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THEORY
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Theory of Mind Deficit in Autistic Disorder

Kelly DeCoste
University of Calgary

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Theory of Mind Deficit in Autistic Disorder

Individuals with Autistic Disorder (AD) are characterized by impairments or
abnormalities in social interactions and communication, and by a restricted repertoire of
behaviors, interests and activities (APA, 2000). Individuals with AD exhibit delays or deficits in
their use of nonverbal behaviors (e.g., eye gaze, posture), a lack of social or emotional
reciprocity, and/or a general lack of awareness of others. Verbal and nonverbal language skills
are also delayed, and these individuals possess restricted, repetitive, and stereotyped patterns of
behavior, interests, and activities (APA, 2000, p. 71). The behavioral manifestations of this
disorder are evident within the first few years of life, and must be present prior to age 3 years to
result in a clinical diagnosis (APA, 2000). Though individuals with Autistic Disorder vary in
terms of the presentation of their symptoms (depending on their chronological age and
developmental level), impairment is always marked and sustained.
Attributing mental states to ones self and others (theory of mind [ToM]; Baron-Cohen,
Leslie, & Frith, 1985) is a complex information processing skill that relies on a network of
cortical areas. Successful ToM requires an ability to understand and separate ones own beliefs
from those of others, and an ability to distinguish beliefs from reality. This paper will explore the
current understanding of a ToM deficit in individuals with AD and provide suggestions for future
research in an attempt to better understand the nature of this disorder.
Theory of Mind
Description
Theory of mind is the ability to attribute mental states to the self and to others (BaronCohen et al., 1985). This skill plays an important role in the success of our daily social
interactions, allowing one to understand and predict the behavior of others. By age 3 or 4,

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typically developing children can predict the behavior of others by reasoning about their mind
using mental state concepts, including desire/goal, perception, and emotion (Saxe, Carey, &
Kanwisher, 2004, p. 91) in conjunction with observable physical cues (e.g., body motions,
emotional expressions). This reasoning has been most commonly tested with false belief tasks
(Wimmer & Perner, 1983), where an individuals ability to explain an action related to an actors
belief is explored. The standard version of this test involves first-order belief questions,
involving the inference of one persons mental state. For instance, the location of an object is
changed without the protagonists knowledge, whereby his/her belief becomes false. The child is
asked questions concerning the protagonists belief regarding the objects location, to predict
where that person will look for the object, and to explain why the individual would do so. These
questions require individuals to focus on the actors belief, and not their own, in order to respond
correctly. False-belief tasks involving reasoning about embedded mental states are also used as a
measure of ToM. These second-order tasks involve attribution of the belief of another persons
belief, and are thus more complex.
The Theory of Mind Hypothesis of Autism
The impaired language and communication skills of individuals with autism lead to social
deficits, as evidenced in impaired social communication and pretend play. In 1985, BaronCohen, Leslie, and Frith put forth a model of autism. They suggested that these difficulties were
the result of failure of a specific cognitive mechanism underlying ToM abilities. Without the
ability to combine information from multiple sources, visual cues (where the individual is
pointing and looking) and verbal cues (what the individual is saying) cannot be effectively
utilized. Unable to infer the beliefs of others, autistic individuals are not able to predict the
behavior of others, and are thus at a social disadvantage. Baron-Cohen et al. believed that the

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majority of autistic children lacked the ability to form second-order representations, and those
who were able to do so, still suffering from social impairments, were qualitatively different from
both their typically developing peers and their autistic counterparts.
Though a Theory of Mind (ToM) deficit has been observed in individuals with AD in
numerous studies (e.g., Baron-Cohen et al., 1985; Castelli, Frith, Happ, & Frith, 2002),
neuroimaging studies over the past two decades examining ToM reasoning are sparse. The
development of functional magnetic resonance imaging (fMRI) brought the ability to observe
hemodynamic changes, which are then used to infer neural activity during task completion.
Using fMRI, researchers have been able to explore the brain regions involved during various
tasks to determine whether there a single underlying mechanism involved in two tasks (Saxe,
Carey, & Kanwisher, 2004) as well as differences between populations.
Imaging Studies
Complex information processing is required to understand the beliefs of others, and to
separate beliefs from reality (as in the false-belief task). Functional imaging studies in this area
have found that this information processing is supported by the integrated activity of frontal and
posterior brain areas. Studies exploring activation using false-belief stories and cartoons
(Gallagher et al., 2000; Saxe et al., 2003), inference of the knowledge and beliefs of Christopher
Columbus (Goel, Grafman, Sadato, & Hallett, 1995) and ToM in geometric shapes (Castelli et
al., 2002) all observed activation in the medial prefrontal cortex (mPFC), temporal poles and
superior termporal sulcus (STS).
Though it is agreed that theoretical thought involves an intricate network of cortical
regions, imaging studies have not always produced consistent results. Carrington and Bailey
(2009) reviewed existing ToM studies and found the mPFC and orbitofrontal cortices (OFC) to

