Explaining Autism Deficits: Theory of Mind vs Executive Function

Autism is a developmental disorder characterized by persistent deficits in social communication and interaction, as well as repetitive and restricted patterns of behavior and interests (American Psychiatric Association, 2013). It has been argued that cognitive deficits may underlie the disorder. Thus, two cognitive theories have been proposed to explain key deficits in autism: theory of mind hypothesis and executive function theory. Each theory offers a different explanation for the deficits seen in autism, with both theories effectively explaining different aspects of autism; however, both theories also have limitations in their explanations. These limitations may prompt future research to consider how different cognitive deficits underlie different domains of autism.

Theory of mind (ToM) can be defined as “the ability to reason about mental states, such as beliefs, desires, and intentions, and to understand how mental states feature in everyday explanations and predictions of people’s behavior” (Apperly, 2012, p.826). Premack and Woodruff (1978) state that an individual has a ToM if they are able to attribute mental states to themselves and others. The ability to draw conclusions about what others believe to be true in a situation enables one to make predictions about what they will do. This is an essential component of social communication and interaction. Difficulty in understanding the minds of others is a central cognitive characteristic of autism, and thus it is suggested that individuals with autism lack a ToM (Baron-Cohen, 2001; Baron-Cohen et al., 1985).

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The ability to employ a ToM has been assessed by false-belief tests. A false-belief test is based on the situation where the one’s own belief varies from another person’s belief, and in order to the pass the test, the individual has to acknowledge that different people may have differing beliefs about a situation. Baron-Cohen et al. (1985) conducted a test of the most basic level of a ToM – a first-order false-belief test. First-order belief attribution refers to the ability of attributing a belief to another person. Findings from the study showed that 85% of typically developing children and 86% of children with Down’s syndrome passed the test. In contrast, 80% of children with autism failed the test. Baron-Cohen et al. (1985) concluded that children with autism were unable to acknowledge the difference between their own knowledge and someone else’s knowledge. Thus, the results supported the hypothesis that children with autism are unable to employ a ToM.

However, it has been found that some individuals with higher-functioning autism can pass the first-order false-belief test (Senju, 2012). This finding is problematic for the ToM hypothesis, as it suggests that the ToM deficit is not universal (Rajendran & Mitchell, 2007). In response to this, Baron-Cohen (1989) conducted a second-order false-belief test. Second-order belief attribution is “the ability to think about another’s person thoughts about a third person’s thoughts about an objective event”. In the study, it was found that 90% of typically developing children and 60% of children with Down’s syndrome passed the test, whilst none of the children with autism passed. It was concluded that even if individuals with autism are able to pass a first-order ToM task, they are unable to pass a second-order task, and therefore do not have a wholly representational ToM (Baron-Cohen, 1989; Rajendran & Mitchell, 2007). Therefore, false-belief tests have demonstrated that individuals with autism lack a complete ToM.

Lacking an ability to impute mental states to others and to the self would cause one to be incapable of effectively communicating and interacting with. A ToM allows one to make sense of utterances by interpreting what the speaker intends to communicate, rather than what is literally said. Individuals with autism have been found to have difficulties making nonliteral interpretations, and tend to interpret speech overly literally. Therefore, it can be suggested that a lack of ToM can account for deficits in pragmatics (Klin, 2000; Baron-Cohen, 2001).

Emotional understanding has also been found to be linked to ToM. Having a ToM enables one to know that behavior has social consequences, as well as facilitating a comprehension of social norm violations. Thus, a deficit in ToM is associated with difficulties in recognizing self-conscious emotions (Heerey et al., 2003). Hillier and Allinson (2002) found that individuals with autism have difficulties in understanding the concept of empathic embarrassment. In addition, it has been found that children with autism are much less able than typically developing children at detecting faux pas, with faux pas referring to the situation where the speaker says something without contemplating if it is appropriate for the listener to hear, and which has unfavorable consequences that the speaker did not mean for. In order to detect a faux pas, one must be able to recognize that the knowledge state of the speaker and that of the listener may differ, as well as appreciate the emotional effect of the utterance on the listener. Thus, the impaired faux pas detection seen in individuals with autism demonstrates their ToM deficit (Baron-Cohen et al., 1999). Therefore, a lack of ToM can explain deficits in emotional understanding.

