11 research outputs found
Behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of autism spectrum disorder and/or attention deficit hyperactivity disorder.
BACKGROUNDS: Atypicalities in tactile processing are reported in autism spectrum disorder (ASD) and attention deficit hyperactivity disorder (ADHD) but it remains unknown if they precede and associate with the traits of these disorders emerging in childhood. We investigated behavioural and neural markers of tactile sensory processing in infants at elevated likelihood of ASD and/or ADHD compared to infants at typical likelihood of the disorders. Further, we assessed the specificity of associations between infant markers and later ASD or ADHD traits. METHODS: Ninety-one 10-month-old infants participated in the study (n = 44 infants at elevated likelihood of ASD; n = 20 infants at elevated likelihood of ADHD; n = 9 infants at elevated likelihood of ASD and ADHD; n = 18 infants at typical likelihood of the disorders). Behavioural and EEG responses to pairs of tactile stimuli were experimentally recorded and concurrent parental reports of tactile responsiveness were collected. ASD and ADHD traits were measured at 24âmonths through standardized assessment (ADOS-2) and parental report (ECBQ), respectively. RESULTS: There was no effect of infants' likelihood status on behavioural markers of tactile sensory processing. Conversely, increased ASD likelihood associated with reduced neural repetition suppression to tactile input. Reduced neural repetition suppression at 10âmonths significantly predicted ASD (but not ADHD) traits at 24âmonths across the entire sample. Elevated tactile sensory seeking at 10âmonths moderated the relationship between early reduced neural repetition suppression and later ASD traits. CONCLUSIONS: Reduced tactile neural repetition suppression is an early marker of later ASD traits in infants at elevated likelihood of ASD or ADHD, suggesting that a common pathway to later ASD traits exists despite different familial backgrounds. Elevated tactile sensory seeking may act as a protective factor, mitigating the relationship between early tactile neural repetition suppression and later ASD traits
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Early Motor Differences in Infants at Elevated Likelihood of Autism Spectrum Disorder and/or Attention Deficit Hyperactivity Disorder.
We investigated infant's manual motor behaviour; specifically behaviours crossing the body midline. Infants at elevated likelihood of Autism Spectrum Disorder (ASD) and/or Attention Deficit Hyperactivity Disorder (ADHD) produced fewer manual behaviours that cross the midline compared to infants with a typical likelihood of developing these disorders; however this effect was limited to 10-month-olds and not apparent at age 5 and 14Â months. Although, midline crossing did not predict ASD traits, it was related to ADHD traits at 2Â years of age. We rule out motor ability and hand dominance as possible explanations for this pattern of behaviour, positing that these results may be a consequence of multisensory integration abilities, and the neurobehavioural shift period, in the first year of life
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Behavioural Measures of Infant Activity but Not Attention Associate with Later Preschool ADHD Traits.
Behavioural Measures of Infant Activity but Not Attention Associate with Later Preschool ADHD Traits.
Mapping infant neurocognitive differences that precede later ADHD-related behaviours is critical for designing early interventions. In this study, we investigated (1) group differences in a battery of measures assessing aspects of attention and activity level in infants with and without a family history of ADHD or related conditions (ASD), and (2) longitudinal associations between the infant measures and preschool ADHD traits at 3 years. Participants (N = 151) were infants with or without an elevated likelihood for ADHD (due to a family history of ADHD and/or ASD). A multi-method assessment protocol was used to assess infant attention and activity level at 10 months of age that included behavioural, cognitive, physiological and neural measures. Preschool ADHD traits were measured at 3 years of age using the Child Behaviour Checklist (CBCL) and the Child Behaviour Questionnaire (CBQ). Across a broad range of measures, we found no significant group differences in attention or activity level at 10 months between infants with and without a family history of ADHD or ASD. However, parent and observer ratings of infant activity level at 10 months were positively associated with later preschool ADHD traits at 3 years. Observable behavioural differences in activity level (but not attention) may be apparent from infancy in children who later develop elevated preschool ADHD traits
Look duration at the face as a developmental endophenotype: elucidating pathways to autism and ADHD.
