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A History and Timeline of Autism

The history of autism as a formal diagnosis began in 1911. Swiss psychiatrist Paul Eugen Bleuler coined the term, using it to describe what he claimed to be the childhood version of schizophrenia.

Since then, our understanding of autism has evolved, culminating in the current diagnosis of autism spectrum disorder (ASD).

Most of the public history of autism has been dominated by allistic (non-autistic) professionals and caregivers. Some of the language in this article includes stigmatizing terminology and ideas that aim to accurately reflect the language used by the cited experts.

1926: Grunya Sukhareva, a child psychiatrist in Kyiv, Russia, writes about six children with autistic traits in a scientific German psychiatry and neurology journal.

1938: Louise Despert, a psychologist in New York, details 29 cases of childhood schizophrenia, some of whom have traits that resemble today's classification of autism.

1943: Leo Kanner publishes a paper describing 11 patients who were focused on or obsessed with objects and had a “resistance to (unexpected) change.” He later named this condition “infantile autism.”

1944: Nazi-funded, Austrian pediatrician Hans Asperger publishes a popularized scientific study on autistic children, a case study describing four children ages 6 to 11. Much of his science was rooted in eugenics and the "race hygiene" politics of the Nazi regime. He notices parents of some of the children have similar personalities or eccentricities, and regards this as evidence of a genetic link. He was foundational to the development of the phased-out functioning labels (high vs. low functioning), and the former DSM diagnosis, Asperger’s syndrome, was named after him.

1949: Kanner proclaims his theory that autism is caused by " refrigerator mothers ," a term used to describe parents who are cold and detached. This theory has long been disproved.

1952: In the first edition of the American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders (DSM), children with autistic traits are labeled as having childhood schizophrenia.

1956: Leon Eisenberg publishes his paper "The Autistic Child in Adolescence," which follows 63 autistic children for nine years and again at 15 years old.

1959: Austrian-born scientist Bruno Bettelheim publishes an article in Scientific American about Joey, a 9-year-old autistic child.

1964: Bernard Rimland publishes Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behavior , challenging the “refrigerator mother” theory and discussing the neurological factors in autism.

1964: Dr. Ole Ivar Lovaas, creator of LGBTQ conversion therapy, begins working on his theory of Applied Behavioral Analysis (ABA) therapy for autistic children. While ABA is the current standard therapy for autistic people, autistic self-advocates draw parallels to the therapy as a form of conversion therapy for autistic people and have begun pushing against its use due to the post-traumatic symptoms individuals experience after ABA.

1965: The Sybil Elgar School begins teaching and caring for autistic children.

1965: A group of allistic parents (people who are not on the autistic spectrum) of autistic children have the first meeting of the National Society of Autistic Children (now called the Autism Society of America ).

1967: Bruno Bettelheim writes Empty Fortress , which reinforces the “refrigerator mother” theory as the cause of autism.

1970s: Psychiatrist Lorna Wing proposes the concept of autism spectrum disorders. She identifies the “triad of impairment,” which includes three areas: social interaction, communication, and imagination.

1975: The Education for All Handicapped Children Act is enacted to help protect the rights and meet the needs of children with disabilities, most of whom were previously excluded from school.

1977: Susan Folstein, M.D., and professor Michael Rutter publish the first study of twins and autism. The study finds that genetics are an important factor for being autistic.

1980: The third edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM-III) includes criteria for a diagnosis of infantile autism for the first time.  

1990: Autism is included as a disability category in the Individuals with Disabilities Education Act (IDEA), making it easier for autistic children to get special education services.

1996: Temple Grandin writes Emergence—Labeled Autistic , a firsthand account of her life with autism and how she became successful in her field.

1998: Andrew Wakefield, M.D. publishes his paper in the Lancet suggesting that the measles-mumps-rubella (MMR) vaccine triggers autism. The theory is debunked by comprehensive epidemiological studies and eventually retracted.

1999: The Autism Society adopts the Autism Awareness Puzzle Ribbon as “the universal sign of autism awareness.” Due to the symbol's implications of autistic people as incomplete and its association with autism hate groups, the autistic community now uses an infinity symbol (black or rainbow-colored) instead.

2003: The Global and Regional Asperger Syndrome Partnership (GRASP), an organization run by people with Asperger’s syndrome and autism spectrum disorders, is formed.

2003: Bernard Rimland, M.D. and Stephen Edelson, Ph.D. write the book Recovering Autistic Children .

2006: Ari Ne'eman establishes the Autistic Self Advocacy Network (ASAN).

2006: Dora Raymaker and Christina Nicolaidis, M.D. start the Academic Autistic Spectrum Partnership in Research and Education (AASPIRE) to provide resources for autistic adults and healthcare providers.

2006: The president signs the Combating Autism Act to provide support for autism research and treatment.

2010: Andrew Wakefield loses his medical license and is barred from practicing medicine, following the retraction of his autism paper.

2013: The DSM-5 combines autism, Asperger’s, and childhood disintegrative disorder into autism spectrum disorder.

2014: The president signs the Autism Collaboration, Accountability, Research, Education and Support (CARES) Act of 2014, reauthorizing and expanding the Combating Autism Act.

2020: The Centers for Disease Control and Prevention estimates one in 54 children has been identified as having an autism spectrum disorder (ASD) diagnosis.

2020: A large-scale genetic sequencing study identifies 102 autism-related genes involved in early brain development.

2023: The Centers for Disease Control and Prevention estimates 1 in 36 children has been identified with autism spectrum disorder (ASD).

Autism research and advocacy continue to build on these past events. As autistic self-advocates are growing in both political power and public presence, they aim to move towards a future of total acceptance and understanding of autistic people.

Advocates also work to provide access to resources to address the current gaps in support that autistic children and adults currently experience.

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The Autism History Project. J. Louise Despert, "Schizophrenia in Children, 1938."

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Sasson NJ, Pinkham AE, Carpenter KL, et al. The benefit of directly comparing autism and schizophrenia for revealing mechanisms of social cognitive impairment .  J Neurodev Disord . 2011;3(2):87-100. doi:10.1007/s11689-010-9068-x

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Folstein S, Rutter M. Infantile autism: a genetic study of 21 twin pairs . J Child Psychol Psychiatry . 1977;18(4):297-321. doi:10.1111/j.1469-7610.1977.tb00443.x

Volkmar FR, Bregman J, Cohen DJ, et al. DSM-III and DSM-III-R diagnoses of autism . Am J Psychiatry . 1988 Nov;145(11):1404-8. doi: 10.1176/ajp.145.11.1404.

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Satterstrom FK, Kosmicki JA, Wang J, et al. Large-Scale Exome Sequencing Study Implicates Both Developmental and Functional Changes in the Neurobiology of Autism . Cell. 2020 Feb 6;180(3):568-584.e23. doi: 10.1016/j.cell.2019.12.036

Shorter E, Wachtel LE. Childhood catatonia, autism and psychosis past and present: is there an 'iron triangle'? . Acta Psychiatr Scand . 2013;128(1):21-33. doi:10.1111/acps.12082

Tateno M, Kikuchi S, Uehara K, et al. Pervasive developmental disorders and autism spectrum disorders: are these disorders one and the same? . Psychiatry Investig . 2011;8(1):67-70. doi:10.4306/pi.2011.8.1.67

By Vincent Iannelli, MD  Vincent Iannelli, MD, is a board-certified pediatrician and fellow of the American Academy of Pediatrics. Dr. Iannelli has cared for children for more than 20 years. 

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The history of autism

It has been more than 50 years since Leo Kanner first described his classic autistic syndrome. Since then, the results of research and clinical work have helped us learn more about autism. More and more people are being diagnosed as autistic, although we still have a long way to go in creating a world that works for autistic people.

Read our charity's timeline below to explore the history of autism, meet some of our 'autism pioneers' and find out more about the incredible work they've done.

Kanner syndrome

• The specific pattern of 'abnormal behaviour' first described by Leo Kanner is also known as 'early infantile autism'. Kanner made no estimate of the possible numbers of people with this condition but he thought that it was rare (Kanner, 1943).
• Over 20 years later, Victor Lotter published the first results of an epidemiological study of children with the behaviour pattern described by Kanner in the former county of Middlesex, which gave an overall prevalence rate of 4.5 per 10,000 children (Lotter, 1966).

The triad of impairments

• In 1979 Lorna Wing and Judith Gould examined the prevalence of autism, as defined by Leo Kanner, among children known to have special needs in the former London Borough of Camberwell.
• They found a prevalence in those with IQ under 70 of nearly 5 per 10,000 for this syndrome, closely similar to the rate found by Lotter. As well as children with Kanner autism, Wing and Gould also found a larger group of children (about 15 per 10,000) who had difficulties with social interaction, communication and imagination (which they referred to as the 'triad' of impairments), as well as a repetitive stereotyped pattern of activities. 
• Although these children did not fit into the full picture of early childhood autism (or typical autism) as described by Kanner, they were described as being on the broader 'autism spectrum'. The total prevalence rate for all autistic children with special needs in the Camberwell study was approximately 20 in every 10,000 children (Wing and Gould, 1979). Gillberg et al (1986) in Gothenburg, Sweden, found very similar rates in children with learning disabilities.
• Other studies in different countries have also looked into autism and numbers of autistic children (but not the whole spectrum). These results range from 3.3 to 60.0 per 10,000. This could be due to differences in definitions or case-finding methods (Wing and Potter, 2002).

Asperger syndrome

Introduction to asperger syndrome.

In 1944, Hans Asperger (read more about the problematic history of Hans Asperger and the removal of Asperger syndrome as a diagnosis ) in Vienna had published an account of children with many similarities to Kanner autism but who had abilities, including grammatical language, in the average or superior range.  There are continuing arguments concerning the exact relationship between Asperger and Kanner syndromes but it is beyond dispute that they have in common the triad of impairments of social interaction, communication and imagination and a narrow, repetitive pattern of activities (Wing, 1981; 1991).

• Stephan Ehlers and Christopher Gillberg published the results of a further study carried out in Gothenburg. This study examined children in mainstream schools. The aim was to find the prevalence of Asperger syndrome and other autism profiles in children with IQ of 70 or above. 
• From the numbers of children they identified, they calculated a rate of 36 per 10,000 for those who definitely had Asperger syndrome and another 35 per 10,000 for those with social difficulties. Some of these children may have fitted Asperger description if more information had been available, but they were certainly on the autism spectrum. Teachers of these children had previously recognised social and/or educational differences, but had not been able to find a reason for these differences.
• For over 30 years, Sula Wolff, in Edinburgh, studied children of average or high ability who had difficulty with social interaction but who did not fit into the triad of impairments. These children represent the most 'subtle' end of the autism spectrum. The majority become independent as adults, many marry, and some display exceptional gifts.
• Why include them in the autism spectrum? As Sula Wolff points out, these children often have a difficult time at school and they need recognition, understanding and acceptance from their parents and teachers. The approach that suits them best is the same as that which is recommended for children with Asperger syndrome and high-functioning autism (as it was then called).
• Sula Wolff quotes Ehlers and Gillberg's study. She considers that their total figure of 71 per 10,000, includes the children she describes.

Autism spectrum

• A survey by the Office of National Statistics of the mental health of children and young people in Great Britain found a prevalence rate of 0.9% for autism or 90 in 10,000 (Green et al, 2005). These were not separated into autism, Asperger syndrome or other profiles on the autism spectrum.
• Gillian Baird and her colleagues published a report of a prevalence study which surveyed a population of children aged 9-10 years in the South Thames region. 
• All children who either already had an autism diagnosis or had social and communication difficulties were selected for screening.
• Children considered to be at risk of being an undetected case because they had a statement of special educational needs were also selected.
• Diagnoses were based on ICD-10 criteria. The results showed a prevalence rate of 38.9 in 10,000 for 'childhood autism', and 77.2 in 10,000 for other conditions on the autism spectrum, giving an overall figure of 116 in 10,000 (Baird et al, 2006).
• In this study very few children were identified with Asperger syndrome. The authors acknowledged that some children in mainstream schools who did not have a statement of special educational needs would have been missed, because of the selection criteria. The authors note that the prevalence estimate found should be regarded as a minimum figure (Baird et al. 2006).
• ICD-10 diagnostic criteria for Asperger syndrome suggests a person who would be diagnosed with Asperger syndrome using the criteria used by Gillberg, would probably receive a diagnosis of childhood autism or atypical autism using the ICD-10 criteria.

Autistic adults

• The Adult Psychiatric Morbidity Survey is the primary data source for monitoring trends in England’s mental health. In 2007 it included  autism for the first time, and found 1% of the population studied were autistic (Brugha, T. et al , 2009).
• The Department of Health then funded a project to build on the APMS study and look more closely at the numbers of autistic adults that were not included in the original study. This included people in residential care settings and those with complex needs. Professor Terry Brugha of the University of Leicester led this study. Brugha also led on autism research for the APMS 2007. Combining its findings with the original APMS, the study found that approximately 1.1% of people in England are autistic (The NHS Information Centre, Community and Mental Health Team, Brugha, T. et al, 2012).

Recent studies from other countries

• The Autism and Developmental Disabilities Monitoring Network in the USA looked at eight-year-old children in 14 states in 2008, and found a prevalence rate of autism within those states overall of  1 in 88, with around five times as many boys as girls diagnosed (Autism and Developmental Disabilities Monitoring Network Surveillance Year 2008 Principal Investigators, 2012).
• The National Center for Health Statistics in the USA published findings from telephone surveys of parents of children aged 6-17 undertaken in 2011-12. The report showed a prevalence rate for autism of 1 in 50, (Blumberg, S .J. et al, 2013).
• A study of a 0-17 year olds resident in Stockholm between 2001-2007 found a prevalence rate of 11.5 in 1,000, very similar to the rate found other prevalence studies in Western Europe, (Idring et al , 2012).
• A much higher prevalence rate of 2.64% was found in a study done in South Korea, where the researchers found two thirds of the people on the autism spectrum were in the mainstream school population, and had never been diagnosed before. (Kim et al, 2011).
• Researchers comparing studies from different parts of the world over the past few years have come up with a more conservative estimate of 62 in 10,000. They conclude that the both the increase in estimates over time and the variability between countries and regions are likely thanks to broadening diagnostic criteria, service availability and increasing awareness of autism among professionals and the public, (Elsabbagh M. et al, 2012).

Stories from the Spectrum

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• Published: 26 October 2016

The origin and natural history of autism spectrum disorders

• James C Harris 1  

Nature Neuroscience volume  19 ,  pages 1390–1391 ( 2016 ) Cite this article

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Refined social phenotyping of syndromic and idiopathic forms of autism, combined with advances in genetics, animal models of syndromes and brain imaging, may facilitate discovery of shared brain mechanisms that will lead to new treatments. The reversal of social deficits in animal models is promising for eventual translation into therapeutics.

