Autism

What does it take to see how autistic people participate in social interactions? And what does it take to support and invite more participation? Western medicine and cognitive science tend to think of autism mainly in terms of social and communicative deficits. But research shows that autistic people can interact with a skill and sophistication that are hard to see when starting from a deficit idea. Research also shows that not only autistic people, but also their non-autistic interaction partners can (...) have difficulties interacting with each other. To do justice to these findings, we need a different approach to autistic interactions—one that helps everyone see, invite, and support better participation. I introduce such an approach, based on the enactive theory of participatory sense-making and supported by insights from indigenous epistemologies. This approach helps counteract the homogenising tendencies of the “global mental health” movement, which attempts to erase rather than recognise difference, and often precludes respectful engagements. Based in the lived experiences of people in their socio-cultural-material and interactive contexts, I put forward an engaged—even engaging—epistemology for understanding how we interact across difference. From this perspective, we see participatory sense-making at work across the scientific, diagnostic, therapeutic, and everyday interactions of autistic and non-autistic people, and how everyone can invite and support more of it. (shrink)

I use critical phenomenological resources in Tetsurō Watsuji and Sarah Ahmed to explore the spatial origin of some social impairments in Autistic Spectrum Disorder (ASD). I argue that a critical phenomenological perspective puts pressure on the idea that social impairments in ASD are exclusively (or even primarily) neurocognitive deficits that can be addressed by focusing on cognitive factors internal to the autistic person — for example, training them to adopt a more neurotypical approach to social cognition. Instead, I argue that (...) the structure and character of some neurotypical spaces may play a regulative role in shaping aspects of at least some of the social impairments autistic people exhibit when they inhabit these spaces. I also briefly consider some possible therapeutic applications of this critical phenomenological approach. (shrink)

This chapter canvases a number of ways that issues surrounding disability intersect with social epistemology, particularly how dominate norms concerning communication and ability can epistemically disadvantage some disabled individuals. We begin with a discussion of how social epistemology as a field and debates concerning epistemic injustice in particular fail to take the problem of ableism seriously. In section two, we analyze the concept of an individual’s “knowledge capacity,” arguing that it can easily misconstrue the extended, social nature of both knowledge (...) and capacity/ability. In section three, we turn to issues of testimony and their relation to debates concerning disability and well-being. We address how the regular lack of uptake of disabled people’s testimony can lead to a number of structural rather than merely individual epistemic injustices, and we also consider how the very nature of some disabilities make testimonial issues more complicated. In our fourth and final section, we discuss various norms of social interaction and how they can systematically disadvantage Autistic people in particular. (shrink)

Synesthesia literally means a “union of the senses” whereby two or more of the five senses that are normally experienced separately are involuntarily and automatically joined together in experience. For example, some synesthetes experience a color when they hear a sound, although many instances of synesthesia also occur entirely within the visual sense. In this paper, I first mainly engage critically with Sollberger’s view that there is reason to think that at least some synesthetic experiences can be viewed as truly (...) veridical perceptions, and not as illusions or hallucinations. Among other things, I explore the possibility that many forms of synesthesia can be understood as experiencing what I will call “second-order secondary properties,” that is, experiences of properties of objects induced by the secondary qualities of those objects. In doing so, I shed some light on why synesthesia is typically one-directional and its relation to some psychopathologies such as autism. (shrink)

Background Genomic research on neurodevelopmental disorders (NDDs), particularly involving minors, combines and amplifies existing research ethics issues for biomedical research. We performed a review of the literature on the ethical issues associated with genomic research involving children affected by NDDs as an aid to researchers to better anticipate and address ethical concerns. Results Qualitative thematic analysis of the included articles revealed themes in three main areas: research design and ethics review, inclusion of research participants, and communication of research results. Ethical (...) issues known to be associated with genomic research in general, such as privacy risks and informed consent/assent, seem especially pressing for NDD participants because of their potentially decreased cognitive abilities, increased vulnerability, and stigma associated with mental health problems. Additionally, there are informational risks: learning genetic information about NDD may have psychological and social impact, not only for the research participant but also for family members. However, there are potential benefits associated with research participation, too: by enrolling in research, the participants may access genetic testing and thus increase their chances of receiving a (genetic) diagnosis for their neurodevelopmental symptoms, prognostic or predictive information about disease progression or the risk of concurrent future disorders. Based on the results of our review, we developed an ethics checklist for genomic research involving children affected by NDDs. Conclusions In setting up and designing genomic research efforts in NDD, researchers should partner with communities of persons with NDDs. Particular attention should be paid to preventing disproportional burdens of research participation of children with NDDs and their siblings, parents and other family members. Researchers should carefully tailor the information and informed consent procedures to avoid therapeutic and diagnostic misconception in NDD research. To better anticipate and address ethical issues in specific NDD studies, we suggest researchers to use the ethics checklist for genomic research involving children affected by NDDs presented in this paper. (shrink)

