Theory of Mind is the ability to infer other persons’ mental states and emotions. It is thought to have evolved as part of the human’s social brain and probably emerged as an adaptive response to increasingly complex primate social interaction.
Brüne and Brüne-Cohrs (2006) explore the ‘evolutionary cost’ of language evolution:
This sophisticated ‘metacognitive’ ability comes at an evolutionary cost, reflected in a broad spectrum of psychopathological conditions. Extensive research into autistic spectrum disorders has revealed that theory of mind may be selectively impaired, leaving other cognitive faculties intact. Recent studies have shown that observed deficits in theory of mind task performance are part of a broad range of symptoms in schizophrenia, bipolar affective disorder, some forms of dementia, ‘psychopathy’ and in other psychiatric disorders.
Now it’s fairly uncontroversial to assert that without the ability of theory of mind humans would have never evolved language (Sperber and Wilson, 2002). This is due to the fact that if one can’t attribute another to have a ‘mind’ like ones own, or assume that other minds hold different information to ones own then one would see little point in trying to share information. (I’m sorry for the amount of ‘ones’ in that sentence).
Sooo, it does not seem presumptuous to assume that people interested in the evolution of language should be interested in theory of mind, in fact for many years evolutionary linguists, psychologists and biologists have been looking into this, but mostly through observing the behaviour of animals, and especially primates to see if they display theory of mind capabilities. A good summary of this work can be found here, and a lot of relevant studies can be found on this blog in the What makes humans unique? posts by Michael. I’m not going to look at the animal data in this post, but instead what the deficiencies in some human conditions can tell us about the evolution of theory of mind. That is, what can autism, schizophrenia, bipolar affective disorder, dementia, ‘psychopathy’ and other psychiatric disorders tell us?
The manifestations of impaired theory of mind are so highly diverse between and within the conditions listed this can contribute to our knowledge of theory of mind. The different components which make up theory of mind can be demonstrated by using the resource of subjects with impaired theory of mind. These subjects can be analysed using both neuroimaging and genetic methods to work out the picture step by step of the faculties that ToM is made up from.
Studies have started to compile a list of the areas of the brain which make up the neural network involved in theory of mind. Abu-Akel (2003) attempts to account for the data observed from psychiatric and developmental disorders in one neurobiological model. He lists the areas of the brain involved as follows: the frontal lobes, the Superior Temporal Sulcus (STS), the anterior cingulate cortex (ACC), and the inferior parietal cortex.
Conditions such as autism have shown us that impaired theory of mind can occur because of genetic factors from birth as well as subjects with acquired brain lesions show us that it can also be secondarily impaired in individuals who had normal theory of mind abilities prior to the event (Stuss et al., 2001)
If one was to try to pin-point some of the genes involved in theory of mind it may get infinitely more complicated than working out the neurological areas involved. I feel, however, that when the technology is available it will through looking at patients with deficits in ToM that the specific mutations will be able to be pinpointed.
I also feel that patients with deficits such as these are underused in language evolution experiments in that laboratory experiments in language evolution are often criticised for the fact that they use modern humans which doesn’t tell us much about the abilities of earlier hominids. But in experiments in pragmatics people with varying abilities in ToM may be able to tell us more about the stages in which we evolved and the capabilities of early humans at these stages of evolution. This is a similar argument to that of the contributions that aphasiology can have to the field, Andreas Kyriacou did a talk at EvoLang in which he put forward the hypothesis that the biologically oldest capacities recruited for language processing are the least likely to suffer selective impairments from brain injuries as they presumably evolved pre-linguistically. Although this hypothesis is centred around capacities for grammar it would be interesting to see if it applied to the different aspects of theory of mind as well.
References
Abu-Akel, 2003. A neurobiological mapping of theory of mind, Brain Res. Rev. 43 , pp. 29–40.
Brüne and Brüne-Cohrs. 2006. Theory of mind—evolution, ontogeny, brain mechanisms and psychopathology. Neuroscience & Biobehavioral Reviews. Volume 30, Issue 4, Pages 437-455
Sperber and Wilson, 2002 . Pragmatics, modularity and mind-reading, Mind Lang. 17, pp. 3–23
Stuss et al., 2001. The frontal lobes are necessary for ‘theory of mind’, Brain 124, pp. 279–286.
