From Wikipedia, the free encyclopedia
Jump to navigation Jump to search

Mind-blindness is a concept of a cognitive divergence where an individual is unable to attribute mental states to others. As a result of this kind of social[1] and empathetic cognitive phenomenon, the individual is incapable of putting themselves "into someone else's shoes" and cannot conceptualize, understand or predict knowledge, thoughts and beliefs, emotions, feelings and desires, behaviour, actions and intentions of another person.[2] Such an ability to develop a mental awareness of what is in the other minds is known as the theory of mind (ToM),[3] and the "mind-blindness" theory asserts that children who delay in this development often are or will be autistic.[4][5] In addition to autism, ToM and mind-blindness research has recently been extended to other fields such as schizophrenia, dementia, bipolar disorders, antisocial personality disorders as well as normal aging.[6]

Relevance and causes[edit]

Theory of mind[edit]

Mind-blindness is a state where the ToM has not been developed, or has been lost in an individual. According to the theory, ToM is implicit in neurotypical individuals. This enables one to make automatic interpretations of events taking into consideration the mental states of people, their desires and beliefs. Simon Baron-Cohen described how an individual lacking a ToM would perceive the world in a confusing and frightening manner, leading to a withdrawal from society.[7]

An alternative approach to the social impairment observed in mind-blindness focuses on the emotion of subjects. Based on empirical evidence, Uta Frith concluded that the processing of complex cognitive emotions is impaired compared to simpler emotions. In addition, attachment does not seem to fail in the early childhood of autistics. This suggests that emotion is a component of social cognition that is separable from mentalizing.[1]

Lombardo and Cohen updated the theory and pinpointed some additional factors that play an important part in ToM of autistic people. They highlighted that the middle cingulate cortex which is outside the traditional mentalizing region was underactive in autistic patients, while the rest of ToM activation was normal. This region was important in deciding how much to invest in a person and hence required mentalization.[8]

Biological basis[edit]

Neural correlates of the ToM point towards three regions of the brains. The anterior paracingulate cortex (Brodmann), is considered at the key region of mentalizing. It is located anterior corpus callosum and the anterior cingulate cortex. This cortex is associated with the medial frontal cortex where activation is associated with the mentalization of states. The cells of the ACC develops at the age of 4 months suggesting that the manifestations of mind-blindness may occur around this time.[2]

In addition to the anterior paracingulate cortex is the superior temporal sulcus and the temporal poles that are involved with the ToM and its nature. However, these areas are not uniquely associated with mentalization. They aid in the activation of the regions that are associated with the ToM. The superior temporal sulcus is involved in the processing of behavioural information while the temporal poles are involved in the retrieval of personal experiences. These are considered important regions for the activation of the ToM regions and are associated with the mind-blindness. The temporal poles provide personal experiences for mentalization such as facial recognition, emotional memory and familiar voices. In patients suffering from semantic dementia, the temporal regions of these patients undergo atrophy and lead to certain deficits which can cause mind-blindness.[2]

Superior temporal sulcus

The amygdala and the orbitofrontal cortex also are a part of the ToM. It is in involved in the interpretation of behaviour which plays an important role in social cognition and therefore contributes to the theory of the mind. It is suspected that the damage to the orbitofrontal cortex brings upon subtle impairments, but not a total loss of the ToM that would to mind-blindness.[2] Some studies[citation needed] have shown that the orbitofrontal cortex is not directly associated with the theory of the mind or mind-blindness. However, a study by Stone and colleagues were able to show impaired ToM on mentalisation tasks.[9]

Since the frontal lobe is associated with executive function, researchers theorize that the frontal lobe plays an important role in ToM and its associated nature. It has also been suggested that the executive function and the theory of mind share the same regions.[10] Despite the fact that ToM and mind-blindness can explain executive function deficits, it is argued that autism is not identified with the failure of the executive function.[11]

Lesion studies show that when lesions are imposed to the medial frontal lobe, performance on mentalization tasks is reduced, similar to typical mind-blindness cases.[12] Patients that experienced frontal lobe injuries due to severe head trauma showed signs of mind blindness, as a result of a lost ToM. However, it is still debated whether the inactivation of the medial frontal lobe is involved in mind-blindness.[13]