Identifying developmental endophenotypes on the pathway between genetics and behavior is critical to uncovering the mechanisms underlying neurodevelopmental conditions. In this proof-of-principle study, we explored whether early disruptions in visual attention are a unique or shared candidate endophenotype of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). We calculated the duration of the longest look (i.e., peak look) to faces in an array-based eye-tracking task for 335 14-month-old infants with and without first-degree relatives with ASD and/or ADHD. We leveraged parent-report and genotype data available for a proportion of these infants to evaluate the relation of looking behavior to familial (n = 285) and genetic liability (using polygenic scores, n = 185) as well as ASD and ADHD-relevant temperament traits at 2 years of age (shyness and inhibitory control, respectively, n = 272) and ASD and ADHD clinical traits at 6 years of age (n = 94).Results showed that longer peak looks at the face were associated with elevated polygenic scores for ADHD (β = 0.078, p = .023), but not ASD (β = 0.002, p = .944), and with elevated ADHD traits in mid-childhood (F(1,88) = 6.401, p = .013, =0.068; ASD: F (1,88) = 3.218, p = .076), but not in toddlerhood (ps > 0.2). This pattern of results did not emerge when considering mean peak look duration across face and nonface stimuli. Thus, alterations in attention to faces during spontaneous visual exploration may be more consistent with a developmental endophenotype of ADHD than ASD. Our work shows that dissecting paths to neurodevelopmental conditions requires longitudinal data incorporating polygenic contribution, early neurocognitive function, and clinical phenotypic variation
Look duration at the face as a developmental endophenotype: elucidating pathways to autism and ADHD.
Identifying developmental endophenotypes on the pathway between genetics and behavior is critical to uncovering the mechanisms underlying neurodevelopmental conditions. In this proof-of-principle study, we explored whether early disruptions in visual attention are a unique or shared candidate endophenotype of autism spectrum disorder (ASD) and attention-deficit/hyperactivity disorder (ADHD). We calculated the duration of the longest look (i.e., peak look) to faces in an array-based eye-tracking task for 335 14-month-old infants with and without first-degree relatives with ASD and/or ADHD. We leveraged parent-report and genotype data available for a proportion of these infants to evaluate the relation of looking behavior to familial (n = 285) and genetic liability (using polygenic scores, n = 185) as well as ASD and ADHD-relevant temperament traits at 2 years of age (shyness and inhibitory control, respectively, n = 272) and ASD and ADHD clinical traits at 6 years of age (n = 94).Results showed that longer peak looks at the face were associated with elevated polygenic scores for ADHD (β = 0.078, p = .023), but not ASD (β = 0.002, p = .944), and with elevated ADHD traits in mid-childhood (F(1,88) = 6.401, p = .013, =0.068; ASD: F (1,88) = 3.218, p = .076), but not in toddlerhood (ps > 0.2). This pattern of results did not emerge when considering mean peak look duration across face and nonface stimuli. Thus, alterations in attention to faces during spontaneous visual exploration may be more consistent with a developmental endophenotype of ADHD than ASD. Our work shows that dissecting paths to neurodevelopmental conditions requires longitudinal data incorporating polygenic contribution, early neurocognitive function, and clinical phenotypic variation
Development of the pupillary light reflex from 9 to 24 months: association with common ASD genetic liability and 3-year ASD diagnosis
Background: Although autism spectrum disorder (ASD) is heritable, the mechanisms through which genes contribute to symptom emergence remain unclear. Investigating candidate intermediate phenotypes such as the pupillary light reflex (PLR) prospectively from early in development could bridge genotype and behavioural phenotype.
Methods: Using eye tracking, we longitudinally measured the PLR at 9, 14 and 24 months in a sample of infants (N = 264) enriched for a family history of ASD; 27 infants received an ASD diagnosis at 3 years. We examined the 9- to 24-month developmental trajectories of PLR constriction latency (onset; ms) and amplitude (%) and explored their relation to categorical 3-year ASD outcome, polygenic liability for ASD and dimensional 3-year social affect (SA) and repetitive/restrictive behaviour (RRB) traits. Polygenic scores for ASD (PGSASD) were calculated for 190 infants.
