectory, progressing from a frontal asymmetry pattern
suggestive of relative left hemisphere activation to relative right hemisphere activation over the
same 6 to 18 month window (Gabard-Durnam et al., 2015). This atypical pattern of frontal
asymmetry has additionally been documented, and linked with characteristics of ASD, in older
children who are diagnosed with autism (Burnette et al., 2011; Sutton et al., 2005), further
supporting the notion that a disruption in rhythmic neural processes is related to ASD
symptomatology.
As hypothesized, the Sibs-ASD group showed greater right frontal asymmetry when
compared to the Sibs-TD group at 18 months. This result is consistent with previous research
(Gabard-Durnam et al., 2015). In addition, within the Sibs-ASD group, increased sensory
seeking was associated with this atypical pattern of greater right frontal asymmetry (i.e.,
relatively reduced alpha power in the right versus left hemisphere) at 18 months of age. This
SENSORY SEEKING IN INFANT SIBLINGS 23
finding suggests that increased sensory seeking in Sibs-ASD may be associated with atypical
organization and maturation of oscillatory processes. It is also possible that greater right frontal
asymmetry may develop as a compensatory neural function due to reduced left cortical activity
in this population, as some previous research suggests that differences in the lateralization of
brain function may occur over development when one hemisphere compensates for reduced
functioning in the other hemisphere (Dehaene-Lambertz, Pena, Christophe, & Landrieu, 2004).
Further research is needed along these lines.
Interestingly, Sibs-TD demonstrated the opposite pattern, with relatively greater left
frontal asymmetry being associated with increased sensory seeking. This result is somewhat
difficult to interpret. We note, however, that there was a fairly limited range of sensory seeking
behavior observed across Sibs-TD. The moderated results that we obtained indicate that
increased seeking, to the extent that it was observed within the TD group, not only tended to co-
occur with a more left lateralized or “typical” resting brain state, but also did not predict future
social deficits. On the whole, these results may suggest that some degree of sensory seeking
behavior may be adaptive. Thus, there is a need for future research to determine at what point,
and in what populations, sensory seeking has implications for social development.
Past work linking frontal asymmetry to hyporesponsiveness in Sibs-ASD (Simon et al.,
under review) and to other symptoms of ASD within children who are diagnosed (Burnette et al.,
2011; Sutton et al., 2005), suggests that atypical frontal asymmetry is not specific to sensory
seeking, but is associated with sensory responsiveness and ASD symptomatology more
broadly. As such, further work is also warranted to elucidate how these early-emerging
oscillatory patterns contribute to atypical development in ASD.
4.4. Limitations and Future Directions
The results of the present study have important implications for understanding the
developmental course of social deficits associated with ASD and the broader autism phenotype,
SENSORY SEEKING IN INFANT SIBLINGS 24
but are limited. Findings are subject, of course, to the limitations of the longitudinal correlational
design. We cannot rule out alternative explanations for any of the associations we have
observed or conclude that any of the links that we have observed are causal in nature. Along
these lines, one possibility is that an unmeasured variable has contributed to one or more of the
relations of interest in this report. For example, it is possible that anxiety in the Sibs-ASD group
contributed to both reduced social orienting and increased sensory seeking during the sensory
assessment. Anxiety is of particular interest because it has previously been linked to ASD
symptomatology, including atypical responses to sensory stimuli (e.g., Mazurek et al., 2013). In
addition, anxiety has been associated with greater right frontal asymmetry (Davidson, Marshall,
Tomarken, & Henriques, 2000; Wiedemann et al., 1999). Future studies should examine the
potential role of anxiety in the relations among sensory seeking, social orienting, and frontal
asymmetry.
Additionally, measurement of sensory seeking and social orienting at a single time point
precludes us from establishing temporal precedence for sensory seeking. The same is true for
the concurrent measurement of frontal asymmetry and seeking behavior. Future studies, with
measurement at additional time points, planned a priori to establish the presence of atypical
frontal asymmetry prior to the emergence of sensory seeking, and to ascertain the presence of
sensory seeking prior to diminished social orienting, would increase our confidence in the
direction of effects suggested here. Further research is also needed to determine whether these
results generalize to other groups at risk for autism spectrum disorder (e.g., premature infants,
infants who are showing red flags but have no family history of ASD), or whether the present
pattern of results is specific to infants who are genetically predisposed to ASD. Finally,
subsequent work should seek to determine how we might best intervene upon atypical sensory
responsiveness in Sibs-ASD, and whether effects of treatment on sensory responses translate
to more optimal developmental outcomes in children who are diagnosed with, or at high risk for,
ASD. Large-scale studies that evaluate which of the variables of interest here (frontal alpha
SENSORY SEEKING IN INFANT SIBLINGS 25
asymmetry, sensory seeking, social orienting), in combination with other brain and behavioral
factors previously observed to covary with social symptoms, show incremental validity or have
“added-value” in predicting future social symptomatology in Sibs-ASD would be helpful for
focusing our efforts at early identification and intervention in infants at heightened risk for ASD.