The Eyes Test, which is an advanced test for ToM, assesses individuals’ ability to deduce the mental state of another person solely from a photograph of the person’s eyes. Further, the test assesses the participant’s ability at reading the mind of another person and at ‘tuning in’ to that person’s mental state (Baron-Cohen, Jolliffe, Mortimore and Robertson, 1997). Baron-Cohen et al. (1997) found that participants with autism were significantly impaired on this task, compared to non-autistic individuals. It can therefore be suggested that a lack of ToM is associated with difficulties in reading social and emotional messages.

Therefore, a lack of ToM among individuals with autism is well supported by previous studies and can specifically explain the nature of the social communication and social interaction impairments. However, there are problems with ToM theory. A lack of ToM does not account for the impaired functioning in the non-social aspect of autism, such as repetitive and restricted behaviors and interests. It has previously been argued that explanatory theories must give a complete account of a disorder. Thus, according to this standard, it is suggested that the ToM account does not explain autism successfully (Frith & Happe, 1994). Another problem for this theory is specificity. Late-signing deaf children have been found to fail standard false-belief tests, indicating that as a group they also lack ToM (Peterson, Wellman & Liu, 2005). In addition, individuals with schizophrenia have also been found to have an impaired capacity to impute mental states to others (Corcoran, Cahill & Frith, 1997). The claim that ToM causes the social impairments in autism is therefore challenged, as other groups who fail false-belief tasks do not necessarily social and communicative deficits that are characteristic of autism. Therefore, evidence disputes the concept that ToM impairments are specific to autism.

It can therefore be argued that the ToM hypothesis may account for some of the cognitive deficits of autism, but that it fails to explain all aspects of the disorder. Thus, other explanatory theories should be considered, such as executive function (EF) theory. EF includes functions such as planning, impulse control, inhibition, mental flexibility, and the initiation and monitoring of action (Hill, 2004). These cognitive functions enable new behavior, and enhance one’s response to unfamiliar, or non-routine, circumstances and events. EF is typically impaired in individuals with frontal lobe damage. Hence, the EF account was conceived from the observation that some symptoms of autism are comparable to those related to specific brain injury. Thus, the EF hypothesis suggests that dysfunction in EF can explain key deficits in autism, particularly repetitive behavior and restricted interests. As EF encompasses a wide range of skills, there is not one exclusive test of EF. Instead, different tasks are conducted to assess its different facets.

A typical task that has been used to assess planning in individuals is the Tower of Hanoi (TOH) task. Planning requires conceptualizing changes from the present situation, looking ahead and making decisions, then executing the plan and amending it accordingly to meet an objective. In the TOH task, participants are required to plan a sequence of moves that rearranges a starting arrangement of rings into a ‘tower’, with the rule that when rings are moved, larger rings cannot be put on top of smaller rings. Findings have shown that individuals with autism have difficulties completing the TOH task, indicating deficits in planning (Hill, 2004; Ozonoff & Jensen, 1999).

Mental flexibility is another aspect of EF which has been frequently assessed. It involves one being able to shift to a different thought or action, in accordance with changes in circumstances. The ability to exhibit such flexibility is a key characteristic of EF. Impaired mental flexibility is indicated by perseverative and fixed behavior. The Wisconsin Card Sorting Task (WCST) has been used to assess mental flexibility. The test requires participants to sort cards according to a rule; a rule which is discreetly changed during the task, meaning that participants have to shift sets accordingly and sort the cards to the new rule (Banich, 2009). WCST studies found that individuals with autism are highly preservative in their response to this task compared to individuals without autism (Liss et al., 2001; Shu, Lung, Tien & Chen, 2001). Specifically, individuals with autism have difficulties in shifting to sort the cards according to the second rule, and they persist with sorting using the first rule, despite making errors. The behavior of perseveration seen in individuals with autism and revealed by the WCST, indicates a deficit in the mental flexibility aspect of EF (Hill, 2004).

