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SPECIAL REPORT: CHILD & ADOLESCENT PSYCHIATRY

Clinicians generally screen children for 

 (ASD) twice, at ages 18 months and 2 years, during routine health maintenance exams. Unfortunately, this neurodevelopmental condition often evades formal diagnosis until a child is 4 years or older.

 To expedite diagnosis, investigators are exploring a variety of artificial intelligence (AI)–based diagnostic systems as well as telehealth- and sensor-based technologies.

ASD affects 1 in 59 children in the United States.

 In many circumstances, a child suspected of having ASD is referred to a multidisciplinary diagnostic team composed of multiple medical and nonmedical specialists. Thus, there are often lengthy wait times for an evaluation. If a child does not meet threshold criteria, the assessment is considered inconclusive and parents must wait until the child is older for repeat assessment.

Many factors may delay the diagnosis. Individuals in poor communities and members of racial minority groups often have limited access to the services.

 In addition, only 60% of pediatricians nationwide screen children for developmental delays despite American Academy of Pediatrics (AAP) recommendations to perform screens at 18- and 24-month wellness checks. Also, screening may not result in appropriate follow-up care. In one study, for example, only two-thirds of those who failed screening were referred for a diagnostic ASD evaluation.

 The screening tools themselves present challenges. For instance, it has been shown that the Modified Checklist for Autism in Toddlers – Revised with Follow-up (M-CHAT-R/F) has a sensitivity as low as 39% in detecting children with ASD.

 has resulted in significant delays in evaluations.

Many tools are available to screen for ASD, including the Ages and Stages Questionnaires, the Communication and Symbolic Behavior Scales, the Parents Evaluation of Developmental Status, the Screening Tool for Autism in Toddlers and Young Children, and the aforementioned M-CHAT-R/F (

). Pediatricians often use M-CHAT-R/F at ages 18 months and 24 months; it queries parents regarding their child’s perception of others, use of gestures, and interactive eye contact, as well as vocal communication and their ability to interact with parents and children. The AAP recommends referral for a diagnostic evaluation when children screen positive or if the pediatrician is suspicious of the diagnosis.

The DSM-5 consolidated previous categories of ASD into 1. To meet ASD criteria, a child must have 3 of 3 symptoms relating to social communication and interaction, plus 2 of 4 symptoms relating to repetitive or restricted behaviors (

This recharacterization and simplification of the elements needed for ASD diagnosis has facilitated its diagnosis by specialists. Many use a chart similar to the 

 as an intake screening form before proceeding with a diagnostic evaluation.

The Autism Diagnostic Observation Schedule (ADOS) test and/or the Autism Diagnostic Interview – Revised (ADI-R) can also be used to evaluate for a suspected diagnosis. The ADOS is an observational play and activity assessment that takes up to an hour to complete, while the ADI-R is a 93-point questionnaire that may take several hours to complete.

 Many developmental pediatricians and child psychologists utilize their own screening methods rather than performing a full ADOS or ADI-R, sometimes using such screening tools as the Social Responsive Scale and the Childhood Autism Rating Scale. Most importantly, although these tools help with diagnosis, ASD is a clinical diagnosis best rendered by clinicians with the training and expertise to do so.

Children affected with ASD are a heterogeneous group, with varying degrees of functional limitations. Many have comorbidities that include seizures, 

, speech delay, and others. Researchers have long looked to sensor-based technologies, many employing AI algorithms, to screen for children with ASD. AI is particularly useful for identifying patterns within data, and it therefore can be advantageous in identifying markers associated with an ASD diagnosis. AI algorithms are only as good as the training datasets inputted into a diagnostic system, but they do have the potential to improve medical care.

Although a complete discussion of sensor technologies is beyond the scope of this article, investigators have had some promising results using sensors to analyze facial expressions, vocalizations, touch sensitivity, eye tracking, movements, and interactions with robots—all of which may help identify children with ASD. Unfortunately, to date, none of these technologies have been proven to be sensitive enough to be used diagnostically.

Developed over several years with National Institutes of Health grant funding, the Naturalistic Observation Diagnostic Assessment (NODA) was developed by Behavior Imaging Solutions. This is a 

 (DTx) that can facilitate the diagnosis of ASD, and it has 2 components. Parents use a smartphone-based application to complete a developmental questionnaire and to record and upload 10-minute videos of their child. NODA scenarios include the child playing alone, the child playing with others, a family mealtime, and a behavior of parental concern.

The web-based portal allows the clinician to analyze submitted videos for features of ASD. The doctor then completes a DSM-5 ASD checklist and considers the diagnosis. The results of several studies have indicated that the BSI system is easy to use and renders diagnoses comparable with those produced by a traditional ADOS evaluation.

 For example, a 2017 study compared the diagnostic accuracy of the NODA system with in-person evaluations by experienced ASD diagnosticians for 40 families who were seeking an ASD evaluation and 11 families with normally developing children. The diagnostic clinicians were blinded as to which group they were evaluating and used ADOS, ADI-R, or other diagnostic tools to render a determination of ASD status for each child. Sensitivity between NODA and the in-person exam was 85%, and the specificity was 94%.

The developer is currently in the process of integrating AI into NODA, using vision algorithms to tag video frames containing suspect diagnostic features. This AI is expected to be incorporated into the portal over the next 2 years and will speed the diagnostic process.

As with many DTx, the ease of use and availability of this system can shorten wait times to diagnosis considerably. Best of all, the evaluation can be done remotely, even in a pandemic, and the specialist can render a diagnosis expediting appropriate interventions for the child with ASD.

Another possibility is using a multimodular AI-based system to diagnose ASD.

 The prescription-only system developed by Cognoa, called Canvas Dx, was granted breakthrough device status via a preliminary submission to the US Food and Drug Administration (FDA), and it recently received FDA authorization.

