Putting theory of mind in its place: psychological explanations of the socio-emotional-communicative impairments in autistic spectrum disorder

Abstract

In this review, the history of the theory of mind (ToM) theory of autistic spectrum disorder (ASD) is outlined (in which ToM is indexed by success on false belief tasks), and the explanatory power and psychological causes of impaired ToM in ASD are critically discussed. It is concluded that impaired ToM by itself has only limited explanatory power, but that explorations of the psychological precursors of impaired ToM have been fruitful in increasing understanding of mindreading impairments in ASD (where ‘mindreading’ refers those abilities that underlie triadic interaction as well as ToM). It is argued that early explanations of impaired mindreading are untenable for various reasons, but that impairments of dyadic interaction in ASD that could lead to impaired ability to represent others’ mental states may be the critical psychological cause, or causes, of impaired ToM. The complexity of causal routes to impaired ToM is emphasized.

Keywords

theory of mind mindreading metarepresentation mentalizing simulation relational/complex reasoning executive function metacognition triadic interaction dyadic interaction

The theory: History and terminology

In 1985, Baron-Cohen, Leslie, and Frith published a paper that radically altered the focus of research into autistic spectrum disorder (ASD), with lasting effects on the understanding of the nature and causes of ASD. In their paper, Baron-Cohen et al. reported a test of the hypothesis that children with ASD lack ‘theory of mind’ (ToM). The term was taken from a paper by Premack and Woodruff (1978) with commentaries by the philosophers Dennett (1978) and Pylyshyn (1978). These philosophers proposed that a critical test of whether or not an individual (human or primate) has a ‘ToM’ is to assess their ability to predict another individual’s behaviour on the basis of their false belief (FB).

Baron-Cohen et al. (1985) assessed this ability in children with ASD using the now classic ‘Sally Ann’ test, based on a paradigm devised by Wimmer and Perner (1983). In this test, a protagonist (‘Sally’) hides a marble in a box and exits; ‘Ann’ enters, takes the marble from the box, places it in a covered basket, and exits; Sally returns – and the child being tested is asked ‘Where will Sally look for her marble?’ To respond correctly, the child must understand that Sally falsely believes that the marble is still in the box, and that this FB will determine where she will look for it. Various precautionary questions are also asked, to ensure that a child who fails has not, for example, forgotten that Sally placed her marble in the box. Another frequently used test of FB understanding is the ‘false appearances’ task in which, for example, a child is shown a matchbox and asked to guess what it contains. Young children almost invariably answer ‘matches’, but are then shown that the matchbox actually contains buttons (or similar small objects). The matchbox is closed again, and the child is asked what another person, who has not been shown the buttons, will think is in the box. To respond correctly, the child must, as in the Sally Ann task, appreciate that this other person will – as they themselves did previously – falsely believe there are matches in the matchbox and will answer accordingly.

Whereas the Sally Ann and false appearances paradigms assess 1st order FB (X falsely believes that z is the case), more difficult tasks were also devised to assess 2nd order FB (X falsely believes that Y falsely believes that z is the case). In their original study, Baron-Cohen et al. (1985) showed that 80% of lower-functioning children with ASD (mean chronological age 11;11 years; mean verbal mental age 5;5 years) failed a 1st order FB task that typically developing (TD) children pass by approximately 4;0 years of age. Non-autistic, ability-matched children with learning disabilities did not show such a high failure rate. In a follow-up study, Baron-Cohen (1989a) used a 2nd order FB task to assess ToM in the 20% of children with ASD who had passed the 1st order task in the original study. All the participants in the ASD group (mean chronological age 15;3 years; mean verbal mental age 7;8 years) failed the 2nd order FB task that TD children pass by approximately 8;0 years.

These findings led Baron-Cohen and his colleagues to argue that impaired ToM, indexed by impaired ability to pass FB tasks, is the psychological¹ cause of social interaction and communication impairments in ASD, in that someone who lacks understanding of other people’s knowledge and beliefs will be socially and communicatively egocentric (Baron-Cohen et al., 1985). Baron-Cohen (1989b) subsequently proposed that impaired ToM might be able to explain all the behaviours diagnostic of ASD, including repetitive behaviours and lack of imagination. This was not, however, a view he held for long, and ‘single cause’ explanations of all the diagnostic features of ASD are not now generally considered tenable (Boucher, 2011; Happé et al., 2006). Correspondingly, the present review assumes that impaired ToM and its precursors may be a critical contributory cause of socio-communicative impairments in ASD, but not of other diagnostic or co-morbid features of behaviour.

Over the next decade, the ‘impaired ToM’ hypothesis became the dominant focus of research into the behavioural precursors of ASD-related behaviours, despite some immediately apparent problems with the hypothesis. The first of these was that – as noted above – a minority of the children with ASD tested by Baron-Cohen et al. (1985) succeeded on the Sally Ann task (as was also shown in numerous subsequent studies: Happé, 1995). This suggested that impaired ToM might not be a universal feature of ASD, thus forfeiting some explanatory power. Baron-Cohen initially countered this difficulty by showing a100% failure rate on a 2nd order FB task, as noted above (Baron-Cohen, 1989a). Shortly afterwards, however, a study by Bowler (1992) showed that adults with Asperger syndrome can pass 2nd order as well as 1st order FB tasks, reviving doubts about the universality of ToM impairment in people with ASD. The issue of universality was only neutralized once it had been shown that able individuals with ASD learn to ‘hack out’ correct responses to 1st and 2nd order FB tasks using compensatory reasoning (Happé, 1995). Reliance on compensatory reasoning implies that people with ASD lack, or have diminished use of, whatever intuitive abilities neurotypical individuals rely on for their understanding of FB.

This inference gains support from evidence that high functioning children and adults with ASD tend to fail on other complex tests involving the ability to understand other minds. Such tests include: (i) the ‘Strange Stories test’, which assesses the ability to understand non-literal uses of language in, for example, bluffing, white lies, irony, sarcasm or metaphor (Happé, 1994; White et al., 2009); (ii) the ‘Eyes test’, in which participants must ‘read’ a person’s state of mind from information around the eyes (Baron-Cohen et al., 1997; Baron-Cohen et al., 2001); and (iii) the ‘Faux Pas test’, which assesses the ability to reason about others’ reactions to socially inappropriate behaviours (Baron-Cohen et al., 1999). Not all of these tests assess the kinds of cognitive capacities that enable TD children to pass FB tasks at around age 4;0 (Perner, 1991). However, they all assess different facets of the (largely intuitive) ability to understand what another person is thinking or feeling. It is therefore more plausible to argue that this ability, or set of abilities, may be universally impaired in people with ASD, rather than failure to pass FB tasks.

A second immediately obvious problem with the suggestion that impaired ToM is a major cause of autism was that a proportion of the comparison group in Baron-Cohen et al.’s (1985) study (children with Down syndrome) also failed the Sally Ann task, indicating that inability to pass FB tasks is not specific to people with ASD. Subsequent research confirmed that various groups of individuals with intellectual disability (ID) are persistently impaired in their ability to pass FB tasks (Yirmiya et al., 1998); also that the ability to pass FB tasks is often delayed in children with significant hearing or visual impairments (Minter et al., 1998; Russell et al., 1998). If impaired ToM causes autism, or at least the socio-communicative impairments typical of autism, this raises the question of why these other groups of individuals who fail FB tasks do not universally show autistic-like social and communicative impairments².

A third problem with the claim that impaired ToM is a major cause of ASD-related behaviours was pointed out by Hobson (1993). Hobson argued that impaired emotion-processing is a universal characteristic of autism, and that the impaired ToM explanation of anomalous socio-communicative behaviour in ASD ignores this.

The final argument against the theory that impaired ToM is a major cause of ASD-related socio-communicative impairments derives from the fact that TD children do not pass FB tasks until approximately 4;0 years of age. Failure on FB tasks cannot therefore explain those ASD-related social and communicative impairments that occur within the first three years of life.