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Historical Perspective

There has been tremendous progress made in the field of autism over the last six decades. While it was once a syndrome that was rarely discussed in public, we find information about autism spectrum disorder (ASD) all around us today — on television and radio, websites and internet searches, public service announcements, and in the views of celebrities sharing their stories. Political leaders discuss the importance of autism diagnosis, cause, and cure, and have earmarked federal dollars for research and treatment initiatives that will be instrumental in furthering the field in the years to come.

Before discussing the current state of autism, however, let’s briefly review the history of this disorder and what we have learned over the years.

In 1943, a doctor named Leo Kanner began observing a group of children who were previously thought to have mental retardation. He noticed that these children had difficulty developing speech, and did not socially interact with their peers. He also noted that these children engaged in ritualized and/or repetitive behaviors to the exclusion of other activities.

These children had difficulties with transitions, and did not like changes in their routines or schedules. Some of them experienced regression in their functioning over time, losing skills that had been established previously. We know Kanner’s description will be familiar to you if you are a parent, caregiver, or teacher of a child on the autism spectrum.

At the time, treatment for autism was very limited. Most of these children were placed in institutions, far from the public eye, to live out their lives. Professionals commonly held the view that “refrigerator mothers” were responsible for the symptoms observed in these children. Deficits in the children’s functioning were assumed to be linked to poor attachment and/or absentee parenting (Bettleheim, 1967). Because parents were often blamed for their children’s disorders, many experienced great shame for having a child with ASD.

Much has changed in the last six decades. We now know that autism, a neurodevelopmental disorder, is most likely caused by a combination of genetic and environmental factors. Although we would like to think that parents are no longer blamed, all-too-frequent examples demonstrate how autism is still widely misunderstood.

Around the same time that Kanner was identifying symptoms of autism, pediatrician Hans Asperger was studying another group of children (Wing & Gould, 1979). These boys and girls were also having problems in social interactions with their peers. Like their counterparts, they exhibited behavioral problems commonly seen in children with autism. However, this group of children did not have deficits in speech and language formation. In fact, these children often spoke early and frequently. They also did not display deficits in adaptive functioning. In other words, these children could feed themselves, dress themselves, participate in their personal care, and function independently in the community. Unlike the group that Kanner observed, most of these children did not have lowered cognitive abilities. They were often very bright and had specific areas of interest in which they could amass large amounts of information.

Unfortunately, Asperger’s research was not discovered until three decades later. It was reintroduced to the field when other individuals interested in ASD began questioning the diagnostic criteria that were used at the time. His work has made a tremendous difference in the way we have come to view and understand the autism spectrum.

A Brief History of Autism Research

Cautionary tales from researchers’ past mistakes

The past six months saw the release of two bestselling books about autism: Steve Silberman’s Neurotribes , and John Donvan and Caren Zucker’s In a Different Key .

Both books chronicle the oftentimes dark history of autism while expressing hope for a better future for people with the condition. They focus on the good work of people—strong-willed parents and devoted advocates—who transformed a once-shameful diagnosis into a widely accepted condition. But they also highlight several missteps by scientists that derailed research and the lives of many people on the spectrum.

This history offers lessons for today’s scientists, ranging from the importance of purging presumptions about autism to the acute need for services that help people, especially adults, with the condition.

The books take the reader back to the infancy of autism research. In the late 1940s, psychiatrists declared that they had found autism’s cause: cold parents—particularly mothers—who did not love their children enough. Leo Kanner , one of the first psychiatrists to study the condition, abandoned his own theory that autism was innate in favor of what would later be called the “ refrigerator mother ” hypothesis.

“If Kanner had really stuck to his guns and gone with his instincts, it’s possible the whole refrigerator-mother theory never would have evolved the way it did,” Donvan says.

Instead, for the next two decades, many psychiatrists focused on treating what they believed were defective mothers and fathers. Research exploring other explanations for the condition stagnated.

Having a scientific orthodoxy can be a positive thing, but it can cause severe damage if it turns out to be inaccurate, Donvan says. “The history of autism has shown that, time and time again—particularly in the early days—researchers failed to examine their own assumptions and biases.”

Flawed assumptions also invade researchers’ attitudes toward people with autism, according to Silberman. He says scientists long viewed people with autism as less than human, rationalizing a range of “treatments” that were more akin to torture than therapy, including electric shocks and physical abuse such as hitting. Although contemporary practitioners have largely abandoned these methods, some continue to use punishment as a means of modifying behavior, he says.

“The first question that should be asked in any research project is, ‘Would you do this to a non-autistic person?’” he says, noting that asking adults with autism for their input is a crucial second step. “Autistic people should be seen as valuable collaborators in your work, rather than as passive subjects.”

Many researchers working in the field today are motivated by a deep desire to help people with autism, Donvan says. But scientists should still ask themselves, “Is there anything I’m doing now that I may regret 20 years from now?”

Some of the researchers who tested electroshock therapy or hallucinogenic drugs in children with autism back in the 1950s and ‘60s did so with the best of intentions, Donvan says. “In light of modern mores and best practices, those choices look bad today,” he says. “But that does not mean those researchers were motivated by cruelty or sadism.”

The 1990s saw a sea change in awareness of autism. People previously diagnosed with childhood schizophrenia or minimal brain damage were recognized as having autism all along. This new awareness sparked the notion of an ‘autism epidemic,’ which drew an influx of research dollars into a once underfunded and overlooked field. But unfortunately, little of this money went toward helping people with autism.

It went largely to uncovering autism’s cause, giving scientists insight into the workings of the brain. It also generated leads for drug targets. But for people with autism and their families, “the tangible benefits remain elusive,” Silberman says.

Researchers know “astonishingly little” about the lives of adults with autism, he adds, including how many of them there are , how other conditions associated with autism affect their lives and how best to translate their abilities into meaningful employment . Likewise, little research focuses on how autism manifests itself in women , or on determining the prevalence of autism in minority communities with limited access to diagnostic services.

There is also little research into better drugs for controlling seizures—one of the leading causes of death among people with autism.

“These are not questions that can be answered by sequencing another set of genomes of people from multiplex families,” Silberman says. “That kind of work is still very much worth doing, but if we’re only doing that kind of long-range research, we’re not really meeting our responsibility as a society to help the autistic people who are all around us lead happier, healthier, more fulfilling and more secure lives.”

For those who are investigating treatments and services for people with autism, Zucker and Donvan warn that the work carries great responsibility. Parents are desperate for guidance about how to help their children, they say—especially in light of the emphasis put on early intervention . As past examples ranging from vitamins to hugging therapy have shown, families will rush to adopt new methods that are prematurely presented as solutions.

“Researchers need to be very, very careful in how they present their findings, so as not to set off hope for a quick, silver-bullet-type solution,” says Donvan.

How researchers talk to the press can shape the public reaction to research. In 1987, for example, The New York Times reported on the work of Ivar Lovaas, a clinical psychologist and pioneer in applied behavior analysis. The story, titled “ Researcher Reports Progress Against Autism ,” described children who were “transformed” into “apparently normal children.”

Although Lovaas never used the word ‘cure’ when talking to the Times , the story implied as much. The fact that his research was preliminary was largely overlooked. Parents frantically flew their children to his lab at the University of California, Los Angeles, even as he hopelessly tried to correct the false headlines.

Today’s scientists should take great care when describing their work and strive to communicate their findings in terms non-experts can understand, Donvan says. “Researchers need to understand that there’s a public that is hanging on their every word.”

This post appears courtesy of Spectrum .

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The History of Autism

Editorial Policy | Research Policy

Learn about major scientific events and changes in scientific understanding that helped us better understand autism spectrum disorder.

The concept of autism was introduced over a century ago as a specific symptom of schizophrenia. Since then, autism has gradually become recognized as a neurodevelopmental disorder. Additionally, the perception of autism has changed from being a psychological problem caused by bad parenting to a disorder caused by biological and environmental factors.

Autism  is recognized by the Diagnostic and Statistical Manual of Mental Disorders, 5th Edition (DSM-5) as a developmental disorder. The criteria for diagnosis have been expanded to include milder symptoms, such as in the case of Asperger’s syndrome. The DSM-5 does not distinguish subcategories of autism spectrum disorder — it looks at deficits in social interactions and repetitive behaviors to help make a diagnosis.

Autism Timeline

Here is a brief timeline describing major developments in the history of autism, including scientific breakthroughs, changes in public perception and controversies:

• 1908 : The German psychiatrist Eugene Bleuler coined the term “autism” to describe symptoms of some severe schizophrenia cases. Autism described as retreating to the inner life to avoid facing the harshness of reality.
• 1943 : Leo Kanner, a child psychiatrist at Johns Hopkins University School of Medicine, identified autism as a separate psychological disorder in children. Kanner described it as early infantile autism, characterized by symptoms including obsessiveness, deficits in social behavior and a need for sameness.
• 1944 : Hans Asperger, a pediatrician at the University of Vienna, described a similar group of symptoms and coined the term “autistic psychopathy.” Asperger was particularly interested in high-functioning individuals who showed social deficits.
• 1967 : Kanner and others theorized that autism stemmed from poor parenting in a child’s early years. According to an article published by Kanner, emotionally cold (or “refrigerator” mothers) may have been responsible for the symptoms of autism in their children. Bruno Bettelheim was a proponent of this theory and popularized the idea of refrigerator mothers.
• 1977 : A study conducted by Susan Folstein and Michael Rutter found that autism had a high chance of occurring in one twin if their identical twin had autism. In the case of non-identical twins, however, there were no occurrences of autism in both siblings. This study showed that genetics plays an important role in the development of autism, challenging the view that autism was caused by bad parenting.
• 1980 : Autism entered the Diagnostic and Statistical Manual of Mental Disorders as a separate entity. Autism was recognized as a developmental disorder separate from schizophrenia, and previous associations with the presence of hallucinations were removed. Autism was divided into four subcategories: infantile autism, residual autism, childhood-onset pervasive developmental disorder and an atypical form.
• 1987 : The DSM-III was revised in 1987 to broaden the concept of autism, and the criteria were expanded to include milder symptoms. The same year, Ivar Lovaas, the pioneer of applied behavioral analysis, published a study showing an improvement in the symptoms of autistic children after intensive behavioral therapy.
• 1988 : The movie “Rain Man” revolved around the story of an autistic savant, Raymond Babbitt, portrayed by Dustin Hoffman. This movie increased public awareness about autism spectrum disorder, but it also generated a stereotype regarding the abilities of people with autism.
• 1990 : In 1990, the U.S. Congress passed legislation to include autism in the category of education disability. This helped individuals with autism qualify for special education.
• 1994 : The DSM-4 was released with Asperger’s syndrome added as a separate subcategory of autism spectrum disorder.
• 1998 : Andrew Wakefield and his colleagues released a report in the Lancet journal suggesting that the measles, mumps and rubella (MMR) vaccine  may predispose children to autism . The study involved only 12 subjects and did not have scientific controls, but it received widespread media attention. This resulted in a decline in MMR vaccination rates.
• 2001 : Use of thimerosal, a mercury-based preservative used in vaccines, was discontinued in childhood vaccines. This was due to the speculation regarding the association between thimerosal and autism. Many scientific studies have reported that there is no association between thimerosal and autism.
• 2009 : A  study published  in 2014 by the Centers for Disease Control and Prevention (CDC) showed that 1 in every 59 children had autism. A similar survey conducted by the CDC in 2002 indicated that every 1 in 150 children had autism. This  rise in autism  is believed to be caused by increased autism awareness and changes in autism diagnosis criteria. However, biological factors such as parents having children at an older age may also be responsible for the increase.
• 2013 : The DSM-5 was released, which combined all the subcategories of autism into a single diagnostic entity called the “autism spectrum disorder.” This was done to address inconsistencies in the criteria used in diagnosis.

Autism Today

Although much scientific progress had been made, there is much more to learn about the causes, diagnosis and best treatment methods of autism.  Current research on autism  is primarily focused on finding genes that predispose people to autism. Other efforts include trying to find differences in brain activity that are specific to people with autism. Some research is aimed at identifying prenatal factors that predispose newborns to autism.

The severity and the type of symptoms present in people with autism vary widely, and the same treatment does not work for everyone. Research is currently underway to assess ways to individualize treatment.

Various non-medication  treatment approaches , including speech therapy, occupational therapy and behavioral therapy, are generally used to address autism symptoms. Applied behavioral therapy has been one of the most effective approaches, teaching people with autism to avoid negative behaviors and display positive ones. Applied behavioral therapy also involves teaching communication and social skills. Some research is focused on improving ways to engage children with autism in a classroom setting.

Medicinal approaches include the use of antipsychotics like risperidone and aripiprazole, and other medications are currently being investigated. People with autism are considered to have disrupted excitation and inhibition levels in the brain, and new drugs that restore these levels are also being investigated. Since changes in the immune system are associated with autism, researchers are also investigating anti-inflammatory drugs that regulate the immune system. Alterations to the nicotine-acetylcholine receptor have also been found in people with autism. Researchers are looking into whether drugs or nicotine itself can have therapeutic potential.

Autism spectrum disorder can sometimes  co-occur with substance use disorders .

Evans, Bonnie. “How autism became autism: The radical transformation of a central concept of child development in Britain.” History of the Human Sciences, March 2013. Accessed September 29, 2019.

Hollander, Eric; Uzunova, Genoveva. “ Are there new advances in the pharmacoth[…] spectrum disorders? ” World Psychiatry, February 2017. Accessed September 29, 2019.

Centers for Disease Control and Prevention. “ Data & Statistics on Autism Spectrum Disorder. ” September 3, 2019. Accessed October 11, 2019.

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The Early History of Autism in America

A surprising new historical analysis suggests that a pioneering doctor was examining people with autism before the Civil War

John Donvan and Caren Zucker

Billy was 59 years old that spring or summer of 1846, when a well-dressed man from Boston rode into his Massachusetts village on horseback, and began measuring and testing him in all sorts of ways. The visitor, as we imagine the scene, placed phrenologist’s calipers on his skull, ran a tape measure around his chest and asked many questions relating to Billy’s odder behaviors. It was those behaviors that had prompted this encounter. In the parlance of the mid-19th century, Billy was an “idiot,” a label that doctors and educators used not with malice but with reference to a concept that owned a place in the medical dictionaries and encompassed what most of us today call, with more deliberate sensitivity, intellectual disability.

Billy’s name (but not the village he lived in) was on a list of the commonwealth’s known “idiots,” hundreds of whom would be visited that year. A few months earlier, the legislature had appointed a three-man commission to conduct, in effect, a census of such individuals. In Billy’s case, however, the man who examined him soon realized that no commonly accepted definition of intellectual impairment quite fit this particular subject. Although Billy was clearly not “normal,” and was considered by his family and neighbors to be intellectually incapacitated, in some ways he demonstrated solid, if not superior, cognition. His ability to use spoken language was severely limited, but he had perfect musical pitch and knew more than 200 tunes. Billy was not the only person whose combination of skills and strengths puzzled the examiners. As the leader of the commission would acknowledge, there were “a great many cases” seen in the course of the survey about which it was “difficult to say whether...the person should be called an idiot.”

