Exploring the ‘fractionation’ of autism at the cognitive level

Abstract

Autism spectrum disorders are defined by difficulties across a range of areas: social and communication difficulties and restricted and repetitive behaviours and interests. It has been suggested that this triad of symptoms cannot be explained by a single cause at the genetic, neural or cognitive level. This article reviews the evidence for a 'fractionable' autism triad at the cognitive level, highlighting questions for future research.

Exploring ‘The autisms’ at a cognitive level

“…Our ToM results at a group level are consistent with other studies of autism (Abell, Happe, & Frith, 2000;Castelli et al, 2002;Salter et al, 2008;White et al, 2009), including all those assessing performance across multiple cognitive domains (Brunsdon et al, 2014;Lai et al, 2012;Lam, 2013;Pellicano et al, 2006). Despite great diversity in the tasks and methods used, ToM is consistently found to be impaired.…”

“…Interindividual heterogeneity addresses a subtly different issue: whether there is any causal mechanism common to all individuals, a notion that is also widely presumed to be true but which has received much less empirical attention (Brunsdon & Happe, 2014). In fact, interindividual heterogeneity has even been suggested to be a more distinct marker for autism than any one neuropathology (Towgood, Meuwese, Gilbert, Turner, & Burgess, 2009), attempting to explain why one study may find support for and the next find no evidence in favour of a particular underlying deficit.…”

“…There is convergence from genetics to neurobiology, with evidence focussing around synaptic function (Zoghbi, 2003) and neural connectivity (Geschwind & Levitt, 2007); further convergence from cellular to systems neuroscience is apparent, with most emphasis placed on the frontal lobes, amygdala and cerebellum (Amaral, Schumann, & Nordahl, 2008). Whilst theories abound at the cognitive level, Theory of Mind (ToM), executive function (EF) and a local processing bias (LB) remain the most prominent (Brunsdon & Happe, 2014;Frith, 2012;Rajendran & Mitchell, 2007) drawing together diverse biological and behavioural findings.…”

“…While such fractionation is evident at the behavioural level, it is still unclear whether the different proposed cognitive impairments in autism are similarly separable (Brunsdon & Happe, 2014); very few studies have examined ToM, EF and LB simultaneously in ASD and these findings have been contradictory (Brunsdon et al, 2014;Lai et al, 2012;Lam, 2013;Pellicano, Maybery, Durkin, & Maley, 2006). Furthermore, only one of these studies (Pellicano et al, 2006) has examined the relationship between cognition and symptomatology, finding no associations, and hence it is unknown whether these cognitive impairments really can explain independent aspects of autistic behaviour.…”

Sensitivity to the prototype in children with high-functioning autism spectrum disorder: An example of Bayesian cognitive psychometrics

“…It has been argued that social and non-social symptoms that are generally associated with ASD are not necessarily inherently linked and may have very different causes at the genetic, neural, and cognitive level (the fractionable autism triad hypothesis, see, e.g., Brunsdon & Happé 2014;Happé & Ronald 2008). Even within the cognitive domain, symptoms related to executive functioning on the one hand and focus on detail and the difficulty to integrate information on the other may not be caused by the same underlying principles (see e.g., Best et al 2008;Happé & Booth 2008;Lawson et al 2004).…”