Given the above problems, it is interesting to consider why the impaired ToM theory so quickly achieved and still maintains such a dominant place in the literature on ASD. The most straightforward reason is that, despite the ability of the most able individuals to hack out solutions to FB tasks, subsequent research strongly suggests that impaired understanding of other minds is a universal feature of people with ASD, as noted above. Moreover, impaired ToM, indexed by impaired ability to pass FB tasks, can undoubtedly help to explain some later-manifesting socio-communicative impairments associated with ASD, such as impaired pragmatics and discourse.

Less obviously, the concept of ToM was – and is – of great interest to philosophers of mind, evolutionary psychologists, anthropologists, ethologists, linguists, developmental psychologists and others, generating thousands of publications and conference papers on the topic (see chapters and references in e.g. Astington et al., 1988; Carruthers and Smith, 1996; Carruthers, 2009 and related commentaries; Whiten, 1991). The neat and memorable term ‘theory of mind’ thus took root in numerous specialist literatures, and people with little or no knowledge of autism frequently assumed that ASD constituted the manifestation of ‘impaired ToM’. This helped to publicize and maintain adherence to the theory that impaired ToM is a major cause of ASD, despite strong counter arguments appearing in the autism literature from an early date (e.g. Boucher, 1996; Hobson, 1991, 1993; Mitchell, 1997; Russell, 1992, 1997).

A further reason why ToM remains an important theme in the ASD literature is that the term quickly lost its tight linkage to the ability to pass FB tasks, and is now frequently used in a much broader sense. This broadening of meaning was preceded by the introduction of the terms ‘mentalizing’ (Frith, 1989) and ‘mindreading’ (Baron-Cohen, 1995) to cover not only the ability to pass FB tasks and other advanced tests of the ability to understand others’ beliefs, knowledge, intentions etc, but also to cover the precursors of these abilities including, for example, joint attention and empathy. Thus, ‘ToM abilities’, ‘mindreading’ and ‘mentalizing’ are now often used interchangeably to include a broad range of psychological processes associated with understanding other minds. In this paper, ‘ToM’ is used in its original narrow sense to refer specifically to the high-level mindreading capacities that TD children develop from around the age of 4;0, whereas ‘mindreading’ will be used to refer to the whole range of capacities and achievements relating to the understanding of minds in neurotypical individuals, from infancy through to adulthood. ‘Mentalizing’ will be used in the sense introduced by Frith (1989) to refer to the ability to represent mental states, whether perceptual, conative, emotional or epistemic.

In the next section, some likely consequences of impaired ToM (as defined here) are indicated. Following this, theories of the psychological causes of impaired ToM are outlined and briefly discussed under headings relating to stages in the development of mindreading abilities in TD children. The paper closes with a short evaluation of the contributions the ‘theory of mind theory’ has made to the understanding of ASD.

Some consequences of impaired theory of mind

Impaired ToM, however caused, will have certain predictable effects on behaviour. These may be most clearly identified by considering some of the behavioural limitations and anomalies of individuals who are not autistic, but who cannot pass FB tasks. Such groups include TD children under the age of approximately 4;0 years; some young children with severe sensory impairments; and individuals of all ages who have moderate or severe ID. In these groups, social interaction and communication are egocentric in so far as their capacities for appreciating and reflecting on others’ points of view, thoughts, knowledge or desires are limited. The resulting socio-communicative deficit manifests in below average socio-communicative abilities in young children with sensory impairments (e.g. Horn et al., 2009) and children with ID (e.g. Dykens et al., 2006). In TD children below the age of 4;0 such limitations are, of course, entirely normal, and older children and adults make allowances for them in social interaction.

Limitations in the ability to appreciate and reflect on others’ points of view, knowledge, beliefs, etc reduce the capacity to make fully mature reciprocal relationships with others. To this extent, there is overlap between some of the behavioural anomalies universal in ASD and those of other groups of individuals who lack ToM. Notably, however, TD infants are by definition not autistic; and individuals with sensory impairments or ID are only rarely diagnosed with co-morbid ASD. This is because individuals these latter groups do not generally lack empathy or the desire for social interaction (e.g. Hosie et al., 1998; Kasari et al., 2003; Tager-Flusberg and Sullivan, 2000). Indeed, individuals with some forms of ID may be affectionate to the extent of being over-friendly and unguarded in their approach to strangers. By contrast, empathy is universally impaired in people with ASD (Baron-Cohen, 2005). Moreover, only a subset of relatively able individuals with ASD will seek out social interaction with strangers, or respond positively to those they do not know well (Wing, 1996).

In conclusion, impaired ToM (as defined here) cannot logically be a major cause, let alone the major cause, of the socio-emotional impairments pathognomic in ASD. However, it is undoubtedly an important contributory cause of these impairments.

Theories of the psychological causes of impaired theory of mind in ASD

Theories implicating capacities that typically developing children develop towards the end of their fourth year

Defective metarepresentation

Baron-Cohen et al. (1985) identified defective metarepresentation as the immediate cause of impaired ToM, defining metarepresentation in terms of a model of cognitive development proposed by Leslie (1987; Leslie and Roth, 1993). A component of this model was a a metarepresentational or ‘theory of mind’ module, or specific learning mechanism, innately programmed to mature at about age 4;0 years in TD children. It was proposed that maturation of this domain-specific module enables TD children to represent in their own mind, and to reflect on, others’ epistemic mental states, and to use these ‘meta-representations’ in reasoning about the behaviour of others. Furthermore, it was proposed that this module is defective in individuals with ASD.

Perner (1991) defined metarepresentation as ‘a representation of the relationship between a representation and what it represents’, and proposed that metarepresentation in this sense is a prerequisite for a range of developments in cognitive reasoning that co-occur at about age 4;0 in TD children, including success on FB tasks. Perner therefore differed from Leslie in that metarepresentation was envisaged as a domain-general, rather than a domain-specific, ability.

Perner initially concluded that impaired (domain-general) metarepresentation could not explain failure on FB tasks in ASD, noting that children with ASD are not impaired on a non-social task (the ‘false photograph’ task) also involving metarepresentation as defined in his model (Leekam and Perner, 1991). Leslie, however (Leslie and Thaiss, 1992) interpreted ASD children’s success on the false photograph task as supporting his definition of metarepresentation as a domain-specific ability, capable of explaining impaired ToM in ASD. Two subsequent studies, however, threw doubt on the domain-specificity of any metarepresentational deficit – or, indeed of whatever impairment of complex reasoning might underlie failure on FB tasks. The first of these, by Russell et al. (1999) demonstrated that children with ASD fail on a false photograph task if the executive demands are made more equivalent to the executive demands of FB tasks (executive dysfunction as a cause of impaired ToM is discussed below). Similarly, Bowler et al. (2005) reported that individuals with ASD failed on a paradigm designed to make exactly comparable demands on cognitive processing capacities as FB tasks, except that there was no requirement to reflect on others’ mental states.

The findings from these two studies strengthen the argument that whatever advances in cognitive development occur in TD children at around age 4;0 have domain-general consequences, and that – for whatever reason – these advances do not proceed normally in individuals with ASD. This impairment of higher-order reasoning in ASD could result from defective metarepresentation with domain-general consequences. However, a pervasive impairment of higher-order thought of the kind envisaged in Perner’s (1991) model, and in many other models of staged developments in the ontogeny or phylogeny of recursive or ‘meta’ thinking (e.g. Dennett, 1996; Karmiloff-Smith, 1992; Rosenthal, 2000; Tallis, 1999; Zelazo and Zelazo, 1998), is inconsistent with the high academic achievements of some individuals with ASD. On the other hand, a domain-general impairment of higher-order thought might explain impaired ToM in individuals with ID without autism, and also contribute to impaired ToM in low-functioning individuals with ASD. However, the challenge is to explain impaired ToM and parallel impairments of non-social reasoning in high-functioning individuals, and the domain-general version of a defective metarepresentation theory is probably too strong to achieve this.