Several theories propose that one of the core functions of inner speech (IS) is to support subjects in the completion of cognitively effortful tasks, especially those involving executive functions (EF). In this paper we focus on two populations who notoriously encounter difficulties in performing EF tasks, namely, people diagnosed with schizophrenia who experience auditory verbal hallucinations (Sz-AVH) and people within the Autism Spectrum Conditions (ASC). We focus on these two populations because they represent two different ways in which IS can (...) fail to help in EF tasks, which can be illustrative for other mental conditions. First, we review the main components of EF (Section 1). Then we explain the functions that IS is taken to perform in the domain of EF (Section 2) and review the evidence concerning problems about EF in the two populations of our study: Sz-AVH (Section 3) and ASC (Section 4). After this we further detail our account about what a properly functioning IS can do for both populations and how different IS profiles may impact EF performance: in the case of Sz-AVH, the uncontrolled and intrusive character of IS negatively affects EF performance, whereas in ASC, EF is not sufficiently supported by IS, given the tendency in this population to present a diminished use of IS (Section 5). We finally briefly discuss Attention Deficit/Hyperactivity Disorder (ADHD) and Developmental Language Disorders (DLD). (shrink)

One way to determine whether a mental condition should be considered a disorder is to first give necessary and sufficient conditions for something to be a disorder and then see if it meets these conditions. But this approach has been criticized for begging normative questions. Concerning autism, a neurodiversity movement has arisen with essentially two aims: advocate for the rights and interests of individuals with autism, and de-pathologize autism. We argue that denying autism’s disorder status could undermine autism’s exculpatory role (...) in cases where individuals with autism are charged with a crime. Our argument raises a dilemma for the neurodiversity movement: advocating for the rights and interests of individuals with autism may require viewing autism as a condition that can be inherently disabling. If this is right, autism’s disorder status might be maintained without deriving this result from any general account of disorder. (shrink)

Although enactive approaches to cognition vary in terms of their character and scope, all endorse several core claims. The first is that cognition is tied to action. The second is that cognition is composed of more than just in-the-head processes; cognitive activities are externalized via features of our embodiment and in our ecological dealings with the people and things around us. I appeal to these two enactive claims to consider a view called “direct social perception” : the idea that we (...) can sometimes perceive features of other minds directly in the character of their embodiment and environmental interactions. I argue that if DSP is true, we can probably also perceive certain features of mental disorders as well. I draw upon the developmental psychologist Daniel Stern’s notion of “forms of vitality”—largely overlooked in these debates—to develop this idea, and I use autism as a case study. I argue further that an enactive approach to DSP can clarify some ways we play a regulative role in shaping the temporal and phenomenal character of the disorder in question, and it may therefore have practical significance for both the clinical and therapeutic encounter. (shrink)

Externalist theories hold that a comprehensive understanding of mental disorder cannot be achieved unless we attend to factors that lie outside of the head: neural explanations alone will not fully capture the complex dependencies that exist between an individual’s psychiatric condition and her social, cultural, and material environment. Here, we firstly offer a taxonomy of ways in which the externalist viewpoint can be understood, and unpack its commitments concerning the nature and physical realization of mental disorder. Secondly, we apply a (...) strongly externalist approach to the case of Autistic Spectrum Disorder, and argue that this condition can be illuminated by appeal to the hypothesis of extended cognition. We conclude by briefly considering the significance this strongly externalist approach may have for psychiatric practice and pedagogy. (shrink)

Autism Spectrum Condition presents a challenge to social and relational accounts of the self, precisely because it is broadly seen as a disorder impacting social relationships. Many influential theories argue that social deficits and impairments of the self are the core problems in ASC. Predictive processing approaches address these based on general purpose neurocognitive mechanisms that are expressed atypically. Here we use the High, Inflexible Precision of Prediction Errors in Autism approach in the context of cultural niche construction to explain (...) atypicalities of the relational self, specifically its minimal, extended, and intersubjective aspects. We contend that the social self in ASC should not be seen as impaired, but rather as an outcome of atypical niche construction. We unpack the scientific, ethical, and practical consequences of this view, and discuss implications for how the challenges that autistic persons face should be approached. (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)

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.