But what diagnosis might have fit better? If Billy were alive today, we think his disability, and that of others documented then in Massachusetts, would likely be diagnosed as autism. True, the actual word “autism” did not exist in their time, so neither, of course, did the diagnosis. But that does not mean the world was empty of people whose behaviors would strike us, in 2016, as highly suggestive of autistic minds.

There are no known biological markers for autism. Its diagnosis has always been a matter of experts closely watching an individual, and then matching what that person says and does against established criteria. Finding it in the past requires finding a witness, also from the past, who was good at observing behaviors and writing down what he saw.

Like that man on the horse, whose devotion to hard data, fortunately for detectives of autism history, was far ahead of his time.

Samuel Gridley Howe, born into a well-to-do Boston family in 1801, was an adventurer, a medical doctor, a visionary educator and a moral scourge. He was also half of what today would be called a power couple. He and his New York-born wife, Julia Ward Howe, operated at the Brahmin level of Boston society, well-connected, well-traveled and with a shared commitment to the anti-slavery cause, which perhaps helped bind them together through their often stormy marriage. Samuel secretly raised funds for John Brown’s violent guerrilla campaign against slavery, and Julia, after visiting Abraham Lincoln at the White House in November of 1861, composed a set of verses whose original intent was to inflame a merciless passion for crushing the Confederacy. Today, with a few word changes, her “Battle Hymn of the Republic” is an American standard, struck up at high-school graduations and when presidents are buried.

Her husband’s most enduring achievement, however, is the 38-acre Perkins School for the Blind, in Watertown, Massachusetts—a storied institution that opened in 1832. Howe was the school’s first and longtime director, and lead designer of its groundbreaking curriculum. His radical idea, which he personally imported from Europe, was that people who are blind can and should be educated. Howe believed in the improvability of people, including those whose physical impairments most of society regarded as divine retribution for sins that they, or their parents, had committed. At the time, few others were interested in sending children who were blind to school: They were regarded as a lost cause.

That Howe would emerge as a thundering advocate for teaching children who were disabled would have stunned those who knew him only in his mischievous younger years. As an undergraduate at Brown University, he kidnapped the university president’s horse, led the animal to the top of a campus building and, the story goes, left it there to be found the next morning. After being caught throwing a stone through a tutor’s window and putting ashes in the man’s bed, Howe was not expelled from Brown but “rusticated”—sent to a remote village to live with a pastor. Around the same time, his mother died; he returned to school a changed man. He graduated in 1821, picked up a medical degree at Harvard in 1824, and then embarked on a lifetime of high-minded challenges, always as a champion of the underdog.

He headed for Greece first, and the front lines of a war, serving as a battlefield doctor on the side of the Greek revolutionaries rising up against Turkish rule. After that, he raised funds for Polish patriots in their struggle to throw off czarist domination. He spent a month of the winter of 1832 in jail in Prussia, where he had been holding clandestine rendezvous with Polish contacts.

Howe had a second reason for making that trip to Prussia. By then, on what seems like a whim, he had agreed to become the first director for the New England Asylum for the Blind. He’d gone to Prussia—and France and Belgium—to see how special education was done. He learned well. Within a decade and a half, Howe was a celebrated educator. His school, renamed after a financial benefactor, Thomas Handasyd Perkins, was a resounding success. Blind children were reading and writing, appreciating poetry, playing music and doing math. One student, Laura Bridgman, who was both deaf and blind, became a worldwide celebrity, especially after Charles Dickens published an account of spending time in her company in January of 1842. Dickens’ description of the girl’s “earnestness and warmth...touching to behold” helped advertise and validate Howe’s conviction that society should believe in the potential of disabled people. Some decades later, the Perkins School would enroll its most famous student—Helen Keller.

Emboldened by the school’s progress with blind students, Howe set out to prove that so-called idiots could learn and also merited a school to go to. For this he was publicly ridiculed—dismissed as a “Don Quixote.” But Howe had allies in the legislature, and in April of 1846, the body resolved to support a survey, led by him, of intellectually impaired citizens “to ascertain their number, and whether any thing can be done for their relief.”

In November 2015, the U.S. Centers for Disease Control and Prevention reported a new estimate of the prevalence of autism in children ages 3 to 17. The figure, 1 in 45, is the highest ever announced by the CDC, up from 1 in 150 in 2007.

Though many news reports described the figure as an alarming jump in the number of people with the condition, in fact no study carried out to date can be said to tell us exactly how much autism exists in the population at any given moment. Instead, there are estimates with wide margins of uncertainty. The reasons are many: inconsistency in how the diagnosis is applied from one locale to another; disparities among different ethnic, racial and socioeconomic groups in the availability of diagnostic services; and greater autism awareness, which tends to drive rates higher in places where the condition is better recognized. Notably, the CDC’s 1-in-45 estimate is based not on direct observation of children, but on interviews with parents, who were asked whether a child in the family had been diagnosed with autism or any other developmental disability. Among the acknowledged limitations of the approach is that it cannot correct for errors or differences in how the diagnosis was made in the first place.

In addition, researchers have continually revised the operative definition of autism, generally in a direction that makes it easier to qualify for the label now than in the past. This has added to the impression that the true, underlying rate is increasing. It may well be that autism is on the rise. But it may also be that we are getting better at finding those people who merit the diagnosis and were once overlooked.

Still, the dominant narrative has been that real rates are going up, and the United States is in the midst of an autism “epidemic,” even though most experts see that as a highly debatable proposition. Moreover, the “epidemic” story has helped crystallize the notion that “something must have happened” in the near past to cause autism in the first place. Most famously, some activists blamed modern vaccines—a now discredited theory. Air and water pollution have also been posited. Such 20th-century factors accord with the history of autism as a diagnosis: The condition was not even named in the medical literature until the late 1930s.

Yet even the man usually credited with first recognizing autism, a Baltimore-based child psychiatrist named Leo Kanner, doubted that the profound impairment in social relatedness he first reported seeing in 11 children in 1943 was, in fact, something new in human history. While a Viennese pediatrician named Hans Asperger described something similar, Kanner’s account was more influential. His contribution, he said, was not in spotting the disparate behavioral traits that constitute autism—strange use of language, a disconnectedness from human interaction and a rigid affinity for sameness, among others—but in seeing that the conventional diagnoses used to explain those behaviors (insanity, feeblemindedness, even deafness) were often mistaken, and in recognizing that the traits formed a distinctive pattern of their own. “I never discovered autism,” Kanner insisted late in his career. “It was there before.”

Looking back, scholars have found a small number of cases suggestive of autism. The best known is the Wild Boy of Aveyron, later given the name Victor, who walked naked out of a French forest in 1799, unspeaking and uncivilized, giving birth to fantastic tales of a child raised by wolves; in recent decades experts have tended to believe that Victor was born autistic and abandoned by his parents. The behavior of the so-called Holy Fools of Russia, who went about nearly naked in winter, seemingly oblivious to the cold, speaking strangely and appearing uninterested in normal human interaction, has also been reinterpreted as autistic. And today’s neurodiversity movement, which argues that autism is not essentially a disability, but, rather, a variant of human brain wiring that merits respect, and even celebration, has led to posthumous claims of autistic identity for the likes of Leonardo da Vinci, Isaac Newton and Thomas Jefferson.

As far as we can determine, we are the first to suggest the diagnosis for Howe’s numerous cases, who appear to constitute the earliest known collection of systematically observed people with probable autism in the United States. We came across them during the fourth year of research for our new book,  In a Different Key: The Story of Autism , by which time our “radar” for autistic tendencies was fairly well-advanced. Granted, retrospective diagnosis of any sort of psychological state or developmental disability can never be anything but speculation. But Howe’s “Report Made to the Legislature of Massachusetts upon Idiocy,” which he presented in February of 1848, includes signals of classic autistic behavior so breathtakingly recognizable to anyone familiar with the condition’s manifestations that they cannot be ignored. Plus, his quantitative approach vouches for his credibility as an observer, despite the fact that he believed in phrenology, which purported to study the mind by mapping the cranium, long since relegated to the list of pseudosciences. Howe’s final report contained 45 pages of tabulated data, drawn from a sample of 574 people who were thoroughly examined by him or his colleagues in nearly 63 towns. The tables cover a wide range of measurements as well as intellectual and verbal capacities. Howe, extrapolating, estimated that Massachusetts had 1,200 “idiots.”

In a Different Key: The Story of Autism

Nearly seventy-five years ago, Donald Triplett of Forest, Mississippi became the first child diagnosed with autism. Beginning with his family’s odyssey, "In a Different Key" tells the extraordinary story of this often misunderstood condition, and of the civil rights battles waged by the families of those who have it.

Billy was Number 27 in the survey. Across 44 columns of data, we learn that he was 5 feet 4 inches tall, his chest was 8.9 inches deep and his head was 7.8 inches in diameter front to back. At least one of his parents was an alcoholic, he had one near relative who was mentally ill or disabled, and Billy himself was given to masturbation. (Howe subscribed to the once commonly held view that masturbation was a cause of mental disability.) Billy was given a low “4” rating in the “Ability to Count” column (where the average was “10”). His “Skill in the Use of Language” was also below average, at “6.” But his “Sensibility to Musical Sounds” was on the high side, at “12.”

As much as Howe favored precise measurement, he was honest in admitting that his tables of data failed to capture essential aspects of Billy’s personality. Rather than gloss over the problem, Howe acknowledged that Billy’s musical gifts and other qualities made it difficult to label the young man as an “idiot.” A striking observation that reinforces the notion that Billy was autistic concerns his spoken language. Howe gave this account: “If he is told to go and milk the cows, he stands and repeats over the words, ‘Billy, go and milk the cows,’ for hours together, or until some one tells him something else, which he will repeat over in the same way.” And yet, Howe reported, Billy was capable of understanding nonverbal communication. “Put a pail in his hand,” he wrote, “and make the sign for milking, and give him a push, and he will go and fill the pail.”

Experts today refer to the tendency to repeat words or phrases as echolalia. It is listed in the latest edition of the Diagnostic and Statistical Manual of Mental Disorders as one of the “stereotyped or repetitive motor movements, use of objects, or speech” that can contribute, in combination with other behaviors, to a diagnosis of autism.

Echolalia does not necessarily persist for life. For example, we have spent time with the first child whom Leo Kanner cited in his groundbreaking 1943 paper, autism’s “Case 1,” Donald Triplett, now a healthy 82 years old. Donald can engage in conversational speech, but he had pronounced echolalic tendencies as a child, when he uttered random-seeming words and phrases such as “trumpet vine,” or “I could put a little comma,” or “Eat it or I won’t give you tomatoes.” It is fascinating that the young Donald demonstrated some other traits that made Billy stand out to Howe back in the 1840s. Like Billy, he had an unusual gift for remembering songs; as a toddler, Donald was singing complete Christmas carols after hearing them just once. Also like Billy, Donald had perfect pitch; when he belonged to a choir, the director relied on Donald to give his fellow choristers their starting note, in lieu of a pitch pipe.

It is often noted that no two people with autism ever have it in exactly the same way. While Billy was reported to be bad at counting, Donald was fascinated by numbers, and could multiply double- and triple-digit numbers in his head instantly and flawlessly.

Howe did discover that same talent for numbers among other people in his study population. One man, Case 360, “has the perception of combination of numbers in an extraordinary degree of activity,” Howe wrote. “Tell him your age, and ask him how many seconds it is, and he will tell you in a very few minutes.” Cases 175 and 192 also confounded Howe, as they were both able to count up to “20,000 and perform many simple arithmetical operations, with a great deal more facility than ordinary persons.”

Finally, Howe drew attention to a young man, Case 25: “This young man knows the name and sound of every letter, he can put the letters into words, the words into sentences and read off a page with correctness; but he would read over that page a thousand times, without getting the slightest idea of the meaning.”

That description is highly reminiscent of the modern idea that autism involves a tendency for “weak central coherence.” It is another way of saying that autistic people are better at processing parts of a pattern—while missing how the parts fit together in the pattern as a whole. (Donald’s mother remarked that he loved going to the movies as a boy, but always came home unaware that the flashing images were meant to add up to a story.)

To be sure, Howe’s cases do not prove there was a lot of autism in his day, or even any. But the concept of autism helps explain some of the cases that puzzled him. We showed Howe’s observations to Peter Gerhardt, chairman of the scientific council of the Organization for Autism Research. Absent some contradictory information, and invoking the precaution about evaluating people one had not met face to face, Gerhardt told us that “autism spectrum disorder would appear to be a far more accurate description” than intellectual disability for those individuals.

Howe may have been primed to spot “outlier” cases as a result of correspondence with a fellow physician named Samuel Woodward, head of a Massachusetts facility then known as the Worcester Lunatic Hospital. The year before Howe undertook his survey, he published a letter in the  Boston Daily Advertiser , citing a report that Woodward had shared with him. Woodward described a group of children in his care who didn’t fit the usual categories. These “little patients have intelligent faces, well-formed bodies, good developments of the head, and active minds,” Howe wrote, citing Woodward: “Their movements are free, easy and graceful, many of them are sprightly, even handsome; they are generally restless, irritable and extremely mischievous, and are rarely able to speak.... No person familiar with these cases would be likely to mistake them for idiots.”

What would their diagnosis be if those children were seen by a neurologist today? James Trent, author of the superb 2012 Howe biography  The Manliest Man , has suggested that this group of children in Worcester would be diagnosed with autism, much as we are suggesting that Howe’s cases were also candidates for the label.

Howe was appalled by the horrifying conditions in which many “idiots” lived—crammed into almshouses, kept in cages, left to wander unwashed and uncared for. He demanded that society do better by this vulnerable group. When the community failed “to respect humanity in every form,” Howe wrote in a letter to a state legislator, it “suffers on account of it” and “suffers therefor [sic] in its moral character.”

Part of his agenda was to persuade the legislature to fund a school for the mentally disabled. He succeeded. After reading an interim report about his survey, lawmakers appropriated $2,500 for the purpose, which allowed Howe to take in ten mentally disabled students at Perkins. He proved, in short order, that they could indeed be educated. Based on that success, Howe founded a second school—the Massachusetts School for the Feeble-Minded, subsequently renamed the Fernald State School, and then the Fernald Center. Unfortunately, in later decades, his innovative facility fell victim to the neglect that defined many similar institutions in the 20th century. More like warehouses than schools, these institutions confined people in overcrowded conditions, while delivering little that could be called education. Despite real efforts at reform in the last part of the 20th century, the center was finally closed for good in 2014.

Howe had begun warning, in the years before his death in 1876, against the trend he saw taking shape, of states moving to segregate disabled people behind institutional walls in distant locations. Howe’s forward thinking had its limits, though. Even with his fervent anti-slavery views, he took the cultural superiority of the white race for granted. And his conviction that women deserved education was tempered by his adamant belief that a wife’s place—including that of his famously activist spouse—was in the home. This early progressive who believed in the perfectibility of people was himself “not a perfect man,” as Trent put it.