Impaired relational or complex reasoning

Frye et al. (1995; see also Zelazo and Frye, 1998) argued that the ability to pass FB tasks involves the use of embedded rules, as shown in square brackets in the following example: ‘If the lights at the crossing are flashing on amber, then [if no pedestrian at the crossing, drive on]; but [if pedestrian attempting to cross, stop]’. In the ‘Sally and the marble’ task the embedded rules are: ‘If searching for the marble, then [if Sally, look in the basket]; but [if me, look in the box]’. Frye and his colleagues demonstrated impairments in children with ASD on these kinds of tasks, regardless of whether or not they involved false belief (Zelazo et al., 2002). Impairments have also been demonstrated on other tasks involving conditional reasoning. In particular, counterfactual reasoning (‘If X had been the case, then it would have been the case that Y…’) was shown to be impaired in ASD in a study by Grant et al. (2004; but see Peterson and Bowler, 2000 for a contrary finding).

Findings of impairment on such tasks add to Bowler et al.’s (2005) observation that individuals with ASD have a particular problem with certain forms of complex reasoning, regardless of whether or not such reasoning entails understanding other minds. Bowler et al. explained their finding in terms of a problem of ‘relational processing’, and specifically a problem of 3-way hierarchical processing, noting that the ability to process 3-way-hierarchic relations is central to Halford’s (1992) concept of information-processing complexity. Similarly, Minshew and colleagues (Minshew et al., 1997; Williams et al., 2006) have argued over many years for a domain-general impairment of ‘complex information processing’ in ASD, identifying this with loss of top-down control (executive dysfunction) and impaired ability to integrate information from distributed brain regions (weak central coherence), associated with impaired brain connectivity (Minshew and Williams, 2007). There is a solid body of behavioural evidence from high-functioning individuals with ASD in support of the hypotheses proposed by Bowler’s and Minshew’s groups, mostly relating to selective memory impairments but also relating to facets of abstract reasoning, as in the Bowler et al. (2005) study. It seems reasonable to suppose that impaired relational or complex reasoning may explain problems of rule-bound or conditional reasoning as well as impairments on non-social analogues of FB tasks. Such impairments would also, inevitably, contribute to failure on advanced tests of ToM. However, impairments of ToM in ASD are more severe and pervasive than the impairments of non-social reasoning that have been demonstrated, and cannot be wholly explained in this way.

Impaired language or use of inner language

There have been several attempts to explain impaired ToM and failure on non-social complex reasoning tasks in terms of either impaired language in general (Happé, 1995; Zelazo, 2004), impaired acquisition of specific syntactic forms in language (De Villiers, 2000), and impaired use of inner language to mediate rule-bound reasoning especially when these rules are arbitrary (Biro and Russell, 2001; Hughes and Russell, 1993). However, none of these suggestions have been reliably supported (for a review of relevant evidence see Colle et al., 2007; see also Lind and Bowler, 2009; Williams et al., 2008). Moreover, although the ability to pass FB tasks is unusually strongly related to overall verbal ability in people with ASD (Happé, 1995; Pellicano, 2007), this relationship almost certainly results from the fact that standard tests of FB involve linguistic comprehension, plus the fact that individuals with ASD who pass ToM tasks do so by using compensatory, language-based strategies (Tager-Flusberg and Joseph, 2005).

Delayed or persistently impaired language development may, however, explain delayed acquisition of ToM in children with severe hearing impairment raised in non-signing environments (Peterson and Siegal, 1999) and in children with specific language impairments (Miller, 2001). The effects of language delay on deaf and language impaired children’s acquisition of ToM are both direct and indirect. Direct effects result from the fact that standard FB tests require linguistic comprehension. Indirect effects result from the fact that impaired language limits social interaction generally, and conversational experience in particular, both of which facilitate – and are probably necessary for – normal acquisition of ToM (Perner et al., 1994). A similar indirect effect of delayed or persistently impaired language in ASD might be argued for. However, social interaction and conversational experience are limited and distorted in children with ASD by other factors with greater significance for impaired ToM than delayed language. Some such factors are considered later in this paper.

Executive dysfunctions

Executive dysfunctions, and specifically a difficulty in inhibiting responses based on reality (‘… the marble (really) is in the basket’), and/or impaired generativity and imagination (‘If pigs could fly, then … ’ – what might follow from this?’), have been proposed as explanations of failure on FB and other, non-social, complex reasoning tasks (Carlson et al., 1998; Hughes, 2001; Russell, 1997; Zelazo and Frye, 1998). There is a solid body of evidence showing that certain facets of executive control are impaired in people with ASD (Hill, 2004; Robinson et al., 2009). Moreover, studies by Joseph and Tager-Flusberg (2004) and by Pellicano (2007) among others, found a strong correlation in people with ASD between performance on executive tasks and FB tasks (plus a moderating role for overall verbal ability). Executive functions develop gradually over the preschool years in TD children, which could explain why TD children do not generally pass FB tasks in their earliest years.

This evidence might appear to support the hypothesis that executive dysfunction underlies impaired ToM in ASD. However, correlation does not indicate direction of cause. In addition, in Joseph and Tager-Flusberg’s (2004) study a proportion of children with ASD had intact ToM co-existing with executive dysfunctions, weakening this hypothesis. Moreover, if executive dysfunctions cause impaired ToM, then children with attention deficit and hyperactivity disorder (ADHD) should have at least as severe impairment of ToM as children with ASD, whereas a study by Perner et al. (2002) showed intact ToM in young children with ADHD. It may be the case, therefore, that ToM is a prerequisite for executive control, as argued by, for example, Carruthers (1996) and Perner and Lang (1999) or that both sets of abilities depend on some other shared factor. In either case, it seems unlikely that executive dysfunction is a major or critical cause of impaired ToM in ASD, although it may have a contributory role.

Conclusion

None of the theories implicating abilities that come on stream in TD children towards the end of their fourth year offers a complete explanation of impaired ToM in ASD. The domain-general version of the defective metarepresentation theory, if interpreted in terms of a pervasive impairment of higher-order thought, is too strong. Impaired relational or complex information processing, limited language ability and specific executive dysfunctions may be contributory factors, but cannot by themselves explain the universal and persistent difficulties that people with ASD, including the most able, have in understanding other minds. The domain-specific version of the defective metarepresentation theory comes closest to explaining why intellectually able and academically successful individuals with ASD nevertheless struggle to understand what another person is thinking, intending etc. However, this theory is pitched at too advanced a level to explain earlier manifestations of impaired mindreading in ASD, such as are considered next.

Theories implicating capacities that typically developing children develop during their second year

Towards the end of the first year of life, TD infants start to manifest early mindreading behaviours such as social referencing, protodeclarative pointing and joint attention (Schaffer, 1996; Trevarthen and Aitken, 2001). During their second or third year – the exact timing is controversial – TD children also demonstrate that they have an intuitive (unconscious, implicit) understanding that another person can hold a false belief, and that their behaviour will be determined by this false belief (Onishi and Baillargeon, 2005; Southgate et al., 2007; Surian et al., 2007). The measure used to assess this implicit ability is anticipatory looking. Thus, if asked where a protagonist will look for a hidden object, TD infants tend to look towards the location associated with a protagonist’s false belief. However, if asked to tell the Tester where the protagonist will look for the hidden object – a test of explicit knowledge – children give the wrong answer³.

Triadic, or 3-way, interactive behaviours such as joint attention and protodeclarative pointing are well known to be delayed or absent in individuals with ASD (Curcio, 1978; Mundy et al., 1986). Moreover, individuals with ASD, including those with Asperger syndrome, perform poorly on anticipatory looking tasks such as those described above (Senju, et al., 2009; Senju et al., 2007a). Some theories that have attempted to explain these phenomena and, thereafter, impaired ToM as defined here, are considered below.

