In Mindblindness, Simon Baron-Cohen presents a model of the evolution and development of "mindreading." He argues that we mindread all the time, effortlessly, automatically, and mostly unconsciously. It is the natural way in which we interpret, predict, and participate in social behavior and communication. We ascribe mental states to people: states such as thoughts, desires, knowledge, and intentions. Building on many years of research, Baron-Cohen concludes that children with autism, suffer from "mindblindness" as a result (...) of a selective impairment in mindreading. For these children, the world is essentially devoid of mental things. Baron-Cohen develops a theory that draws on data from comparative psychology, from developmental, and from neuropsychology. He argues that specific neurocognitive mechanisms have evolved that allow us to mindread, to make sense of actions, to interpret gazes as meaningful, and to decode "the language of the eyes." A Bradford Book. (shrink)

We use a new model of metarepresentational development to predict a cognitive deficit which could explain a crucial component of the social impairment in childhood autism. One of the manifestations of a basic metarepresentational capacity is a ‘ theory of mind ’. We have reason to believe that autistic children lack such a ‘ theory ’. If this were so, then they would be unable to impute beliefs to others and to predict their behaviour. This hypothesis was tested using Wimmer (...) and Perner’s puppet play paradigm. Normal children and those with Down’s syndrome were used as controls for a group of autistic children. Even though the mental age of the autistic children was higher than that of the controls, they alone failed to impute beliefs to others. Thus the dysfunction we have postulated and demonstrated is independent of mental retardation and specific to autism. (shrink)

An examination of the controversial "theory of mind" hypothesis, which states that children with autism are unable to comprehend other people's mental states. The theory relates to the most fundamental questions of normal development as well as to autism i.

Why do children with autism have such trouble developing normal social understanding of other people's feelings? This new edition updates the field by linking autism research to the newest methods for studying the brain.

We take a fresh look at emotion recognition in autistic children, by testing their recognition of three different emotions (happy, sad, and surprise). The interest in selecting these is that whereas the first two are typical “simple” emotions (caused by situations), the third is typically a “cognitive” emotion (caused by beliefs). Because subjects with autism have clear difficulties in understanding beliefs, we predicted they would show more difficulty in recognising surprise. In contrast, as they have no difficulty in understanding situations (...) as causes of emotion, we predicted they would not show deficits in recognising happy and sad. These predictions were borne out, in a comparison with a group of normal children and in a group of subjects with mental handicap. This result shows the importance of fine-grain analysis in emotion-recognition tasks, and is discussed in relation to affective and theory of mind models of autism. (shrink)

A total of 378 mathematics undergraduates (selected for being strong at “systemizing”) and 414 students in other (control) disciplines at Cambridge University were surveyed with two questions: (1) Do you have a diagnosed autism spectrum condition? (2) How many relatives in your immediate family have a diagnosed autism spectrum condition? Results showed seven cases of autism in the math group (or 1.85%) vs one case of autism in the control group (or 0.24%), a ninefold difference that is significant. Controlling for (...) sex and general population sampling, this represents a three- to sevenfold increase for autism spectrum conditions among the mathematicians. There were 7 of 1,405 (or 0.5%) cases of autism in the immediate families of the math group vs 2 of 1,669 (or 0.1%) cases in the immediate families of the control group, which again is a significant difference. These results confirm a link between autism and systemizing, and they suggest this link is genetic given the association between autism and first-degree relatives of mathematicians. (shrink)

Cognitive developmentalists have had a long-standing interest in neurodevelopmental conditions, such as autism. This is not only out of a desire to understand the causes of such atypical development, in order to advance medical science and develop interventions. It is also because studying the processes that cause atypicality can sometimes throw light on typical development. It is this two-way influence that characterises the field of developmental psychopathology. In this chapter, we focus on autism. We bring out this interaction between what (...) we now understand about autistic cognition, and how this has helped us understand ‘normality’. (shrink)

Most scientists and theorists concerned with the problem of consciousness focus on our consciousness of the physical world (our sensations, feelings, and awareness). In this paper I consider our consciousness of the mental world (our thoughts about thoughts, intentions, wishes, and emotions).The argument is made that these are two distinct forms of consciousness, the evidence for this deriving from studies of autism. Autism is a severe childhood psychiatric condition in which individuals may be conscious of the physical world but not (...) of the mental world. Relevant experimental evidence is described, including some recent neuroimaging studies pointing towards the neural basis of our consciousness of the mental. (shrink)