Cognoa AI software was trained on datasets that were compiled from ADOS and ADI-R score sheets of children aged between 18 and 84 months, supplied by numerous ASD evaluation and treatment centers. Cognoa’s system includes: 1) a parental questionnaire; 2) a questionnaire filled out by the patient’s pediatrician; and 3) an analysis of 2 to 3 uploaded short videos, each 1 to 2 minutes long, of the child during mealtime or play at home. The videos are analyzed and scored by trained analysts for features of ASD who respond to a behavior questionnaire. AI algorithms analyze the questionnaires and video report and render a decision regarding whether the child has or does not have ASD, or if the valuation is inconclusive.

...the system could identify children with ASD with sensitivity and specificity as high as 90% and 83%, respectively.

Study results validated Cognoa’s system; 375 sample patients evaluated over 2 years, indicating that the system could identify children with ASD with sensitivity and specificity as high as 90% and 83%, respectively.

More recently, the company completed a double-blind clinical trial at 14 sites around the United States, utilizing an improved algorithm to gather data. The trial involved 425 participants aged between 18 and 72 months whose parents or doctors expressed concern about their development but had not previously been evaluated for ASD. Each child was assessed twice: once using Cognoa’s diagnostic, and once by a specialist clinician based on DSM-5 criteria. The study ran from July 2019 through May 2020, so some of the children were evaluated remotely during the pandemic via telemedicine. According to the company, the tool performed equally well when administered remotely and showed that Cognoa’s diagnostic is highly accurate across males and females as well as ethnic and racial backgrounds.

 remains a challenge, and recent advances in technology may expedite the identification of affected children so the child can receive early interventions. Looking ahead, various smart device-based applications are either in development or will soon be available to assist parents in socializing ASD children. Progress is being made, and soon parents and providers will leverage technologic advances to better identify ASD.

is clinical assistant professor of pediatrics at Geisel School of Medicine at Dartmouth University and an editorial advisory board member of Contemporary Pediatrics, a sister publication of

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Prevalence of autism spectrum disorder among children aged 8 years – Autism and Developmental Disabilities Monitoring Network, 11 sites, United States, 2014.

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Clinical features of children with autism who passed 18-month screening.

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Screening and referral practices for autism spectrum disorder in primary pediatric care.

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Diagnosing autism spectrum disorders in pre-school children using two standardized assessment instruments: the ADI-R and the ADOS.

AI in pediatrics: past, present and future. 

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A novel system for supporting autism diagnosis using home videos: iterative development and evaluation of system design.

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The potential of a store and forward tele-behavioral platform for effective treatment and research of autism.

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Investigating the accuracy of a novel telehealth diagnostic approach for autism spectrum disorder.

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Use of artificial intelligence to shorten the behavioral diagnosis of autism.

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Machine learning approach for early detection of autism by combining questionnaire and home video screening.

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https://cognoa.com/ai-driven-autism-diagnosis-aid-receives-fda-authorization/

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Multi-modular AI approach to streamline autism diagnosis in young children.

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https://www.cdc.gov/ncbddd/autism/hcp-screening.html

Autism spectrum disorder often evades formal diagnosis until a child is 4 years or older, but these artificial intelligence and telehealth systems may be able to help facilitate diagnosis. 

Facilitating Autism Diagnosis

Conversations in Critical Psychiatry is an interview series that explores critical and philosophical perspectives in psychiatry and engages with prominent commentators within and outside the profession who have made meaningful criticisms of the status quo.

Robert Chapman, PhD (they/them or he/him) is a philosopher in the United Kingdom (UK). They are an associate of the department of philosophy at the University of Bristol, UK, focusing on the philosophy of neurodiversity. They have published widely on issues in philosophy of disability, the ethics of autism, and critical neurodiversity studies, and are currently writing their first book on the philosophy of neurodiversity. Their Shirley Foundation-funded doctoral research was carried out at the University of Essex between 2013 and 2018 and focused on the ethics of autism. They have taught at the University of Essex, King’s College London and the University of Bristol. They are proudly neurodivergent and disabled. They also blog for 

Dr Chapman’s work on the intersection of neurodiversity and psychiatry has had a substantial impact on my own thinking, and their writings have consistently forced me, and many others, to rethink long-standing assumptions related to pathology and medical care. Among Dr Chapman’s writings, of particular note are: “Neurodiversity Theory and its Discontents: Autism, Schizophrenia, and the Social Model of Disability,”

 “The Reality of Autism: On the Metaphysics of Disorder and Diversity,”

 and “Neurodiversity and the Social Ecology of Mental Functions.”

 In recent years, the neurodiversity perspective has not only emerged as a vital player in our philosophical understanding of health and disease, but also has also had begun to shape how societies relate to disabled individuals. Furthermore, the neurodiversity perspective and sister movements such as Mad Pride center the voices of mad and neurodivergent individuals, transforming what has so far been, in the words of Michel Foucault, PhD, “a monologue of reason about madness,” to a dialogue enabling collective self-reflection on the relational nature of dysfunction and disability.

: Let’s start by an introduction to the neurodiversity movement and the neurodiversity paradigm. What is neurodiversity and where does it clash with mainstream medical thinking?

: The neurodiversity movement is a social justice movement pushing for a shift away from the default pathologizing of mental, developmental, and cognitive disability, and towards what I have called a 

 approach to understanding disablement. It all started when autistic individuals began meeting and raising consciousness online in the 1990s. Many realized they were tired of being represented as tragic deviations from supposedly normal functioning, and they were also often traumatized by ensuing attempts to treat or cure their autism. Eventually, as a new way to challenge how we think about normality, they began to talk about whether the principle that increased biodiversity is necessary for a robust ecosystem also applied to neuro-cognitive diversity within species. Just as we value, see beauty in, and try to conserve biodiversity, why not think about neuro-cognitive diversity in the same way? Based on this, Judy Singer, a member of these communities and, at the time, a sociology student, coined the term 

 and called for a “politics of neurological diversity” in her 1998 thesis. Singer circulated her thesis, which was grounded in the theories of disability studies, among other autistic activists before publishing a revised version as a book chapter in 1999.