Generativity is a facet of EF that refers to the ability to generate novel ideas (Bishop & Norbury, 2005). It has been suggested that impairments in generativity may be underlie the lack of spontaneity and initiative observed in individuals with autism. In addition, such an impairment may be associated with the repetitive patterns of behavior and dislike of change seen in autism (Turner, 1997). Generativity has been investigated through pretend play, with findings showing that while children with autism could engage in pretend play, they showed difficulties in spontaneously producing pretend play (Jarrold, Boucher & Smith, 1996). It was suggested that this impairment was due to generativity problems (Jarrold et al., 1996).

Verbal and ideational fluency tests have also been used to assess generativity. Standard verbal fluency tasks involve producing as many words as possible within specific category (Shao, Janse, Visser & Meyer, 2014), whilst a classic ideational fluency task requires the participant to generate all possible uses for a familiar object (Snyder, Mitchell, Bossomaier & Pallier, 2004). Findings from both types of tasks suggested that individuals with autism have impairments in generating novel responses and behavior. Furthermore, a correlational link in individuals with autism between poor performance on ideational fluency tasks and repetitive behavior in everyday life has been found. Turner (1999) suggests that such a generativity impairment would prevent the performance of routine behavior where unusual circumstances are encountered, or adjustment is required. Further, a deficit in the ability to generate novel ideas and behavior would be predicted to result in behavior that is restricted in range, lacking in spontaneity, novelty, and variability, marked by repetition (Turner, 1999). Thus, the generativity facet of EF can be used to explain repetitive and restricted behaviors and interests shown in individuals with autism.

Therefore, findings show that impaired EF can explain deficits in autism that cannot be accounted for by a lack of ToM. However, the EF account does have limitations. Firstly, there is an issue of universality. Pellicano, Maybery, Durkin & Maley (2006) reported that EF deficits were found in only half of the individuals with autism in their study. Furthermore, Baron-Cohen, Wheelwright, Stone & Rutherford (1999) found EF to be intact or even superior in their sample. Thus, while such impairments in EF are common, they are not necessarily a universal feature of autism. Therefore, it cannot necessarily be said that impaired EF is the underlying cause of the disorder.

Secondly, the EF account lacks specificity. It has been found that there are several disorders, such as ADHD and Tourette’s syndrome, which share EF problems with autism. In response to this, it has been proposed that the particular type of dysfunction in EF may differ across conditions. Ozonoff & Jensen (1999) found that individuals with autism had difficulties on the WCST and TOH, indicating mental flexibility and planning problems, but showed no difficulties on an inhibition test (the Stroop test). In contrast, individuals with ADHD were found to have difficulty on the Stroop test, but not the WCST or TOH. Thus, it has been proposed that there is a specific pattern of EF deficits that discriminates autism from other disorders (Hill, 2004b). Considering individual domains within EF may help to explain the nature of impairments in autism, as well as address the specificity issue for the EF account of autism.

Despite limitations, Happe and Ronald (2008) suggest that satisfactory accounts do exist for each of the triad domains (impaired social interaction, impaired communication, and restricted and repetitive behaviors and interests). However, they also argue that there is not a single unitary account that can provide an explanation for both social and non-social deficits in autism. For example, ToM hypothesis can effectively explain the social interaction and communication impairments but fails to explain the non-social aspects, whilst the EF account can explain the non-social features such as repetitive and restricted behaviors, but cannot necessarily account for the social deficits. Thus, Happe, Ronald and Plomin (2006) argue that attempts to find a single cognitive explanation for deficits in autism should be stopped, in favor of strong explanations for each separate aspect of the triad. Consistent with this argument, it has been found that individuals with autism may be affected differently in these three, potentially independent, domains. Happe and Ronald (2008) found that although social interaction, communication, and restricted and repetitive behaviors and interests do occur together at rates that are above-chance, the three areas are considerably independent. Further, Pellicano et al. (2006) found that the domains of ToM and EF appeared to be unrelated to each other. Such findings have provided support for a fractionable autism triad theory, which proposes that there may be different cognitive functions underlying the distinct domains of autism. Thus, future research could consider that multiple cognitive accounts may apply, which each explain the distinct parts of the autism triad.

