Project Description
To address the prevalence of multiple cognitive atypicalities in children with autism, their unaffected co-twins and a control group
To investigate the predictions of the ‘fractionated triad’ theory
- if cognitive atypicalities are relatively independent from one another
- if different cognitive atypicalities underlie the distinct symptom domains of autism
To examine the heritability of cognitive atypicalities and the genetic and environmental overlap between cognitive atypicalities and autism using genetic model-fitting analyses
To examine if there are different subgroups of autism based on behavioural symptoms, and whether these subgroups differ in terms of age, gender, IQ, diagnosis, cognitive profiles, and comorbid symptoms.
Thesis Abstract
The behavioural symptoms of autism spectrum disorder (ASD) are thought to reflect underlying cognitive deficits/differences. Single cognitive deficit models of ASD have attempted to reduce the varied behavioural symptoms of the disorder to a single underlying cognitive deficit. However, there is a need to move on from these single cognitive deficit accounts of ASD. Therefore, the main focus of the thesis is to explore the potential for a multiple cognitive model of ASD using the predictions of the fractionated triad account.
The data that is examined in the thesis originated from the Twins Early Development Study (TEDS) where one or both children met diagnostic criteria for ASD. A subsample of adolescents took part in the Social Relationship (SR) study. Overall, 181 adolescents with a diagnosis of ASD and 73 unaffected co-twins were included in the SR sample, plus an additional 160 comparison control participants.
The findings in this thesis do not support a strong version of the fractionated account of ASD, in which distinct causes at the genetic and neural levels relate to distinct deficits at the cognitive level, and are associated with distinct symptoms of ASD at the behavioural level. There were some selective relationships between cognitive atypicalities and the behavioural symptoms of ASD, but these differed depending on the diagnostic symptom measure used. A weaker version of the fractionated theory is supported in which multiple cognitive deficits characterise ASD, and these cognitive deficits relate to distinct symptoms, as in the strong version, but a single cognitive deficit can explain more than one symptom domain, and more than one cognitive deficit can explain a single symptom domain. General interpretations are discussed using the framework of the fractionated triad theory of ASD. The limitations of the current thesis and potential future research are also considered.
Project Publications
Brunsdon, V. E. A., Colvert, E., Ames, C., Garnett, T., Gillan, N., Hallett, V., Lietz, S., Woodhouse, E., Bolton, P., & Happé, F. (2015). Exploring the cognitive features in children with autism spectrum disorders, their co-twins, and typically-developing children within a population-based sample. Journal of Child Psychology and Psychiatry, 56, 893-902. doi: 10.1111/jcpp.12362
Brunsdon, V. E. A., & Happé, F. (2014). Exploring the ‘fractionation’ of autism at the cognitive level. Autism, 18, 17 - 30. doi: 10.1177/1362361313499456