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be most consistently identified, in 93% of studies (e.g., Happ et al., 1996; Gallagher et al.,
2000). The consistency of these findings has resulted in these areas being deemed critical for
ToM reasoning (Gallagher et al., 2000) and may play the dominant role in this system,
possessing top-down control over the other areas involved (Frith, 2003). Other common areas
revealed in their analysis were the anterior temporal lobe (including the amygdala), superior
temporal region, and anterior- and paracingulate cortices; identified in 38%, 50%, 55% and 58%
of studies respectively.
Though these differences may initially seem disparaging, they are likely the result of
methodological differences, including differences in the paradigm used (e.g., stories, cartoons,
games), mental states explored, and the associated language demands. Evidence for this possible
explanation is found in a study comparing a ToM story (verbal) and cartoon (visual) task in
typically developing adults. In this study, Gallagher et al. (2000) found overlap in activation of
the mPFC; in the visual task, BA8 was activated, while activity during the verbal task revealed
activity in BA8 and 9. These researchers believed that, as the tasks were not matched for
difficulty, the level of ToM reasoning necessary may have differed, accounting for the broader
region of activation. Some individuals with autism were able to pass simple ToM tasks in a study
by Happ (1994). However, they were unable to do so when the task involved higher levels of
mentalizing (e.g., white lies, double bluffs). Upon examination of those individuals, certain
trends emerged: They were generally older and had higher verbal skills than those who did not
pass the ToM tasks, and would qualify for a diagnosis of Asperger syndrome as opposed to AD.
A later study conducted in 1996 (Happ et al.) found that, though individuals with Aspergers
were successful on ToM tasks, they did not perform as well as controls. Scans revealed adjacent
cortical activity in the left mPFC when compared to controls, with activation of Brodmanns area

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(BA) 9/10 (compared to BA8/9). Though BA9/10 were activated in controls in this study, it was
to a lesser extent. Finally, in a study by Takeuchi, Harada, & Nishitani (2002), fMRI was used to
explore brain activation during a ToM story task compared to a physical story task in individuals
with autism and a control group. Where the controls showed dominant activation in the left
frontal lobe, individuals with autism showed diffuse activation in the bilateral frontal lobes, with
increased activation in the right hemisphere.
Taken together, these findings highlight the existence of an intricate neural network
responsible for normal ToM reasoning, and though all of these findings suggest a deficiency in
the cognitive system underlying ToM, results must be interpreted with caution. Until these
studies can be replicated using larger sample sizes, generalizability is questionable. Similarly,
given the heterogeneity of studies (e.g., methodology, population-base), comparison of findings
must be considered limited.
Limitations
Use of False-Belief Tasks
Debate exists whether success with false belief tasks is indicative of ToM reasoning or
whether it may be better explained as the result of the inhibitory demands placed on the child
(Saxe et al., 2004) as children must be able to inhibit the incorrect answer (the true location of
the object) to succeed in this task. In fact, children who possess better inhibitory control and
planning skills have been found more likely to pass these tests (Tager-Flusberg, 2007). Similarly,
Bloom and German (2000) believe that more than ToM is necessary to pass false belief tasks,
and that ToM is more complex than just passing a false belief task. Future studies would be well
served to find alternate measures of ToM to compare to existing findings to determine its
efficacy as measure of ToM.

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ToM in Autism
One explanation for autistic individuals passing ToM tasks is that these individuals do not
utilize the same cognitive system as their typically developing peers (Tager-Flusberg, 2007).
Instead, they may approach these problems as they would logical-reasoning tasks, using
language and reasoning as opposed to mental reasoning. Tager-Flusberg (2007) made a
distinction between a linguistically mediated theory of mind used by higher functioning autistic
individuals and the traditional ToM skills based on social insights. Support for this distinction
was found in Frith and Friths (2003) study that found activation in problem-solving cortical
areas in individuals with autism who successfully completed ToM tasks. Again, further
exploration is needed to confirm these findings, but this finding seems initially promising given
that it is higher functioning autistic individuals who have had success with ToM tasks.
Critical Areas
While neuroimaging studies have provided us with evidence of areas that are involved in
ToM tasks, they do not necessarily indicate that those areas are necessary for success in these
tasks. In addition, it may be possible that damage to one part of the system may not be sufficient
to affect ToM performance. One major assumption underlying all of these studies is that ToM
mechanisms are shared by all typically developing individuals. This may be too big an
assumption to make. Individual variations are apparent in the ability of members of the general
population to adapt their behavior based on the mental states they attribute to others. It is
possible that this reflects differences in strategies and/or differences in the underlying cognitive
areas used. Additionally, discrepant findings in the existing studies may reflect the fact that not
only can a brain region perform multiple cognitive functions, but the same cognitive function
could be performed by multiple regions, although the precise implementation of that function