To conclude, cognitive theories can provide good explanations for key deficits in autism. A lack of ToM can account for the social deficits seen in autism, as findings have shown that the inability to impute mental states to others explains impairments in social communication and interaction. However, the theory lacks specificity, as ToM impairments have been found in other disorders. Furthermore, the ToM hypothesis cannot account for the non-social deficits seen in autism. In contrast, a dysfunction in EF can explain the non-social impairments in autism, as the EF account explains that impaired EF can result in repetitive and restricted behaviors and interests. Despite the plausible explanation for non-social deficits, the EF account lacks universality as not all individuals with autism have been found to have EF deficits. As well as this, the account lacks specificity, as other disorders have been found to share EF problems. It may be helpful to consider distinct domains within EF to help to explain the nature of deficits in autism, compared to other disorders. As neither the EF account nor the ToM hypothesis can explain all deficits seen in autism, it has been suggested that a fractionated triad theory may be the best solution to explaining all deficits in autism. Future research should consider such a theory, as effective interventions could be implemented to efficaciously address different domains of the disorder.

References

1. American Psychiatric Association. (2013). Diagnostic and Statistical Manual of Mental Disorders: DSM-5/ American Psychiatric Association (Fifth edition ed.). Washington, DC American Psychiatric Association.
2. Apperly, I. A. (2012). What Is 'Theory of Mind'? Concepts, Cognitive Processes and Individual Differences. The Quarterly Journal of Experimental Psychology, 65(5), 825-839. doi:10.1080/17470218.2012.676055.
3. Banich, M. T. (2009). Executive Function: The Search for an Integrated Account. Current Directions in Psychological Science, 18(2), 89-94. doi:10.1111/j.1467-8721.2009.01615.x.
4. Baron-Cohen, S. (2001). Theory of Mind in Normal Development and Autism. Prisme, 34(1), 174-183. Retrieved from https://www.researchgate.net/publication/238603356_Theory_of_Mind_in_normal_development_and_autism
5. Baron-Cohen, S., Jolliffe, T., Mortimore, C., & Robertson, M. (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 and Allied Disciplines, 38(7), 813-822. doi:10.1111/j.1469-7610.1997.tb01599.x.
6. Baron-Cohen, S., Leslie, A. M., & Frith, U. (1985). Does the Autistic Child Have a 'Theory of Mind'? Cognition, 21(1), 37-46. doi:10.1016/0010-0277(85)90022-8.
7. Baron-Cohen, S. (1989). The Autistic Child's Theory of Mind: A Case of Specific Developmental Delay. Journal of Child Psychology & Psychiatry & Allied Disciplines, 30(2), 285-297. doi:10.1111/j.1469-7610.1989.tb00241.x.
8. Baron-Cohen, S., O'Riordan, M., Stone, V., Jones, R., & Plaisted, K. (1999). Recognition of Faux Pas by Normally Developing Children and Children with Asperger Syndrome or High-Functioning Autism. Journal of Autism & Developmental Disorders, 29(5), 407-418. doi:10.1023/A:1023035012436.
9. Baron-Cohen, S., & Wheelwright, S. (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 & Psychiatry & Allied Disciplines, 42(2), 241-251. doi:10.1111/1469-7610.00715.
10. Baron-Cohen, S., Wheelwright, S., Stone, V., & Rutherford, M. (1999). A Mathematician, a Physicist and a Computer Scientist with Asperger Syndrome: Performance on Folk Psychology and Folk Physics Tests. Neurocase, 5(6), 475-483. doi:10.1080/13554799908402743.