Frith and Frith proposed that a neural network that comprised the medial prefrontal cortex, the anterior cingulate cortex and the STS, is crucial for the normal functioning of ToM and self monitoring. This so formed dorsal system is crucial for social cognition. Disruption of this neural network leads to mind-blindness in schizophrenic individuals.[14]

Another clue towards a possible explanation of mind-blindness in autistics was done by Castelli and colleagues. They were able to show that the connectivity between occipital and the temporo-parietal regions were weaker in the autistic group than the control group. The under activation of this network may inhibit the interactive influences between regions that process higher and lower perceptual items.[1]

Relationship to diagnostic criteria[edit]

Relationship to autism[edit]

Mind-blindness is usually associated with autistic people. Lower performance on the mentalization tasks were the first screening task used to diagnose the autism, with a good prediction level.[1]

Cohen proposed the mind-blindness theory of autism as "deficits in the normal process of empathising". He described empathising to include the ToM, mind reading and taking an intentional stance. According to this view empathising includes the ability to attribute mental states and to react in an appropriate emotional manner which is appropriate to another's mental state. More deficits tend to occur in reference to one's own mental states compared to the other's mental states. It has been proposed that autistic people undergo a specific developmental delay in the area of metarepresentational development. The delay facilitates mind-blindness.[15]

There is some evidence that suggests that certain patients develop a rudimentary ToM and do not suffer from complete lack of ToM causing mind-blindness.[15] A study by Bowler concluded that mind-blindness and social impairment is not as straightforward as previously thought. It showed that a complete possession of ToM was not enough to protect from social impairments in autistic people. Conversely the absence or impairment of the ToM that leads to mind-blindness does not lead to social impairments.[16]

The social and cognitive differences seen in autistic people are often attributed to mind blindness. Abnormal behaviour of autistic children is perceived to include a lack of reciprocity. Some cases in which mind-blindness manifests includes the child being totally withdrawn from social settings as well as not being able to make eye contact, while in other cases the individual may attempt to interact with other people. However, global asocial behaviour is not the rule in autism. Cohen described the cognitive/mind-blindness effects in autistic people as a "triad of deficits." The triad consists of deficits in social, communication and imagination of others' minds.[15]

Ozonoff and colleagues were able to discriminate between autistic people diagnosed with Asperger's syndrome and other autistic people by their ability to solve ToM tasks. It is because those diagnosed with AS seem more neurotypical in early childhood development. The siblings of individuals diagnosed with AS were shown to have a lesser variant of ToM deficits. This shows that the cognitive deficits affecting ToM play a central role in the phenotype expressed in AS diagnoses.[17]

Relationship to schizophrenia[edit]

People with schizophrenia also show deficits associated with mind-blindness.[3] However, there is an ongoing debate as to whether individuals with schizophrenia have an impaired ToM leading to mind-blindness or display an exaggerated ToM. Unlike autism, schizophrenia is a late onset condition. It is speculated that this difference in the condition may account for differences seen in the ToM abilities.[18] Brain lesion studies show that there are differences seen in the laterality of brain that account for mind-blindness. It is unknown whether the ToM in schizophrenia deteriorates in the affected person as the condition progresses.[6]

The cognitive impairment linked to mind-blindness is best explained by a modular theory; the domain specific capabilities that account for mindreading and mentalization are lost in schizophrenia. Furthermore, Frith has predicted that the extent of mind-blindness depends on whether the objective/behavioural or subjective symptoms of ToM abilities prevail.[1] Patients with the behavioural symptoms perform the poorest in ToM tasks, similar to autistic subjects, while patients displaying subjective/experiential symptoms have a ToM. However, these patients are impaired in using contextual information to infer what these mental states are.[6]


The mind-blindness theory helps to explain the impairment in the social development of individuals as well as the impairment in the communication skills of autistics. However one of the most important limitations of this theory is that it is unable to explain the highly repetitive behaviours which is a characteristic trait attributed to autistic people. This triad is explained through the process of systemising.[15] The theory also did not account for the motor problems and the superior rote memory skills that were associated with autism.[1] These aspects along with the highly repetitive behaviours formed the triad of strengths. Simon Baron-Cohen himself has acknowledged that the theory, while adept at explaining the communications difficulties experienced by autistic people, fails to explain such patients' penchants for narrowly defined interests, an important step to proper diagnosis. Furthermore, mind-blindness seems decidedly non-unique to autistic people, since conditions ranging from schizophrenia to various narcissistic personality disorders and/or anti-social personality disorders all exhibit mind-blindness to some degree.[4]