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may vary from region to region (Carrington & Bailey, 2009, p. 2328). Combined with
methodological differences, this may account for some of the discrepant findings. More
importantly, though, it may reveal a potential flaw in the assumption underlying ToM research.
Generalizability
Existing studies are limited by their use of small sample sizes in cross-sectional designs,
calling into question the generalizability of their findings. Comparisons across studies are further
hindered by the heterogeneity in population and methodologies used. In addition, the majority of
existing research into ToM has been done with adult subjects. As the critical age range for the
development of ToM is 10-48 months (Saxe et al., 2004), future studies using pediatric
populations are needed to develop an understanding of this skill across development.
Regionality
Activation of the same brain area(s) in imaging studies is taken as an indirect measure of
the same mechanisms underlying two tasks. However, brain areas can measure over 10 square
centimeters (Saxe et al., 2004). As such, it is possible that the shared activation, assumed to
reflect a shared underlying mechanism, may actually be distinct a result of separate subregions.
Analyzing the results of individual subjects performing different tasks within the same scan can
help provide evidence that a shared brain region is involved. This relates to a further limitation of
most studies the use of group analyses. Averaging data across subjects can result in a blurring
of the data (Saxe et al., 2004, p. 92) as a result of physical and functional differences between
individuals. Again, future research addressing these areas of concern will be invaluable in
furthering our understanding of ToM processing.
Underconnectivity Theory of Autism

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Just, Cherkassky, Keller, & Minshew (2004) proposed a theory of autism whereby the
deficits exhibited by autistic individuals results from decreased functional connectivity in the
underlying neural system, resulting from lowered coordination and communication between
these neural areas. Deficits in social interactions, heavily reliant on the integration of information
from various sources, arise from this deficit in integration. This is consistent with suggestions
arising from the earlier work of Frith (2001), as well as findings from Castelli et al. (2002), Just
et al. (2006) and Kana et al. (2009) in support of this hypothesis individuals with autism may
experience ToM difficulties as a result of the underconnectivity between the frontal and posterior
regions involved in ToM. This theory of a deficit in integration of information processing may be
able to explain not only the ToM impairments, but also those of face processing, language and
executive function, and deserves further study.
Conclusion
Theory of mind is a complex information processing skill that relies on an intricate
cortical network. Though much remains to be learned about ToM in autistic individuals, it
appears that the social and communicative impairments experienced by these individuals can be
attributed to differences in this network. Establishing the underlying neural mechanisms and the
precise role each area plays in ToM is a task for future research. Existing imaging studies are in
their infancy and comparison and generalization of the evidence presented here must be
considered limited as a result of heavy reliance on false-belief tasks, small sample sizes and
differences in subject-base and methodology.

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References

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders
(4th ed., text rev.). Washington, DC: Author.
Baron-Cohen, S., Leslie, A. M., & Frith, U. (1985). Does the autistic child have a theory of
mind? Cognition, 21, 37-46. Retrieved from http://www.autismtruths.org/pdf/3
.%20Does%20the%20autistic%20child%20have%20a%20theory%20of%20mind_SBC
.pdf
Bird, C. M., Castelli, F., Malik, O., Frith, U., & Husain, M. (2004). The impact of extensive
medial frontal lobe damage on theory of mind and cognition. Brain, 127, 914-928. doi:
10.1093/brain/awh108
Bloom, P., & German, T. P. (2000). Two reasons to abandon the false belief task as a test of
theory of mind. Cognition, 77, 25-31. Retrieved from http://www.debralieberman.com
/downloads/courses/625/bloom_german_2000.pdf
Carrington, S. J., & Bailey, A. J. (2009). Are there theory of mind regions in the brain? A review
of the neuroimaging literature. Human Brain Mapping, 30, 2313-2335. doi:
10.1002/hbm.20671
Castelli, F., Frith, C., Happ, F., & Frith, U. (2002). Autism, Asperger syndrome and brain
mechanisms for the attribution of mental states to animated shapes. Brain, 125, 18391849. doi: 10.1093/brain/awf189
Frith, U. (2001). Mind Blindness and the brain in autism. Neuron, 32, 969-979. doi:
10.1016/S0896-6273(01)00552-9