11. Bishop, D. V. M., & Norbury, C. F. (2005). Executive Functions in Children with Communication Impairments, in Relation to Autistic Symptomatology. 1: Generativity. Autism, 9(1), 7-27. doi:10.1177/1362361305049027.
12. Boucher, J. (2012). Putting Theory of Mind in Its Place: Psychological Explanations of the Socio-Emotional-Communicative Impairments in Autism Spectrum Disorder. Autism, 16(3), 226-246. doi:10.1177/1362361311430403.
13. Brunsdon, V. E. A., & Happé, F. (2014). Exploring the 'Fractionation' of Autism at the Cognitive Level. Autism: The International Journal of Research and Practice, 18(1), 17-30. doi:10.1177/1362361313499456.
14. Corcoran, R., Cahill, C., & Frith, C. D. (1997). The Appreciation of Visual Jokes in People with Schizophrenia: A Study of 'Mentalizing' Ability. Schizophrenia Research, 24(3), 319-327. doi:10.1016/S0920-9964(96)00117-X.
15. Frith, U. (1996). Cognitive Explanations of Autism. Acta Paediatrica, 85(416), 63-68. doi:10.1111/j.1651-2227.1996.tb14280.x.
16. Frith, U., & Happe, F. (1994). Autism: Beyond 'Theory of Mind'. Cognition, 50(1-3), 115-132. doi:10.1016/0010-0277(94)90024-8.
17. Frith, U., & Happe, F. (1999). Theory of Mind and Self-Consciousness: What Is It Like to Be Autistic? Mind & Language, 14(1), 1-22. doi:10.1111/1468-0017.00100.
18. Gilbert, S. J., & Burgess, P. W. (2008). Executive Function. Current Biology, 18(3), R110-R114. doi:10.1016/j.cub.2007.12.014.
19. Happé, F., Booth, R., Charlton, R., & Hughes, C. (2006). Executive Function Deficits in Autism Spectrum Disorders and Attention-Deficit/Hyperactivity Disorder: Examining Profiles Across Domains and Ages. Brain and Cognition, 61(1), 25-39. doi:10.1016/j.bandc.2006.03.004.
20. Happé, F., Ronald, A., & Plomin, R. (2006). Time to Give Up on a Single Explanation for Autism. Nature Neuroscience, 9(10), 1218-1220. doi:10.1038/nn1770.
21. Happe, F., & Ronald, A. (2008). The 'Fractionable Autism Triad': A Review of Evidence from Behavioural, Genetic, Cognitive and Neural Research. Neuropsychology Review, 18(4), 287-304. doi:10.1007/s11065-008-9076-8.
22. Heerey, E. A., Keltner, D., & Capps, L. M. (2003). Making Sense of Self-Conscious Emotion: Linking Theory of Mind and Emotion in Children with Autism. Emotion, 3(4), 394-400. doi:10.1037/1528-3542.3.4.394.
23. Hill, E. L. (2004a). Executive Dysfunction in Autism. Trends in Cognitive Sciences, 8(1), 26-32. doi:10.1016/j.tics.2003.11.003.
24. Hill, E. L. (2004b). Evaluating the Theory of Executive Dysfunction in Autism. Developmental Review, 24(2), 189-233. doi:10.1016/j.dr.2004.01.001.
25. Hillier, A., & Allinson, L. (2002). Understanding Embarrassment Among Those with Autism: Breaking Down the Complex Emotion of Embarrassment Among Those with Autism. Journal of Autism & Developmental Disorders, 32(6), 583-592. doi:10.1023/A:1021259115185.
26. Jarrold, C., Boucher, J., & Smith, P. K. (1996). Generativity Deficits in Pretend Play in Autism. British Journal of Developmental Psychology, 14(3), 275-300. doi:10.1111/j.2044-835X.1996.tb00706.x.
27. Klin, A. (2000). Attributing Social Meaning to Ambiguous Visual Stimuli in Higher-Functioning Autism and Asperger Syndrome: The Social Attribution Task. Journal of Child Psychology and Psychiatry, 41(7), 831-846. doi:doi.org/10.1111/1469-7610.00671.