Modularist theories

Baron-Cohen (1995) argued that impaired triadic relating and thereafter impaired ToM resulted from a defective ‘shared attention mechanism’, using again the kind of cognitive model originally outlined by Leslie (1987; Leslie and Roth, 1993). The circularity of this explanation was, however, quickly evident – also its failure to explain those forms of triadic relating that involve emotion-perception – and Baron-Cohen moved on, as will be described in a later subsection.

Leslie himself has continued to update his model of cognitive development, and has argued that metarepresentational capacity normally develops over two stages, one of which comes on stream in the TD child’s second or third year, and which is defective in individuals with ASD (Leslie et al., 2004). Although it may be the case that some form of representational ability more advanced than that available during the first year of life enables TD children to succeed on the anticipatory looking task, Leslie’s theory fails to explain why children with ASD have impaired dyadic (2-way, ‘one-on-one’) as well as triadic relating abilities – an issue considered below.

Defective mentalizing (‘weak form’)

From an early stage, Frith (1989) preferred the term ‘mentalizing’ to ‘ToM’, defining mentalizing as the ability to represent not only the epistemic mental states of others, such as their knowledge and beliefs, but also mental states relating to perceptions, emotions and desires. Frith proposed – and maintains (Frith, 2003; Frith and Frith, 2010) – that individuals with ASD lack the ability to represent others’ mental states, and that this can explain impaired triadic relating and, thereafter, impaired ToM. Frith (1989) initially ascribed impaired mentalizing to weak central coherence, that is, a bias towards processing detail as opposed to wholes (Frith, 1989). Later, however, she argued that impaired mentalizing and weak central coherence are independent causes of the social and non-social impairments in autism, respectively, and that mentalizing is an innate capacity not in need of further explanation (Frith, 2003). To this extent, the theory might be described as modularist. The theory has an advantage over other modularist theories in that it predicts problems of emotion-sharing, as well as impaired perception- and knowledge-sharing. However, like other theories reviewed in this section, it has the disadvantage that it cannot explain the impairments of dyadic relating that are also characteristic of individuals with ASD.

Defective mentalizing (‘strong form’). In a speculative expansion of the defective mentalizing theory, Frith and Happé (1999; see also Frith, 2003; Happé, 2003) suggested that impaired mentalizing in ASD may not be confined to representing the mental states of other people, but may extend to representing one’s own mental states. Frith and Happé suggest that this version of the defective mentalizing theory might explain why individuals with ASD have impaired self-concept and self-awareness, or what Frith (2003) memorably termed ‘the absent self’.

The ability to represent and to reflect on one’s own mental states is sometimes referred to as ‘metacognition’ in contradistinction to ‘mindreading’, referring to the ability to represent and reflect on others’ mental states (Carruthers, 2009). ‘Metacognition’ originally referred to the ability to reflect on and reason about one’s own knowledge and beliefs (Flavell, 1979), and is now sometimes used to cover a broad range of self-regulatory abilities (Dinsmore et al., 2008). However, Carruthers’ usage is adopted here.

The strong defective mentalizing theory hypothesizes that metacognition is impaired in people with ASD. However, such evidence as is available does not clearly support this prediction. Positive evidence comes from a review of literature on the development of self-concept in ASD by Lind (2010) who concluded that knowledge of own psychological characteristics is somewhat impaired in ASD, whereas knowledge of own physical characteristics is unimpaired. Results of studies by Hill et al. (2004) and by Williams and Happé (2010) indicating impaired knowledge of own emotions and of own intentions, respectively, also support the impaired metacognition hypothesis. On the other hand, a study by Farrant et al. (1999a) showed impaired ‘knowledge of learning’ relative to ability matched TD children, although not relative to children with ID; and another study by the same group (Farrant et al., 1999b) showed that metamemory is unimpaired. Moreover, a direct test of introspection (Hurlburt et al., 1994) showed that high-functioning individuals with ASD have access to their own mental states, especially those consisting of visual imagery. Finally, the experience of talking to very high-functioning individuals with ASD, such as ‘JS’ (described in Boucher, 2007; see also numerous quotes from firsthand accounts included in Boucher, 2009), also casts doubt on any claim that access to, or representations of, one’s own mental states is severely or pervasively impaired in ASD. JS, for example, is analytic and articulate about the strategies he uses to overcome his social and cognitive lacunae, and about his inner experiences of stress. It might be suggested that these reflections on his inner world are constructed from the suggestions of others. However, his self-reflections and those of other high-functioning individuals are often detailed, colourful and idiosyncratic, contradicting this suggestion.

Clearly more tests of metacognition in ASD are needed to resolve this issue. However, the contradictory findings suggest that if metacognition is impaired in ASD the impairment is neither absolute nor severe, a conclusion that tends to disconfirm the strong version of the defective mentalizing theory.

Defective simulation

In this theory, ‘simulation’ is defined as the ability to access one’s own mental states and to use these as the basis for imagining (i.e. internally representing) what other people are perceiving, feeling and thinking – to ‘put oneself in another person’s shoes’. The case for simulation as the necessary prerequisite for ToM has been strongly argued for in the philosophy literature (Goldman, 1993, 2006), and was first proposed as the main cause of impaired ToM in ASD by Harris (1989, 1991; see also Oberman and Ramachandran, 2007).

The impaired simulation theory resembles the strong – but not the weak – version of the defective mentalizing theory in that it predicts that metacognition in ASD will be significantly impaired. As noted above, such evidence as is available concerning metacognition in ASD does not clearly support this prediction, although there is sufficient positive evidence to suggest that metacognition may be mildly or selectively impaired in ASD⁴. Moreover, like other theories reviewed in this subsection, the impaired simulation theory fails to explain those anomalies of dyadic interaction in ASD that are not dependent on either representation of, or access to representations of, mental states.

Conclusion

Modularist theories, including the weak version of the defective mentalizing theory, are likely to be correct in as far as they identify impaired representation of others’ mental states as directly and importantly contributing to impairments of triadic relating and ToM in ASD. However, these theories do not explain why representational abilities of others’ mental states is impaired, other than positing innate mechanisms. Nor do they attempt to explain why dyadic relating, which is not dependent on the ability to represent mental states, is invariably impaired in people with ASD. These theories are, therefore, incomplete rather than incorrect. Both the strong version of the defective mentalizing theory and the defective simulation theory are, on the other hand, probably incorrect.

Theories implicating capacities available to typically developing infants within their first year

Typically developing infants spontaneously engage in dyadic social interactions (sometimes referred to as ‘primary intersubjectivity’) from the first year of life. For example, within their first two months TD infants will smile in response to another’s smile and hold another’s face-to-face gaze as if entranced. Within the first six months they engage in face-to-face lap play, initiating and turn-taking in ‘protoconversations’ or games such as peek-a-boo (Stern, 1985; Trevarthen, 1980). Dyadic interaction in TD infants is characterized by emotion-sharing; by spontaneous imitation of the other person’s movements, vocalizations and emotional expressions; by preferential responsiveness to social stimuli; and by rhythmicity and synchronicity in the timing of infant-carer interactions (Sigman et al., 2004). Retrospective analysis of family videos indicates that infants under 1;0 year old who are later diagnosed with ASD do not voluntarily or willingly engage in these kinds of behaviours. For example, they dislike social touch; do not make sustained eye contact; lack the usual preferential responses to the human voice, and do not readily respond to their own name (Adrien et al., 1993; Baranek, 1999; Osterling and Dawson, 1994). Behaviours associated with ASD do not always manifest in the first year of life (Rapin, 2006). However, dyadic interaction remains an essential component of social behaviour in neurotypical children and adults, especially within intimate relationships. By contrast, dyadic relating impairments are a consistent feature of behaviour in ASD, as is clear from evidence reviewed next.