5. Conclusions
The present study found that sensory seeking behaviors may serve as an early marker
for social deficits, or an endophenotype, in ASD. Infant siblings of children with ASD
demonstrate increased sensory seeking at 18 months, and sensory seeking is related to later
social symptomatology at 36 months. In addition, results provide insight into the mechanisms by
which sensory seeking might impact later social development by showing that the predictive
relationship between sensory seeking and social deficits at 36 months is mediated by social
orienting. Finally, findings suggest that resting frontal asymmetry is a potential neural marker of
atypical sensory seeking in this high-risk population. Further research is needed to increase our
confidence in the associations suggested here, to determine whether findings generalize to
other populations at high-risk for ASD, and to guide clinical practice with infants who present
with atypical patterns of sensory responsiveness.
Acknowledgments
The work described was supported by NIH U54 HD083211 (PI: Dykens), NICHD R01
HD057284 (PI: Stone), the Marino Autism Research Institute, the Wallace Foundation, the
Simons Foundation Autism Research Initiative, and by CTSA award No. KL2TR000446 from the
National Center for Advancing Translational Sciences. Its contents are solely the responsibility
of the authors and do not necessarily represent the official views of the National Center for
SENSORY SEEKING IN INFANT SIBLINGS 26
Advancing Translational Sciences, or the National Institutes of Health. The authors would like to
thank the laboratory of Dr. Grace Baranek for guidance in using the SPA and Warren Lambert
for his statistical support. The authors declare no conflicting interests.
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Figure A.1. Risk group differences in early sensory seeking. Sibs-ASD = Infant siblings of
children diagnosed with autism spectrum disorder. Sibs-TD = Infant siblings of typically
SENSORY SEEKING IN INFANT SIBLINGS 36
developing children. Sensory seeking aggregate = average of z-scores for seeking intensity
(sum of seeking ratings across eight novel toys) and seeking inventory (sum of discrete seeking
behaviors across 12 categories) component variables derived from the Sensory Processing
Assessment (Baranek, 1999). Error bars represent standard error of the mean. * p < .05.
Figure A.2. Risk group differences in resting frontal asymmetry. Sibs-ASD = Infant siblings of
children diagnosed with autism spectrum disorder. Sibs-TD = Infant siblings of typically
developing children. Frontal asymmetry = log right alpha power - log left alpha power (log R –
log L). Note that negative scores for frontal asymmetry reflect relatively greater right hemisphere
SENSORY SEEKING IN INFANT SIBLINGS 37
activation (i.e., a more atypical pattern at this chronological age), whereas positive scores reflect
relatively greater left hemisphere activation (i.e., a more typical pattern at this chronological
age). Error bars represent standard error of the mean. * p < .05.
Figure A.3. Relation between resting frontal asymmetry and early sensory seeking. Sibs-TD =
Infant siblings of typically developing children. Sibs-ASD = Infant siblings of children diagnosed
with autism spectrum disorder. Sibs-ASD-Dx ASD = Infant siblings of children diagnosed with
autism spectrum disorder who are diagnosed with autism spectrum disorder at 36 months.
Sensory seeking aggregate = average of z-scores for seeking intensity (sum of seeking ratings
across eight novel toys) and seeking inventory (sum of discrete seeking behaviors across 12
SENSORY SEEKING IN INFANT SIBLINGS 38
categories) component variables derived from the Sensory Processing Assessment (Baranek,
1999). Note that negative scores for frontal asymmetry reflect relatively greater right hemisphere
activation (i.e., a more atypical pattern at this chronological age), whereas positive scores reflect
relatively greater left hemisphere activation (i.e., a more typical pattern at this chronological
age).
SENSORY SEEKING IN INFANT SIBLINGS 39
Figure A.4. Relation between early sensory seeking and social orienting. Sibs-TD = Infant
siblings of typically developing children. Sibs-ASD = Infant siblings of children diagnosed with
autism spectrum disorder. Sibs-ASD-Dx ASD = Infant siblings of children diagnosed with autism
spectrum disorder who are diagnosed with autism spectrum disorder at 36 months. Sensory
seeking aggregate = average of z-scores for seeking intensity (sum of seeking ratings across
eight novel toys) and seeking inventory (sum of discrete seeking behaviors across 12
categories) component variables derived from the Sensory Processing Assessment (Baranek,
1999).
SENSORY SEEKING IN INFANT SIBLINGS 40
Figure A.5. Relation between early sensory seeking and future social symptomatology. Sibs-TD
= Infant siblings of typically developing children. Sibs-ASD = Infant siblings of children
diagnosed with autism spectrum disorder. Sibs-ASD-Dx ASD = Infant siblings of children
diagnosed with autism spectrum disorder who are diagnosed with autism spectrum disorder at
36 months. Sensory seeking aggregate = average of z-scores for seeking intensity (sum of
seeking ratings across eight novel toys) and seeking inventory (sum of discrete seeking
behaviors across 12 categories) component variables derived from the Sensory Processing
Assessment (Baranek, 1999).
