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Theory of mind in autism, schizophrenia, and in-between

Published online by Cambridge University Press:  26 June 2008

Ahmad Abu-Akel
Affiliation:
8015 Airlane Avenue, Los Angeles, CA 90045. abuakel@hotmail.com
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Abstract

Autism and schizophrenia are presented as the extremes of disorders affecting the social brain. By viewing human cognition impairment in terms of competence and performance, a variety of social brain disorders can be identified along the autistic-psychotic continuum.

Type
Open Peer Commentary
Copyright
Copyright © Cambridge University Press 2008

The target article discusses disorders affecting the social brain on “a continuum of human cognitive architecture from mechanistic to mentalistic cognition” (sect. 8, para. 2) in which autism and schizophrenia are the extremes. Within these extremes, there is a variety of conditions that manifest varying degrees of disturbances to the social brain. Theory of mind, which is the ability to represent and apply mental states to both self and other, has become a corollary construct by which we evaluate social cognition in developmental and psychiatric disorders. Theory-of-mind impairment can thus be a result of a disturbance in the ability to represent mental states to self and/or other (i.e., an impairment of competence), as well as in the ability to apply mental states to self and/or other (i.e., an impairment of performance).

By invoking the competence-performance theory of mind paradigm (Abu-Akel Reference Abu-Akel2003), we are now in a position to introduce some of the in-between cases to the extremes proposed by Crespi & Badcock (C&B). Impairment of competence is associated with individuals with autism who lose the ability to manifest an understanding of both self and other's mental states. Schizophrenic patients with passivity phenomena also fall within this category. These individuals, however, appear only to lose their ability to represent their own mental states (Mlakar et al. Reference Mlakar, Jensterle and Frith1994). Impairment of performance, on the other hand, is associated with individuals with delusional and paranoid schizophrenia, negative symptom schizophrenia, and Asperger's syndrome. In the case of paranoid or delusional schizophrenia, we observe theory of mind impairments that result from an over-attribution of mental states to self or others (i.e., hyper-theory of mind) (Abu-Akel & Bailey Reference Abu-Akel and Bailey2000). Asperger's syndrome and negative symptom schizophrenia seem to maintain an understanding of mental states, but have a deficit in the ability to manifest this understanding in real-life situations (Bowler Reference Bowler1992). Bowler has shown that although patients with Asperger's syndrome as well as patients with negative symptom schizophrenia perform well on theory-of-mind tasks in laboratory settings, they failed to demonstrate their knowledge of mental states in real life.

The C&B autistic-psychotic continuum can therefore be further enhanced by incorporating how disorders of the social brain vary along the lines of their ability to represent mental states (i.e., competence) as well as their ability to apply mental states (i.e., performance). It would be intriguing to uncover the extent to which disorders of performance and disorders of competence are etiologically related, within and across groups of disorders, in terms of the role genetic imprinting has in the development of social cognition.

References

Abu-Akel, A. (2003) A neurobiological mapping of theory of mind. Brain Research Review 43:2940.CrossRefGoogle ScholarPubMed
Abu-Akel, A. & Bailey, A. L. (2000) The possibility of different forms of theory of mind impairment in psychiatric and developmental disorders [Letter to the editor]. Psychological Medicine 30:735–38.CrossRefGoogle ScholarPubMed
Bowler, D. M. (1992) “Theory of mind” in Asperger's syndrome. Journal of Child Psychology and Psychiatry, and Allied Disciplines 33:877–93.CrossRefGoogle Scholar
Mlakar, J., Jensterle, J. & Frith, C. (1994) Central monitoring deficiency and schizophrenic symptoms. Psychological Medicine 24:557–64.CrossRefGoogle ScholarPubMed