A primary goal of Howe’s pioneering mental health survey was to discover the root cause of intellectual disability. In that respect, of course, he failed. But conceding that “the whole subject of idiocy is new,” Howe expressed hope in 1848 that his data would be of use to future generations trying to understand mental disability. “Science,” he said, “has not yet thrown her certain light upon its remote, or even its proximate causes.”

A century and a half later, we’re in much the same position in regard to autism. Still not sure how good we are at gauging autism in the population—or even at defining its boundaries—we wait for science to illuminate the mystery of its origins. Howe’s careful humanitarian work strongly suggests that answers may yet be found in the undiscovered past.

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John Donvan and Caren Zucker | READ MORE

John Donvan and Caren Zucker began covering autism in 2000 for ABC News, where Donvan is a correspondent and Zucker is a producer. After nearly a decade of television stories on the subject, they cowrote In a Different Key: The Story of Autism . On Twitter, Donvan is @JohnDonvan, and Zucker is @caren_zucker.

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Tracing the Origins of Autism: A Spectrum of New Studies

The etiology of a medical condition might seem an unlikely subject to arouse intense feelings. Yet few medical disorders have stirred up as much passion and divisiveness among scientists and the general public as autism has in recent years. The heat of the controversy has even attracted attention from periodicals such as The Wall Street Journal , the Columbia Journalism Review , and Wired magazine—seemingly improbable forums for a medical debate. Why all the furor?

At the eye of the storm is the startling climb in the numbers of children who have been diagnosed with one of the autism spectrum disorders (ASDs). The most severe ASD is autistic disorder (which often is called simply “autism”); other forms include Asperger syndrome and the much rarer childhood disintegrative disorder. In the United States, the diagnosis of ASDs increased roughly 10-fold over the course of a decade, from 4–5 children per 10,000 in the 1980s to 30–60 children per 10,000 in the 1990s, according to a report in the August 2003 Journal of Autism and Developmental Disorders . The 5 May 2006 issue of Morbidity and Mortality Weekly Report describes the results of two parent surveys from 2003 and 2004, which suggested that 55–57 children per 10,000 had autism (however, an editorial note points out that, due to the nature of the surveys, parents of children with other ASDs may have reported their children as having autistic disorder).

Some scientists believe that much of the upsurge is the result of increased awareness of ASDs or changes in diagnostic criteria, which would suggest that the true prevalence of the disorders has been stable over time. Others disagree. “It is premature to state that there is no increase in prevalence,” says W. Ian Lipkin, a professor of neurology, anatomy, and neurobiology at Columbia University. “None of the studies to date has been designed to definitively address the issue.”

The prevalence of ASDs plays into the fundamental question of what causes these disorders. If the number of cases is truly on the rise, then it would seem likely that some change in the environment is driving up the total. That’s partly what has divided scientists into opposing camps—they cannot agree on the relative importance of genetic and environmental factors in the disorders’ etiology.

Alas, answering the prevalence question might not end that debate. “Even if the prevalence of autism were stable,” says Lipkin, “you would not be able to rule out the possibility of an environmental trigger.” That’s because very little is known about the mechanisms that cause autism, be they environmental or genetic.

“The study of autism was, until recently, largely dominated by the field of psychology, where characterizing the behaviors and developing reliable instruments for diagnosis have been major areas of research over the past few decades,” says Irva Hertz-Picciotto, an epidemiologist at the University of California, Davis.

Indeed, the core symptoms of ASDs—social disinterest, repetitive and overly focused behavior, and problems in communication, usually appearing before 3 years of age—have been well described. Much less research has focused on the causes of these symptoms.

Several investigations dating back to the 1970s indicate that identical twins have a much higher concordance rate of ASDs than fraternal twins, according to a report in the Spring 1998 issue of Mental Retardation and Developmental Disabilities Research Reviews . Those studies provide some of the best evidence that these disorders have a strong genetic component. But the identity of the genes involved, much less how they produce ASDs, has not been established. Moreover, the concordance rate for identical twins is not 100%, which suggests that at least some cases must be associated with environmental or epigenetic factors.

A few cases of ASDs have been clearly linked to environmental insults. These include prenatal exposure to chemical agents such as thalidomide and valproic acid, as well as to infectious agents such as the rubella and influenza viruses. Here again, the concordance rate is not 100%, which suggests that a genetic predisposition is necessary for chemical and microbial factors to act as triggers.

Tantalizing clues like these are prompting scientists to reconsider the research agenda for ASDs. Martha Herbert, a pediatric neurologist at Harvard Medical School, and her colleagues have been applying the methods of genomics to identify environmentally responsive genes that might be important in these disorders.

“When you realize that the widespread changes we’re seeing in autistic brains may occur in parallel with or even downstream from widespread changes in the body—such as in the immune system—and that these changes may be environmentally triggered, you start looking for ways to think more broadly about genetic vulnerability. It can’t be just about ‘brain genes,’” Herbert says.

Some new epidemiological studies also are looking for gene–environment interactions. According to Diana Schendel, an epidemiologist and project officer for autism research at the CDC, which funds one of the projects, these initiatives will be able to examine many possible causal pathways to ASDs, including both genetic and environmental causes that may lead to the development of the disorders in different subgroups of children.

Some of these projects are already under way, whereas others will begin soon. All of the scientists involved, however, believe their research will finally provide some of the answers that everyone has been looking for.

The Childhood Autism Risks from Genetics and the Environment (CHARGE) project is unique among the large ASD epidemiological studies. It focuses solely on autistic disorder, and it emphasizes a search for environmental factors—including a broad array of chemicals in food, consumer products, and ambient air, as well as infectious and medical exposures—that might be linked to the disorder. The study is funded by the NIH.

CHARGE is a case–control study in which a group of autistic children aged 2 to 5 years is compared to a group of age-matched controls in a population-based study. “Because of the California Department of Developmental Services’ system of Regional Centers [nonprofit corporations that coordinate health care services and support for citizens with developmental disabilities], we have a handle on enumerating a high proportion of the children newly diagnosed with autism in our defined area over a specific time period,” says Hertz-Picciotto, the principal investigator of the CHARGE study. “Similarly, we can enumerate the children in the same area and time period who are not cases. We then sample from both.”

The project was initiated in 2002 with the goal of recruiting 1,000 to 2,000 children. Half of the children will be autistic. The other half will make up two control groups: one group of children with developmental delays (but not an ASD) and a second group of children selected from the general population without regard to developmental characteristics.

The advantage of the case–control design is that scientists can acquire large numbers of children with the disorder. By comparison, in a cohort design researchers would need a very large sample size, given the prevalence of autism, to acquire the same number of cases.

Hertz-Picciotto expects to have enrolled nearly 700 children by August 2006, the end of the first funding period. “I’ve applied for another five-year grant,” she says, “and I hope to be funded to enroll nine hundred in that round, which would bring us to sixteen hundred children.”

The CHARGE team is looking at possible exposures during the prenatal period and early childhood. Some of the data will be gathered through comprehensive interviews with parents, but Hertz-Picciotto admits that this is not the best way to look for exposures. “You ask people questions, and their answers may be colored by the fact that they know they have a child with a condition,” she says. “They may spend a lot of time thinking about what they might have done or what might have gone wrong, and they may have preconceived ideas about what caused [the disorder]. They might not be as objective.” Such problems with postdiagnosis interview information are recognized as a weakness of retrospective studies.

The scientists are getting around this issue by examining each child’s medical records and those of the mother during pregnancy and delivery—nonsubjective data gathered in the course of routine obstetric care. They are also collecting blood, urine, and hair specimens that will be analyzed in the laboratory.

The study has already provided some intriguing leads. “We’re finding that the immune system seems to function at a lower level in autism,” says Hertz-Picciotto. “That’s an important clue. It could mean that whatever causes autism also disrupts the immune system, or it could be that the immune system disrupts neural development so that something goes awry in laying down brain circuitry prenatally or in the early postnatal period.” [For more information on the CHARGE study, see p. 1119, this issue.]

The Autism Birth Cohort (ABC) Study, now under way in Norway, is a large prospective design that is expected to gather information on 100,000 babies. The work is being led by scientists at the Mailman School of Public Health at Columbia University, who are collaborating with colleagues at the Norwegian Institute of Public Health, with funding from the U.S. National Institute of Neurological Disorders and Stroke.

“When you want to know why some people are more at risk than others in a population, then that’s best answered using a cohort design,” says Ezra Susser, an epidemiologist at Columbia University and a co-investigator on the ABC project. “When we think about environmental causes of [ASDs], we’re probably interested in phenomena that occur prior to birth or perhaps shortly after birth. So you want to collect prospective data from people as early as possible in pregnancy.” Because ASDs are not common, the study will need large numbers of children to have enough statistical power, according to Susser.

So far the ABC team has recruited 75,000 pregnant Norwegian mothers, but Susser is hoping for more. “We’ve got enough to look for an environmental risk factor, but you need larger numbers for studying gene–environment interactions, which could turn out to be important,” he says. It’s possible the team could acquire greater numbers by collaborating with other studies. One candidate for collaboration is the Avon Longitudinal Study of Parents and Children in the United Kingdom, which is looking at the complex ways in which environmental features may relate to optimal development and health in children. But there’s been no agreement yet, Susser says.

Even so, the ABC scientists are optimistic about their study. “Little is known about the natural history of [ASDs],” says Lipkin, who is the principal investigator of the project. “By starting prenatally, we’re collecting detailed, critical information about environmental exposures in an unbiased fashion.”

The scientists are also collecting plasma, serum, RNA, and DNA. “We have extraordinary biological materials,” says Lipkin. “We can pursue biomarkers as well as exposure to toxicants and infection. We also have maternal DNA, paternal DNA, and the child’s DNA [so-called trio data]; thus we can look for the appearance of novel mutations,” he adds.

The ABC researchers will follow the children through time, with parents answering questionnaires about the health and social interactions of their children as they reach 6, 18, and 36 months of age. “It may be that the developmental trajectory tells us much more than a single time point can ever tell us about the pathogenesis of [ASDs],” says Mady Hornig, a physician-scientist at Columbia University who participates in the project.

Despite their enthusiasm for the project’s potential, the ABC scientists feel they could accomplish much more if they only had the funding. “The pity of it is we have no money to do the biological work,” says Lipkin. “We can collect the samples and do the questionnaires, but we’ve been unable to get funding to look for any of the environmental factors. We’re collecting blood, but we won’t know whether there’s a biomarker until we do a biomarker analysis. We have funds to collect RNA, but in order to do the transcript profiling we need approximately four hundred dollars per sample,” he says.

Lipkin adds that there’s only so much that one can do with questionnaire data. “We do ask about infection and diet, but that’s not the same as having a lab value that can validate what was reported, and then look at a direct correlation with the outcome,” he says.

Lipkin believes that part of the problem is that searching for environmental factors goes against the current research paradigm in ASDs. “The focus is on genetic factors,” he says. “Infectious diseases, toxicology, and immunology receive short shrift. The ABC is clearly the right opportunity to pursue these other leads because we have the ideal samples to survey prenatally and postnatally,” he says.

The scientists are just now receiving the responses to the 36-month questionnaire. “It’ll probably be another two years before we have our first report,” Hornig says. Funds are now in place to study the children at 36 months; however, the team hopes to follow them for a lifetime, according to Hornig.

In response to the Children’s Health Act of 2000, the CDC established and funds six Centers for Autism and Developmental Disabilities Research and Epidemiology (CADDRE) to investigate potential risk factors for ASDs. The multisite approach offers a study group that is geographically and demographically more representative of the general U.S. population than a smaller regional study could provide, according to Craig Newschaffer, an epidemiologist and principal investigator at the Johns Hopkins Bloomberg School of Public Health CADDRE site.

According to Newschaffer, the CADDRE sites will use a case cohort design in which the exposure patterns of the ASD cases are compared to a random sample of children living in the same geographic area. A third study group, consisting of neurodevelopmentally impaired children who do not have an ASD, will round out the sample populations. The investigators hope to enroll a total of 650 to 900 children, aged 3 to 5 years, in each study group across all the sites, making CADDRE the largest study of its kind in the United States, says Newschaffer. A uniform protocol across the sites will allow the scientists to pool their data.

CADDRE will collect and archive blood, cheek cell, and hair samples from the children in order to investigate a broad range of potential risk factors. “We’re not focused on the environment as much as CHARGE is,” says Newschaffer, “but we are collecting data on questionnaires and reviewing medical records on exposure, in addition to the biosampling for exposures.”

The scientists should have sufficient numbers to look at gene–environment interactions. “We are collecting DNA from the parents and the kids from each of the groups. We’ll have trio data in each of the three groups, a potentially powerful design,” says Newschaffer.

CADDRE scientists will also characterize the behavior of the children, as well as describe any comorbid medical conditions and atypical physical features. The goal is to sort out different etiologic subgroups within the autism spectrum. As Newschaffer explains, “There are a lot of possible reasons why we’ve had a hard time coming up with genetic and nongenetic risk factors. One of them is that autism is likely a heterogeneous condition, with different etiologies producing kids with what appear to be similar phenotypic profiles. If you don’t separate out the different etiologic groups, it’s going to be very hard to find an association with a gene or an exposure. If we limit our analyses to kids that have a certain profile, we’re going to be able to make some informed guesses about what profiles might allow risk factors to emerge,” he says. The CADDRE sites will begin recruiting children into the study in the fall of 2006.

More Studies, More Acronyms

There are several other smaller epidemiological studies in the works. In California, scientists are tapping into specimen banks that have stored blood samples taken from mothers during pregnancy and from their children at birth. The Early Markers for Autism (EMA) study employs a case–control design, with about 100 children with an ASD (primarily autism), 100 who are developmentally delayed, and 200 from the general population. “We can correlate what’s happening in the mom and the baby, which is really exciting,” says Lisa Croen, a perinatal epidemiologist at the Kaiser Permanente Division of Research in California and the project’s principal investigator.

EMA is a multidisciplinary collaboration with epidemiologists, geneticists, immunologists, neurovirologists, and endocrinologists, according to Croen. “Because autism is so complex, it’s important for all these researchers to communicate with each other. I think EMA is a model for how to do research in autism,” she says. EMA is unique, according to Croen, because the study will be looking for biological markers of ASDs very early in development, during gestation, and at birth. “This allows us to focus on mechanisms that may be leading to autism rather than mechanisms that are consequences of having autism,” she says.

The EMA scientists are investigating genetic and nongenetic factors, with a focus on the immune dysregulation hypothesis of ASDs. “We’re measuring different kinds of immune markers, including immunoglobulin levels and antibodies to specific infectious agents, cytokines, and autoantibodies,” says Croen. “We’re looking for things that distinguish kids who are subsequently diagnosed with autism from those who aren’t. This will help us understand the pathobiology of autism—the mechanisms that are leading to the dysregulation in development.”