SENSORY SEEKING IN INFANT SIBLINGS 41
Figure A.6. Conditional indirect effect between early sensory seeking and future social
symptomatology through social orienting, according to risk group. Figure A depicts the
conceptual model for the moderated mediation relation. Figure B represents the significant
SENSORY SEEKING IN INFANT SIBLINGS 42
mediation relation within the Sibs-ASD group, product of a * b paths reflecting the indirect effect
= .41; 95% CI [.05, .84]. Note that both the a path, representing the association between
sensory seeking and social orienting, and the b path, representing the association between
social orienting and future social symptomatology when controlling for sensory seeking, are
statistically significant. The c’ path, representing the association between sensory seeking and
future social symptomatology when controlling for social orienting, is non-significant. Thus,
reduced social orienting accounts for the observed association between sensory seeking and
future social symptomatology in Sibs-ASD. Sibs-ASD = Infant siblings of children diagnosed
with autism spectrum disorder. Sibs-TD = Infant siblings of typically developing children. Values
in Figure B are standardized coefficients. * p < .05. ** p < .001. ns = non-significant result.
SENSORY SEEKING IN INFANT SIBLINGS 43
Figure A.7. Outcome group differences in early sensory seeking. Sibs-TD = Infant siblings of
typically developing children. Sibs-ASD-No ASD = Infant siblings of children diagnosed with
autism spectrum disorder who do not receive a diagnosis of ASD. Sibs-ASD-Dx ASD = Infant
siblings of children diagnosed with autism spectrum disorder who do receive a diagnosis of ASD
at 36 months. Sensory seeking aggregate = average of z-scores for seeking intensity (sum of
seeking ratings across eight novel toys) and seeking inventory (sum of discrete seeking
behaviors across 12 categories) component variables derived from the Sensory Processing
Assessment (Baranek, 1999). * p < .05. ** p < .005. ns = non-significant result. Error bars
represent standard error of the mean.
-0.6
-0.4
-0.2
0.0
0.2
0.4
0.6
0.8
1.0
1.2
1.4
Sibs-TD Sibs-ASD-No ASD Sibs-ASD-Dx ASD
Sensory Seeking Aggregate Score at 18 mos
ns
*
**
SENSORY SEEKING IN INFANT SIBLINGS 44
6. Appendices
Table A.1
Sample Characteristics at Time 1
Characteristic
Sibs-ASD
Sibs-TD
Chronological Age In Months
18.24 (.42)
18.34 (.29)
Sex (Male : Female)
8 : 12
10 : 10
Mullen Early Learning
Composite †
103.05 (12.69)
110.42 (7.46)*
Mullen Receptive Language †
43.40 (6.76)
47.11 (4.76)
Mullen Expressive Language †
50.50 (8.69)
54.58 (7.62)
Note. * p < .05. Mullen = Mullen Scales of Early Learning (Mullen, 1995). Early Learning
Composite is a standard score. Receptive and Expressive language scores are T-scores. Sibs-
ASD = Infant siblings of children diagnosed with autism spectrum disorder. Sibs-TD = Infant
siblings of children with typical developmental histories.
†Mullen Scales of Early Learning were collected when infants were 12 months old as part of the
larger study of social-emotional development.
SENSORY SEEKING IN INFANT SIBLINGS 45
Table A.2
Results of Regression Analyses for Effect of Frontal Asymmetry on Sensory Seeking by Risk
Group
Unstandardized
Coefficients
Standardized
Model
B
SE
Beta
t
Significance
1
Constant
-.231
.147
-1.563
.126
Seeking
-.811
.414
-.307
-1.959
.058
2
Constant
-.610
.170
-3.585
.001
Seeking
.610
.482
.230
1.266
.214
Risk Group
.490
.259
.267
1.891
.067
Seeking x
Risk Group
-2.458
.727
-.636
-3.380
.002*
Note.* p value for effect of interest < .05. Models exclude Sib-TD infant who unduly influenced
analyses.
SENSORY SEEKING IN INFANT SIBLINGS 46
Table A.3
Results of Regression Analyses for the Effect of Sensory Seeking on Social Orienting by Risk
Group
Unstandardized
Coefficients
Standardized
Model
B
SE
Beta
t
Significance
1
Constant
2.279
.119
19.089
.000
Seeking
.570
.128
.590
4.448
.000*
2
Constant
2.219
.265
8.366
.000
Seeking
.136
.361
.140
.376
.709
Risk Group
-.175
.309
-.099
-.566
.575
Seeking x
Risk Group
.642
.389
.557
1.649
.108
Note.* p value for effect of interest < .05. Models exclude Sib-TD infant who unduly influenced
analyses.
SENSORY SEEKING IN INFANT SIBLINGS 47
Table A.4
Results of Regression Analyses for the Effect of Sensory Seeking on Social Symptomatology by
Risk Group
Unstandardized
Coefficients
Standardized
Model
B
SE
Beta
t
Significance
1
Constant
2.020
.134
15.032
.000
Seeking
.376
.136
.411
2.777
.008*
2
Constant
1.337
.171
7.824
.000
Seeking
-.229
.193
-.249
-1.186
.243
Risk Group
1.083
.229
.599
4.734
.000
Seeking x
Risk Group
.672
.238
.564
2.822
.008*
Note.* p value for effect of interest < .05. There was no evidence of undue influence on
analyses.
