Abstract
SummaryBackgroundRisk markers for later autism identified in the first year of life present plausible intervention targets during early development. We aimed to assess the effect of a parent-mediated intervention for infants at high risk of autism on these markers.MethodsWe did a two-site, two-arm assessor-blinded randomised controlled trial of families with an infant at familial high risk of autism aged 7–10 months, testing the adapted Video Interaction to Promote Positive Parenting (iBASIS-VIPP) versus no intervention. Families were randomly assigned to intervention or no intervention groups using a permuted block approach stratified by centre. Assessors, but not families or therapists, were masked to group assignment. The primary outcome was infant attentiveness to parent. Regression analysis was done on an intention-to-treat basis. This trial is registered with ISCRTN Registry, number ISRCTN87373263.FindingsWe randomly assigned 54 families between April 11, 2011, and Dec 4, 2012 (28 to intervention, 26 to no intervention). Although CIs sometimes include the null, point estimates suggest that the intervention increased the primary outcome of infant attentiveness to parent (effect size 0·29, 95% CI −0·26 to 0·86, thus including possibilities ranging from a small negative treatment effect to a strongly positive treatment effect). For secondary outcomes, the intervention reduced autism-risk behaviours (0·50, CI −0·15 to 1·08), increased parental non-directiveness (0·81, 0·28 to 1·52), improved attention disengagement (0·48, −0·01 to 1·02), and improved parent-rated infant adaptive function (χ2[2] 15·39, p=0·0005). There was a possibility of nil or negative effect in language and responsivity to vowel change (P1: ES–0·62, CI −2·42 to 0·31; P2: −0·29, −1·55 to 0·71).InterpretationWith the exception of the response to vowel change, our study showed positive estimates across a wide range of behavioural and brain function risk-markers and developmental outcomes that are consistent with a moderate intervention effect to reduce the risk for later autism. However, the estimates have wide CIs that include possible nil or small negative effects. The results are encouraging for development and prevention science, but need larger-scale replication to improve precision.FundingAutistica, Waterloo Foundation, Autism Speaks, and the UK Medical Research Council.
Highlights
Interpretation With the exception of the response to vowel change, our study showed positive estimates across a wide range of behavioural and brain function risk-markers and developmental outcomes that are consistent with a moderate intervention effect to reduce the risk for later autism
Evidence from prospective studies suggests that about 20% of infants who have an older sibling with autism spectrum disorder (ASD) develop ASD themselves,[1] and a further 20–30% develop broader social and communication-development disorders.[2]
These early developmental markers of later ASD are paralleled by reported perturbations in parent–infant interactions from at least 8 months of age in high-risk compared with low-risk parent–infant dyads.[8]
Summary
Evidence from prospective studies suggests that about 20% of infants who have an older sibling with autism spectrum disorder (ASD) develop ASD themselves,[1] and a further 20–30% develop broader social and communication-development disorders.[2] Several specific infant behavioural and neural atypicalities have been identified during the first year of life associated with this later diagnosis of ASD; these include reduced behavioural attention to social scenes,[3] declining attention to eyes,[4] and attenuated neural response to eye gaze,[5] and from 14 months altered attention disengagement[6] and atypical infant temperament.[7] These early developmental markers of later ASD are paralleled by reported perturbations in parent–infant interactions from at least 8 months of age in high-risk compared with low-risk parent–infant dyads.[8] These perturbations are associated with infant atypicalities in infant gaze processing,[9] and by age 14 months are themselves predictive of ASD diagnosis at 3 years.[10] Taken together, these findings suggest that initial neurodevelopmental atypicalities in ASD, associated with changes to dyadic interaction with caregivers might represent increasingly atypical trajectories on the path to later ASD diagnosis Such a model does not imply that interaction cycles are a cause of ASD, but that altered social interactions might maintain or perhaps amplify pre-existing vulnerability. In the context of atypical neurodevelopment, Down’s syndrome, cerebral palsy, and learning disabilities can all be associated with altered parental responding and raised directiveness towards the Lancet Psychiatry 2015; 2: 133–40
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