Defective emotion-processing

Kanner (1943) hypothesized that autism results from ‘an innate inability to form the usual biologically provided affective contact with people’. This hypothesis lay dormant until developed by Hobson (1993; see also Hobson, 2002). Hobson, like Kanner, assumed that TD infants are biologically prewired to relate emotionally to people, and hypothesized that lack of an innate capacity for emotional reciprocity not only diminishes the baby’s desire for social contact but also impairs their unconscious realization that other people have emotions corresponding to their own. As a result, they fail to appreciate that people, unlike tables and chairs, have experiences and feelings ‘like me’, and miss out on the foundational stage of internally representing others’ mental states.

Some other theorists have posited a lack of innate capacities for empathy in ASD (Brothers, 1997; Baron-Cohen, 2005). ‘Empathy’ may refer to the reflexive mirroring of others’ expressions of emotion – ‘contagious empathy’. Alternatively the term may refer to a combination of these involuntary responses with a cognitive understanding of the causes or content of the other person’s expressed emotion – ‘cognitive empathy’ or ‘feelings’ (Le Doux, 1996; Singer, 2006). There is evidence of impaired contagious empathy in ASD (Ben Shalom et al., 2006; Charman et al., 1997; Minio-Paluello et al., 2009; Senju et al., 2007b) such as would impoverish the sharing of emotions in dyadic interactions.

A further set of theories focusing on defective emotion-processing identify failure to experience social reward (variously interpreted) as a fundamental cause of early occurring ASD-related behaviours (Loveland, 2001; Mundy, 1995; 2003; Sigman and Capps, 1997).

Defective imitation

Rogers and Pennington (1991) argued that a fundamental deficit in imitation would have a cascade of effects on emotion-sharing, triadic relating and ToM. Similarly, Meltzoff and Gopnik (1993) suggested that the first step along the route to acquiring a ToM occurs when TD babies imitate the facial postures or hand gestures of another person and understand that ‘Here is something like me’. They argued that defective imitation in babies with incipient ASD would deprive them of this critical experience. Subsequent studies of young children with early signs of autism have confirmed the prediction that defective imitation and impaired ToM are related in children with ASD (Gopnik et al., 2001; Rogers et al., 2003; see also Charman et al., 1997).

Williams et al. (2001) and also Oberman and Ramachandran (2007) have taken this argument a step further, suggesting that both imitation and the ability to simulate or imagine the mental states of others are mediated by mirror neurons (Gallese and Goldman, 1998; Gallese et al., 2004), and that the mirror neuron system may be impaired in ASD. Evidence relating to mirror neurons in ASD and the power they may have to explain critical ASD-related behaviour is, however, controversial (Southgate and Hamilton, 2008).

Defective social orienting

‘Social orienting’ refers to the innate bias in TD neonates and very young infants to attend and respond to significant social stimuli in preference to non-social stimuli (e.g., Dawson et al., 1998). A considerable body of evidence suggests that young children with ASD lack this kind of preferential responsiveness to social stimuli (see for example Dawson et al., 2004; Klin, 1991; Leekam et al., 2000; Leekam and Ramsden, 2006).

Defective timing

Social stimuli, notably faces, voices and body movements, are dynamic in the sense of moving through time, and it has been argued for many years that interactive timing is crucial for the normal development of dyadic and thereafter triadic relating (Newson and Newson, 1975; Trevarthen and Aitken, 2001; Feldman, 2007). It has been suggested that problems of timing and time perception are endemic in people with ASD (Boucher, 2001), and that defective timing mechanisms may underlie the failure of infants with incipient ASD to engage in normal two-way social interaction, with a cascade of negative effects (Newson, 1984; Wimpory et al., 2002).

Conclusion

The convergence of opinion onto problems of dyadic relating as the root cause of impaired mindreading in ASD is noteworthy, and although none of the above theories has been conclusively shown to be the critical cause, all are plausible candidates. Moreover, the theories are not mutually exclusive, and the direction of cause and effect between some of the behaviours emphasized could run either way (Leekam, 2005). This leaves open the possibility that impaired dyadic interaction arises in different ways in different individuals, with a cascade of effects that include impaired triadic interaction and impaired ToM. However, theories that envisage that in dyadic relating TD infants share others’ mental states (either through imitation or through an inbuilt co-experiencing of others’ emotions as in contagious empathy) may be best able to explain defective mentalizing, and hence impaired mindreading, in ASD.

Contributions of the ToM theory to understanding social, emotional and communicative impairments in ASD

The demonstration by Baron-Cohen and his colleagues in the 1980s that children with ASD fail on FB tasks was the first evidence of impaired ability of people with ASD to understand what is going on in other people’s minds – what is here referred to as ‘mindreading’. The demonstration of impaired mindreading constituted a major advance in understanding some of the most consistent socio-communicative impairments characteristic of people with ASD. However, the acquisition of a ToM such as enables neurotypical individuals to pass FB tasks, understand non-literal uses of language in lying, bluffing, irony and so on, and to reason about the niceties of intentions and feelings that underlie certain social conventions, can explain only the highest level of mindreading ability. People with moderate or severe forms of ID commonly lack high-level mindreading abilities, but are not generally autistic. Impaired ToM therefore has limited power to explain the full set of socio-emotional-communicative anomalies associated with ASD.

The demonstration of failure on FB tasks did, however, set in train multiple investigations of earlier manifestations of impaired mindreading in ASD and associated theorizing concerning the psychological causes of impaired mindreading generally. At first, only potential explanations of impaired ToM itself were proposed; then potential explanations of impaired triadic interaction; and now the main focus is on impaired dyadic interaction (also known as primary intersubjectivity). It is concluded that certain impairments at this most fundamental level of interacting with and learning about others would lead to the kind of difficulties in the representation of others’ thoughts and feelings that have been the focus of the majority of theoretical explanations of impaired ToM in ASD. However, evidence of impaired performance by people with ASD on reasoning tasks that resemble FB tasks in form and complexity, but which do not require the representation of the mental states of others, suggest that two major factors contribute to impaired ToM: some as-yet-to-be-established impairment(s) of dyadic relating, plus a domain-general problem in complex reasoning.

However, this is to over-simplify. The possible contributions of impaired language and executive dysfunction to impaired ToM are mentioned above. More importantly, the interconnectedness of the kinds of impairments of dyadic relating that have been emphasized in various explanatory theories indicates ways in which a cascade and then a tangle of secondary effects that become causes of other effects, which in turn become causes of further effects, would build up. Two accounts that attempt to dissect the tangled causal pathways underlying impaired socio-emotional-communicative behaviour in ASD can be found in Belmonte (2009) and Gallagher (2004). These two publications are salutary not only in demonstrating the complexity of the arguments but also in demonstrating the continuing controversies in the field (Rajendran and Mitchell, 2007), which have, of necessity, been underplayed in this short review.

Footnotes

Notes

References

Adrien

Lenoir

Martineau

Perrot

Hameury

Larmande

(1993) Blind ratings of early symptoms of autism from family home movies. Journal of the American Academy of Child and Adolescent Psychiatry 32: 617–627.

Astington

Harris

Olson

(1988) Developing Theories of Mind. Cambridge: Cambridge University Press.

Baranek

(1999) Autism during infancy: A retrospective video-analysis of sensori-motor and social behaviours at 9–12 months of age. Journal of Autism and Developmental Disorders 29: 213–224.

Baron-Cohen

(1989a) The autistic child’s theory of mind: A case of specific developmental delay. Journal of Child Psychology and Psychiatry 30: 285–297.

Baron-Cohen

(1989b) Do autistic children have obsessions and compulsions? British Journal of Clinical Psychology 28: 193–200.

Baron-Cohen

(1995) Mindblindness: An Essay on Autism and Theory of Mind. Cambridge, MA: MIT Press.

Baron-Cohen

(2005) The Empathising System: A revision of the 1994 model of the Mindreading System. In: Ellis

Bjorkland

(eds) Origins of the Social Mind. New York: Guilford Press, 468–492.

