Psychiatric Annals

CME Article 

Autism Spectrum Disorder: A Concept in Evolution

Ahsan Nazeer, MD; Nehdia Hashemi, MD; Nazish Imran, FRCPsych; Muhammad Waqar Azeem, MD

Abstract

Autism is a fascinating topic that has attracted the interest of researchers and the lay public alike. The history of autism is filled with accomplishments of people who were astute observers of childhood psychopathology. Autism spectrum disorder affects a diverse group of children who share certain commonalities. There are ongoing attempts to understand its etiology and to refine diagnostic criteria for improved and timely recognition. In recent years, rapidly evolving research has highlighted the limits of our understanding of a disorder that at one time was considered rare, but now presents itself in 1 in every 59 children in the United States. This article particularly focuses on the history of autism as well as the changing criteria in the Diagnostic and Statistical Manual of Mental Disorders. [Psychiatr Ann. 2019;49(3):103–108.]

Abstract

Autism is a fascinating topic that has attracted the interest of researchers and the lay public alike. The history of autism is filled with accomplishments of people who were astute observers of childhood psychopathology. Autism spectrum disorder affects a diverse group of children who share certain commonalities. There are ongoing attempts to understand its etiology and to refine diagnostic criteria for improved and timely recognition. In recent years, rapidly evolving research has highlighted the limits of our understanding of a disorder that at one time was considered rare, but now presents itself in 1 in every 59 children in the United States. This article particularly focuses on the history of autism as well as the changing criteria in the Diagnostic and Statistical Manual of Mental Disorders. [Psychiatr Ann. 2019;49(3):103–108.]

Few medical disorders in recent years have caused so much controversy and passion, and triggered such an intense debate among academicians, scientists, and the lay public as autism. Autism has attracted the attention of celebrities, journalists, bloggers, and parents. Hundreds of forums have been created about autism for the hotly contested debate on the prevalence, causation, and treatments. Most of this attention is because of the startling rise in the number of children who were diagnosed with autism spectrum disorder (ASD) during the last decade. Prevalence studies have shown that the diagnosis of ASD has increased from 3 to 4 children per 10,000 in the 1940s to 1 in 59 in 2018.1 This estimate reflects a 15% increase in the prevalence in ASD from 2016 when the reported rates were 1 in 68.2 It is important to note, however, that these numbers from both 2016 and 2018 are not the result of direct observation of the children and instead are the result of parental surveys in which they were asked whether a child in the family has been diagnosed with autism. There are obvious limitations in this method including not being able to correct for errors in how and by whom the diagnosis is made.

The reported increase in the prevalence leads to the debate about how much of this increase is the result of broadened diagnostic criteria and increased awareness and how much of this can be attributed to the environmental and genetic factors.3,4 Numerous studies have looked at the role of different etiological factors and the changes in prevalence rates; however, the results are constrained by methodological limitations.5,6 Nevertheless, popular parental views that vaccines and thimerosal are the cause of autism have been discredited.7,8

Throughout history, we have struggled to understand the concepts of disease and disability along with the boundaries between “normality” and “abnormality.” Again and again humans have turned to their internal prejudices to explain deviant behaviors with mysticism and religion. As late as the 19th century, people were called “idiots,” not by prejudice or malice, but because this was a mainstream concept, present in the medical literature, describing people that we used to label as “mentally retarded.” Today by exercising much intellectual sensitivity we call them people who have “intellectual disability.” Although autism was not formally recognized until the mid-20th century when Donald Triplett became the first person to receive this diagnosis, descriptions of these people were found in State surveys commissioned to investigate “idiocy.”9 One such survey, commissioned by the Boston State legislature in 1846, and conducted by a group of three men, found “a great many cases” of people who were intellectually incapacitated but, in some cases, displayed “superior cognition.” As the diagnosis of autism did not exist at that time, those people could well have been diagnosed as having autism by using the criteria that we use today.10 One of those men who led the survey was Samuel Howe, a distinguished graduate of Harvard Medical School and the founding director of the Perkins School for the Blind. He opened the school in 1832 with the resounding idea that blind people (“idiots” by definition at that time) can and should be educated. He promoted the idea to the Massachusetts State legislature and led the survey with the sole aim “to ascertain their number, and whether anything can be done for their relief.” A few years later, the Perkins School enrolled Helen Keller, who became one of their most celebrated students.

