Compare, contrast, and where possible synthesise, two major psychological approaches to understanding the core deficits of autism.

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Compare, contrast, and where possible synthesise, two major psychological approaches to understanding the “core deficits” of autism.

      Sithy Laura Haddow

    Word Count: 2,339

Compare, contrast, and where possible synthesise, two major psychological approaches to understanding the “core deficits” of autism.

Autism is widely recognised as constituting a social/cognitive behavioural and language disorder (Paul, 1987; Rutter, 1978; Wing, 1981).  The special population suffering from this disorder display an array of complex behaviours resulting in difficulties in diagnosis.  It seems pertinent at this stage to clarify the commonly accepted criteria for differentiating between the core impediments and the less central characteristics of any condition (Pennington & Ozonoff, 1991; Rapin, 1987; Sigman, 1994).  Primary deficits require commonality of the disorder amongst sufferers, and specificity to the disorder (Happe, 1994).  Although there is some dispute about the detailed attributes of autism, there is general consensus that it is diagnostically characterised by behavioural difficulties in social reciprocity, pragmatic communication and range of interests and activities (American Psychiatric Association, 1994; Rutter & Bailey, 1993; Rutter & Schopler, 1992).  These characteristics form the basis of Wing’s (1988) triad of impairments and comply with the prevailing criteria.  Similarly, any underlying cognitive psychological model or deficit attempting to explain these core deficits is also required to be universal amongst sufferers and specific to the disorder.  The challenge is to propose a psychological model which can account for, not only autistic people’s striking handicaps but also their unimpaired or even superior skills, commonly referred to as islets of ability (Happe, 1994).    

The notion that a cognitive dysfunction could possibly underlie the developmental disorder autism (Hermelin & O’Connor, 1970) ignited the proposal of many theories regarding the nature of such a cognitive dysfunction.  These have included abnormalities in sensory modulation (Ornitz, 1985), arousal and attention (Dawson & Lewy, 1989), affective and interpersonal relatedness (Hobson, 1989), and language (Rutter, 1978).  However, two psychological models in particular have stimulated a considerable degree of interest over the last decade.  These encompass the “theory-of-mind” deficit and the executive dysfunction hypothesis.  Both models recognise that the disorder is not directly caused by a cognitive deficit and appreciate the overwhelming evidence of an organic cause (Coleman & Gillberg, 1985; Schopler & Mesibov, 1987; Gillberg, 1991) but are equally aware that a cognitive deficit may drive a number of developmental conditions resulting in specific symptoms of the disorder.

Currently, the relationship between the theory of mind and executive function deficit has not been clearly established.  Indeed, these two psychological deficits may act as independent and parallel cognitive operations (Ozonoff, 1997) or there may be possible connections between the two models.  One deficit may be generated by the other, or both may result from a third shared impairment (Ozonoff, 1995; Rutter & Bailey, 1993).  The umbrella term “executive functions” refers to a number of higher cognitive skills, and thus, it is probable there will be some degree of overlap with the theory of mind conception (Baron-Cohen & Swettenham, 1997).  

At a superficial level, these prominent psychological models represent quite different deficits and are distinctly different in the behavioural abnormalities they explain.  The theory-of-mind or “mentalising” deficit, initially originated from Leslie’s (1987) model of first- and second-order representations.  He insists an inability to form second-order representations would lead to a lack of mentalising (Baron-Cohen, 1987), in that autistic individuals may have problems attributing independent mental states to one self and others, impairing their ability to predict and explain behaviour.  This difficulty in tuning into the minds of others has been consistently confirmed by an abundance of experimental testing procedures (Baron-Cohen, Leslie, & Frith, 1985; Baron-Cohen & Cross, 1992; Perner, Leslie, & Leekham, 1989; Tager-Flusberg, 1992) and is a feature of many first-hand accounts (Blackburn, 2000; Lawson, 2001).  Indeed, one first-hand account simply expressed, “I don’t feel the emotions of others” (Lawson, 2001, p. 180-182).  Such a deficit, Frith (1989) suggests, holds excessive explanatory power in explaining the abnormal social, communicative and imaginative development shown by the majority of autistic individuals.  Their striking inability to pretend, in fact, generated the theory of mind model and it was thought their inability to distinguish the independent functioning of others’ minds led to significant social impairment.  Finally, as Happe (1994, p.49) stated, “the characteristic communicative impairments would follow from an inability to represent intentions, or recognise utterances as interpretations of a speaker’s thoughts.” 

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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 ...

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