Baron-Cohen

Jolliffe

Mortimore

Robertson

(1997) Another advanced test of theory of mind: evidence from very high functioning adults with autism or Asperger Syndrome. Journal of Child Psychology and Psychiatry 38: 813–822.

Baron-Cohen

Leslie

Frith

(1985) Does the autistic child have a ‘theory of mind’?. Cognition 21: 37–46.

10.

Baron-Cohen

O’Riordan

Stone

Jones

Plaisted

(1999) Recognition of faux pas by normally developing children and children with Asperger syndrome or high-functioning autism. Journal of Autism and Developmental Disorders 29: 407–418.

11.

Baron-Cohen

Wheelwright

Hill

Raste

Plumb

(2001) The ‘Reading the Mind in the Eyes’ Test Revised Version: A study with normal adults, and adults with Asperger Syndrome or High-Functioning Autism. Journal of Child Psychology and Psychiatry 42: 241–252.

12.

Belmonte

(2009) What’s the story behind the ‘Theory of Mind’ and autism?. Journal of Consciousness Studies 16: 118–139.

13.

Ben Shalom

Mostofsky

Hazlett

Goldberg

Landa

(2006) Normal physiological emotions but differences in expression of conscious feelings in children with high functioning autism. Journal of Autism and Developmental Disorders 36: 395–400.

14.

Biro

Russell

(2001) The execution of arbitrary procedures by children with autism. Development and Psychopathology 13: 97–110.

15.

Boucher

(1996) What could possibly explain autism?. In: Carruther

Smith

(eds) Theories of Theory of Mind. Cambridge: Cambridge University Press, 223–241.

16.

Boucher

(2001) Lost in a sea of time: Time-parsing and autism. In: Hoerl

McCormack

(eds) Time and Memory. Oxford: Clarendon Press, 111–135.

17.

Boucher

(2007) Memory and generativity in very high functioning autism: A firsthand account and an interpretation. Autism 11: 255–264.

18.

Boucher

(2009) The Autistic Spectrum: Characteristics Causes, and Practical Issues. London: Sage.

19.

Boucher

(2011) Redefining the concept of autism as a unitary disorder: Multiple deficits of a single kind?. In: Fein

(ed.) The Neuropsychology of Autism. Oxford: Oxford University Press, 469–482.

20.

Bowler

(1992) Theory of mind in Asperger’s syndrome. Journal of Child Psychology and Psychiatry 33: 877–893.

21.

Bowler

Briskman

Gurvidi

Fornells-Ambrojo

(2005) Autistic and non-autistic children’s performance on a non-social analogue of the false belief task. Journal of Cognition and Development 6: 259–283.

22.

Brothers

(1997) Friday’s Footprint: How Society Shapes the Social Mind. Oxford: Oxford University Press.

23.

Carlson

Moses

Hix

(1998) The role of inhibitory control in young children’s difficulties with deception and false belief. Child Development 69: 672–691.

24.

Carruthers

(1996) Autism as mindblindness: An elaboration and partial defense. In: Carruthers

Smith

(eds) Theories of Theories of Mind. Cambridge: Cambridge University Press, 257–273.

25.

Carruthers

(2009) How we know our own minds: the relationship between mindreading and metacognition. Behavioural and Brain Sciences 32: 121–138.

26.

Carruthers

Smith

(1996) Theories of Theory of Mind. Cambridge: Cambridge University Press.

27.

Charman

Swettenham

Baron-Cohen

Cox

Baird

Drew

(1997) Infants with autism: An investigation of empathy, pretend play, joint attention, and imitation. Developmental Psychology 33: 781–789.

28.

Colle

Baron-Cohen

Hill

(2007) Do children with autism have a theory of mind? A non-verbal test of autism vs. specific language impairment. Journal of Autism and Developmental Disorders 37: 716–723.

29.

Curcio

(1978) Sensorimotor functioning and communication in mute autistic children. Journal of Autism and Childhood Schizophrenia 2: 264–287.

30.

Dawson

Meltzoff

Osterling

Rinaldi

Brown

(1998) Children with autism fail to orient to naturally occurring social stimuli. Journal of Autism and Developmental Disorders 28: 479–485.

31.

Dawson

Toth

Abbott

Osterling

Munson

Estes

(2004) Early social attention impairments in autism: Social orienting, joint attention, and attention to distress. Developmental Psychology 40: 271–283.

32.

Dennett

(1978) Beliefs about beliefs. Behavioral and Brain Sciences 4: 568–570.

33.

Dennett

(1996) Kinds of Minds. New York: Basic Books.

34.

De Villiers

(2000) Language and theory of mind: What are the developmental relationships?. In: Baron-Cohen

Tager-Flusberg

Cohen

(eds) Understanding Other Minds: Perspectives from Developmental Cognitive Neuroscience (2nd edition). Oxford: Oxford University Press, 83–123.

35.

Dinsmore

Alexander

Loughlin

(2008) Focusing the conceptual lens on metacognition, self-regulation, and self-regulated learning. Educational Psychology Review 20: 391–409.

36.

Dykens

Hodapp

Evans

(2006) Profiles and development of adaptive behavior in children with Down syndrome. Down Syndrome Research and Practice 9: 45–50.

37.

Farrant

Blades

Boucher

(1999a) Recall readiness in high functioning children with autism. Journal of Autism and Developmental Disorders 29: 259–366.

38.

Farrant

Boucher

Blades

(1999b) Metamemory in relatively able children with autism. Child Development 70: 107–131.

39.

Feldman

(2007) Parent-infant synchrony and the construction of shared timing; physiological precursors, developmental outcomes, and risk conditions. Journal of Child Psychology and Psychiatry 48: 329–354.

40.

Flavell

(1979) Metacognition and cognitive monitoring. American Psychologist 34: 906–911.

41.

Frith

(1989) Autism: Explaining the Enigma. Oxford: Blackwell.

42.

Frith

(2003) Autism: Explaining the Enigma (2nd edition). Oxford: Blackwell.

43.

Frith

(2010) The social brain: Allowing humans to boldly go where no other species has been. Philosophical Transactions of the Royal Society of London B, Biological Sciences 365: 165–176.

44.

Frith

Happé

(1999) Theory of mind and self-consciousness: What is it like to be autistic?. Mind and Language 14: 1–22.

45.

Frye

Zelazo

Palfai

(1995) Theory of mind and rule-based reasoning. Cognitive Development 10: 483–527.

46.

Gallagher

(2004) Understand interpersonal problems in autism: Interaction theory as an alternative to theory of mind. Philosophy Psychiatry, and Psychology 11: 199–217.

47.

Gallese

Goldman

(1998) Mirror neurons and the simulation theory of mind-reading. Trends in Cognitive Sciences 2: 493–501.

48.

Gallese

Keysers

Rizzolatti

(2004) Trends in Cognitive Sciences 8: 396–403.

49.

Goldman

(1993) The psychology of folk psychology. Behavioral and Brain Sciences 16: 15–28.

50.

Goldman

(2006) Simulating Minds: The Philosophy Psychology, and Neuroscience of Mindreading. Oxford: Oxford University Press.

51.

Gopnik

Capps

Meltzoff

(2001) Early theories of mind: What the theory theory can tell us about autism. In: Baron-Cohen

Tager-Flusberg

Cohen

(eds) Understanding Other Minds: Perspectives from Developmental Cognitive Neuroscience. Oxford: Oxford University Press.

52.

Grant

Riggs

Boucher

(2004) Counterfactual and mental state reasoning in children with autism. Journal of Autism and Developmental Disorders 34: 177–188.

53.

Halford

(1992) Children’s Understanding: The Development of Mental Models. Hillsdale, NJ: L Erlbaum.

54.

Happé

(1994) An advanced test of theory of mind: Understanding of story characters’ thoughts and feelings by able autistic, mentally handicapped, and normal children and adults. Journal of Autism and Developmental Disorders 24: 129–154.