Extreme conditions like savantism, autism or synaesthesia, which have a neurological 2AH, UK basis, challenge the idea that other minds are similar to our own. In this paper we report a single case study of a man in whom all three of these conditions co-occur. We suggest, on the basis of this single case, that when savantism and synaesthesia co- occur, it is worthwhile testing for an undiagnosed Autism Spectrum Condition (ASC). This is because savantism has an established association with (...) ASC, and the combination of ASC with synaesthesia may increase the likelihood of savantism. The implications of these conditions for philosophy of mind are introduced. (shrink)

Since its inception the ‘mindblindness’ theory of autism has greatly furthered our understanding of the core social-communication impairments in autism spectrum conditions . However, one of the more subtle issues within the theory that needs to be elaborated is the role of the ‘self’. In this article, we expand on mindblindness in ASC by addressing topics related to the self and its central role in the social world and then review recent research in ASC that has yielded important insights by (...) contrasting processes relating to both self and other. We suggest that new discoveries lie ahead in understanding how self and other are interrelated and/or distinct, and how understanding atypical self-referential and social-cognitive mechanisms may lead to novel ideas as to how to facilitate social-communicative abilities in ASC. (shrink)

Barresi & Moore contrast two theories of autism: (1) in autism there is a general inability to integrate first and third person information (of any kind), and (2) in autism there is a specific inability to represent an agent's perceptual or volitional mental state being about another agents mental state. Two lines of experimental evidence suggest that the first of these is too broad, favoring instead the more specific “theory of mind” account.

Howe et al. suggest that most talents can be explained in terms of practice and other environmental effects, and only exceptionally by innate factors. This commentary provides an illustration of one such exception: performance on the Embedded Figures Test by people with autism and their relatives.

The shared circuits model (SCM) is a bold attempt to explain how humans make sense of action, at different levels. In this commentary we single out five concerns: (1) the lack of a developmental account, (2) the absence of double-dissociation evidence, (3) the neglect of joint attention and joint action, (4) the inability to explain discrete emotion perception, and (5) the lack of predictive power or testability of the model. We conclude that Hurley's model requires further work before it could (...) be seen as an improvement over earlier models. (shrink)

We begin this chapter with a review of the history of synaesthesia and a comparison of what we consider to be either genuine or inauthentic manifestations of the phenomenon. Next, we describe the creation and development of synaesthetic consistency tests and explore reasons why assessing consistency became the most widely used method of confirming the genuineness of synaesthesia. We then consider methodologies that demonstrate synaesthesia's authenticity by capitalizing on properties other than consistency. Finally, we discuss how together, consistency tests and (...) other methodologies are helping researchers determine prevalence and elucidate the mechanisms of synaesthesia. (shrink)

Functionalism offers an account of the relations that hold between behavioural functions, information and neural processing, and conscious experience from which one can draw two inferences: for any discriminable difference between qualia there must be an equivalent discriminable difference in function; and for any discriminable functional difference within a behavioural domain associated with qualia, there must be a discriminable difference between qualia. The phenomenon of coloured hearing synaesthesia appears to contradict the second of these inferences. We report data showing that (...) this form of synaesthesia is genuine and probably results from an aberrant projection from cortical language areas to a region specialized for the perception of colour. Since functionalism purports to be a general account of consciousness, one such negative instance, if it can be further sustained empirically, is sufficient to invalidate it. (shrink)