 This became a founding text of the movement, which rallied around both Singer’s concept as well as existing themes from disability studies.

 was proposed a bit later, in 2012, by autistic scholar Nick Walker, PhD (she/her),

 who was also a graduate student at the time. By then the ideas initially developed by Singer were increasingly being adopted by individuals with other diagnoses such as bipolar, dyspraxia, and attention-deficit/hyperactivity disorder (ADHD). Walker was interested in the philosophical implications of this broader application and how it challenged theoretical assumptions and cultural and scientific practices. Walker proposed a distinction between the 

, which she took to be dominant and to rest on a relatively restricted conception of neurological, cognitive, and developmental normality, and the emerging 

, which begins from the acknowledgement that neurological diversity is natural and beneficial for the cognitive and cultural richness of the species. On this paradigm, instead of being labelled medically 

, those who are more enabled in a given society are considered more 

, while those who diverge further from functional norms are more 

. Walker argued that developing and cultivating such a paradigm shift, to then be adopted for research, policy, and practice, would be necessary for the long-term emancipation and well-being of neurodivergent individuals. Although Walker's chapter was relatively brief, it became highly influential within the movement, and I count it as another of the seminal texts of neurodiversity theory.

: You have talked about neurodiversity as a sociopolitical idea, centered around social models of disability, as well as neurodiversity as a scientific concept, offering a new way of thinking about function and dysfunction. Can you elaborate on these strands of neurodiversity (among other strands) and the shape they have taken in your own work?

: I see the cultural paradigm shift as quite similar to the change we have been seeing regarding the LGBT community, away from pathologization and towards pride, acceptance, and inclusion. The neurodiversity movement is also part of the broader disability rights and justice movement. With neurodiversity, while there is a long way to go, we are already seeing, for instance, neurodiversity paradigm vocabularies being used in newspapers and magazines, and a shift to disability rights-based practices for neurodivergent individuals in schools and workplaces.

Among other things, researchers increasingly recognize neurodivergent strengths alongside limitations.

Accompanying this, a scientific paradigm has also been emerging, albeit in a somewhat piecemeal way. More neurodivergent individuals have become involved in research, and more neurotypical researchers have begun to listen to neurodivergent perspectives. This is beginning to change how researchers formulate hypotheses and produce knowledge. Among other things, researchers increasingly recognize neurodivergent strengths alongside limitations, study cognitive problems as relational rather than as arising from individual deficits, and view neurodivergent disablement and distress based on a social model of disability rather than a medical model.

In my own work, I developed the ecological model of functioning to help clarify and formalize the theoretical basis of the emerging shift in the scientific paradigm, and to challenge the default pathologization of neurodivergence. I became interested in developing a new model of mental functioning partly because neurodiversity proponents had long been (successfully) using the social model of disability, and yet many researchers were still dismissing the idea that things like autism were not pathological. I realized that this was, at least in part, because the social model of disability leaves the dominant notion of individual dysfunction or impairment relatively intact, which is important because individual dysfunction is a core part of the definition of mental disorder (or of somatic disorder for that matter). As such, even the most successful application of the social model, while vital in other ways, is insufficient for undermining the ascription of neurological or mental illness, disorder, or pathology. After all, we can and do use social model interventions for things everyone agrees are genuine pathologies, such as dementia. Thus, I realized we needed an alternative model of functioning to augment alternative models of disablement and to help shift the paradigm.

Traditionally mental functions and dysfunctions have been determined through what I call “individualist comparativist” models, which compare all individuals to an aggregated norm and then rank them in levels of functioning. These models—which I date back to Darwin’s half-cousin, the eugenicist Francis Galton—seek to be continuous with the kind of evolutionary biology that focuses on individual fitness or adaption, and they thus rank fitness levels from highest to lowest in members of a population. If we accept these models, then it seems like an objective fact that members of low-ranked groups such as autistics and dyspraxics are naturally dysfunctional, and hence pathological, in comparison to neurotypicals—even if the social model can be helpful for alleviating disablement. The continued use of these models reifies neurodivergent disablement as natural fact and also lends scientific authority to the normalization of neurodivergence.

By contrast, the ecological model, as the name indicates, is more influenced by how ecologists talk about functioning. Ecologists tend to be less interested in ranking individual fitness levels, and more interested in how broader systems function as a whole, how functions emerge from the relations between organisms, and how the dominance of some forms of organisms can be harmful for the functioning of others. Bearing this in mind, in 

 I drew on theoretical and empirical research to argue that many neurodivergent functions, or relational functions that emerge from group neurodiversity, are overlooked on the traditional models.

 To avoid these problems, I then combined the arguments of neurodiversity proponents with ecological functional models to propose a preliminary ecological model in line with Walker’s call for a paradigm shift. To the extent this proves to be useful for researchers, I hope it will help with the scientific paradigm shift by orientating researchers towards asking different questions, formulating different hypotheses, and ultimately producing knowledge that helps us move beyond the default pathologizing of neurodivergent disability, and which supports a broadly conservationist approach to neurodiversity.

: How does your ecological model of mental functions play out within psychiatry and in the context of existing philosophical debates about neuropsychiatric dysfunction?