We argue that the notion of "mental institutions"-discussed in recent debates about extended cognition-can help better understand the origin and character of social impairments in autism, and also help illuminate the extent to which some mechanisms of autistic dysfunction extend across both internal and external factors (i.e., they do not just reside within an individual's head). After providing some conceptual background, we discuss the connection between mental institutions and embodied habits of mind. We then discuss the significance of our view (...) for understanding autistic habits of mind and consider why these embodied habits are sometimes a poor fit with neurotypical mental institutions. We conclude by considering how these insights highlight the two-way, extended nature of social impairments in autism, and how this extended picture might assist in constructing more inclusive mental institutions and intervention strategies. (shrink)

Autism has been defined as a disorder of social cognition, interaction and communication where ritualistic, repetitive behaviors are commonly observed. But how should we understand the behavioral and cognitive differences that have been the main focus of so much autism research? Can high-level cognitive processes and behaviors be identified as the core issues people with autism face, or do these characteristics perhaps often rather reflect individual attempts to cope with underlying physiological issues? Much research presented in this volume will point (...) to the latter possibility, i.e. that people on the autism spectrum cope with issues at much lower physiological levels pertaining not only to Central Nervous Systems (CNS) function, but also to peripheral and autonomic systems (PNS, ANS) (Torres, Brincker, et al. 2013). The question that we pursue in this chapter is what might be fruitful ways of gaining objective measures of the large-scale systemic and heterogeneous effects of early atypical neurodevelopment; how to track their evolution over time and how to identify critical changes along the continuum of human development and aging. We suggest that the study of movement variability—very broadly conceived as including all minute fluctuations in bodily rhythms and their rates of change over time (coined micro-movements (Figure 1A-B) (Torres, Brincker, et al. 2013))—offers a uniquely valuable and entirely objectively quantifiable lens to better assess, understand and track not only autism but cognitive development and degeneration in general. This chapter presents the rationale firstly behind this focus on micro-movements and secondly behind the choice of specific kinds of data collection and statistical metrics as tools of analysis (Figure 1C). In brief the proposal is that the micro-movements (defined in Part I – Chapter 1), obtained using various time scales applied to different physiological data-types (Figure 1), contain information about layered influences and temporal adaptations, transformations and integrations across anatomically semi-independent subsystems that crosstalk and interact. Further, the notion of sensorimotor re-afference is used to highlight the fact that these layered micro-motions are sensed and that this sensory feedback plays a crucial role in the generation and control of movements in the first place. In other words, the measurements of various motoric and rhythmic variations provide an access point not only to the “motor systems”, but also access to much broader central and peripheral sensorimotor and regulatory systems. Lastly, we posit that this new lens can also be used to capture influences from systems of multiple entry points or collaborative control and regulation, such as those that emerge during dyadic social interactions. (shrink)

In Gennaro (2016), I had originally replied to Fred Adams and Charlotte Shreve’s (2016) paper entitled “What Can Synesthesia Teach Us About Higher Order Theories of Consciousness?,” previously published in Symposion. I argued that H.O.T. theory does have the resources to account for synesthesia and the specific worries that they advance in their paper, such as the relationship between concepts and experience and the ability to handle instances of ‘pop-out’ experiences. They counter-reply in Adams and Shreve (2017) and also raise (...) further objections to H.O.T. theory which go well beyond the scope of their 2016 paper. In this paper, I offer additional replies to the points they raise in Adams and Shreve (2017). (shrink)

It often seems incorrect to say that psychiatric conditions are diseases, and equally incorrect to say that they are not. This results in what would seem to be an unsatisfactory stalemate. The present essay examines the considerations that have brought us to such a stalemate in our discussions of autism. It argues that the stalemate in this particular case is a reflection of the fact that we need to find the logical space for a position that rejects both positive and (...) negative answers. It then suggests one way in which we might find such space, by applying Michael Dummett’s notion of semantic disharmony. (shrink)