Paul Eugen Bleuler and Leo Kanner

Autism is a word based on Greek “autos” or “self” to describe “self-absorption” or “withdrawal from reality” and is used by Eugen Bleuler as one of the pathognomonic features of schizophrenia. He introduced this term in 1911 to describe the “most severe schizophrenics who live in the world of their own.” The use of the word “autism” in schizophrenia continued to be prevalent throughout the 1920s and 1930s to describe certain subcategories of schizophrenia to discuss the “autistic thinking” of people who did not display any positive symptoms, including delusions or hallucinations. However, because of the lack of an agreed upon definition, “autism” as a term has been deleted from the major diagnostic systems as a component of schizophrenia.11,12

In 1943, Leo Kanner, an Austrian-American psychiatrist recounted 11 case studies in his seminal paper, “Autistic Disturbances of Affective Contact.”13 He described these children as being born without the ability to make social relationships and used the term “autism,” which was previously used by Bleuler, to describe this psychopathology. Some of the phenotypic elements that he identified included profound inability to develop relationships, obsessive desire for sameness, fascination with inanimate objects, aloofness, lack of imagination, and language that did not serve the purpose of adequate communication with others.14 Since no one before Kanner had published a series of such cases, no information existed about the prevalence of autism before his time. Kanner was aware of the previous use of the word “autism” and its association with schizophrenia and noted that “this is not withdrawal in the accepted sense of this word and a specific kind of contact with the external world is a cardinal feature of the illness. Nevertheless, in full recognition of all of this, I was unable to find a concise expression that would be equally or more suitably applicable.” In later years, Kanner used the term “early infantile autism” to describe the same set of characteristics.15,16 However, the use of the word “autism,” which was initially used to describe adult schizophrenia, caused significant confusion in the way autism and psychosis were conceptualized over the next 30 years.

Hans Asperger and Lorna Wing

At about the same time, Hans Asperger, an Austrian pediatrician, described a similar set of symptoms in the children from his clinic that he called “little professors.” Interestingly, he described a form of autism that was different from what was noted by Kanner. Although Asperger's children shared some of the similar symptoms, including communication difficulties, repetitive behaviors, inability to make friends, and unusual sensory responses, their symptoms did not include cognitive disabilities or symptoms of schizophrenia. He also reported that the syndrome is not particularly rare, as he had seen more than 200 children with a similar set of criteria in his clinic. He named this condition “autistic psychopathy.”17

Although Kanner's work was known internationally, Asperger's accounts of “autistic psychopathy” did not get the attention of scholars outside of German literature, until Lorna Wing, an English psychiatrist described her work in the seminal article, “Asperger's Syndrome: A Clinical Account.”18 Because of the concern that autistic psychopathy would equate to sociopathic behavior, she advocated a “neutral” term “Asperger's syndrome” over “autistic psychopathy.” Wing is also widely credited with considering autism as a spectrum disorder, instead of a single entity.

Even though there were individual differences in the initial accounts by Kanner and Asperger, there were also significant similarities, as noted in Table 1.19

Comparison of Leo Kanner's and Hans Asperger's Accounts on Autism

Table 1.

Comparison of Leo Kanner's and Hans Asperger's Accounts on Autism

Bruno Bettelheim and Bernard Rimland

At the time of Sigmund Freud's death in 1939, psychoanalysis was the dominant method of understanding and treating people with psychological disorders. Freud's work was based on the concept of unconscious mind and emotional disturbances resulting from early childhood experiences. He conceptualized these disturbances/imbalances as the root of the development of psychopathology. During the mid-20th century, psychoanalysis remained the predominant model to understand autism as well, and by doing so, the emphasis was placed on the mother's role in fostering ego development. These theories created a sense that the mother's continued guidance is important for the normal development of a healthy child. Developmental disorder like autism were thus attributed, directly or indirectly, to maternal negligence or transgression during the early childhood period. In the post-World War (WW)-II period, psychoanalytic accounts gradually gave way to object-relations accounts; however, until the late 1970s, mother-blaming continued to be the main descriptor of many forms of child psychopathology.20,21