: It may be helpful to look at this historically. The modern debate could be dated to the 1960s, when the antipsychiatrist Thomas Szasz, MD, argued that mental illness was a myth and that psychiatry was a pseudoscience. Szasz was happy to acknowledge that neurological illnesses exist. But he nonetheless held that there could be no mental illnesses, since for him, an illness must be biological (including neurological) by definition. The Szaszian position, while challenging the pathologization of emotional distress, is entirely continuous with the Galtonian project of ranking neurocognitive functions in relation to an assumed norm. This challenged the psychoanalytic psychiatry of the time, which was not based on biological research, and pushed psychiatry towards the more biocentric and cognitivist models that are still used today. While this argument still has some influence, contemporary psychiatry has largely neutralized Szasz’s critique not just by analyzing the conceptual flaws of his arguments, but also by finding ample evidence that biological processes in some form or another, though they may not take the form of discrete dysfunctions, are part of the story for many conditions listed as mental disorders. In many ways contemporary psychiatry has thus become more Szaszian, although nobody likes to admit that.

By contrast, while they have some surface overlap with Szasz in that they challenge pathologization, the neurodiversity perspective and my ecological model present a novel philosophical position that is equally at odds with mainstream psychiatry and the Szaszian tradition (including its various offshoots within critical psychiatry). At base, the ecological model rejects the assumption that humans have enough neurocognitive uniformity across the species that legitimizes the notions of normal neurological functioning. Instead, my model begins with the acknowledgement that we are a neurologically diverse species, and the insight that neurocognitive functions and dysfunctions are (at least in significant part) relationally produced and upheld, both between different minds, and between mind and environment. It is not just that cognitive niche construction enables or disables different forms of functioning, it is also that a trait associated with individual disability may contribute to functioning at the group level, while a trait associated with individual ability may contribute to maladaptive group functioning. So things are a lot more complex than being normal or abnormal.

Part of the significance of adopting this model is that we recognize more neurodivergent mental functions, and that many dysfunctions are relational, often stemming in part from the neurotypical side, rather than being intrinsic to neurodivergent individuals. Simultaneously, by incorporating a social model analysis of cognitive niche construction, this also allows us to shift to viewing neurodivergent abilities as forms of marginalized functioning rather than inherent dysfunction. This model challenges the idea that many neurodivergent individuals necessarily have neurological or cognitive pathologies, as well as the idea that neurotypicals are necessarily superior, while fully acknowledging the fact of neurodivergent disablement. Moreover, unlike the Szaszian critique of psychiatric pathologization, this model is compatible with disability justice more broadly, because it applies equally to learning and cognitive disabilities and neurodevelopmental disabilities, instead of reinforcing their pathologization. More concretely, I thus hope the model will help reorientate the surrounding biopolitics, away from the normalizing tendencies developed by 19th-century eugenicists, and towards a conservationist approach to studying and supporting human neurodiversity.

: A common objection that is raised against neurodiversity is that the framework applies poorly to severely disabled individuals who have high support needs, and may live in specialized settings. Given that this may be on the minds of many readers as well, I think it is worth bringing up here.

: This is a very important question on a complex topic. I will restrict myself to a pair of key points. First, the form of neurodiversity that I, and I believe most proponents, endorse does not deny that there are different forms of disability, and that in some cases much more direct support is needed (even if we have critiqued the utility of terms like 

). In fact, the clear implication of adopting social models of disability (not to mention my ecological model of functioning) would be that individuals with more complex disabilities should get more support, not less.

A key point of contention, of course, regards whether we prefer to see complex disabilities more as mental pathologies to be treated, or marginalized minorities to be supported. This brings me to my second point. Because my approach to neurodiversity is based on a disability justice perspective, it relies more on standpoint epistemology, centering the lived experience of marginalized individuals or groups. My own view, then, is that we need to do more to center the voices of those with intersecting disabilities and high support needs when talking about those who sit at the same intersections (as I wrote about 

 At the moment, we have no data on the views of those considered severe on such topics. Interestingly, though, just looking through texts written by nonverbal autistics with intersecting disabilities and high support needs, it is quite easy to find many who hold views consistent with the neurodiversity perspective, as I have 

 Indeed, some of the most influential neurodiversity proponents, notably the late Mel Baggs, were labelled severe and had high support needs. So, we cannot assume that everyone with higher support needs would reject the neurodiversity perspective. My hope is that empirical researchers will, where possible, survey the preferences of those with high support needs in a more systematic way. As a philosopher I do not have the right resources to do that kind of research, but I can say I do think that should be the starting point of any conversation on this.

: A related issue is that of whether the neurodiversity movement rejects medical care per se. My understanding is that the proponents of neurodiversity movements are not against the use of medical interventions, but these medical interventions need to be offered on terms that are acceptable to and desired by neurodivergent individuals. Is that an accurate characterization? What do you think medical care would look like within a neurodiversity paradigm?

: Views differ among neurodiversity proponents, but for the most part, I think you are right. The key thing most are against is the default assumption that neurodivergent individuals should be normalized, and, in turn, most are against the invariably harmful attempts to cure us or to prevent neurodivergence from existing. What we want is support so neurodivergent individuals of all abilities can thrive. In certain respects, medical care would not change all that much. For instance, when it comes to depression, the neurodiversity paradigm, although it is certainly not committed to these, may be compatible with a range of existing approaches found in many forms of psychotherapy. And, for that matter, it is equally consistent with alternative approaches from beyond the Western medical tradition.

But there are certain things most neurodiversity proponents are very against. An example of this is Applied Behavior Analysis (ABA), which was initially used as gay conversion therapy and is still used on autistics. Traditional ABA uses a system of punishments and rewards to alter behaviors, although more recently punishments have become less popular. Today it is often touted as the gold standard of autism interventions, despite the protests of many autistic individuals who are clear that their experience of ABA was dehumanizing, focused on normalization, and traumatized them. Myself and my co-author Virginia Bovell recently reviewed the evidence and ethical arguments for or against ABA for a forthcoming book chapter. We found the evidence stacked up against the moral permissibility of ABA. I have uploaded a 

 and I invite anyone who is skeptical of worries regarding ABA and normalization to read through and assess the reasoning and evidence we present.

