The executive function deficit, on the other hand, describes a set of related, high-level cognitive skills (Volkmar, Lord, Bailey, Schutz & Klin, 2004) that allows individuals to plan, initiate and perform goal directed behaviour (Oates & Grayson, 2004). These executive functions consist of the ability to inhibit or delay inappropriate prepotent stimuli and have sufficient functioning in planning, working memory and shifting attention flexibly in order to achieve strategic goal-directed behaviour (Baddeley, 1991; Goldman-Rakic, 1987; Pennington, 1994; Shallice, 1988). Impairments on executive function tasks have been consistently found across many studies amongst autistic individuals of differing ages and functioning levels, using a diverse range of measures (Pennington & Ozonoff, 1996). The early 1990s saw the development of the “Executive dysfunction” hypothesis (ED) which has since been theoretically linked to the presence of repetitive or perseverative behaviours often found in autistic people (Baron-Cohen & Swettenham, 1997). However, it appears this hypothesis not only explains their cognitive inflexibility but also provides invaluable insight into Wing’s (1988) triad of handicaps in social relations, communication and imagination.
It is widely recognised that autistic children demonstrate a striking poverty in imaginative pretend play (Sigman & Ungerer, 1981; Ungerer & Sigman, 1981; Wing, Gould, Yeates, & Brierley, 1977; Wing & Gould, 1979) and the “mentalising” deficit is extraordinarily specific in predicting these difficulties in pretend play. They present a particular pattern of difficulty in that they are, when prompted, able to participate in object substitution and can treat an object as if it were a person who talks, acts, and even sees. On the other hand, they have difficulty attributing psychological states, particularly those they do not share, to other people or objects. Since pretend play often calls for the attribution of beliefs to dolls, autistic children are generally found to be impeded in this area (Harris, 1995). According to this hypothesis, an inability to infer certain mental states will have negative effects not only on imaginative but also social and communicative abilities (Harris, 1995).
Yet, autistic children’s imaginative poverty is not only expressed in their lack of pretend play, but also in their limited repertoire of interests and repetitive or stereotype activities. Although not a core deficit, one of the standard symptoms of autism is an incessant need for the upholding of routine. This “obsessive desire for the preservation of sameness” (Kanner, 1943, p. 9) and seeming cognitive inflexibility may underpin one of the primary deficits in imagination. Indeed, it is at this point that the “mentalising” deficit falls down in its attempts to explain this “insistence on sameness.” It is not clear how the apparent inability to understand psychological experience can explain the inflexibility displayed by autistic children not only in play, but also in everyday life (Harris, 1995). Although this theory has speculated that the strong need for routine and orderliness is triggered by socially-induced anxiety in a world of unpredictable actions (Baron-Cohen, 1989), there is no evidence to suggest this is the case.
It is at this point that the mentalising deficit hypothesis and the executive dysfunction hypothesis diverge in their interpretations of the imaginative poverty in autism. Cognitive inflexibility has been conceptualised as a central cognitive characteristic, in contrast to the mentalising deficit which has postulated it merely as a symptom of social anxiety. On the basis of a relatively large body of research Hughes (2001) and Harris (1993) have both indicted that this impediment in cognitive flexibility may be the result of an underlying executive dysfunction deficit; a deficit in disengaging from the external context.
Pretend play involves a level of executive control that is guided, not by the current external context but rather, by an internally-formulated plan. This necessary shift in the locus of control may be impeded or delayed in autistic children adversely affecting imagination and pretend play. It helps explain why they will not spontaneously engage in pretending but when provided with a physical or verbal cue, the control is partly shifted back to the external contextual frame and they are thus, sufficiently able to generate pretence (Harris, 1995). In a similar way, this deficit in disengaging from the external context can help explain autistic individuals’ insistence on sameness and limited range of interests and activities. Their actions remain repetitive and rigid as a result of their inability to disengage from the external situation.
An impediment in disengaging from the external context and such cognitive inflexibility will not only adversely affect imagination but will also have detrimental effects on social and communicative abilities. An inability to shift attention set flexibly may restrict the flow and richness of conversations. Indeed, autistic individuals are known for their largely one-sided conversations, exemplified by their long monologues. This may ultimately hinder their social interactions. An example of an impeded interaction between parent and child is that of “joint attention;” an activity known to be deficient in many autistic individuals. This involves the child directing the parent’s attention to a certain object. Among other things, it is essential for the child to disengage from the object and switch attention flexibly between the parent and the object. However, an autistic person may present significant problems in doing so, ultimately affecting the quality of the interaction (Hughes, 2001). It seems both theory of mind and executive dysfunction hypotheses hold similar explanatory power in explaining the triad of impairments diagnostically characterised in autism and yet “insistence on sameness;” a non-social deficit is not so easily explained by the mentalising deficit. Indeed, at this stage, the evidence appears to point towards these two models representing separate modular cognitive impairments.