55.

Happé

(1995) The role of age and verbal ability in the Theory of Mind task: Performance of subjects with autism. Child Development 66: 843–855.

56.

Happé

(2003) Theory of mind and the self. Annals of the New York Academy of Sciences 1001: 134–144.

57.

Happé

Ronald

Plomin

(2006) Time to give up on a single explanation for autism. Nature Neuroscience 9: 1218–1220.

58.

Harris

(1989) Children and Emotion. Oxford: Blackwell.

59.

Harris

(1991) The work of the imagination. In: Whiten

(ed.) Natural Theories of Mind. Oxford: Blackwell, 283–304.

60.

Hill

(2004) Evaluating the theory of impairments of executive function in autism. Developmental Review 24: 189–233.

61.

Hill

Berthoz

Frith

(2004) Brief report: Cognitive processing of own emotions in individuals with autistic spectrum disorder and in their relatives. Journal of Autism and Developmental Disorders 34: 229–235.

62.

Hobson

(1991) Against the theory of mind. British Journal of Developmental Psychology 9: 33–51.

63.

Hobson

(1993) Autism and the Development of Mind. Hove: Erlbaum.

64.

Hobson

(2002) The Cradle of Thought. London: Macmillan.

65.

Horn

Pisoni

Sander

Miyamoto

(2009) Behavioral assessment of prelingually deaf children before cochlear implantation. The Laryngoscope 115: 1603–1611.

66.

Hosie

Gray

Russell

Scott

Hunter

(1998) The matching of facial expressions by deaf and hearing children and their production and comprehension of emotion lables. Motivation and Emotion 22: 293–313.

67.

Hughes

(2001) Executive dysfunction in autism: Its nature and implications for the everyday problems experienced by individuals with autism. In: Burack

Charman

Yirmiya

Zelazo

(eds) The Development of Autism: Perspectives from Theory and Research. Mahwah, NJ: Erlbaum, 255–275.

68.

Hughes

Russell

(1993) Autistic children’s difficulty with mental disengagement from an object: Its implications for theories of autism. Developmental Psychology 29: 498–510.

69.

Hurlburt

Happé

Frith

(1994) Sampling the form of inner experience in three adults with Asperger syndrome. Psychological Medicine 24: 385–395.

70.

Joseph

Tager-Flusberg

(2004) The relationship of theory of mind and executive functions to symptom type and severity in children with autism. Development and Psychopathology 16: 137–155.

71.

Kanner

(1943) Autistic disturbances of affective contact. Nervous Child 2: 217–250.

72.

Karmiloff-Smith

(1992) Beyond Modularity. Cambridge, MA: MIT Press.

73.

Kasari

Freeman

Bass

(2003) Empathy and response to distress in Down syndrome children. Journal of Child Psychology and Psychiatry 44: 424–431.

74.

Klin

(1991) Young autistic children’s listening preferences in regard to speech: A possible characterization of the symptom of social withdrawal. Journal of Autism and Developmental Disorders 21: 29–42.

75.

Le Doux

(1996) The Emotional Brain. New York: Simon and Schuster.

76.

Leekam

(2005) Why do children with autism have a joint attention impairment?. In: Eilan

Hoerl

McCormack

Roessler

(eds) Joint Attention: Communication and Other Minds. Oxford: Oxford University Press, 205–229.

77.

Leekam

Lopez

Moore

(2000) Attention and joint attention in preschool children with autism. Developmental Psychology 36: 261–273.

78.

Leekam

Perner

(1991) Does the autistic child have a metarepresentational deficit?. Cognition 40: 203–218.

79.

Leekam

Ramsden

(2006) Dyadic orienting and joint attention in preschool children with autism. Journal of Autism and Developmental Disorders 36: 185–197.

80.

Leslie

(1987) Pretense and representation in infancy: The origins of theory of mind. Psychological Review 94: 412–427.

81.

Leslie

Friedman

German

(2004) Core mechanisms in ‘theory of mind’. Trends in Cognitive Sciences 8: 528–533.

82.

Leslie

Roth

(1993) What autism teaches us about metarepresentation. In: Baron-Cohen

Tager-Flusberg

Cohen

(eds) Understanding Other Minds: Perspectives from Autism. Oxford: Oxford Medical Publications, 83–111.

83.

Leslie

Thaiss

(1992) Domain-specificity in conceptual development: Evidence from autism. Cognition 43: 225–251.

84.

Lind

(2010) Memory and the self in autism spectrum disorder: A review and theoretical framework. Autism 14: 430–456.

85.

Lind

Bowler

(2009) Language and theory of mind in autism spectrum disorder: The relationship between complement syntax and false belief task performance. Journal of Autism and Developmental Disorders 39: 929–937.

86.

Lockl

Schneider

(2006) Precursors of metamemory in young children: The role of theory of mind and metacognitive vocabulary. Metacognition and Learning 1: 15–31.

87.

Loveland

(2001) Toward an ecological theory of autism. In: Burack

Charman

Yirmiya

Zelazo

(eds) The Development of Autism: Perspectives From Theory and Research. Mahwah, NJ: Lawrence Erlbaum Associates, 17–38.

88.

Meltzoff

Gopnik

(1993) The role of imitation in understanding persons and developing theories of mind. In: Baron-Cohen

Tager-Flusberg

Cohen

(eds) Understanding Other Minds: Perspectives from Autism. Oxford: Oxford University Press, 335–366.

89.

Miller

(2001) False belief understanding in children with specific language impairment. Journal of Communication Disorders 34: 73–86.

90.

Minio-Paluello

Baron-Cohen

Avenanti

Walsh

Aglioti

(2009) Absence of embodied empathy during pain observation in Asperger Syndrome. Biological Psychiatry 65: 55–62.

91.

Minshew

Goldstein

Siegel

(1997) Neuropsychologic functioning in autism: Profile of a complex information processing disorder. Journal of the International Neuropsychological Society 3: 303–317.

92.

Minshew

Williams

(2007) The new neurobiology of autism. Archives of Neurology 64: 945–950.

93.

Minter

Hobson

Bishop

(1998) Congenital visual impairment and theory of mind. British Journal of Developmental Psychology 16: 183–196.

94.

Mitchell

(1997) Introduction to Theory of Mind. London: Arnold.

95.

Mundy

(1995) Joint attention and socio-emotional approach behaviour in children with autism. Development and Psychopathology 7: 63–82.

96.

Mundy

(2003) The neural basis of social impairments in autism: The role of the dorsal medial-frontal cortex and anterior cingulate system. Journal of Child Psychology and Psychiatry 44: 793–809.

97.

Mundy

Sigman

Ungerer

Sherman

(1986) Defining the social deficit in autism: The contribution of nonverbal communication measures. Journal of Child Psychology and Psychiatry 27: 657–669.

98.

Newson

(1984) The social development of the young autistic child. Paper given at the National Autistic Society Conference, Bath, UK.

99.

Newson

(1975) Intersubjectivity and the transmission of culture: On the social origins of symbolic functioning. Bulletin of the British Psychological Society 28: 437–447.

100.

Oberman

Ramachandran

(2007) The simulating social mind: The role of the mirror neuron system and simulation in the social and communicative deficits of autism spectrum disorders. Psychological Bulletin 133: 310–327.

101.

Onishi

Baillargeon

(2005) Do 15-month-old infants understand false beliefs?. Science 308: 255–258.

102.

Osterling

Dawson

(1994) Early recognition of children with autism: A study of first birthday home videos. Journal of Autism and Developmental Disorders 24: 247–257.

103.

Pellicano

(2007) Links between theory of mind and executive function in young children with autism: Clues to developmental primacy. Development Psychology 43: 974–990.

104.

Perner

(1991) Understanding the Representational Mind. Cambridge, MA: MIT Press.

105.

Perner

Kain

Barchfield

(2002) Executive control and higher-order theory of mind in children at risk of ADHD. Infant and Child Development 11: 141–158.