While I advocate moving towards a neurodiversity paradigm, I do not simply dismiss those autistic individuals who see themselves as ill and who wish to be cured. To help make sense of this from a neurodiversity paradigm perspective, I—somewhat tentatively—

 which refers to when the inner identity or goals of an individual clash with their neurotype to the extent that this becomes distressing. In such a case, I leave it open whether the individual wishes to focus more on changing their self-image (eg, through talking therapy) or their neurotype (eg, through biomedical intervention). Of course, at this point, there is no biomedical intervention for autism, and it looks to me like the whole project of trying to treat or cure autism itself has catastrophically failed. So, with autism, I would imagine that focusing on one’s identity rather than one’s neurotype would be better in practice, even for those autistic individuals who hold out hope for a neurotype change. But in other cases, neurodivergent individuals do use biomedical intervention, as can be seen with ADHD or bipolar. While I agree with many critiques of the pharmaceutical industry, I fiercely support those who find medication helpful, and am strongly against the kind of med-shaming that occurs among some critics of psychiatry. In the long run, though, I would hope that, if the neurodiversity paradigm were widely implemented, then the need and desire for medication would lessen, since educational, occupational, and social expectations and environments would also change accordingly.

: Neurotype dysphoria reminds me of the now obsolete category of ego-dystonic homosexuality and the on-going debates around gender dysphoria. At some point it was considered okay, but it is no longer considered ethically acceptable for a medical professional or psychologist to engage in interventions with the attempted aim of converting the homosexual orientation of an individual distressed by it to heterosexual orientation. Do you think the case of autism is significantly different in certain respects that neurotype dysphoria will not run into the same ethical issues as ego-dystonic homosexuality?

: Just to be clear: I am firmly against attempts to develop a cure for autism. I do not think it is morally permissible to spend limited research funds on something most autistic individuals, including myself, see as a form of eugenics. The neurotype dysphoria concept was more meant to acknowledge the very real suffering of those who do wish for a cure. Right now, we live in a world where some neurodivergent individuals consider themselves ill and do not feel that the neurodiversity paradigm has the conceptual space to acknowledge this. I wanted to find a way to acknowledge this kind of experience while also refraining from pathologizing the neurotype itself.

Another reason I suggested it was that I suspect a lot of individuals experience milder manifestations of neurotype dysphoria (I certainly have, although not to the point of ever wanting a profound change). I imagine even some neurotypicals experience neurotype dysphoria. So I hope that this concept will be helpful for a variety of individuals, including for some pro-cure autistics, but it should not be seen as legitimizing the search for a cure. And to be clear, I do not think the term will work for everyone or cover every issue. It will likely only be temporarily useful, as is the case with all such concepts. If social conditions change, the notion will become obsolete, perhaps even unacceptable. If that happens, I will welcome that as a sign of social progress.

: When it comes to how we conceptualize autism within the context of neurodiversity, I am often unclear on where autism ends and other mental health problems begin. For example, parents of autistic children often seek help for a variety of problematic behaviors, such as repetitive banging or hitting of head; biting of hands and fingers; extreme sensitivity to commonplace sights, sounds, or smell; or inability to tolerate even minor changes in daily routine. When you think of autism, where do you position these behaviors within the fuzzy construct? Do you see them as distinct from, or peripheral to, the core autistic self?

: The first thing to say is that I advocate moving away from notions such as the 

 altogether, if by that we mean something that all autistic individuals share, and which is distinctive of autism. That would contradict all the historical, biological, psychological, and sociological research on autism, which, as I have argued in a number of places, shows it to be a shifting, culturally bound construct that maps on to different rough clusters of neurocognitive dispositions at different times. Saying that, I do not think that the kind of things you describe are core parts of anyone’s authentic self. They are things anyone might experience or do in certain harmful environments. Autistic individuals are subjected to such environments more than most, and therefore tend to do these kinds of things more. Of course, that this is so will also reflect the various neurocognitive tendencies associated with autism to some extent, but for the most part it seems more helpful to focus on the environment.

: You have been quite critical of some strong social constructionist positions which argue for the rejection of all psychiatric categories, including categories such as autism, on the basis that they lack a neurobiological essence and are therefore invalid medical constructs. You have argued that such denial of autism as a category erases autistic culture and deprives them on their disabled identity. Can you elaborate on this?

: Well, I am a constructivist myself, and I have often critiqued biocentric and essentialist depictions of mental disabilities. But yes, I am equally against a specific kind of constructivism that stems from the Szaszian antipsychiatry tradition, which argues that both the concept of mental disorder, and specific classifications, are just myths. My issue here is part theoretical, and about how this position is not really convincing once critically assessed. I covered this in detail in my article “

 which provided a clear rebuttal of recent Szaszian and critical characterizations of autism as a myth, and clarified how autism is both constructed and part of material reality. But my worry is also in part political, which I did not explain in the article and is worth clarifying here.

I do not believe that Szasz’s ontology, even in its updated form, is compatible with service-user liberation in the long run.

To cut to the core issue, I find Szasz’s position abhorrent since, based on his hard-right political views, he developed his theoretical critique of psychiatry to establish that individuals who claim to have mental illnesses are essentially all just impersonating or role-playing, pretending to be ill to avoid responsibility, which may arguably be considered as malingering, despite Szasz’s caveat that the mentally ill individual may be lying “both to himself and others.”

 This boils down to the fact that Szasz thought service users were essentially all liars and that this needed to be exposed. Until recently, many on the left, such as Peter Sedgwick, thus critiqued Szasz, and in reply Szasz was openly disdainful of progressives, and happy to gloat about how his theorizing was grounded in a neoliberal, Hayekian politics. In the past decade or so, though, many Szaszian medical professionals have combined the Szaszian analysis with social justice rhetoric to reframe the Szaszian ontology as somehow progressive, even as a critique of neoliberalism. To do this, they essentially keep the Szaszian ontology (biological essentialism about health) and theory (that mental illness is therefore a myth, and diagnoses are lies), but reverse the historical narrative, suggesting that the psychiatrists were the first to suggest these fictional diagnoses, and that service users have since been tricked into believing them.