The three-year EMA is currently in its last year. “We still have lots of analyses to do,” says Croen, “but we’re beginning to write some papers. We’re finding differences between the children in levels of certain proteins measured in the circulating blood collected from mothers during pregnancy. I think the study has much to contribute to our understanding of the biology of what might be going wrong.”

Croen is also an investigator on the California Autism Twin Study (CATS), which expects to recruit 300 identical and fraternal twin pairs born between 1987 and 1999 in which at least one of the twins has an ASD. Comparing the twin pairs will allow the scientists to estimate the heritability of ASDs—the relative genetic and environmental contributions to the disorder. “Knowing the behavioral and developmental differences between the twins might help us understand the effects of gene expression, the in utero environment, and environmental triggers,” Croen says.

Hertz-Picciotto is also excited about a five-year study that she and her colleagues hope to begin soon. Unlike CHARGE, the new effort, called MARBLES (Markers for Autism Risk in Babies—Learning Early Signs), will be a prospective study in which data will be gathered before the children are diagnosed. Pregnant women who already have at least one child with autism will be enrolled right at the beginning of pregnancy. The mothers will keep diaries about their symptoms and health-related events, and the researchers will collect cord blood samples and placentas.

Based on previous research, Hertz-Picciotto expects that about 1 in 10 siblings of the autistic children will also have the disorder, and perhaps 1 in 4 or 5 will be “on spectrum” with a related but less severe condition such as Asperger syndrome, or with some symptoms of the broad behavioral phenotype, such as language delays and atypical social skills. “This work is complementary to the case–control approach, and should provide us with a lot of information that will build on what we find in CHARGE. It should be a phenomenal resource,” she says.

You Say You Want a Revolution

In April 2004, the U.S. DHHS issued a publication, Congressional Appropriations Committee Report on the State of Autism Research , describing recommendations made by a panel of expert scientists convened by the Interagency Autism Coordinating Committee (IACC). The IACC panel suggested an ambitious agenda, which included the goal of identifying environmental risk factors and their associated developmental windows within a four- to six-year period, as well as identifying genetic and nongenetic causes of ASDs and their interactions within seven to ten years.

Hertz-Picciotto, a member of the IACC panel, thinks these goals should be taken with a grain of salt. “I’m optimistic that we will have identified some environmental risk factors, and may have excluded a few others, between 2008 and 2010—but by no means will we have the final word. The genetics and the gene–environment interactions may be even tougher. Unfortunately, I don’t see enough groups working on the environmental contribution to autism, so it may be slower than projected,” she says.

Mark Blaxill, vice president of SafeMinds, a parent-led advocacy group, also believes that environmental risk factors don’t receive enough consideration. “The CDC has not addressed the crisis in autism responsibly,” he says. “They should be raising the alarm, and they have failed to do so. They should be asking why so many children are sick. Instead, they’ve tried to suggest a degree of doubt about the increases, and that diverts attention and funding from environmental causes.”

Schendel responds, “It is clear that more children than ever before are being classified as having an ASD. It is important that we treat common developmental disorders, and especially the ASDs, as conditions of urgent public health concern. The CDC’s efforts in addressing this public health concern include funding for ASD monitoring programs to understand ASD trends, funding for research into the genetic and environmental causes of ASDs, and education and outreach programs to promote early identification and timely intervention for all children with developmental problems.”

Despite the promise of the new epidemiological studies, some researchers are still dismayed, as one scientist put it, that “geneticists are running the show, and ignoring the environmental aspects.” What would it take for things to change? Blaxill invokes the ideas of philosopher Thomas Kuhn, who suggested that scientific revolutions occur when an old paradigm is replaced by a new one. “I believe we’re in the middle of a paradigm shift,” Blaxill says. “The dramatic explosion of autism rates does not fit the genetic model. It’s an anomaly that will kill the old paradigm.”

Reported Cases of ASDs in the United States and Outlying Areas

Studies of Environmental Factors in Autism Spectrum Disorders (ASDs)

Key to U.S. Funding Agencies: NIMH—National Institute of Mental Health; NINDS—National Institute of Neurological Disorders and Stroke; NIH—National Institutes of Health

Other Major Environmental Health–Related Studies

Key to U.S. Funding Agencies: CDC—Centers for Disease Control and Prevention; EPA—Environmental Protection Agency; JDRF—Juvenile Diabetes Research Foundation; NCI—National Cancer Institute; NIAID—National Institute of Allergy and Infectious Diseases; NICHD—National Institute of Child Health and Human Development; NIDCR—National Institute of Dental and Craniofacial Research; NIDDK—National Institute of Diabetes and Digestive and Kidney Diseases; NIEHS—National Institute of Environmental Health Sciences; NIH—National Institutes of Health

Groundbreaking study connects genetic risk for autism to changes observed in the brain

A groundbreaking study led by UCLA Health has unveiled the most detailed view of the complex biological mechanisms underlying autism, showing the first link between genetic risk of the disorder to observed cellular and genetic activity across different layers of the brain.

The study is part of the second package of studies from the National Institutes of Health consortium, PsychENCODE. Launched in 2015, the initiative, chaired by UCLA neurogeneticist Dr. Daniel Geschwind, is working to create maps of gene regulation across different regions of the brain and different stages of brain development. The consortium aims to bridge the gap between studies on the genetic risk for various psychiatric disorders and the potential causal mechanisms at the molecular level.

"This collection of manuscripts from PsychENCODE, both individually and as a package, provides an unprecedented resource for understanding the relationship of disease risk to genetic mechanisms in the brain," Geschwind said.

Geschwind's study on autism, one of nine published in the May 24 issue of Science , builds on decades of his group's research profiling the genes that increase the susceptibility to autism spectrum disorder and defining the convergent molecular changes observed in the brains of individuals with autism. However, what drives these molecular changes and how they relate to genetic susceptibility in this complex condition at the cellular and circuit level are not well understood.

Gene profiling for autism spectrum disorder, with a few exceptions in smaller studies, has long been limited to using bulk tissue from brains from autistic individuals after death. These tissue studies are unable to provide detailed information such as the differences in brain layer, circuit level and cell type-specific pathways associated with autism as well as mechanisms for gene regulation.

To address this, Geschwind used advances in single-cell assays, a technique that makes it possible to extract and identify the genetic information in the nuclei of individual cells. This technique provides researchers the ability to navigate the brain's complex network of different cell types.

More than 800,000 nuclei were isolated from post-mortem brain tissue of 66 individuals from ages 2 to 60, including 33 individuals with autism spectrum disorder and 30 neurotypical individuals who acted as controls. The individuals with autism included five with a defined genetic form called 15q duplication syndrome. Each sample was matched by age, sex, and cause of death balanced across cases and controls.

Through this, Geschwind and his team were able to identify the major cortical cell types affected in autism spectrum disorder, which included both neurons and their support cells, known as glial cells. In particular, the study found the most profound changes in the neurons that connect the two hemispheres and provide long range connectivity between different brain regions and a group of interneurons, called somatostatin interneurons that are important for maturation and refinement of brain circuits.

A critical aspect of this study was the identification of specific transcription factor networks -- the web of interactions whereby proteins control when a gene is expressed or inhibited -- that drive these changes that were observed. Remarkably, these drivers were enriched in known high-confidence autism spectrum disorder risk genes and influenced large changes in differential expression across specific cell subtypes. This is the first time that a potential mechanism connects changes occurring in brain in ASD directly to the underlying genetic causes.

Identifying these complex molecular mechanisms underlying autism and other psychiatric disorders studied could work to develop new therapeutics to treat these disorders.

"These findings provide a robust and refined framework for understanding the molecular changes that occur in brains in people with ASD -- which cell types they occur in and how they relate to brain circuits," Geschwind said. "They suggest that the changes observed are downstream of known genetic causes of autism, providing insight into potential causal mechanisms of the disease."

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Quantitative Biology > Quantitative Methods

Title: unraveling the autism spectrum heterogeneity: insights from abide i database using data/model-driven permutation testing approaches.

Abstract: Autism Spectrum Condition (ASC) is a neurodevelopmental condition characterized by impairments in communication, social interaction and restricted or repetitive behaviors. Extensive research has been conducted to identify distinctions between individuals with ASC and neurotypical individuals. However, limited attention has been given to comprehensively evaluating how variations in image acquisition protocols across different centers influence these observed differences. This analysis focuses on structural magnetic resonance imaging (sMRI) data from the Autism Brain Imaging Data Exchange I (ABIDE I) database, evaluating subjects' condition and individual centers to identify disparities between ASC and control groups. Statistical analysis, employing permutation tests, utilizes two distinct statistical mapping methods: Statistical Agnostic Mapping (SAM) and Statistical Parametric Mapping (SPM). Results reveal the absence of statistically significant differences in any brain region, attributed to factors such as limited sample sizes within certain centers, noise effects and the problem of multicentrism in a heterogeneous condition such as autism. This study indicates limitations in using the ABIDE I database to detect structural differences in the brain between neurotypical individuals and those diagnosed with ASC. Furthermore, results from the SAM mapping method show greater consistency with existing literature.

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Recent study reveals possible origins of autism

“At birth, the physical appearance and behavior of a child who will develop autism over the next few years are indistinguishable from that of a neurotypical child. Indeed, in most cases the fate of the child with regard to autism is not set at birth,” Naviaux said. 

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Autism in the Twentieth Century: An Evolution of a Controversial Condition

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• First Online: 17 September 2019

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• Michelle O’Reilly 5 ,
• Jessica Nina Lester 6 &
• Nikki Kiyimba 7  

Part of the book series: Mental Health in Historical Perspective ((MHHP))

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Autism spectrum disorder (i.e. autism) is clinically conceptualised as a lifelong neurodevelopmental condition diagnosed by examining impairments in communication, social interaction, and a rigidity in thinking. The twentieth century was an important one for autism as it was labelled and classified during this time, along with a rise of many different voices and perspectives regarding its classification as a psychiatric disability. On one hand, great advancements have been made in terms of understanding the condition, the aetiology, and treatments, and on the other, there has been a rise of critical thinking and political issues for the inclusion agenda. This chapter discusses these movements and changes in thinking.

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Autism Spectrum Disorder

What Is Autism Spectrum Disorder?

Autism Spectrum Disorders: Developmental History of a Concept

Introduction.

Clinically, autism spectrum disorder (henceforth, autism) has been described as a lifelong neurodevelopmental condition characterised by impairments in social interaction, communication, and rigidity in thinking. Additionally, autistic individuals are typically characterised as having executive functioning difficulties (i.e. self-regulation skills), sensory processing problems (i.e. the brain processing information from the senses), difficulties with sleep and food, limited theory of mind (i.e. the ability to see things from the point of view of others), and the possibility of various co-morbid mental health conditions. 1 Despite such descriptions, autism, as we now know it, is a relatively new condition. In less than a century, a whirlwind of ideas, movements, and positions have littered the autism literature, with a critical polemic threaded through the narratives of various autistic individuals, political advocates, writers, and academic scholars. Indeed, autism is a by-product of many (even conflicting) disciplinary knowledges, institutional discourses, and histories. 2

The twentieth century was a significant and powerful century for autism, and for some, it has been classified and understood as a ‘ twentieth-century disorder ’. 3 Not only were there clinical advances in terms of it being recognised, labelled, and identified and appearing in the classification systems for mental illness, but there was also the rise of pharmacology for treatment and the increased role of psychiatry for identifying and managing autism. Importantly, the twentieth century also saw a rise of critical rhetoric, challenges, political ideologies, and a range of movements, such as anti-psychiatry, critical psychiatry, neurodiversity, consumerism, and social models of disability. All these movements and perspectives made visible a struggle to invent, reconfigure, and reinvent the meaning of autism, with some challenging the position of autism as a mental health difficulty, that is, a psychiatric disability. Indeed, even in the historical present, the classification of autism as a mental health condition is controversial and contested. Later in the twentieth century, autism became redefined as a spectrum, which served to acknowledge the great heterogeneity within the meaning of autism and developed more refined ideas around the so-called impairments associated with it.

In this chapter, we overview some of the historical changes and, in doing so, highlight some challenges of labels and language that shroud those who are named autistic and/or take up this identity label. We also note the shifts in thinking that have challenged the psychiatric and psychological framing of autism. The residue of the twentieth-century tensions that is the genetic revolution, the diagnostic medicalisation, and the empowerment of neurodiversity has spilled over into the twenty-first century, leaving us with an array of critical discourses and challenges around what many now describe as a spectrum condition. That is, we are left with a patchwork of different perspectives and ideas regarding what constitutes autism, the language of autism, how autism should be researched, and the most appropriate healthcare pathways and other service provisions for those diagnosed. This chapter explores how this fractured view of one ‘mental health difficulty’ came to be. In so doing, we thread through our own position, that of social constructionism, not denying the reality of the autistic community, but acknowledging differences in views and the importance of language and meaning. Indeed, we recognise that for some autism is celebrated, treated as difference, and tensions of medical notions and impairments are proposed, and yet for others, autism is seen as disabling, the diagnosis is stressful, and treatments are actively sought. The range of perspectives that grew from the twentieth century are considered throughout. We do however insert a caveat here and note that the history of autism is vast and spans multiple disciplines and fields, and thus what follows can only ever represent a snapshot of history and inevitably misses out some of the developments that occurred throughout that century and some scholarly contributions. The chapter is only ever intended as a summary.

Early History of Autism

Importantly, the concept of autism did not specifically exist prior to the 1940s, although the notion was introduced by Bleuler in his work on schizophrenia in 1911. However, it was the work of two pioneering practitioners that identified some of the core characteristics that distinguished it as a discrete concept. First, the work of Leo Kanner, following his seminal child psychiatry text in 1935, introduced the world to the condition, autism. 4 Kanner was an Austrian psychiatrist who wrote a paper describing the behaviour he had observed in eleven children. He conceptualised these characteristics as a need for sameness, aloneness, and obsessions. It was common at this time for children with these types of behaviours to be classified as schizophrenic, so Kanner’s work was important for distinguishing between the two groups. However, it should be noted here that the credit given to Kanner has created some tension and criticism. 5 Second, was the work of Hans Asperger who was writing in parallel with Kanner and wrote about the characteristics of children in similar ways. 6 Asperger was a German paediatrician who observed the behaviour of four boys who he argued were showing challenges in forming friendships, displayed a general lack of empathy towards others, had clumsy movements, and had difficulties with communication. While this work became considerably influential, it did not reach the mainstream literature until after he died. It was Asperger who noted that children with this syndrome could flourish, and in some cases show signs of genius, and expressed the insight that autism may exist on a continuum. 7 It was this notion that resurfaced, as British psychiatrist Lorna Wing introduced the notion of a spectrum. 8

Kannerand Asperger laid a foundation therefore for understanding the behaviours of these children, and Kanner particularly argued that no single factor could explain it. However, the influence of psychoanalysis was strong during this time, and therefore, there was also a powerful promotion of the idea that there were psychodynamic causes. 9 This domination of psychoanalytic theory at this time formed the basis of a culture that blamed mothers for their child’s psychological problems. 10 A hugely influential theory in the 1960s, long since discredited, was that autism was associated with a certain style of parenting, with a cold and unavailable mother leading the child to shut down emotionally. 11 Bettelheim referred to this as the ‘ refrigerator mother ’ 12 and resulted in many mothers feeling to blame for their child’s condition. This has been argued to be particularly problematic, given that evidence suggests that Bettelheim faked his medical credentials. 13

Nonetheless, there is some persistence of mother-blaming even today, 14 despite the neurodevelopmental positioning of autism 15 and despite the extensive criticism. 16 Historically it has always been women who have carried this parental burden, as they were argued to fail to conform to the idealised view of motherhood. 17 There was a shift in thinking as psychoanalytic views lost some favour, and science took over as the predominant explanatory framework, and yet the blaming rhetoric underwent a subtle shift as mothers were not blamed via their parenting skills and style, but via their genes. The genetic and medical revolution in psychiatry positioned the aetiology of autism and other mental illnesses as having a biological origin. 18 This is something we return to shortly.