Another issue associated with the mind-blindness theory is that researchers are unable to predict whether the social deficits are a primary or secondary result of mind-blindness. In addition, Klin and his fellow researchers highlighted another limitation that was that the mind-blindness theory failed to delineate whether the ToM deficits are a generalised deficit or a specific discrete of a mechanism.[19] Stuart Shanker also argued in favour of Klin's argument, that a major part of the mind-blindness theory depicts the ToM as an autonomous cognitive capacity compared to being part of a more general ability for reflective thinking and empathy.[20]

A boy with autism, obsessively stacking cans.

Other researchers have pointed out the inherent flaws of assuming autistic traits develops from a "theory of mind" deficit, pointing out that this presupposes autistic traits derives from a single, core insufficiency within the brain. This contrasts, they say, with the very same researchers' description of autism as a "puzzle", which implies a far more diverse range of causes than a single, unifying theory.[21]

Many have also pointed out that Mind-blindness wrongly categorizes autism as a problem to be fixed, rather than a condition to be accommodated. This assumes an inherent lack of intelligence in autistic people, which ignores the nuanced view of intelligence (as in varying types of intelligence) that has been observed in cognitive research.[21]

The drawbacks in the Mind-blindness theory of autistic people paved way for the E-S theory which helps to explain the observations seen in these individuals. The E-S theory accounts for both the triad of deficits which is the loss of empathising and the triad of strengths is related to hyper systemisation of certain behaviours. The theory also helps to explain the exaggerated male spectrum termed as the extreme male behavior.[22]

See also[edit]