While I have every sympathy with other service users who, like me, are angry with psychiatry and the misleading claims many clinicians and researchers have often made, I do not believe that Szasz’s ontology, even in its updated form, is compatible with service-user liberation in the long run. It undermines and gaslights those service users who do find a medicalized approach helpful and who seek diagnosis and recovery (eg, from eating disorders). It is also harmful when we consider that many of us have reclaimed psychiatric terms such as autistic to form minority cultures and join with the broader disability rights movement to resist the medicalized approach. Instead of supporting our self-emancipation and recognizing the nuanced positions we have on the metaphysics of diagnosis, professionals and critics working within a Szaszian ontology (where they identify as Szaszian or not) still routinely reduce us to gullible victims, since there is not really any space for a more nuanced analysis within their framework. To me, such contemporary critical positions mainly function to erase our agency, identities, voices, and cultures, and to undermine our efforts to resist the medicalized approach.

: Something you have articulated quite well is the idea that pathologizing first happens in society and that psychiatrists just officially medicalize ways of being that have already by pathologized by the society in some way. You write, “psychiatrists can, for the most part, only medicalize differences that have already implicitly been deemed pathological by the society they live in. For instance, psychiatrists only classified homosexuality as a mental disorder—and, importantly, only could have done so—because society was already deeply homophobic, and had already decided that being gay was a fundamentally bad, sick, thing. Today, if UK psychiatrists tried to re-medicalise being gay, they simply would not be able to because society would be so outraged... It is society that mainly decides who is pathological or not, not psychiatry...”

 How do you think this insight should inform individuals, both within and outside psychiatry, who are concerned about over-medicalization and wish to counter it?

: Okay so this again relates back to the contemporary Szaszian reduction of neurodivergent individuals to victims of psychiatric lies. More specifically, I wrote this in response to the oft-repeated Szaszian claim that psychiatry, and in particular the DSM taskforce, is a uniquely powerful force that is medicalizing normality. I call this “the DSM conspiracy narrative,” since it presents the fact that taskforce members vote on diagnostic classifications as some kind of shocking truth about psychiatry, which is taken to show it to be some kind of elite conspiracy with the power to decide who is normal or not. To be clear, I agree that we do often wrongfully pathologize normal variations, and I also think there are a number of hugely significant problems with the DSM (I am currently writing a book that locates that basis of the DSM conception of mental disorder in 19th-century eugenic theory and which argues that it is still bound up with this way of thinking). But despite being among the harshest critics of the DSM and all it represents, I also think this particular narrative is deeply problematic and that ultimately it reinforces disempowering ableist narratives that undermine our individual and collective agency.

There are a number of interrelated issues here. First consider that, at least in the UK where I live, it is unthinkable that psychiatrists could pathologize homosexuality today. Once we accept this, it becomes apparent that, not just what psychiatrists do medicalize but what they could medicalize, is in large part already set by social forces outside their control. I emphasized this because I think any realistic attempt to resist wrongful pathologization must take this as the starting point of its analysis rather than by framing psychiatry, or the DSM taskforce, as some kind of elite conspiracy that has the power to decide who is normal or not. If anything, for the most part DSM taskforce votes on diagnoses are channeling the already settled outcomes of wider public debates that have already taken place in the years leading up to each DSM revision. Second, it is also important to note here that researchers voting on classifications is consistent with how classifications are decided in the rest of medicine, not to mention in science more generally. While this conspiracy narrative has clearly been good for Szaszian clinical professionals to generate tabloid headlines or book sales, it is at base a distraction that will not be helpful for emancipating those who are mentally disabled or distressed in the long run.

Importantly, my distaste for the DSM conspiracy narrative also relates back to my worries about the erasure of neurodivergent agency. A big part of why challenging this narrative is important is that over many decades, countless neurodivergent individuals have been part of debates regarding how we are categorized. Many have campaigned for the inclusion or expansion of DSM classifications, just as many have campaigned for the removal or contraction of others. As just one example, it is worth reading Kapp and Ne’eman’s 

 on how autistic advocates were part of the construction of autism in the DSM-5. This is important to note because it means our neurodivergent agency is part of diagnostic looping effects that determine each DSM edition, just like the agency of other actors, such as pharmaceutical corporations or DSM taskforce members. Given this, any given DSM vote on diagnostic classifications should be seen—albeit to varying extents in each case—as the outcomes of decades’ long co-construction rather than something solely determined by medical professionals and corporate interests. While I am all for critiquing and eventually abolishing the DSM or specific diagnoses, I would urge critics, whether within or outside psychiatry, to recognize that analyses which overlook the fact that the DSM is co-constructed with significant input from individuals with mental illnesses or neurodivergent individuals are not just misleading, they also actively erase our agency and histories, and contribute to ableist tropes about us being powerless and passive victims.

: There are increasing efforts to apply the neurodiversity paradigm to conditions such as ADHD, dyslexia, and even conditions such as schizophrenia and personality disorders. I wonder what the boundaries of the neurodiversity paradigm are, what falls within its scope and what does not. It seems to me to be an open question. This is also presumably not a binary issue, that is, there are likely situations where the neurodiversity paradigm may apply, but only partly so (which I suspect will be the case for many psychiatric conditions). There are clearly some limits to the neurodiversity paradigm, so as the neurodiversity paradigm is increasingly studied and increasingly applied, what are your thoughts on how the over-application of neurodiversity may be avoided by activists and scholars of today and tomorrow?