This is a review of Susan Greenfield's 2015 book 'Mind Change: How Digital Technologies Are Leaving Their Mark On Our Brains'. Greenfield is a neuroscientist and a member of the UK House of Lords, who argues that digital technologies are changing the human environment "in an unprecedented way," and that by adapting to this environment, "the brain may also be changing in an unprecedented way." The book and its author have created a surprising amount of controversy. I discuss both Greenfield's (...) book and a prominent critique by Bell et al. (2015). The exchange points to some flaws in Greenfield's argument and represents an interesting debate about the public role of scientists, but it does not undermine the value of the book as a springboard for discussions about possible policies and future research. (shrink)

One of the central claims of the neurodiversity movement is that society should accommodate the needs of autistics, rather than try to treat autism. People have variously tried to reject this accommodation thesis as applicable to all autistics. One instance is Pier Jaarsma and Stellan Welin, who argue that the thesis should apply to some but not all autistics. They do so via separating autistics into high- and low-functioning, on the basis of IQ and social effectiveness or functionings. I reject (...) their grounds for separating autistics. IQ is an irrelevant basis for separating autistics. Charitably rendering it as referring to more general capacities still leaves us mistaken about the roles they play in supporting the accommodation thesis. The appeal to social effectiveness or functionings relies on standards that are inapplicable to autistics, and which risks being deaf to the point of their claims. I then consider if their remaining argument concerning autistic culture may succeed independently of the line they draw. I argue that construing autistics' claims as beginning from culture mistakes their status, and may even detract from their aims. Via my discussion of Jaarsma and Welin, I hope to point to why the more general strategy of separating autistics, in response to the accommodation thesis, does not fully succeed. Finally, I sketch some directions for future discussions, arguing that we should instead shift our attention to consider another set of questions concerning the costs and extent of change required to accommodate all autistics. (shrink)

If one can judge a society by how it treats its prisoners, one can surely judge a society by how it treats cognitively- and learning-impaired children. In the United States children with physical and cognitive impairments are subjected to higher rates of corporal punishment than are non-disabled children. Children with disabilities make up just over 13% of the student population in the U.S. yet make up over 18% of those children who receive corporal punishment. Autistic children are among the most (...) likely to receive corporal punishment. -/- Although they may deny or redescribe particular instances of corporal punishment or their use of restraints, educators defend such actions as legitimate punishment. In this paper, I assess the logic underlying the use of restraints and corporal punishment on autistic children by educators. The rationalizations for the corporal punishment or restraint of autistics stems from the educator’s desire to control the autistic children so as to end typical autistic behaviors such as rocking, repetitive verbalizations, or “flapping” but also the autistic child’s non-affective responses such as not appearing to feel remorse or shame or the absence of a verbal acknowledgement of remorse or shame. The educators assume that the autistic’s failure to exhibit the desired responses is evidence of the autistic’s moral incorrigibility and is, therefore, evidence of the appropriateness of corporal punishment. But this assumption of the incorrigibility of the autistic child is questionable. -/- Indeed accepting this incorrigibility assumption reveals two important problems. First, instructors using physical punishment on autistic children do not understand autism. Second, they are not working with a tenable conception of punishment. Any action undertaken to induce socially acceptable behaviors (whether it be the end of autistic acts or responses such as remorse) is to fail to understand what the legitimate punishment of children is about. (shrink)

In this chapter, I describe my “post-diagnosis” experiences as the parent of an autistic child, those years in which I tried, but failed, to make sense of the overwhelming and often nonsensical information I received about autism. I argue that immediately after being given an autism diagnosis, parents are pressured into making what amounts to a life-long commitment to a therapy program that (they are told) will not only dramatically change their child, but their family’s financial situation and even their (...) entire mode of existence. Moreover, despite information overload, many treatment programs for autism rely on empty jargon and make completely unrealistic promises, so parents are left feeling overwhelmed and panicked. Even well respected therapy programs encourage parents to spend liberally. Indeed, autistic therapists, who help construct what I refer to as the Culture of Autism, advise parents to commit to a minimum of 35 to 45 hours of intensive therapy every week. The implications are clear: for a parent who works full-time, their autistic child becomes a second full-time job. Autism is big business right now, and therapists are pushing parents to the brink of desperation. So it is not too surprising that there is a desperate cry for a more permanent solution—which is why researchers seek to cure autism. But there are two ways to conceptualize cure. A Therapeutic Cure model (TC) conceives of a cure as a beneficial treatment for the patient that eliminates or ameliorates the harms of the disease or condition. But the notion of a therapeutic cure for autism is highly implausible, given the complexities of autism. Indeed, at this point, the vast majority of researchers have come to the conclusion that the idea of a therapeutic cure for autism is simply a non-starter. Therefore the bulk of research seeking a cure for autism focuses instead on a second approach, which I refer to as the Negative Eugenics Cure model (NEC). With this model, the intention is to eliminate the disease or condition without regard for the health or well-being of the organism carrying the disease or condition. So, with regard to autism, researchers are focusing on identifying genetic markers for autism that can be detected in utero, or in embryos, so that autistic fetuses can be eliminated and autism eradicated by preventing the existence of autistic individuals. I review both models and argue that both fail to provide convincing arguments that the “solution” either offers is desirable. Both rest on the assumption that autism renders a life not worth living which, all things considered, is false. Instead of pushing to cure autism, an idea pervasive in this Culture of Autism, I contend that autistics are individuals with lives worth living. Moreover, rather than expend millions on research to search for the means to eliminate autism, we should instead expend our resources to ensure autistic individuals have access to support they may need. If the phenomenology of autism were better understood and appreciated, the panicked demand for a cure for autism might abate and perhaps autism could be seen as having value in and of its own right. (shrink)