  1. ^ a b c d e f Frith, Uta (20 December 2001). "Mind Blindness and the Brain in Autism". Neuron. 32 (6): 969–979. doi:10.1016/S0896-6273(01)00552-9. PMID 11754830.
  2. ^ a b c d Gallagher, Helen L.; Frith, Christopher D. (1 February 2003). "Functional imaging of 'theory of mind'". Trends in Cognitive Sciences. 7 (2): 77–83. doi:10.1016/S1364-6613(02)00025-6. PMID 12584026.
  3. ^ a b Pijnenborg et al. (June 2013). "Insight in schizophrenia: associations with empathy". European Archives of Psychiatry and Clinical Neuroscience. 263 (4): 299–307. doi:10.1007/s00406-012-0373-0. PMID 23076736.
  4. ^ a b Baron-Cohen, Simon (25 March 2009). "Autism: The Empathizing-Systemizing (E-S) Theory". Annals of the New York Academy of Sciences. 1156, The Year in Cognitive Neuroscience: 68–80. doi:10.1111/j.1749-6632.2009.04467.x. PMID 19338503.
  5. ^ Jurecic, Ann (Spring 2006). "Mindblindness: Autism, Writing, and the Problem of Empathy". Literature and Medicine. 25 (1): 1–23. doi:10.1353/lm.2006.0021.
  6. ^ a b c Brune, M. (1 January 2005). ""Theory of Mind" in Schizophrenia: A Review of the Literature". Schizophrenia Bulletin. 31 (1): 21–42. doi:10.1093/schbul/sbi002. PMID 15888423.
  7. ^ Baron-Cohen, Simon (1990). "Autism: a specific cognitive disorder of 'mind-blindness". International Review of Psychiatry. 2 (1): 81–90. doi:10.3109/09540269009028274.
  8. ^ Lombardo, Michael V.; Baron-Cohen, Simon (1 March 2011). "The role of the self in mindblindness in autism". Consciousness and Cognition. 20 (1): 130–140. doi:10.1016/j.concog.2010.09.006. PMID 20932779.
  9. ^ Stone, V.E.; Baron-Cohen, S.; Knight, R.T. (September 1998). "Frontal lobe contributions to the theory of mind". Journal of Cognitive Neuroscience. 10 (5): 640–656. doi:10.1162/089892998562942. PMID 9802997.
  10. ^ Josef Perner & Birgit Lang (1 September 1999). "Development of theory of mind and executive control". Trends in Cognitive Sciences. 3 (9): 337–344. doi:10.1016/s1364-6613(99)01362-5. PMID 10461196.
  11. ^ Carruthers, Peter (1996). "Chapter 16. Autism as Mind-Blindness: an elaboration and partial defence (pp. 257 ff.)". In Carruthers, Peter; Smith, Peter K. (eds.). Theories of Theories of Mind. Cambridge University Press. ISBN 978-0-521-55916-4.
  12. ^ Havet-Thomassin, P. Allain, F. Etcharry-Bouyx, & D. le Gall (2006). "What about theory of mind after severe brain injury?". Brain Injury. 20 (1): 83–91. doi:10.1080/02699050500340655. PMID 16403703.CS1 maint: Uses authors parameter (link)
  13. ^ Bird, C. M. (14 January 2004). "The impact of extensive medial frontal lobe damage on 'Theory of Mind' and cognition". Brain. 127 (4): 914–928. doi:10.1093/brain/awh108. PMID 14998913.
  14. ^ Frith, Uta; Frith, C.D (October 2001). "The biological basis of social interaction". Current Directions in Psychological Science. 10 (5): 151–155. doi:10.1111/1467-8721.00137.
  15. ^ a b c d Baron-Cohen, S. (1 July 2004). "The cognitive neuroscience of autism". Journal of Neurology, Neurosurgery, and Psychiatry. 75 (7): 945–948. doi:10.1136/jnnp.2003.018713. PMC 1739089. PMID 15201345.
  16. ^ Bowler, Dermont. M. (July 1992). "Theory of Mind in Asperger's syndrome". Journal of Child Psychology and Psychiatry. 33 (5): 877–893. doi:10.1111/j.1469-7610.1992.tb01962.x.
  17. ^ Ozonoff, S; Rogers, S. & Pennington, B. (November 1991). "Asperger's syndrome: Evidence for an empirical distinction from high-functioning autism". Journal of Child Psychology and Psychiatry. 32 (7): 1107–1122. doi:10.1111/j.1469-7610.1991.tb00352.x.CS1 maint: Multiple names: authors list (link)
  18. ^ Langdon, Robyn (2007) [2005]. "Chapter 21. Theory of Mind in Schizophrenia (pp. 323 ff.)". In Malle, Bertram F.; Hodges, Sara D. (eds.). Other Minds. How Humans Bridge the Divide Between Self And Others. New York City: Guilford Press. ISBN 978-1-593-85468-3.
  19. ^ Klin, Ami., Folkmar, Fred R., Sparrow, Sara S. (July 1992). "Autistic Social Dysfunction: Some limitations of the Theory of Mind hypothesis". Journal of Child Psychology and Psychiatry. 33 (5): 861–876. doi:10.1111/j.1469-7610.1992.tb01961.x.CS1 maint: Multiple names: authors list (link)
  20. ^ Shanker, S. (1 October 2004). "The Roots of Mindblindness". Theory & Psychology. 14 (5): 685–703. doi:10.1177/0959354304046179.
  21. ^ a b Smukler, David (February 2005). "Unauthorized Minds: How 'Theory of Mind' Theory Misrepresents Autism". Mental Retardation. 43 (1): 11–24. doi:10.1352/0047-6765(2005)43<11:UMHTOM>2.0.CO;2. PMID 15628930.
  22. ^ Baron-Cohen, S.; Knickmeyer, Rebecca S.; Belmonte, Mathew S. (4 November 2005). "Sex Differences in the Brain: Implications for Explaining Autism". Science. 310 (5749): 819–823. doi:10.1126/science.1115455. PMID 16272115.


  • Geoffrey Cowley, "Understanding Autism," Newsweek, July 31, 2000.
  • Simon Baron-Cohen, "First lessons in mind reading," The Times Higher Education Supplement, July 16, 1995.
  • Suddendorf, T., & Whiten, A. (2001). "Mental evolution and development: evidence for secondary representation in children, great apes and other animals." Psychological Bulletin, 629–650.