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Cognitive and Biological Pathways to Anxiety in Children and Adolescents with Autism Spectrum Disorders
Children and adolescents with autism spectrum disorder (ASD) have a high prevalence of co-occurring anxiety disorders compared to their non-ASD peers (~40%). Anxiety in young people without ASD has previously been associated with changes in cognitive processing and physiological reactivity. However, there has been little research investigating different cognitive and biological pathways that may be associated with anxiety in ASD and how these pathways may relate to each other.
Objectives:
The objectives of this study were as follows; 1) to investigate whether differences in cognitive processing biases and/or differences in physiological responsiveness to psychosocial stress, measured via heart rate and salivary cortisol, are significantly related to anxiety symptoms and diagnoses, 2) to use structural equation modelling to examine the associations between cognitive and physiological processes in relation to heightened anxiety in ASD, and 3) to use receiver operating characteristic (ROC) analysis to examine how well changes in cognitive and physiological parameters predicated anxiety diagnoses.
Methods:
This study included 55 boys with ASD (two groups: 34 with a co-occurring anxiety disorder, 21 without) and 28 male controls, aged 10 – 16 years and with a full-scale IQ ≥70. Anxiety diagnoses were assessed prospectively using the Child & Adolescent Psychiatric Assessment. Participants completed a series of clinical, cognitive (attention bias/interpretation bias) and biological measures (salivary cortisol/heart rate (HR) response to social stress). After comparing the three groups on task performance structural equation modelling was used, within the ASD groups, to investigate the relationships between the cognitive and biological variables and anxiety.
Results:
Results indicated that children with ASD and co-occurring anxiety disorders display more attentional and interpretational biases and a reduced heart rate and cortisol response to social stress compared to those with ASD only and healthy controls. Our SEM model revealed that both attentional biases and physiological responsiveness are significant, but unrelated, predictors of anxiety symptoms in ASD. Finally, ROC analysis revealed that while both HR (AUC = 0.94) and cortisol (AUC = 0.89) were strong predictors of anxiety diagnosis, attentional bias was not (AUC = 0.56).
Conclusions:
Anxiety in children with ASD appears to be related to both cognitive and physiological factors via two independent pathways and may partially explain the high prevalence of anxiety. This has implications for both our understanding of the aetiology of anxiety in ASD and may also inform the development of novel treatment strategies.