: This is an important question I have grappled with a lot. Personally, I think it is better to ask 

 we can include an individual or group within the paradigm rather than 

 we can. Based on this, I have argued (eg, 

) that there should be room for a non-Galtonian conception of pathology within the neurodiversity paradigm, so we can include those who prefer to see themselves as ill without pathologizing those who do not.

But I think you are really asking about which standard we should use to determine what counts as pathology once we reject the Galtonian approach. Neurodiversity proponents do not yet have a clear way of distinguishing genuine pathology from marginalized functioning. Some critics see this as a weakness of the neurodiversity paradigm, and they suggest that the neurodiversity paradigm leads to some kind of naïve, antiscientific relativism. But I think that is far too hasty. Exactly where health ends and pathology begins has always been a problem and always will be. And really it is a philosophical and pragmatic issue rather than a scientific one. While this is a problem for neurodiversity proponents, it is equally a problem for everyone else, including for critics of neurodiversity. Those who dismiss the neurodiversity paradigm for encountering a problem that is equally shared by everyone else overlook this.

Personally, I advocate what I hope will be a more inclusive and liberatory approach, again by incorporating standpoint epistemology alongside social and ecological models of disability and functioning. Instead of trying to come up with more and more refined ways of objectively demarcating health from illness, I think it is probably better to move towards incorporating the perspectives of those classified into whether they should be counted as pathological or not. If people diagnosed with schizophrenia (or whatever other name they chose) came to find the depathologization useful, then I would fully endorse including them in that kind of analysis. By the same token, if they mainly found this way of looking at it unhelpful and, on reflection, preferred to see themselves as mentally ill, then I would begin with that as the starting point of any future analysis. In general, I think that whether a disability is depathologized has to be the product of consciousness raising from within to be emancipatory. If it was enforced from the outside then it may end up being epistemically oppressive. The approach I advocate thus avoids simplistic claims to objectivity and is more about opening up conceptual and existential space for those who are marginalized and for groups to collectively reimagine what their disablement means to them.

Just to be clear, this is a pragmatist approach rather than an anything goes kind of relativism. (Here I agree with Robert Spitzer, MD, architect of the DSM-III, who 

 that whether we call schizophrenia a disorder should ultimately be a pragmatic consideration.) I see individual and group preference as a key factor in whether we should focus more on, say, medical intervention or societal acceptance, for any given trait or disability. But sometimes different factors might conflict. If someone tried to use neurodiversity paradigm vocabulary to justify support for, say, harmful, unethical behavior, then that would be a clear co-option and abuse of the framework. In general, the kinds of things I am happy to endorse depathologizing—voice hearing, autistic stimming, hyperactivity, and so forth—are not intrinsically harmful.

: What hopes do you have for the future of neurodiversity theory and practice?

: I am excited about how neurodiversity theory and neurodiversity studies have been coming on in leaps and bounds over the past few years especially. We have talked about the need for a new paradigm in the 

 sciences for decades but a shift has not happened, mainly because nobody has come up with a workable alternative (and yes I am aware of the existing attempts). I believe that neurodiversity proponents have actually been getting on and building the basis for a different paradigm, even though it is still very much a work in progress. This has been led by grass roots advocates and has been strengthened more recently due to a concentrated effort of neurodivergent individuals to train in a variety of fields to further develop the paradigm.

But there is still a lot of work to do and there are a lot of problems and barriers we are facing. One thing I often worry about is how the vocabularies of neurodiversity are being co-opted by already established neurotypical clinicians, researchers, corporations, and so forth in ways that function to uphold rather than challenge the status quo. Many of the leading pathology paradigm theorists of autism have now rebranded themselves as neurodiversity advocates without giving up on their harmful, pathology paradigm theories and commitments. My hope is that the more radical, liberating aspects of the movement will prevail.

This brings me to a second point, which regards my hopes for institutional support. I hope educational and research institutions will make meaningful moves to support neurodiversity research by neurodivergent researchers. There are many disabling barriers in academia that are stifling for neurodivergent students and researchers and may have multiple marginalizing characteristics. Moreover, while an increasing number of neurodivergent individuals have now trained as scholars and are producing important neurodiversity paradigm research, there are few stable jobs for us in universities given that our approach often defies traditional boundaries and expectations. This is despite the interest many students have in learning about neurodiversity theory and the impact neurodiversity paradigm research and advocacy is having. By the end of the decade, I hope to see universities establish neurodiversity research centers, neurodiversity studies degrees, and neurodiversity studies lectureships. I would also like to see neurodiversity theory modules increasingly included in clinical training, not to mention in humanities and social science degrees.

Finally, within the neurodiversity movement, there are still remnants of the pathology paradigm that I think need to be overcome. For instance, some neurodiversity proponents still see neurotypes as natural kinds with timeless biological essences. I hope we can overcome this kind of biological essentialism since it is theoretically untenable and in my view contributes to a lot of needlessly toxic discourse. Relatedly, we also need to have more of a widespread acknowledgement that neurotype is, to some extent, fluid, and that even neurotypicals become neurodivergent if they live long enough. Working towards a more fluid and inclusive understanding of neurological identification will, I hope, not just be more liberating for neurodivergent individuals, but also help establish how the neurodiversity paradigm will be better for everyone. After all, even neurotypicals cannot live up to the ideal of normalcy. They have closer proximity to the ideal, sure. But since nobody is wholly normal, adherence to the ideal is, I think, harmful in other ways even for those who are temporarily enabled by it.

The opinions expressed in the interviews are those of the participants and do not necessarily reflect the opinions of 

is a psychiatrist in Cleveland, Ohio, and Clinical Assistant Professor of Psychiatry at Case Western Reserve University. He is a member of the executive council of Association for the Advancement of Philosophy and Psychiatry and has been actively involved in initiatives to educate psychiatrists and trainees on the intersection of philosophy and psychiatry. He is also a member of the

Dr Aftab and Dr Chapman has no relevant financial disclosures or conflicts of interest.