106.

Perner

Lang

(1999) Development of theory of mind and executive control. Trends in Cognitive Sciences 3: 337–344.

107.

Perner

Ruffman

Leekam

(1994) Theory of mind is contagious: You catch it from your sibs. Child Development 65: 1228–1238.

108.

Peterson

Siegal

(1999) Representing inner worlds: Theory of mind in autistic, deaf and normal hearing children. Psychological Science 10: 126–129.

109.

Peterson

Bowler

(2000) Counterfactual reasoning and false belief understanding in children with autism, children with severe learning difficulties and children with typical development. Autism 4: 391–405.

110.

Premack

Woodruff

(1978) Does the chimpanzee have a ‘theory of mind’?. Behavioral and Brain Sciences 4: 515–526.

111.

Pylyshyn

(1978) When is attribution of beliefs justified?. Behavioral and Brain Sciences 4: 492–593.

112.

Rajendran

Mitchell

(2007) Cognitive theories of autism. Developmental Review 27: 224–260.

113.

Rapin

(2006) Language heterogeneity and regression in the autism spectrum disorders. Clinical Neuroscience Research 6: 209–218.

114.

Robinson

Goddard

Dritschel

Wisley

Howlin

(2009) Executive functions in children with Autism Spectrum Disorders. Brain and Cognition 71: 362–368.

115.

Rogers

Hepburn

Stackhouse

Wehner

(2003) Imitation performance in toddlers with autism and those with other developmental disorders. Journal of Child Psychology and Psychiatry 44: 763–781.

116.

Rogers

Pennington

(1991) A theoretical approach to the deficits in infantile autism. Development and Psychopathology 3: 137–162.

117.

Rosenthal

(2000) Metacognition and higher-order thoughts. Consciousness and Cognition 9: 231–242.

118.

Ruffman

Perner

(2005) Do infants really understand false belief?. Trends in Cognitive Sciences 9: 462–463.

119.

Russell

(1992) The theory-theory: So good they named it twice?. Cognitive Development 7: 485–519.

120.

Russell

(1997) How executive disorders can bring about an inadequate ‘theory of mind’. In: Russell

(ed.) Autism as an Executive Disorder. Oxford: Oxford University Press, 256–304.

121.

Russell

Saltmarsh

Hill

(1999) What do executive factors contribute to the failure on false belief tasks by children with autism?. Journal of Child Psychology and Psychiatry 40: 859–868.

122.

Russell

Hosie

Gray

Scott

Hunter

Banks

Macaulay

(1998) The development of theory of mind in deaf children. Journal of Child Psychology and Psychiatry 39: 903–910.

123.

Schaffer

(1996) Social Development: An Introduction. Cambridge MA: Blackwell.

124.

Senju

Maeda

Kikuchi

Hasegawa

Tojo

Osanai

(2007a) Absence of contagious yawning in children with autism spectrum disorder. Biology Letters 3: 706–708.

125.

Senju

Southgate

Miurab

Matsuib

Hasegawac

Tojod

(2007b) Absence of spontaneous action anticipation by false belief attribution in children with autism spectrum disorder. Development and Psychopathology 22: 353–360.

126.

Senju

Southgate

White

Frith

(2009) Mindblind eyes: An absence of spontaneous theory of mind in Asperger syndrome. Science 325: 883–885.

127.

Sigman

Capps

(1997) Children with Autism: A Developmental Perspective. Cambridge, MA: Harvard University Press.

128.

Sigman

Dijamco

Gratier

Rozga

(2004) Early detection of core deficits in autism. Mental Retardation and Developmental Disabilities Research Reviews 10: 221–233.

129.

Singer

(2006) The neural basis and ontogeny of empathy and mind reading: Review of literature and implications for future research. Neuroscience and Biobehavioural Reviews 30: 855–863.

130.

Southgate

Senju

Csibra

(2007) Action anticipation through attribution of false belief. Psychological Science 18: 587–592.

131.

Southgate

Hamilton

(2008) Unbroken mirrors: Challenging a theory of autism. Trends in Cognitive Sciences 12: 225–229.

132.

Stern

(1985) The Interpersonal World of the Infant: A View from Psychoanalysis and Developmental Psychology. New York: Basic Books.

133.

Surian

Caldi

Sperber

(2007) Attribution of beliefs in 13-month-old infants. Psychological Science 18: 580–586.

134.

Tager-Flusberg

Joseph

(2005) How language facilitates the acquisition of false belief understanding in children with autism. In: Astington

Baird

(eds) Why Language Matters in Theory of Mind. Oxford: Oxford University Press, 298–318.

135.

Tager-Flusberg

Sullivan

(2000) A componential view of theory of mind: Evidence from Williams syndrome. Cognition 76: 59–89.

136.

Tallis

(1999) The Explicit Animal: A Defence of Human Consciousness (2nd edition). London: Palgrave Macmillan.

137.

Trevarthen

(1980) The foundations of intersubjectivity: Development of interpersonal and co-operative understanding in infants. In: Olson

(ed.) The Social Foundations of Language and Thought. New York: WW Norton, 316–342.

138.

Trevarthen

Aitken

(2001) Infant intersubjectivity: Research, theory, and clinical applications. Journal of Child Psychology and Psychiatry 42: 3–48.

139.

White

Hill

Happé

Frith

(2009) Revisiting the Strange Stories: revealing mentalizing impairments in autism. Child Development 80: 1097–1117.

140.

Whiten

(1991) Natural Theories of Mind. Oxford: Blackwell.

141.

Williams

Goldstein

Minshew

(2006) Neuropsychologic functioning in children with autism: Further evidence for disordered complex information-processing. Child Neuropsychology 12: 279–298.

142.

Williams

Happé

(2010) Representing intentions in self and other: Studies of autism and typical development. Developmental Science 13: 307–319.

143.

Williams

Happé

Jarrold

(2008) Intact inner speech use in autism spectrum disorder: Evidence from a short-term memory task. Journal of Child Psychology and Psychiatry, 44: 51–58.

144.

Williams

Whiten

Suddendorf

Perrett

(2001) Imitation, mirror neurons and autism. Neuroscience and Biobehavioural Reviews 25: 287–295.

145.

Wimmer

Perner

(1983) Beliefs about beliefs representation and constraining function of wrong beliefs in young children’s understanding of deception. Cognition 13: 103–128.

146.

Wimpory

Nicholas

Nash

(2002) Social timing, clock genes and autism: A new hypothesis. Journal of Intellectual Disability Research 46: 352–358.

147.

Wing

(1996) The Autistic Spectrum. London: Constable.

148.

Yirmiya

Erel

Shaked

Solomonica-Levi

(1998) Meta-analyses comparing theory of mind abilities of individuals with autism, individuals with mental retardation, and normally developing individuals. Psychological Bulletin 124: 283–307.

149.

Zelazo

(2004) The development of conscious control in childhood. Trends in Cognitive Sciences 8: 12–17.

150.

Zelazo

Frye

(1998) Cognitive complexity and control: The development of executive function in childhood. Current Direction in Psychological Science 7: 121–126.

151.

Zelazo

Jacques

Burack

Frye

(2002) The relation between theory of mind and rule use: Evidence from persons with autism-spectrum disorders. Infant and Child Development 11: 171–195.

152.

Zelazo

(1998) The emergence of consciousness. In: Jasper

Descarries

Castellucci

Rossingnol

(eds) Consciousness: At the Frontiers of Neuroscience. Advances in Neurology 77. New York: Lippincott-Raven Press, 149–165.

Supplementary Material

Please find the following supplemental material available below.

For Open Access articles published under a Creative Commons License, all supplemental material carries the same license as the article it is associated with.

For non-Open Access articles published, all supplemental material carries a non-exclusive license, and permission requests for re-use of supplemental material or any part of supplemental material shall be sent directly to the copyright owner as specified in the copyright notice associated with the article.

0.00 MB