Results: While infants showed a decrease in latency between 9 and 14 months, higher PGSASD was associated with a smaller decrease in latency in the first year (β = â.16, 95% CI = â0.31, â0.002); infants with later ASD showed a significantly steeper decrease in latency (a putative âcatch-upâ) between 14 and 24 months relative to those with other outcomes (typical: β = .54, 95% CI = 0.08, 0.99; other: β = .53, 95% CI = 0.02, 1.04). Latency development did not associate with later dimensional variation in ASD-related traits. In contrast, change in amplitude was not related to categorical ASD or genetics, but decreasing 9- to 14-month amplitude was associated with higher SA (β = .08, 95% CI = 0.01, 0.14) and RRB (β = .05, 95% CI = 0.004, 0.11) traits.
Conclusions: These findings corroborate PLR development as possible intermediate phenotypes being linked to both genetic liability and phenotypic outcomes. Future work should incorporate alternative measures (e.g. functionally informed structural and genetic measures) to test whether distinct neural mechanisms underpin PLR alteration
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Parent-infant interaction trajectories in infants with an elevated likelihood for autism in relation to 3-year clinical outcome.
Publication status: PublishedFunder: European Autism Interventions (EUâAIMS): A Multicentre Study for Developing New Medications; Grant(s): 115300Funder: European Federation of Pharmaceutical Industries and Associations companiesFunder: European Union's Horizon 2020 research and innovation programmeFunder: European Federation of Pharmaceutical Industries and Associations; doi: http://dx.doi.org/10.13039/100013322Funder: Autism Speaks; doi: http://dx.doi.org/10.13039/100000073Funder: Autistica; doi: http://dx.doi.org/10.13039/100011706Funder: SFARI; doi: http://dx.doi.org/10.13039/100014370Developmental antecedents of autism may affect parent-infant interactions (PII), altering the context in which core social skills develop. While studies have identified differences in PII between infants with and without elevated likelihood (EL) for autism, samples have been small. Here, we examined whether previously reported differences are replicable. From a longitudinal study of 113 EL and 27 typical likelihood infants (TL), 6-min videotaped unstructured PII was blind rated at 8 and 14âmonths on eight interactional qualities. Autism outcome was assessed at 36âmonths. Linear mixed-effects models found higher parent sensitive responsiveness, nondirectiveness, and mutuality ratings in TL than EL infants with and without later autism. PII qualities at 8 (infant positive affect, parent directiveness) and 14âmonths (infant attentiveness to parent, mutuality) predicted 3-year autism. Attentiveness to parent decreased between 8 and 14âmonths in EL infants with later autism. This larger study supports previous findings of emerging alterations in PII in this group and extends on this by detecting earlier (8-month) predictive effects of PII for autism outcome and a more marked trajectory of decreased social attentiveness. The findings strengthen the evidence base to support the implementation of early preemptive interventions to support PII in infants with early autism signs
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Mid-childhood autism sibling recurrence in infants with a family history of autism.
Publication status: PublishedAutism sibling recurrence in prospective infant family history studies is ~20% at 3âyears but systematic follow-up to mid-childhood is rare. In population and clinical cohorts autism is not recognized in some children until school-age or later. One hundred and fifty-nine infants with an older sibling with autism underwent research diagnostic assessments at 3âyears and mid-childhood (6 to 12âyears (mean 9)). We report the autism sibling recurrence rate in mid-childhood and compare developmental and behavioral profiles at mid-childhood and 3âyears in those with earlier versus later recognized autism, and those who had, or had not, received a community autism diagnosis. The autism recurrence rate in this sample in mid-childhood was 37.1%, 95% CI [29.9%, 44.9%] and higher in boys than girls. Around half of those diagnosed with autism in mid-childhood had not received a diagnosis at 3âyears. Later, diagnosis was more common in girls than boys. While some had sub-threshold symptoms at 3, in others late diagnosis followed a largely typical early presentation. Sibling recurrence based on community clinical diagnosis was 24.5%, 95% CI [18.4%, 31.9%]. Those who also had a community diagnosis tended to be older, have lower adaptive function and higher autism and inattention symptoms. Notwithstanding limitations of a single site study, modest sample size and limits to generalisability, autism sibling recurrence in family history infants may be higher in mid-childhood than in studies reporting diagnostic outcome at 3âyears. Findings have implications for families and clinical services, and for prospective family history studies