I admit to not having read the links you provide, but from my personal experience (which I acknowledge may have no further meaning), but… my 25+ years dealing with brain injured people tells me that the injuries dealing with the most “modern” brain entities are the ones where language incapacity is most problematic.
The “older” the brain structure that is injured, the more likely the subject is to die or be incapable of verbal communication.
And that fits with the hypothesis!
Andreas Kyriacou said that the biologically ‘oldest’ capacities recruited for language processing are the least likely to suffer selective impairments from brain injuries, these impairments will be more serious or even fatal, indeed if damage to these areas occurs it is more likely not to be selective to a specific function and so will be more devasting to the overall language function. The more ‘modern’ linguistic capacities will be more likely to be selectively impaired and so language incapacity will be the most problematic in these cases, as you said.
Thanks for the comment.
I like the idea of using these types of patients in lang-evo lab experiments. It’s probably far too early to ask, but are you thinking of pursuing this for your MSc project? Anyway, on a semi-related note: Language as a window into sociability.
Interesting article. That reminds me of some iterated learning studies done by Alex Mesoudi where the they fed participants ‘stories’ with varying degrees of social or factual content to see which came out with the most details intact at the end.
Presumably if the same tests were done on individules with Williams syndrome these findings would be exaggerated, or with Autism, inverted.
R.e. my MSc project, I am getting increasingly fascinated by psychological disorders so I am interested in doing something along them lines, however it is quite early, I need to do a lot more reading/research and I’m not sure how easy it would be for an MSc student to have access to patients with disorders???
(Quote above is from Mesoudi, A. (2007). Using the methods of experimental social psychology to study cultural evolution. Journal of Social, Evolutionary & Cultural Psychology, 1(2), 35-58.)
I’m not sure how easy it would be for an MSc student to have access to patients with disorders???
I might be able to put you in contact with someone based in Edinburgh who managed to get access with, and run experiments on, patients with certain psychological disorders. I do remember him saying it was quite arduous to go through the whole ethics procedure etc. Also, I think he only managed to get about 7 patients…
I’m coming to this a bit late, via Dorothy Bishop’s work, but wanted to make a point about the way developmental disorders are construed. Theory of mind, like autism, dyslexia, SLI and many other developmental disorders, is a conceptual construct. These constructs are reliable, in that there is usually a high degree of agreement about the phenomena they map onto. They also have face validity, because the phenomena they map onto do exist in the real world. (Some people are unable to tell what other people are thinking, others have impaired social interaction and communication coupled with restricted and repetitive behaviours, some do have difficulty learning to read, and others do have difficulty with specific aspects of language acquisition without any obvious cause.)
However, that reliability and face validity does not mean that it’s safe to assume that everyone showing ToM impairments has the same underlying cause for the impairment. Nor that everyone diagnosed with autism has the same underlying cause for their autism. And so on. All the constructs listed above are impairments in highly complex sets of behaviours, so there are many possible ways for the complex behaviour in question to be disrupted.
For example; an important component of ToM is the ability to discriminate between different facial expressions and to associate those expressions with emotional states or likely actions. It’s been estimated that the prevalence of congenital prosopagnosia (difficulty in recognizing faces) might run at around 2.5% in a large population. People with face-recognition problems report, variously; not seeing faces as faces but as collections of facial features, being unable to recognize facial expressions, being unable to discriminate between some facial expressions, discriminating between facial expressions but not knowing what emotional state they are related to, or having no awareness of what another person might be experiencing in specific circumstances. In other words, one of the components of ToM is itself complex and can be subject to a range of different disruptions.
Also, the efficacy of ToM in a given individual is often measured in terms of ‘false belief’ tests. People vary widely as to how many levels of belief attribution they can handle, and the number of levels of belief attribution children can manipulate increases as they get older. A very young child might be able to cope with “Johnny is sad” (first-order belief). An older child might be able to cope with “ Billy thinks Johnny is sad” (second-order belief), then later “Billy’s mum thinks that Billy thinks Johnny is sad” (third-order belief). Make some of those beliefs false ones and you have a task that puts a considerable load on working memory, a component itself vulnerable to a variety of disruptions during development.
In order to find the genes responsible for ToM, one would need first to decompose the components of ToM to the simplest level possible, and to take into account the structural and physiological factors involved in the functioning of each component. This is not an intractably complex task, but does involve first asking precisely what we mean by ToM (and autism and dyslexia and SLI etc) and whether our current definitions are in fact unhelpfully complex.