1. Chapman R. Neurodiversity theory and its discontents: autism, schizophrenia, and the social model of disability. In: Tekin S and Bluhm R, eds. 

The Bloomsbury Companion to Philosophy of Psychiatry

2. Chapman R. The reality of autism: on the metaphysics of disorder and diversity. 

3. Chapman R. Neurodiversity and the social ecology of mental functions. 

4. Singer J. ‘Why can’t you be normal for once in your life?’ From a ‘problem with no name’ to the emergence of a new category of difference. In: Corker M and French S, eds. 

5. Walker N. Throw away the master’s tools: liberating ourselves from the pathology paradigm. In: Bascombe J, ed. 

. Autistic Self Advocacy Network; 2012:225–237.

Multiply-disabled autism and intersectional feminism

. September 2, 2019. Accessed September 21, 2021. 

Are the voices of the “severely” autistic being silenced?

. September 10, 2019. Accessed September 21, 2019. 

Health and Wellbeing for a Neurodiverse Age

. June 26, 2020. Accessed September 21, 2021. 

The Myth of Mental Illness: Foundations of a Theory of Personal Conduct

Will opposing psychiatric labels stop over-medicalisation?

. October 12, 2020. Accessed September 21, 2021. 

12. Kapp SK, Ne’eman A. Lobbying autism’s diagnostic revision in the DSM-5. In: Kapp S, ed. 

Autistic Community and the Neurodiversity Movement: Stories From the Frontline

13. Spitzer RL. The diagnostic status of homosexuality in DSM-III: a reformulation of the issues. 

Is neurodivergence to be cured or is it a healthy part of our social ecology?

The Neurodiversity Paradigm in Psychiatry: Robert Chapman, PhD

Rashmi Parmar, MD, gives an overview on autism. Examples of signs and symptoms in children include trouble having a back-and-forth conversation, difficulty establishing eye contact, and difficulty reading facial expressions.

is a double board-certified adult and child psychiatrist with Community Psychiatry based in Newark, CA. She earned her medical degree at Terna Medical College & Hospital in Mumbai, India.

More than 3.5 million Americans have Autism Spectrum Disorder. How can you recognize the signs in children? 

Common Signs and Symptoms of Autism Spectrum Disorder in Children

 and autism spectrum disorders is in its infancy, there has been much controversy and confusion. Over the years, more patients and their families are seeking guidance from doctors on using cannabis to alleviate symptoms. From preventing seizures to calming aggression, a slow trickle of research is suggesting that cannabidiol (CBD), a component of cannabis, may be the wonder drug families have been searching for. But does it hold up to this standard? Should we be recommending it to patients? How do we weigh the benefits and the risks?

Unfortunately, many clinicians lack adequate training on the subject, making them unprepared to have a meaningful discussion with patients and families. Efforts to advance research have been limited for technical and logistical reasons, often leaving doctors with just as many questions as patients.

is a genus of flowering plants belonging to the family Cannabaceae that includes 3 species: cannabis sativa, indica, and ruderalis. Marijuana specifically refers to the parts of the cannabis plant that contains high amounts of delta-9-tetrahydrocannabinol (THC). Medicinal use of the cannabis plant dates back thousands of years in cultures all around the world. Today, it is used to treat an assortment of conditions, such as arthritis, cancer, HIV/AIDS, glaucoma, seizures, and more.

Used recreationally, it produces a high or mind-altering effect when smoked or consumed. It is also used therapeutically. The National Institute on Drug Abuse 

 as “using the whole, unprocessed marijuana plant or its basic extracts to treat symptoms of illness and other conditions.”

The plant produces more than 500 different chemical substances. These include 100 unique cannabinoids, which bind to the CB1 and CB2 receptors in the body’s endocannabinoid system. CB1 receptors are more common in the central and peripheral neurons, while CB2 receptors are expressed only in peripheral tissues, predominating the immune system.

THC and CBD are 2 cannabinoids found in cannabis that have particular clinical importance.

In medical applications, THC is typically used to relieve pain, nausea, insomnia, and poor appetite. THC is a partial agonist of the CB1 and CB2 receptors.

, which is why it is included in so many recreational marijuana products.

CBD is less controversial than THC because it does not produce mind-altering or euphoric effects. It has low affinity for CB1/CB2, acting as an antagonist.

 It affects various receptor systems in the body (TRPV1, GPR55, PPAR.) Of note is its agonism on the 5HT1A (serotonin) receptor at high concentrations to help with anxiety, sleep, pain perception, and nausea.

 It also appears to be a partial dopamine receptor agonist, pointing toward its possible antipsychotic properties. Additionally, CBD appears to influence the glutamate-GABA system.

Endocannabinoids are naturally occurring lipid mediators in the body that bind to the cannabinoid receptors. Unlike other neurotransmitters, they are produced on demand in the body and are quickly inactivated. The most common ones include: N-arachidonoylethanolamine (anandamide), 2-arachidonylglycerol (2-AG), and 2-arachidonylglyceryl ether.

Anandamide, also known as the “bliss molecule,” is currently one of the most-studied endocannabinoids.

 The cannabinoid receptor system has a very complex role in the body, which includes regulation of cell function, maintenance of homeostasis, motor coordination (basal ganglia), brain reward system, stress response, memory function (hippocampus), appetite, modulation of pain, and reduction of inflammation. 

Anandamide causes inhibition of the release of neurotransmitters such as glutamate and gamma aminobutyric acid (GABA). It also affects norepinephrine, dopamine, serotonin, histamine, prostaglandins and opioids.

 An imbalance in the GABA and glutamate system is often linked with 

Cannabis is prescribed as a treatment for autism in 14 states. Is it the wonder drug patients and families have been waiting for? 

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Common Signs and Symptoms of Autism Spectrum Disorder in Children

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