28. Liss, M., Fein, D., Allen, D., Dunn, M., Feinstein, C., Morris, R., . . . Rapin, I. (2001). Executive Functioning in High-Functioning Children with Autism. Journal of Child Psychology and Psychiatry, 42(2), 261-270. doi:10.1111/1469-7610.00717.
29. Mitchell, P., Saltmarsh, R., & Russell, H. (1997). Overly Literal Interpretations of Speech in Autism: Understanding That Messages Arise from Minds. Journal of Child Psychology and Psychiatry, 38(6), 685-691. doi:10.1111/j.1469-7610.1997.tb01695.x.
30. Morton, J., & Frith, U. (1995). Causal Modeling: A Structural Approach to Developmental Psychopathology. In D. Cicchetti, & D. J. Cohen (Eds.), Developmental psychopathology (1st ed., pp. 357-390). New York: Wiley.
31. Ozonoff, S., & Jensen, J. (1999). Brief report: Specific Executive Function Profiles in Three Neurodevelopmental Disorders. Journal of Autism & Developmental Disorders, 29(2), 171-177. doi:10.1023/A:1023052913110.
32. Ozonoff, S., & McEvoy, R. E. (1994). A Longitudinal Study of Executive Function and Theory of Mind Development in Autism. Development and Psychopathology, 6(3), 415-431. doi:10.1017/S0954579400006027.
33. Pellicano, E., Maybery, M., Durkin, K., & Maley, A. (2006). Multiple Cognitive Capabilities/Deficits in Children with an Autism Spectrum Disorder: 'Weak' Central Coherence and Its Relationship to Theory of Mind and Executive Control. Development and Psychopathology, 18(1), 77-98. doi:10.1017/S0954579406060056.
34. Peterson, C. C., Wellman, H. M., & Liu, D. (2005). Steps in Theory-of-Mind Development for Children with Deafness or Autism. Child Development, 76(2), 502-517. doi:10.1111/j.1467-8624.2005.00859.x.
35. Premack, D., & Woodruff, G. (1978). Does the Chimpanzee Have a Theory of Mind? Behavioral & Brain Sciences, 1(4), 515-526. doi:10.1017/S0140525X00076512.
36. Rajendran, G., & Mitchell, P. (2007). Cognitive Theories of Autism. Developmental Review, 27(2), 224-260. doi:10.1016/j.dr.2007.02.001.
37. Romine, C. B., Lee, D., Wolfe, M. E., Homack, S., George, C., & Riccio, C. A. (2004). Wisconsin Card Sorting Test with Children: A Meta-Analytic Study of Sensitivity and Specificity. Archives of Clinical Neuropsychology, 19(8), 1027-1041. doi:10.1016/j.acn.2003.12.009.
38. Senju, A. (2012). Spontaneous Theory of Mind and Its Absence in Autism Spectrum Disorders. The Neuroscientist, 18(2), 108-113. doi:10.1177/1073858410397208.
39. Shao, Z., Janse, E., Visser, K., & Meyer, A. S. (2014). What Do Verbal Fluency Tasks Measure? Predictors of Verbal Fluency Performance in Older Adults. Frontiers in Psychology, 5(772), 1-10. doi:10.3389/fpsyg.2014.00772.
40. Shu, B., Lung, F., Tien, A. Y., & Chen, B. (2001). Executive Function Deficits in Non-Retarded Autistic Children. Autism, 5(2), 165-174. doi:10.1177/1362361301005002006.
41. Snyder, A., Mitchell, J., Bossomaier, T., & Pallier, G. (2004). The Creativity Quotient: An Objective Scoring of Ideational Fluency. Creativity Research Journal, 16(4), 415-420. doi:10.1080/10400410409534552.
42. Tager-Flusberg, H. (2007). Evaluating the Theory-of-Mind Hypothesis of Autism. Current Directions in Psychological Science, 16(6), 311-315. doi:10.1111/j.1467-8721.2007.00527.x.
43. Turner, M. (1997). Towards an Executive Dysfunction Account of Repetitive Behaviour in Autism. In J. Russell (Ed.), Autism as an Executive Disorder (pp. 57-100). Oxford: Oxford University Press.
44. Turner, M. A. (1999). Generating Novel Ideas: Fluency Performance in High-Functioning and Learning Disabled Individuals with Autism. Journal of Child Psychology and Psychiatry, 40(2), 189-201. doi:10.1111/1469-7610.00432.