THEORY OF MIND DEFICIT

11

Frith, U., & Frith, C. (2003). Development and neurophysiology of mentalizing. Philosophical
Transactions of the Royal Society London B Biological Sciences, 358, 459473. doi:
10.1098/rstb.2002.1218
Gallagher, H. L., Happ, F., Brunswick, N., Fletcher, P. C., Frith, U., & Frith, C. D. (2000).
Reading the mind in cartoons and stories: An fMRI study of theory of mind in verbal
and nonverbal tasks. Neuropsychologia, 38, 11-21. doi: 10.1016/S0028-3932(99)00053-6
Goel, V., Grafman, J., Sadato, N., & Hallett, M. (1995). Modeling other minds. NeuroReport, 6,
1741-1746. Retrieved from http://ovidsp.ovid.com.ezproxy.lib.ucalgary.ca/ovidweb
.cgi?ID=hkn001admin&CSC=Y&PASSWORD=hkn00199&SEARCH=%2209594965%22.is+and+%226%22.vo+and+%2213%22.ip+and+
%221741%22.pg&T=JS&D=ovft&NEWS=N&MODE=ovid&PAGE=fulltext
Happ, F. G. (1994). The role of age and verbal ability in the theory of mind task performance of
subjects with autism. Child Development, 66, 843-855. Retrieved from http://www.jstor
.org/stable/1131954
Happ, F. G., Ehlers, S., Fletcher, P., Frith, U., Johansson, M., Gillberg, C., Frith, C. (1996).
Theory of mind in the brain. Evidence from a PET scan study of asperger syndrome.
NeuroReport, 8, 197-201. Retrieved from http://sfxhosted.exlibrisgroup.com/calgary?ctx
_ver=Z39.88-2004&ctx_enc=info%3Aofi%2Fenc%3AUTF8&rfr_id=info:sid/summon
.serialssolutions.com&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.ati
tle=%27Theory+of+mind%27+in+the+brain.
+Evidence+from+a+PET+scan+study+of+Asperger+syndrome&rft.jtitle=Neuroreport&r
ft.au=Happ%2C+F&rft.au=Ehlers%2C+S&rft.au=Fletcher%2C+P&rft.au=Frith

THEORY OF MIND DEFICIT

12

%2C+U&rft.au=Johansson%2C+M&rft.au=Gillberg%2C+C&rft.au=Dolan
%2C+R&rft.au=Frackowiak%2C+R&rft.au=Frith%2C+C&rft .date=1996-1220&rft.issn=09594965&rft.volume=8&rft.issue=1&rft.spage=197&rft
_id=info:pmid/9051780&rft.externalDocID=9051780
Just, M. A., Cherkassky, V. L., Keller, T. A., Kana, R. K., & Minshew, N. J. (2006). Functional
and anatomical cortical underconnectivity in autism: Evidence from an fMRI study of an
executive function task and corpus callosum morphometry. Cerebral Cortex, 17, 951-961.
doi: 10.1093/cercor/bhl006
Just, M. A., Cherkassky, V. L., Keller, T. A., & Minshew, N. J. (2004). Cortical activation and
synchronization during sentence comprehension in high-functioning autism: evidence of
underconnectivity. Brain, 127, 1811-1821. doi: 10.1093/brain/awh199
Kana, R. K., Keller, T. A., Cherkassky, V. L., Minshew, N. J., & Just, M. A. (2009). Atypical
frontal-posterior synchronization of theory of mind regions in autism during mental state
attribution. Social Neuroscience, 4, 135-152. doi: 10.1080/17470910802198510
Levy, F. (2007). Theories of autism. Australian and New Zealand Journal of Psychiatry, 41, 859868. doi:10.1080/00048670701634937
Saxe, R., Carey, S., & Kanwisher, N. (2004). Understanding other minds: Linking developmental
psychology and functional neuroimaging. The Annual Review of Psychology, 55, 87-124.
doi: 10.1146/annurev.psych.55.090902.142044
Tager-Flusberg, H. (2007). Evaluating the theory-of-mind hypothesis of autism. Current
Directions in Psychological Science, 16, 311-315. Retrieved from http://www.bu.edu
/autism/files/2010/03/2007-HTF-ToM1.pdf

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Takeuchi, M., Harada, M., & Nishitani, H. (2002). Deficiency of theory of mind in autism
estimated by fMRI. International Congress Series, 1232, 737-740. doi:10.1016/S05315131(01)00821-4

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