No two individuals with the autism diagnosis are ever the same—yet many practitioners and parents can recognize signs of ASD very rapidly with the naked eye. What, then, is this phenotype of autism that shows itself across such distinct clinical presentations and heterogeneous developments? The “signs” seem notoriously slippery and resistant to the behavioral threshold categories that make up current assessment tools. Part of the problem is that cognitive and behavioral “abilities” typically are theorized as high-level disembodied and modular functions—that (...) are assessed discretely (impaired, normal, enhanced) to define a spectral syndrome. Even as biology reminds us that organic developing bodies are not made up of independent switches, we remain often seduced by the simplicity of mechanistic and cognitive models. Developmental disorders such as autism have accordingly been theorized as due to different modular dysfunctions—typically of cortical origin, i.e., failures of “theory of mind” (Baron-Cohen et al., 1985), of the “mirror neuron system” (Ramachandran and Oberman, 2006), of “weak central coherence” (Happe and Frith, 2006) or of the balance of “empathizing” and “systemizing” (Baron-Cohen, 2009), just to list a few. -/- The broad array of autonomic (Ming et al., 2005; Cheshire, 2012) and sensorimotor (Damasio and Maurer, 1978; Maurer and Damasio, 1982; Donnellan and Leary, 1995; Leary and Hill, 1996; Donnellan and Leary, 2012; Donnellan et al., 2012) differences experienced and reported by people with autism have by such theories typically been sidelined as “co-morbidities,” possibly sharing genetic causes, but rendered as incidental and decisively behaviorally irrelevant symptoms—surely disconnected from cognition. But what if the development of cortically based mental processes and autonomous control relies on the complexities and proper function of the peripheral nervous systems? Through such an “embodied” lens the heterogeneous symptoms of autism invites new interpretations. We propose here that many behavioral-level findings can be re-defined as downstream effects of how developing nervous systems attempt to cope and adapt to the challenges of having various noisy, unpredictable, and unreliable peripheral inputs. (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)

Some researchers and autistic activists have recently suggested that because some ‘autism-related’ behavioural atypicalities have a function or purpose they may be desirable rather than undesirable. Examples of such behavioural atypicalities include hand-flapping, repeatedly ordering objects (e.g., toys) in rows, and profoundly restricted routines. A common view, as represented in the Diagnostic and Statistical Manual of Mental Disorders (DSM) IV-TR (APA, 2000), is that many of these behaviours lack adaptive function or purpose, interfere with learning, and constitute the non-social behavioural (...) dysfunctions of those disorders making up the Autism Spectrum. As the DSM IV-TR continues to be the reference source of choice for professionals working with individuals with psychiatric difficulties, its characterization of the Autism Spectrum holds significant sway. We will suggest Extended Mind and Enactive Cognition Theories, which theorize that mind (or cognition) is embodied and environmentally embedded, as coherent conceptual and theoretical spaces within which to investigate the possibility that certain repetitive behaviours exhibited by autistics possess functions or purposes that make them desirable. As lenses through which to re-examine ‘autism-related’ behavioral atypicalities, these theories not only open up explanatory possibilities underdeveloped in the research literature, but also cohere with how some autistics describe their own experience. Our position navigates a middle way between the view of autism as understood in terms of impairment, deficit and dysfunction and one that seeks to de-pathologize the Spectrum. In so doing we seek to contribute to a continuing dialogue between researchers, clinicians and self- or parent advocates. (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.