Contextualising Children

An important advancement during the first half of the twentieth century that has important implications for the development of an understanding of autism was the view of children and childhood in relation to the role of psychiatry and psychology. As Steve Taylor observes in Chapter 4 , a significant period of history for child mental health was the introduction of a universal education system. In Europe and North America in the late nineteenth century, there was a new formalisation of public and private education. 19 Karim reported that it was this formalisation of education that provided a platform for adults to recognise physical and mental health conditions in the young, which subsequently in the twentieth century led to the creation of sub-disciplines such as educational psychology, social care, and developmental psychology. The increase in the social surveillance of children with the advent of compulsory education indeed engendered the necessary social conditions for the creation of autism. 20 Further, developmental psychology was especially influential and is generally credited as beginning with the work of Wilhelm Preyer in 1882 and G. Stanley Hall through his introduction of the first American Journal of Child Psychology in 1891. 21 Notably, such work at the time, into the early twentieth century was heavily influenced by the notion of the ‘normal’ child, underpinned by psychoanalytic ideas of childhood, which was strengthened by the specialised work of Anna Freud, Melanie Klein, and Jacques Lacan, amongst others.

The field of psychiatry also recognised the relevance and importance of treating children separately from adults, and it was in 1935 that the first child psychiatry textbook was produced by Leo Kanner. This was in parallel with the US work by Douglas Thom who developed the Boston Habit Clinic designed to help parents manage their child’s everyday difficulties. This was considered necessary as following the Second World War there was recognition that children too needed help with their mental health. 22 Child psychiatry therefore became a separate sub-discipline of medicine, and one that recognised that specialist attention that was developmentally appropriate was needed, with the foundation of the American Academy of Child and Adolescent Psychiatry happening in 1953. 23 By the 1960s and 1970s, therefore, specific treatments designed for children had been developed within psychiatry and psychology. 24 Furthermore, during this period, family therapy emerged and gained popularity as it viewed the child as part of a complex social system. 25 However, it was the focus on pharmacological treatments for children that raised controversy in the later part of the twentieth century and continues today. 26 Thus, by the late twentieth century, child mental health was treated as distinctive and separate by a range of health services, including psychiatry, nursing, psychology, and education. Such services for children relied on childhood being constructed as a series of stages, with a separate focus on adolescence.

Diagnosing Autism: The Introduction of Standardised Manuals

A crucial historical moment in conceptualising autism was the development of standardised manuals. We present an overview of the main diagnostic manual, the Diagnostic and Statistical Manual of Mental Disorders (DSM) to demonstrate some of the key shifts in thinking about autism. While we recognise that there was some influence of the International Classification of Diseases (ICD), this system was much broader and contained physical illness, whereas the DSM was designed specifically for mental illness. The DSM was designed so that those working in the field of mental health were able to classify the full range of mental health conditions based on standardised criteria for diagnosis. 27 In other words, the DSM defined what does and does not constitute an illness and by default implies what constitutes normality and therefore a ‘healthy mind’. 28

The development of the DSM and the role of psychiatry have to some extent influenced how ‘normal’ is viewed, and the American Psychiatric Association decided to unify the diagnostic processes with the creation of DSM-I. Notably, however this single manual was not published until 1952. 29 This first edition represented an important paradigmatic change about the conceptualisation of mental illness and was a milestone in the creation of diagnostic categories. This first version contrasted two core groups of conditions, those caused by organic brain dysfunction and those with aetiology in environmental circumstances. 30 The second version, DSM-II, was developed quite quickly because of concerns about inconsistencies in the first. This version had 193 diagnostic categories, was heavily influenced by psychoanalysis, and launched in 1968. 31 This version of the DSM transformed psychiatry from a field that was concerned with pathology, to one that was more concerned with the boundaries of normality. 32 During this time, the rise of psychopharmacology was influencing more biological and neurological explanations of mental illness. Consequently, the diagnostic criteria were proposed as ways to ensure that standardisation could be achieved. 33

The notion of standardisation underpinned new changes to the system, and in the resulting DSM-III, there were substantial changes from DSM-II. DSM-III contained criteria which identified categories but moved to a multi-axial system for diagnoses, 34 and while the revision began in 1974, it was not published until 1980. 35 This version held nearly 500 pages and 265 categories. 36 The USA was especially influential here with its insurance health system, as they demanded more precise diagnostics and were more reluctant to fund long-term therapies like psychotherapy. 37 What is especially relevant to our discussion in this chapter is that it was the advent of DSM-III in 1980 that recognised autism as a distinct conceptual category, almost 40 years after its inception by Kanner. 38

It was this point in the twentieth century, with the inclusion of autismon the DSM-III that the work of Kannerand Asperger were revived by two British professionals who coined the notion of autistic spectrum disorder 39 and the triad of impairments became part of common clinical discourse. 40 This triad consisted of three core characteristics of autism;

Impairments in social interaction

Impairments in communication

Restrictive repetitive patterns of behaviour.

This was later reconfigured in the twenty-first century as a dyad of impairments and reconstructed as autism spectrum disorder, but the notion of the spectrum has been maintained.

A quick succession of revisions occurred after this with DSM-III- R , to DSM-IV, and DSM-IV- R which each reflected a round of changes. Again, relevant to our discussion, is that DSM-IV saw the inclusion of Asperger’s Syndrome and this was viewed as distinct to autism. 41 Those with Asperger’s Syndrome were seen as having normal or higher levels of intellectual ability, and those with the diagnosis often argue that this is fundamental to their identity. 42

DSM 5: Autism in the Twenty-First Century

DSM-5 is the first of the manuals in the twenty-first century and reflects the modern revision from DSM-IV- R . Notably, this version was represented with numbers rather than Roman numerals. This new version, DSM-5, has created a great deal of controversy and was created during a period of critical thinking around mental illness more generally. The development of DSM-5 began at the end of the twentieth century and unlike its predecessors was subject to public scrutiny because of the rise of the internet. 43 By 2010, the first draft was posted online and returned over 8000 comments, with 2000 further comments in 2011 on the revision. 44 By this point, the DSM had grown to 947 pages and 541 diagnostic categories. 45

This new version of DSM had some important changes for autism. While the notion of the spectrum was maintained, other changes were more controversial. For example, this version saw the removal of Asperger’s Syndrome as a distinct classification. Indeed, Asperger’s Syndrome had a short shelf-life in terms of official diagnosis, as it was not formally recognised until the 1990s and was then removed in 2013, being subsumed under the general category of autism spectrum disorder. The rationale for its removal was to reflect the shift from a categorical system to a dimensional one. 46 This however has caused great unrest in the autistic community, 47 as new interest groups have emerged claiming that classifications are a blueprint for their identity and not just an arbitrary means for classifying conditions. 48

The criteria for diagnosing autism also shifted, as there was a move away from a triad of impairments, to a dyad of impairments, as we noted earlier. Thus, there were now just two domains of difficulties—social communication and restrictive and repetitive patterns of behaviour. 49 However, Wing et al. argued that there were relevant clinical reasons why social interaction and communication were treated separately on the triad, and therefore, collapsing them into one domain was viewed as inappropriate. 50

The shifts in diagnosis and classification from the original version in 1952 to the latest version in 2013 have shaped and impacted on the meaning of autism and the language used to describe it. Autism is a condition that has invoked a great deal of debate and controversy in terms of the language and labels used and adopted and this has not been straightforward. As Kenny et al. noted,

Tensions surrounding the language of autism are attributable, in part, to the very different ways that autism touches people’s lives; some experience it personally, others through their children and others still might only encounter autism in some aspect of their lives – at school, at work, in the community or through friends and family. 51

The terms used and the language adopted around autism have changed over time, with a range of different conceptualisations of the condition, including, autism, autistic spectrum disorder, autism spectrum disorder, autism spectrum condition, Asperger’s syndrome, pervasive developmental disorder, and high functioning autism. 52 The different labels used are loaded with category rich inferences, and these can have different meanings for different individuals and their families.

The tensions and debates within public and academic communities regarding the most appropriate ways to conceptualise autism has been a consequence of growing disquiet about the role of psychiatry and the influence of medicine, as well as the rise of critical perspective. 53 During the twentieth century, there was a shift towards person-first language when describing individuals diagnosed with autism, so that the person came first, and the disability came after, that is, person with autism. 54 Over time however, this position has changed and further controversy about descriptive language has been proposed. Disability-first language is now more generally accepted to be the most appropriate way of describing autism, that is, an autistic person. This is because disability-first language adheres to the principle of putting a positive pronoun in front of the noun and thus removes the suggestion that autism is intrinsically negative. 55 This is especially important for the autism community who often view their autism as an accepted and instrumental part of their identity. 56 A good example of this was offered by Hagan who argued that society would not describe someone who was creative as ‘a person with creativity’, they would be a creative person and as such treats the creativity as part of who they are. 57 Perhaps unsurprisingly then, research has shown that diagnosed individuals tend to favour the concept of ‘autistic person’, but interestingly professionals still favour ‘person with autism’. 58

The Genetic Revolution

An important contribution to the rise of science and medicine was advances in the study of genetics. Psychiatry and medicine advocated organic causes of mental illness, and geneticists began to seek ways to isolate the gene(s) responsible for autism. This notion of aetiology had important implications for how we view autism and for the position of autistic people in society. The geneticisation of deviance worked to provide accounts for behaviour that failed to conform to social norms and thus provided new ways of thinking about stigma. 59 In other words, those with diagnosed conditions were now constructed as less blameworthy for their condition where it had a biological origin rather than a psychosocial one. 60

Such a turn to science has had consequences for research and funding. The field of autism research became reenergised by genetics studies. This generally increased pace in the late-1990s, when a link between two chromosomes, 15q and 7q, were identified as connected to autism. 61 Consequently, large funding streams have been provided to further the credibility of genetic explanations, so that the aetiology may be uncovered, and medical treatments created that target the core symptoms. However, it is arguably concerning that this energy has resulted in a dominance of genetics in the study of autism at the expense of other kinds of necessary and needed research. Statistics from the UK have shown that autism research is now preoccupied with biomedical issues, as 56% of studies have explored brain, biology, and condition, and a further 15% on aetiology, and only 18% on interventions, 5% on services, and 5% on diagnosis. 62 The picture is similar in the USA, which spends 18 times the amount of the UK, but again biologically grounded work receives significantly greater income than other areas. 63

The inappropriateness of this lack of balance in research funding streams has been positioned from a range of different views. For example, some have argued that autism is an incredibly complex and heterogeneous condition, and it is unlikely that scientists will be able to isolate a single autism gene. 64 Arguably more concerning is the risk or threat perceived by the autistic community in terms of the potential for genetic testing, which may put mothers under pressure to terminate their pregnancy. 65 Waltz noted that for autism this is especially concerning as the spectrum is broad and it is likely that multiple genes are connected, and this termination potential may threaten the lives of autistic people who could be functional in society. Some scholars have extended this argument further by claiming that the genetic focus in autism research reflects a new wave of eugenics. 66

The diversion of research resources to genetics research is also problematic for those already diagnosed as autistic. Critics and autistic advocates have argued that by prioritising genetics research, necessary finances have been diverted away from those who need support now. 67 Arguably, there is a need for more research which focuses on the agendas that matter to autistic people and their families. 68 In our own work, we found that genetics research and the notion of a cure for autism was a low priority for autistic people and their families, and what they really wanted was more work to help them manage difficult behaviour, challenging sleep patterns, coping with adversity, and improving quality of life. 69 The research base that has an impact on the lives of autistic people and their families is insufficient, and medical and genetic evidence is inconclusive or contested. 70 It seems therefore that the priorities of medical researchers and funding councils are at odds with autistic self-advocates and families. 71 In practice, this means there is a gap between our knowledge and practice, and we need to advance our research to meet the needs of those who would benefit from it most, by focusing on issues that affect people’s daily lives. 72 Specifically, we argue that there is a need for much more qualitative research that promotes the need to listen to the voices of autistic people and their families and allows for an exploration and focus on their views, opinions, and experiences.

The Challenge of Anti and Critical Psychiatry

The dominance of genetics and medicine in the field of autism has caused tensions for scholars and advocates throughout the twentieth century and into the twenty-first. As the different versions of the DSM evolved and changed, and the dominance of genetics and pharmacology grew, there was a notable shift in thinking about psychiatry as a discipline, the conceptualisation of mental illness (and more specifically tensions in classifying autism that way), and the ways in which diagnosed individuals ought to be treated and embedded in society. By the mid-twentieth century, there was a great deal of tension regarding the turn to science and medicine for answers regarding mental illness, and questions were raised about the credibility of categorising illness purely in biological ways and treatment with medications. Notably, movements during this latter half of the century were the anti-psychiatry and the critical psychiatry movement, which gained momentum as new and different critical arguments emerged.

It was during the 1960s that the international anti-psychiatry movement was recognised as such, as was a term coined by David Cooper. 73 This movement was noted to be motivated by anger and the perceived arbitrariness of diagnosis. 74 Those advocating anti-psychiatry called for a paradigm shift in terms of understanding mental illness and argued that patients were being marginalised. 75 Fundamentally those taking this position opposed the use of medication, which was the main form of treatment in the field. Furthermore, they opposed the power of psychiatrists and considered the practices to be coercive (see, e.g., Foucault). 76 The mid-twentieth century therefore saw three critical periods of anti-psychiatry, as noted by Furnham:

The early 1950s, where there was a conflict between psychiatrists adopting psychoanalytic perspectives and those new ideas around biology.

The 1960s saw a range of influential figures, such as Szasz, Basaglia, Foucault, Laing, and Cooper, from within and outside of psychiatry.