If each of the subtypes of autism is defined simply as constituted by a set of symptoms, then the criteria for its observation are straightforward, although, of course, some of those symptoms themselves might be hard to observe definitively. Compare with telling whether or not someone is bleeding: while it might be hard to tell if someone is bleeding internally, we know what it takes to find out, and when we have the right access and instruments we can settle the (...) issue. But matters are not so simple for the autism subtypes. For one thing, how do we settle which symptoms to group together under one heading? One key difference between “autism disorder” and “Asperger’s disorder” is that the former exhibit language delays (sometimes extreme), whereas the latter do not. But is that a sign of genuinely distinct conditions or is that an artifact of the distinct groups of subjects that Leo Kanner and Hans Asperger worked with? And in general, although there are certainly types of behavior that are taken to be indicative of autism, none by itself is taken by diagnosticians to be either necessary or sufficient for a definitive diagnosis for any of the autism subtypes. What is the diagnostician to do? This is not merely an academic issue, as many parents can attest. Are we in a situation, then, that each practitioner has his or her own “pet” signs that are the “real keys” to the diagnosis? That would suggest that the term “autistic” might meet the fate of the outdated term “neurotic,” which turned out to be a pseudo-scientific term for an inexact clumping together of unrelated phenomena. The assumption amongst specialists seems to be that we will reach the point with "autism" that we have with "water": there will be a root essence to autism whose presence or absence settles a diagnosis. If that is to be the case, however, we have to settle the level of application of the concept. Does the term apply to people who exhibit particular behaviors? Or is it possible to exhibit “autistic” behaviors without actually being autistic, because autism is instead a particular feature of the mind (as, for example, in Baron-Cohen’s “impaired theory of mind module” theory, discussed below) which usually but not necessarily has behavioral effects? Or is autism located instead in the brain, perhaps in damage to key areas, which in turn would typically have an effect on modules of the mind? Or perhaps autism is located in genetics or biology, so that some people with damage to the brain caused by accidents so that they exhibit autistic symptoms would not actually be autistic. Conversely, supposing one had an “autistic brain” but showed none of (or not a sufficient number of) the symptoms, would one not be autistic? The assumption is that the genotypes and phenotypes will line up neatly, but if they do not, what happens to the concept “autistic?” (There is an analogy in the philosophy of sex and gender: androgen insensitive individuals tend to self-identify as female and have outward female traits, but have XY chromosomes—should we go with chromosomes or self-identity in assigning sex category?) Finally, the implications for these complications for diagnosis and categorization, with the attendant social and medical implications is discussed. The typical assumption of the medical profession is that autism cannot be “cured.” That assumes that autism is not simply the symptoms. However, at the same time, the tests used to diagnose ASDs work simply from the symptoms (for example, Baron-Cohen’s Sally/Anne test, which ASD children of a certain age almost all fail, but which practically no ASD adult fails). This implies an inherent confusion over the status of the concept. I conclude that attempts to make sense of some true or accurate summary of what it is to be autistic (such as one would find in the DSM) are almost certainly misguided and will vanish into history along with “neurotic.” But as with racial terms, which are similarly shifting and perverse, the term has already passed into the public sphere and will have a lasting and dangerous influence beyond its short scientific shelf-life. (shrink)

The fifth edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) was published in 2013 containing the following changes from the previous edition: gone are the subcategories ‘Autistic Disorder,’ ‘Asperger Syndrome’ and ‘PDD-NOS,’ replaced by the single diagnosis ‘Autism Spectrum Disorder,’ and there is a new category ‘Social Communication Disorder.’ In this paper I consider what kind of reasons would justify these changes if one were (a) a realist about autism, or (b) one were a constructivist. I explore (...) various analyses of autism in the research literature that portray it as essentially either a psychological, neurological or genetic phenomenon, and discuss these by reference to the diagnostic criteria and by analogy with the way we understand race and sex categories. I conclude that no realist reasons are available to justify the changes in the diagnostic criteria, and further, that the only way the changes could be justified is if one takes the position that the DSM categories are social constructs. I conclude by exploring what implications follow from this. (shrink)

This book examines autism from the tradition of analytic philosophy, working from the premise that Autism Spectrum Disorders raise interesting philosophical questions that need to be and can be addressed in a manner that is clear, jargon-free, and accessible. The goal of the original essays in this book is to provide a philosophically rich analysis of issues raised by autism and to afford dignity and respect to those impacted by autism by placing it at the center of the discussion.

Reappraisal is an adaptive emotion regulation strategy associated with favourable mental health outcomes. It is unclear whether the adaptive outcomes of habitual reappraisal are associated with better implementation of reappraisal when faced with negative affective situations. The current study aimed to examine whether habitual reappraisal predicts the implementation of instructed reappraisal and to evaluate the potential moderating effects of situational factors, namely – emotional intensity and reappraisal affordance. To address this question, 100 participants reported their habitual reappraisal tendency and were (...) asked to imagine themselves in different hypothetical interpersonal situations. Participants rated emotional intensity levels and reappraisal affordance for each situation, followed by instructions to implement reappraisal. Implementation success was measured by self-reported affect pre-and-post-implementation. Results indicated that habitual reappraisal was associated with greater reappraisal implementation success. While higher intensity scores predicted greater reappraisal implementation success, intensity did not moderate the association between habitual reappraisal and reappraisal implementation success. Reappraisal affordance did not predict reappraisal implementation success, nor did it moderate the association between habitual reappraisal and reappraisal implementation success. Our findings suggest that individual-centred factors play a significant role in reappraisal implementation success, while the effects of situation-centred factors demand further investigation. (shrink)

The professor of psychopathology Simon Baron-Cohen claims that males are on average stronger at systematizing than empathizing and females are on average stronger at empathizing than systematizing. Systematizing is defined as the drive to construct or understand systems. In this paper, I observe that Baron-Cohen overlooks certain examples of systems, examples which lead to doubts about his claim.

The professor of psychopathology Simon Baron-Cohen is well-known for his thesis that males are on average better at systematizing than empathizing and females are on average better at empathizing than systematizing. In this paper, I note an ambiguity in how he defines systematizing.