The ability of a group of adults with high functioning autism (HFA) or Asperger Syndrome (AS) to distinguish moral, conventional and disgust transgressions was investigated using a set of six transgression scenarios, each of which was followed by questions about permissibility, seriousness, authority contingency and justification. The results showed that although individuals with HFA or AS (HFA/AS) were able to distinguish affect-backed norms from conventional affect-neutral norms along the dimensions of permissibility, seriousness and authority-dependence, they failed to distinguish moral and (...) disgust transgressions along the seriousness dimension and were unable to provide appropriate welfare-based moral justifications. Moreover, they judged conventional and disgust transgressions to be more serious than did the comparison group, and the correlation analysis revealed that the seriousness rating was related to their ToM impairment. We concluded that difficulties providing appropriate moral justifications and evaluating the seriousness of transgressions in individuals with HFA/AS may be explained by an impaired cognitive appraisal system that, while responsive to rule violations, fails to use relevant information about the agent’s intentions and the affective impact of the action outcome in conscious moral reasoning. (shrink)

This article attempts to show why an experimental hypothesis is plausible and merits testing; in brief, the hypothesis is that autism begins with a failure in early learning and that changing the environment of early learning would dramatically change its incidence. Strong statistical evidence supporting this hypothesis has been published by Waldman et al. , but to date this evidence has largely been ignored, perhaps because it challenges prevalent beliefs about autism. This article also suggests that the current epidemic of (...) autism is serious enough, and intellectually mysterious enough, to merit attention from a wider community of brain scientists: New ideas are needed. A confirmation of this article’s hypothesis would have interesting implications for brain science. (shrink)

This article attempts to show why an experimental hypothesis is plausible and merits testing; in brief, the hypothesis is that autism begins with a failure in early learning and that changing the environment of early learning would dramatically change its incidence. Strong statistical evidence supporting this hypothesis has been published by Waldman et al., but to date this evidence has largely been ignored, perhaps because it challenges prevalent beliefs about autism. This article also suggests that the current epidemic of autism (...) is serious enough, and intellectually mysterious enough, to merit attention from a wider community of brain scientists: New ideas are needed. A confirmation of this article’s hypothesis would have interesting implications for brain science. (shrink)

Several recent lines of inquiry have pointed to the amygdala as a potential lesion site in autism. Because one function of the amygdala may be to produce autonomic arousal at the sight of a significant face, we compared the responses of autistic children to their mothers’ face and to a plain paper cup. Unlike normals, the autistic children as a whole did not show a larger response to the person than to the cup. We also monitored sympathetic activity in autistic (...) children as they engaged in a wide range of everyday behaviours. The children tended to use self-stimulation activities in order to calm hyper-responsive activity of the sympathetic (`fight or flight’) branch of the autonomic nervous system. A small percentage of our autistic subjects had hyporesponsive sympathetic activity, with essentially no electrodermal responses except to self-injurious behaviour. We sketch a hypothesis about autism according to which autistic children use overt behaviour in order to control a malfunctioning autonomic nervous system and suggest that they have learned to avoid using certain processing areas in the temporal lobes. (shrink)

"Our literature is replete with complaints about the chaotic state of the systematics of psychoses and every psychiatrist knows that it is impossible to come to any common understanding on the basis of the old diagnostic labels. ... Thus, not even the masters of science can make themselves understood on the basis of the old concepts and with many patients the number of diagnoses made equals the number of institutions they have been too. ... Errors are the greatest obstacles to (...) the progress of science; to correct such errors is of more practical value than to achieve new knowledge. We have here eliminated chaos of terms behind which useful concepts of disease were mistakenly sought; we have eliminated a veritable forest of boundary posts, not one of which indicated any natural line of demarcation. ... By the term „dementia praecox“ or „schizophrenia“ we designate a group of psychoses whose course is at times chronic, at times marked by intermittent attacks, and which can stop or retrograde at any stage, but does not permit a full restitutio ad integrum. The disease is characterized by a specific type of alteration of thinking, feeling, and relation to the external world which appears nowhere else in this particular fashion." Eugen Bleuler. Dementia Praecox or the Group of Schizophrenias. Translated by Joseph Zinkin. International Universities Press, New York, 1950. (shrink)