In the 1970s and 1980s, American and European sociology joined the debate, particularly in relation to labelling ideas and stigma, and popular media began to spotlight the practices of the profession. 77

It was thus during the 1980s that anti-psychiatry began to lose its momentum, as psychiatrists began responding to the critique, changing their practices, and working in a more biopsychosocial way. This biopsychosocial perspective of formulating and working with mental illness began to address some of those concerns about treatment of the mentally ill. 78 Thus, anti-psychiatry as a movement failed to establish itself as a mainstream ideology embraced by mental health professionals. 79 A further paradigmatic shift occurred therefore in the 1990s, with a softer critique of psychiatry emerging under a new guise of critical psychiatry. 80 The notion of critical psychiatry was coined by David Ingleby through the collection of essays into a monologue. 81 This recognised the change from focusing on the institution to the community but retained recognition of the difficulties of psychiatry and the political issues surrounding the field. This movement began to gain some acceptance, even amongst those practicing psychiatry. 82

The focus for critical psychiatry was that psychiatry was a powerful field, and this should be moderated by the voices of service users as central to decisions made. 83 This movement thus proposed two core issues with psychiatry. First, they argued that there are challenges to the scientific basis of psychiatric classification, and second, they noted moral problems that are a consequence of diagnosis. 84 The reliance on science and the turn to genetics were viewed as fundamentally problematic, as the biological basis of mental illness was argued to be overstated as the evidence fails to offer sufficient support for this thesis. 85

One of the core concerns in the rising movements that had varying degrees of opposition to psychiatry, particularly from those concerned with autism, was that mental illness, and in this case autism, was being over-medicalised and thus ignoring the ecological and systemic frameworks around an individual. The significantly progressive number of diagnostic categories with each version of the DSM was argued to be increasingly medicalising behaviour of individuals, reducing social expectations of normal behaviour. 86 Such an increase of conceptualisations of abnormality created by diagnostic manuals is a cause for concern, particularly in the context of autism, and the medicalisation of autism has been especially contested.

The concept of medicalisation refers to the process of human experience being reduced to medical terms and definitions. 87 It is this medical vocabulary that validates professionals’ determination of what constitutes sickness, and who qualifies as being categorised as psychiatrically disabled. 88 For the critical psychiatrists, psychiatry is a discipline that medicalises the mind as a way of legitimising the requirement of medicine to manage conditions 89 and this perpetuates an illusion that medicine provides a theoretically viable view of disability, which in turn, is tied to the notion of recovery and the restoration of the healthy mind. 90 In other words, this perspective constructs the person’s illness as dispositional, and those who are unable to be ‘fixed’ by medicine are inappropriately labelled as deficient in some way. 91 Such a goal of normalisation denies agency to those with disabilities 92 and risks judgements of laziness, weakness or belligerence. 93 By the end of the twentieth century, healthcare was seen as consumer-driven and patient-centred, and these changes increased the tension between rising medicalisation and increased resistance to it. 94 Furthermore, the DSM-5 was argued to rely more heavily on medicalisation than any of its predecessors, 95 because of lowered thresholds, which separate individuals from the optimal society. 96

For autism, these arguments are especially pertinent. The autism diagnostic process lacks definitive measures, and while there are tools to facilitate the process, the decision relies mostly on the subjective judgement of professionals applying the criteria, and thus, the power of medicine to define, diagnose, and treat autism has come under criticism. 97 There is therefore an extensive literature that expresses dissatisfaction with the medicalisation of autism as failing to adequately meet the needs of the autistic community. 98 This has been further hindered by the medicalised notions of deficit and cure, as medicalisation has encouraged the search for a cure. 99 Through this, autism has been constructed as a biological fact 100 and the social and cultural aspects inherent to the language of autism have been given less attention. 101 Consequently, autistic people and their families are frequently renegotiating what constitutes normal behaviour and such deviations from the norm are called to account. 102

The ambition to ‘fix’ disability is central to medicalised practices, and for many autistic people, this provides a perspective that they are ‘broken’ in some way. 103 Such ideas are co-constructed by the mental health profession and taken directly from medical, psychological, neurological, and developmental positions of autism as grounded in the criteria created through DSM-5. 104 Importantly, autistic individuals do not use the same knowledge spheres or frames of reference as professionals, and their relationships with services can be stressful and in some cases conflicting. 105

It may seem that medicalisation as a concept is negative; yet, notably medicalisation is not inherently problematic. The view of medicalisation as being viewed as good or bad rests on the implicit definitions of health and illness and a critical perspective regarding the effectiveness of medicine to address the well-being of the individual. 106 Indeed, the founders of medicalisation theory, such as Peter Conrad, described medicalisation as value neutral. 107 Furthermore, it must be recognised that medicalisation does serve some function for patients and families. It provides a basis to legitimise concerns that may otherwise be dismissed, and although there are risks that society takes on psychiatric concepts as identity terms, access to support largely relies on medics to confirm the nature of the problems. 108 Thus, the medical hegemonic position on autism underpins a legislative requirement to access services, as without an official diagnosis and label families are not entitled to help. 109 The flip side to this, however, is that parents may fear that if they fail to follow medical advice they will be morally implicated in any later negative experience. 110

Despite the value neutral nature of medicalisation, it has brought with it a very particular orientation to mental health; that is, one focused on ‘fixing’ the presumably ‘broken’ individual. In contrast to this, more social constructionist understandings afford nuanced and layered understandings of difference and disability. More particular to autism, there is a need to shift away from a focus on the medicalisation to language, with its overreliance on medical explanations regarding autism. 111 Such an overreliance might lead to the mismeasurement of the autistic experience. 112 Indeed, this shift has implications for whether autism might be viewed as a natural identity or a dilemma. 113 This focus on language and the social construction of disability and normal identity were encapsulated by a related movement, that of neurodiversity.

Neurodiversity: Empowering Autism

The language that we use has the power to reflect and shape people’s perceptions of autism. 114

A core focus of the neurodiversity movement is on the language we use around autism. This movement rejects medicalised negative concepts such as ‘disorder’, ‘deficit’, and ‘impairment’ and instead reconstitutes autism as a way of being. 115 The neurodiversity movement therefore directly challenged framing autism in a medicalised way. The notion of neurodiversity can be traced to Australian sociologist Judy Singer and journalist Harvey Blume, and it became popular with civil rights groups in the late-1990s. 116 The popularity of neurodiversity as a movement arose mostly online in response to what was argued to be a marginalisation of autistic people. 117 Thus, this movement sought to establish a culture where autistic people could have pride in their autistic identity and provide mutual support in self-advocacy. 118

An underpinning principle of neurodiversity was the foundational idea of a ‘differently wired brain’. 119 This movement has been instrumental in advocating strength-based discourses for autism, 120 but also for other brain-related conditions. 121 For autism, neurodiversity has two main claims as outlined by Jaarsma and Welin:

That autism is simply a natural variation in humans, and being neuro-diverse or neurotypical, reflect different ways of being human.

That neurodiversity connects to human rights, political issues, and non-discrimination of autistic people. 122

This movement therefore became associated with the struggle for civil rights for those individuals diagnosed with neurodevelopmental conditions 123 and as such became a counter-argument for the deficit model to prevent discrimination. 124 This is important, as society tends to be organised around neurotypical values and by contrast autism is positioned as a deficit. 125

As will be seen in Chapter 8 , an important aspect of neurodiversity is that the autistic community were instrumental in its promotion and development. Indeed, there are many autistic self-advocates who have celebrated autism as part of their identity and see their autism as a natural variation. 126 Some of these people have expressed fears that the seeking of a ‘cure’ may result in the eradication of autism. 127 It was argued therefore that by constructing autism as synonymous with impairments, it raises questions about what it means to be human, and those failing to conform to the dominant ideology are positioned as impaired. 128

We would note here that not all those in the autistic community advocate a neuro-diverse position, and it is important to have some balance in these arguments. Some neurodiversity movement advocates have acknowledged that some aspects of autism can cause distress and their amelioration or control is sometimes useful, and they do not oppose all forms of intervention and treatment. 129 Notably, some parents of children with autism do actively pursue treatments for their child and may even seek a cure for the condition. 130 Parents of course should have the right to seek early intervention for their offspring and have the freedom to work in ways they see as best for their child. 131 For those promoting neurodiversity, there is a position of promoting well-being and adaptive functioning to support autistic people. 132 The balance therefore is to support the notion for treatment, support, and services to overcome some of the potentially disabling effects of the condition, while steering away from medicalisation, negative language of deficiency, and damaging stereotypes that reify difference. 133 Neurodiversity as a movement and the construct of an autistic disability do not have to be incongruent, as individuals may have areas of strength and celebrate their identity, while still having some difficulties. 134

A central underpinning concern that has arisen from medicalisation and from neurodiversity therefore is the way in which autism is classified. While medicalisation advocates the appropriateness of autism as a mental health condition, as reified through its presence on the DSM, neurodiversity tempers this position, critically questioning the ‘deficit’ associated with such constructions. Ultimately, therefore, questions have been raised as to whether autism should be viewed by medicine, and by society more widely, as a psychiatric disability. The rise of the neurodiversity movement in the latter part of the twentieth century had a significant impact on the way we view autism and contributed greatly to this debate. The construction of autism as a psychiatric category, as a mental health condition, and as a disability is therefore dependent upon different points of view, different theoretical frameworks, subscription to different disability models, and personal experiences and viewpoints.

In our own work, we attempt to strike a balance between recognising the real distress of some families and the severity of symptoms for some children, against the critical and imperative challenges to the notion of deficit and the importance of empowering autistic people. It is important to be aware that for some families the diagnosis of autism is stressful, and the condition can have some disabling effects on the autistic person and their families. 135 For others, a more positive view of autism is necessary and the language surrounding the autistic identity is crucial in challenging deficit, stigma, and unacceptable stereotyping. Arguably, we should not see dysfunction, but we should see difference. 136

This is a helpful perspective that has been recognised in research with autistic people and those who live or work with them. In our own research on this issue, we considered how the notion of a disability might be understood discursively in relation to autism. 137 Using focus groups with a range of stakeholders, including autistic adults, parents of autistic children, mental health practitioners, researchers, and service managers, we found that the notion of a disability is fluid, contestable, and socially constructed. For example, an autistic adult in the focus groups argued that autism is not a disability:

I’m a great believer that ↑autism 138 its elf actually isn’ t a disability in any way at a::ll (.) in fact there are many areas where I would argue that my autism >is a s↑trength. 139

However, a mother of an autistic daughter, actively disagreed, noting that autism is a disability:

I kinda disagree< because (0.6) wouldn’t you say that (0.4) <some of th::e> the like from the < tri age> of autism (0.2) >the symptoms< (.) ↑a::re a symptom of the condition which is autism…….So it is a disa bility. 140

There was little agreement amongst participants as to whether autism constitutes a psychiatric disability as discussions permeated the boundaries of normality versus abnormality, disability versus ability, and medicalisation versus neurodiversity. While there was some acceptance that, clinically, categorisation and diagnosis were essential for support and service provision, and that some autistic people encountered more severe levels of difficulty than others, there was also an advocacy that autism was a fundamental characteristic of personhood and should not be characterised in limiting ways.

Drawing Conclusions: Our Personal View of Autism in the Twentieth Century

Our focus has predominantly been the evolution of autism throughout the twentieth century, exploring the various paradigmatic shifts that occurred and polar arguments that developed to influence our thinking around autism. However, these influences, research ideas, medical ideologies, genetic revolution, critical discourses, movements, and personal advocacies have all influenced our understanding of autism today. We now have a fractured view of a heterogeneous condition with a spectrum of characteristics, and of autistic people being different and reflecting a multitude of identities, views, opinions, and experiences. The twenty-first century is now plagued by the notion of an autism epidemic, and medicalised questions about where such an influx of autistic individuals has come from. This means that parents are thrown into a ‘ minefield of conflicting information ’. 141 Indeed, the volume of information is a confusing and time-consuming area for parents. 142 Yet, in some ways, this has been positioned as hope for parents, as ‘the first decade of the new century was a time of hope for many families, as parents told me they felt optimistic that science was on the verge of finally unravelling the mystery of their children’s condition’. 143

Such ‘hope’ and challenges related to autism are important as the ‘epidemic’ of the twenty-first century has become part of the medical rhetoric. There are few epidemiological studies of autism, but it is generally agreed that the prevalence currently stands at approximately 1% of the population. 144 Similarly, in childhood, a total prevalence of 116.1 per 10,000 was presented. 145 Baird et al. argued that the rates of autism are now much greater than was previously seen, and yet the reasons for such an increase in incidence are unclear. 146 The consequences of this growth have meant that services are having to rapidly expand to meet the greater demands. 147 Such an increase has however been controversial, as some have argued that it reflects an exaggeration of the existence of the condition, and others claiming it reflects the broader criteria. 148 It is therefore arguably not a new scientific discovery, but a shifting cultural and social practice regarding the social construction as to what counts as normal. 149

We conclude our chapter by presenting our perspective on this controversial issue and in so doing recognise the validity in different perspectives. In a personal and professional sense, we acknowledge our own experiences of autism. The lead author (O’Reilly) is an academic psychologist who has a brother diagnosed with autism, currently living in an institution due to the severity of his condition and the expanse of personal need. Furthermore, in addition to the academic position, O’Reilly also works as a research consultant for a Child and Adolescent Mental Health Service and therefore works alongside a multi-disciplinary team of mental health practitioners. The second author (Lester) is a former autism teacher in the USA, has a niece diagnosed with autism, and is now an academic working in educational autism research. The third author (Kiyimba) is an academic and chartered clinical psychologist, who specialises in trauma, and has worked professionally both with clients with autism, and as a clinical supervisor of mental health professionals working with autism, as well as supervising professionals who are autistic themselves. In outlining this personal position, we reflexively acknowledge that no text can ever be produced without influence and some imposition of the values and experiences of the writer, and our views and motivations are inspired and underpinned by our personal circumstances.

Thus, in our work on autism, we favour social constructionism as a guiding theoretical position, recognising the importance of language, and taking a child-centred and family-centred approach to research. We see the value of balancing the perspectives of psychiatrists, psychologists, other mental health professionals, autistic people, autistic advocates, families, and other stakeholders. The focus, for us, should be on meaning-making, that is, on the language used in different contexts and the impact that this has. In taking this social constructionist position, we do not deny the reality of autistic people or their families. This was eloquently expressed in a recent text by Thomas et al.:

This is not to deny the reality of mental health issues within people’s lives, but rather to acknowledge that if we are to comprehend the ubiquity and impact of mental distress within a contemporary UK context, then we need to recognise the ways that particular types of scientific knowledge and particular narratives of distress have been invested with meaning and authority, and as such, have the potential to become tools for use in the pursuit of broader political agendas. 150

The twentieth century saw many changes in the scientific and medical community understanding of autism. What we understand about autism is ‘constantly in flux’. 151 Autism as a condition has created much interest, amongst researchers, scientists, the public, and the media, and this is likely due to the multiplicity of meanings. 152 We have argued that autism is a social construct. In so doing, we have recognised that for some autistic people, their autism is celebrated, but for other families it is distressing, and they struggle to cope with what they frame as adversity. 153 We have woven a narrative that is congruent with the autonomy of those with lived experiences, have favoured a person-centred position, and explored alternative ways of thinking about the pervasive medicalised discourses that have constructed autism as a psychiatric disability. We have recognised that there are economic, institutional, and social consequences of adopting different social constructions of autism. 154 Through our exploration of the different arguments, we have shown how the dominant ideas of the impaired autistic person have become reified through medical rhetoric and the genetic revolution. We argued that psychiatry and other mental health professions have an important place for autism but acknowledge that the embracing of biopsychosocial framings of autism within those fields is important. We also noted that social constructionism provides a way for easing some of the tensions and a focus on language sets autism centre stage and challenges narrow interpretations of normality. The neurodiversity movement will be considered in greater depth by Erika Dyck and Ginny Russell in Chapter 8 .