Yet, it has been hypothesised that theory of mind impairments may share similar underpinnings with executive function deficits. Russel, Mauthner, Sharpe and Tidswell (1991) illustrated how an inability to engage in deception, commonly thought to be a theory of mind impairment might be recast as an executive function deficit, representing an inability to disengage from the external context and orient behaviours instead by internal rules. It is possible that autistic children’s mentalising abilities are, in fact, intact but they unable to use these capabilities due to their problems with inhibiting a prepotent stimulus. However, this “lack of inhibition” interpretation of theory of mind tasks has been found not to be a viable explanation in certain experiments measuring “mentalising” abilities where autistic children still display problems (Leslie & Frith, 1988; Baron-Cohen, 1989).
Frye and colleagues (in press) and Ozonoff (in press) have arrived at similar conclusions concerning the relationship between executive function and theory of mind measures. They have suggested that these independent tasks, although decidedly dissimilar at the content level, are unexpectedly similar at a process level of analysis (Ozonoff, 1997). The smarties task, a standard false-belief measure (Perner et al., 1989) and the Tower of Hanoi task, an executive function measure both involve sequential analysis of information and the embedded use of “if-then” rules” (Frye Zelazo, & Palfai, in press; Hughes & Russel, 1993). Thus, impairment in executive function and the capacity to employ “if-then” strategic rules may result in failure on both theory of mind and executive function measures (Frye et al., in press; Ozonoff, in press), regardless of functional abilities in mentalising.
Although some of these findings point towards the theory of mind deficit being reducible to the executive dysfunction model of autism, there is evidence somewhat to the contrary. Ozonoff and colleagues (1991) found that “Asperger’s syndrome” and autistic subjects presented executive function problems on the Tower of Hanoi and the WSCT test but only the autistic sample failed to display problems on the mentalising tasks. Considering Asperger’s syndrome is a disorder thought to be on the autistic spectrum with the same underlying cognitive deficit, it has been argued that the executive dysfunction model is a better possibility than the theory of mind deficit with reference to the primary impairment in autism. These findings indicate that some people with autism, in particular individuals with Asperger’s syndrome, present deficient executive function abilities but a seemingly intact theory of mind. Essentially, this suggests that one deficit is not generated by the other and specifically, theory of mind may not be reducible to executive function. Ozonoff and colleagues have further speculated that both deficits may be the result of a third shared impairment and have proposed this may entail damage to the prefrontal cortex (Ozonoff, Pennington, & Rogers, 1991). This is by no means an unreasonable assumption since both executive function and theory of mind share the frontal origin in the brain.
There is no doubt that difficulties in “mindreading” and executive functions hold much explanatory power in explaining the striking triad of handicaps in autism but both theories, particularly the theory of mind model, are less helpful in explaining the preservation of some functions, namely the non-social deficits. Indeed, the mentalising deficit does provide some form of explanation for the islets of ability, good rote memory and above-average intelligence sometimes found in autistic children by suggesting these are skills which require only primary representations, rather than an amalgam of both primary and secondary (Happe, 1994). The executive dysfunction hypothesis accounts for, to a significant degree, the remaining non-social deficit in autistic children’s strong need for sameness. A brief mention of another prominent psychological model, the “central coherence” theory (Frith,1989; Happe, 1994) seems appropriate, as this deficit appears to account for not only the social but also the non-social features of autism. It postulates a deficiency in processing local versus global information and incoming stimuli in context (Happe, 1996) however, this theory is in need of rigorous experimental testing. Although the theory of mind deficit and executive dysfunction hypothesis have extended our understandings of the experiences of many, perhaps most people with autism, neither psychological model is universal nor specific to autism signifying that neither can claim to be the core, cognitive deficit of autism with the potential to explain the condition psychologically (Happe, 1994). Further generation of underlying cognitive deficits are essential for enhancing our understandings of autism and ultimately, facilitating effective early intervention methods.
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