Khalid Karim, Alvina Ali, and Michelle O’Reilly, A Practical Guide to Mental Health Problems in Children with Autistic Spectrum Disorder: ‘It’s Not Just Their ASD!’ (London: Jessica Kingsley Publishers, 2014).

Majia Nadesan, Constructing Autism: Unravelling the ‘Truth’ and Understanding the Social (New York: Routledge, 2005).

Nadesan, Constructing Autism , 29.

Leo Kanner, “Autistic Disturbances of Affective Contact,” Nervous Child 2 (1943): 217–250.

Steve Silberman, Neuro - Tribes (London: Allen & Unwin, 2015).

Hans Asperger, “ Die ‘Autistischen Psychopathen’ im Kindesalter [Autistic Psychopaths in Childhood]” (in German), Archiv für Psychiatrie und Nervenkrankheiten 117 (1944): 76–136.

Silberman, Neuro - Tribes.

Lorna Wing, “Language, Social and Cognitive Impairments in Autism and Severe Mental Retardation,” Journal of Autism and Developmental Disorders 11, no. 1 (March 1981): 31–44.

Khalid Karim, “The Value of Conversation Analysis: A Child Psychiatrist’s Perspective,” in The Palgrave Handbook of Child Mental Health: Discourse and Conversation Studies , eds. Michelle O’Reilly and Jessica Nina Lester (Basingstoke: Palgrave Macmillan, 2015), 25–41.

Michelle Lafrance and Suzanne McKenzie-Mohr, “The DSM and Its Lure of Legitimacy,” Feminism and Psychology 23, no. 1 (February 2013): 119–140.

Bruno Bettelheim, The Empty Fortress (New York: Free Press, 1967).

Sometimes this is referred to as the ‘icebox’ mother.

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Acknowledgements

We are very grateful to two reviewers who provided very useful feedback on this chapter. We thank Professor Katherine Runswick-Cole, University of Sheffield (UK) and Professor Jason Lee, De Montfort University (UK).

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O’Reilly, M., Lester, J.N., Kiyimba, N. (2020). Autism in the Twentieth Century: An Evolution of a Controversial Condition. In: Taylor, S.J., Brumby, A. (eds) Healthy Minds in the Twentieth Century. Mental Health in Historical Perspective. Palgrave Macmillan, Cham. https://doi.org/10.1007/978-3-030-27275-3_7

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How Did Applied Behavior Analysis (ABA) Start?

Explore how Applied Behavior Analysis (ABA) started and its role in revolutionizing autism treatment.

Understanding Autism

Autism, or Autism Spectrum Disorder, is a complex neurological and developmental condition that affects millions of people worldwide. The understanding and awareness of this condition have grown over the years, but there is still much to learn.

Definition of Autism

Autism Spectrum Disorder (ASD) is a developmental disorder that affects communication and behavior. It includes a wide "spectrum" of symptoms, skills, and levels of disability. People with ASD often have ongoing social problems that include difficulty communicating and interacting with others. They might also exhibit repetitive behaviors as well as limited interests or activities.

Symptoms can vary widely from person to person, hence the term "spectrum" in ASD. For some, ASD can significantly interfere with daily life, while others may experience minor issues and lead normal lives. It's important to note that there is no "typical" person with ASD; every individual's experience with the disorder can be unique.

Prevalence of Autism

According to the Centers for Disease Control and Prevention (CDC), autism affects an estimated 1 in 54 children in the United States today. It is reported to occur in all racial, ethnic, and socioeconomic groups, and is about 4 times more common among boys than among girls.

The prevalence of autism in adults is harder to determine, but estimates suggest that roughly 1 in 45 adults in the U.S. are on the autism spectrum. The condition tends to be lifelong, although symptoms may change over time or with therapy and support.

This understanding of autism lays the groundwork for a deeper exploration of the history and evolution of Applied Behavior Analysis (ABA), a key treatment method for ASD. Further sections will delve into the origins, principles, applications, effectiveness, and criticisms of ABA.

History of Applied Behavior Analysis (ABA)

To understand the role of Applied Behavior Analysis (ABA) in autism treatment, it's crucial to delve into its origins and how its techniques have developed over time.

Origins of ABA

Applied Behavior Analysis owes its roots to the field of behaviorism, a psychological perspective emphasizing the scientific study of observable behaviors. The primary force behind the development of ABA was B.F. Skinner, a psychologist known for his work in the area of operant conditioning.

Operant conditioning is a learning process where behavior is influenced by its consequences. If a behavior leads to a desirable outcome, it's likely to be repeated, whereas if it leads to an undesirable outcome, it's likely to be avoided. Skinner's theories formed the foundation for ABA, which essentially applies these principles to real-world situations.

ABA emerged as a distinct field in the 1960s, spearheaded by psychologists like Jack Michael, Donald Baer, and Montrose Wolf. They published a seminal paper titled "Some Current Dimensions of Applied Behavior Analysis," outlining the fundamental characteristics of ABA. This publication widely recognized as marking the official beginning of ABA.

Development of ABA Techniques

Once the foundational principles were established, the development of specific ABA techniques began. Early ABA programs were mainly focused on teaching simple skills through repetition and reinforcement. However, as the field evolved, the techniques became more sophisticated and diverse.

ABA techniques are now designed to help individuals learn a wide range of skills, from basic tasks like dressing and feeding themselves to complex social and communication skills. The techniques are also tailored to the individual's specific needs and abilities, reflecting a shift towards more personalized and holistic approaches.

One significant development was the introduction of discrete trial training (DTT). This technique involves teaching skills in a structured, step-by-step manner, often using physical prompts and rewards. It has proven particularly effective in teaching new behaviors to individuals with autism.

Another key technique is natural environment training (NET), which emphasizes teaching skills in the context where they will be used. This approach helps individuals generalize the skills they learn to different situations, enhancing their ability to navigate the world independently.

The development of ABA techniques continues to this day, with ongoing research and innovation driving the field forward. The goal remains the same: to help individuals with autism live more fulfilling, independent lives.

Principles of Applied Behavior Analysis

Understanding the principles of Applied Behavior Analysis (ABA) is crucial to appreciate how this method has been used in autism treatment. ABA is built on three fundamental principles: behavior modification, positive reinforcement, and data collection.

Behavior Modification

Behavior modification is a central tenet of ABA, focusing on changing behaviors that are socially significant. In the context of autism treatment, it means altering behaviors that may hinder an individual's ability to learn or interact with others.

A behavior analyst first assesses the individual's behavior in different environments, such as home, school, and community. The objective is to understand the factors that trigger the behavior (antecedents) and the outcomes that maintain it (consequences). This approach allows the analyst to develop strategies that modify the antecedents and consequences, thus changing the behavior.

For example, if a child with autism engages in self-injury when asked to complete a difficult task, the behavior analyst might modify the antecedent by breaking down the task into smaller, more manageable parts.

Positive Reinforcement

Positive reinforcement is another key principle of ABA. It involves providing a reward immediately after a behavior, encouraging the individual to repeat that behavior in the future. The reward, or positive reinforcer, can be anything that the individual finds motivating.

In a therapy session, a child might receive a favorite toy or snack for correctly answering a question or completing a task. Over time, this reinforcement helps the child associate positive outcomes with the desired behavior, increasing the likelihood that the behavior will occur again in the future.

It's important to note that what works as a positive reinforcer for one individual might not work for another. Therefore, the behavior analyst needs to identify specific reinforcers for each individual based on their preferences and motivations.

Data Collection

The third principle of ABA is data collection. Behavior analysts collect data to measure the individual's progress and the effectiveness of the intervention. This data helps them make informed decisions about modifying the intervention as needed.

Data collection involves recording the frequency, duration, and intensity of targeted behaviors. For example, if a behavior analyst is working with a child to reduce tantrums, they might record how often the tantrums occur, how long they last, and how intense they are.

This data provides a quantifiable measure of the child's behavior, allowing the behavior analyst to track changes over time and adjust the intervention as necessary. Regular data collection is essential for ensuring that ABA interventions are effective and meet the individual's unique needs.

In conclusion, the principles of behavior modification, positive reinforcement, and data collection form the foundation of ABA. These principles guide the development and implementation of interventions, ultimately helping individuals with autism improve their behaviors and quality of life.

Applications of ABA

The principles and techniques of Applied Behavior Analysis (ABA) have been used in multiple fields to bring about significant behavioral changes. Two key areas where its application has been particularly notable are in the treatment of autism and in education.

ABA in Autism Treatment

ABA has been recognized as a successful method for treating individuals with autism. In the context of autism, ABA focuses on improving specific behaviors such as social skills, communication, and academics, as well as adaptive learning skills, such as fine motor dexterity, hygiene, grooming, domestic capabilities, punctuality, and job competence.

ABA interventions for autism often involve one-on-one treatment plans that are tailored to each individual's needs and abilities. These plans involve regular, often daily, therapy sessions where the individual works with a therapist on a variety of skills and behaviors. The frequency and intensity of these sessions can vary depending on the individual's needs and progress.

A key element of ABA in autism treatment is the use of positive reinforcement. This involves rewarding the individual for demonstrating desired behaviors, which increases the likelihood of these behaviors being repeated in the future. Over time, this reinforcement can help individuals with autism to develop and improve their social and communication skills, leading to improved quality of life and greater independence.

ABA in Education

Beyond autism treatment, ABA has also been applied in education settings to support the learning and development of all students, not just those with special needs. In an educational context, ABA strategies can be used to help students improve their academic skills, reduce problematic behaviors, increase motivation and engagement, and improve social and communication skills.

For example, teachers may use positive reinforcement to encourage students to complete their homework, participate in class discussions, or demonstrate positive social behaviors. They may also use data collection methods to track a student's progress and make adjustments to their teaching strategies as needed.

ABA can also be used in the development of individualized education programs (IEPs) for students with special needs. These programs, which are tailored to each student's unique abilities and challenges, can help to ensure that students receive the support they need to succeed in the classroom.

Overall, the application of ABA in both autism treatment and education demonstrates the versatility and effectiveness of this approach. By focusing on improving specific behaviors through the use of positive reinforcement and data collection, ABA can support individuals in developing new skills and achieving their full potential.

Effectiveness of ABA

Applied Behavior Analysis (ABA) has demonstrated effectiveness in many areas, particularly in the treatment of autism. However, like any therapeutic approach, its efficacy can vary from individual to individual. In this section, we'll examine the research supporting ABA and share some success stories.

Research on ABA

Numerous scientific studies have highlighted the benefits of ABA for individuals with autism. Much of this research has focused on early intervention, with findings indicating that ABA can significantly improve language skills, social interactions, and adaptive behaviours.

A meta-analysis of 22 studies, published in the Journal of Autism and Developmental Disorders, found that ABA interventions led to positive outcomes in intellectual functioning, language development, and adaptive behavior. The study also noted that ABA-based interventions were more effective when delivered in intensive, comprehensive formats.

Furthermore, a review of 13 studies published in Behavior Modification concluded that ABA is effective at improving a variety of behaviors in children with autism, including social-communication skills and reduction of problem behaviors.

While these studies provide strong support for the use of ABA in autism treatment, more research is needed to understand the long-term effects and to identify the most effective strategies for different individuals.

Success Stories

In addition to empirical research, countless success stories attest to the effectiveness of ABA in improving the lives of those with autism. Many parents and professionals report significant improvements in children's abilities to communicate, interact socially, and perform daily tasks after receiving ABA therapy.

One well-documented success story is that of a boy named Jack. Diagnosed with autism at age three, Jack was largely nonverbal and had difficulty interacting with others. After two years of intensive ABA therapy, Jack's language skills improved dramatically, and he was able to engage in conversations, make friends, and participate in mainstream education.

Another success story involves a girl named Emily. After starting ABA therapy at age four, Emily made significant strides in her ability to communicate, maintain eye contact, and engage in play with her peers. Her parents attribute much of her progress to the individualized approach of ABA, which focused on her unique needs and strengths.

While these stories are certainly encouraging, it's important to remember that every individual with autism is unique. What works for one person may not work for another, and progress can often be slow and require ongoing commitment. However, the potential for improvement with ABA is evident, and many families and professionals consider it an invaluable tool in autism treatment.

Criticisms and Controversies

While Applied Behavior Analysis (ABA) has had a significant impact on the field of autism treatment, it has not been without its criticisms and controversies.

Ethical Concerns

Some ethical concerns raised about ABA involve the fundamental principle of behavior modification. Critics argue that ABA, in its attempts to change 'problem' behaviors, often dismisses or fails to consider the importance of these behaviors to the individual with autism. These behaviors, although considered disruptive or socially unacceptable, may serve as essential coping mechanisms for the individual.

Another ethical concern is the potential for ABA to be misused in a manner that is controlling or overly restrictive, leading to a violation of the individual's dignity or autonomy. This concern emphasizes the necessity for ABA practitioners to adhere strictly to ethical guidelines that prioritize respect for the individual's rights and dignity.

Alternative Approaches

In response to the criticisms of ABA , several alternative approaches to autism treatment have emerged. These approaches often focus on understanding the individual’s unique experience of autism and promoting skills that enable them to navigate the world on their own terms.

One such alternative approach is the Developmental, Individual differences, Relationship-based (DIR) model. This approach emphasizes understanding the unique developmental profile of each child and using that understanding to guide intervention strategies.

Another alternative approach is the Social Communication, Emotional Regulation, and Transactional Support (SCERTS) model. This model prioritizes social communication and emotional regulation as key areas of development for children with autism.

It's important to note that these alternative approaches are not necessarily in opposition to ABA, but rather offer additional perspectives and strategies. Many practitioners and researchers advocate for an integrative approach that incorporates elements from ABA and alternative models, depending on the needs and preferences of the individual with autism.

The evolution of autism treatment, including how ABA started and developed, continues to be a dynamic field. As our understanding of autism deepens, it is crucial that our treatment approaches evolve to reflect this understanding, placing the needs and rights of individuals with autism at the center.

‍[1]: https://www.autismspeaks.org/expert-opinion/what-discrete-trial-training

[2]: https://www.webmd.com/mental-health/what-is-applied-behavior-analysis

[3]: https://www.ncbi.nlm.nih.gov/books/NBK459285/

[4]: https://www.cdc.gov/mmwr/preview/mmwrhtml/ss6302a1.htm

[5]: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9114057/

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