Although, Bruno Bettelheim is usually considered responsible for the introduction of the “refrigerator mother” theory, this idea that the mother's behavior leads to childhood psychopathology predates his work. The concept of “schizophrenogenic mother” by Fromm-Reichmann and D.W. Winnicott's theories of object relation that emphasized the mother's role in the success and failure of achieving stable egos may have given an initial impute to mother blaming. Bettelheim was a professor of psychology and child-development specialist at the University of Chicago. From the 1940s to 1970s, he also served as director of the Sonia Shankman Orthogenic School at the University, which was a residential treatment facility for children with behavioral disorders. Through his work at the Orthogenic School and publication of the book The Empty Fortress,22 Bettelheim became an influential figure in promoting the “refrigerator mother” theory. Building upon that work, he expanded on the idea that autism is an emotional disorder that is caused by the psychological harm brought upon some children by their own mothers.22,23 Substantiated by his own 10-month experience at Dachau concentration camp in WWII, his theories compared the lives of autistic children to the experience of prisoners in Nazi concentration camps. Mainly due to his charisma, and a plain-spoken approach, his theories were widely accepted by the general public during the 1950s and 1960s.24

Bernard Rimland, a psychologist, founded the Autism Society of America in 1965 and the Autism Research Institute in 1967. He was critical of Bettelheim's theories and stressed that autism had a neurologic basis, thus emphasizing an organic basis of the disorder. He published a book, Infantile Autism: The Syndrome and Its Implications for a Neural Theory of Behavior, in 1964 with a foreword by Kanner who by that time had changed his views toward a neurologic basis of autism.25 Rimland was also concerned about the increase in the prevalence of autism and hypothesized that vaccinations, especially thimerosal, might be the cause of this increase. His status in the public's perception has lent credibility in the eyes of many that vaccines indeed might be the cause of this condition, an assertion that is still being hotly debated by the public and scientists alike.26

Autism Across Diagnostic and Statistical Manuals

In the Diagnostic and Statistical Manual of Mental Disorders (DSM)-I (1952) and DSM-II (1968), autistic-like symptoms were labeled under “childhood schizophrenia.”27,28 Rutter's studies played an important role in the validation of the syndrome and identifying the prognostic significance of early speech and language development and intelligence.29 Kolvin contributed much by his comparative studies distinguishing early childhood schizophrenia and autism by considering family history, the trajectory of the diseases, phenomenology, and associated symptoms.30 By 1979, the idea that autism is an early form of “childhood schizophrenia” was abandoned.31

Kanner had described social difficulties and “insistence on sameness” as the central features of autism.32 However, with rapidly evolving research during the 1970s, it became clear that speech and language problems are also a major source of disability in children with autism.

By the time autism was included in DSM-III in 1980,33 there was a consensus that social deficits, resistance to change, speech and language problems, and onset during early years characterized autism. Autism was included under the broader category of Pervasive Developmental Disorder (PDD). DSM-III saw most of the specific symptoms of autism being captured with the introduction of “infantile autism.” Both infantile autism and childhood-onset PDD could also be diagnosed as “fully present,” or in a “residual state” where signs of odd communication and social awkwardness persist but current clinical presentation no longer meets full criteria. DSM-III also allowed for the diagnosis of atypical PDD for the cases in which distortions of social and language development cannot be classified as either infantile autism or childhood-onset PDD.33

The separation of core symptoms of autism into three domains of impairment—reciprocal social interaction, communication, and restricted or repetitive behaviors—were formalized in DSM-III-R34 and a more polythetic definition of autism started to take shape. The diagnostic subgroups were reduced to autistic disorder and PDD NOS (not otherwise specified).

Around the same time DSM-III-R was introduced, significant changes occurred in the educational landscape in the US. Before the 1960s children with disabilities either were excluded from the public education system or categorized under “mental retardation” and “learning disabled.” During the first half of the 1960s, a presidential panel was convened, calling for the education of all disabled children. The Elementary and Secondary Education Act was created in 196535 that allowed for the accessibility of free education for children with disabilities. In 1975, the US Congress approved the Public Law 94-142 Education of All Handicapped Children Act,36 mandating financial support for all children with developmental disabilities to receive education. This law was reauthorized in the 1990s as the Individuals with Disabilities Education Act;37 these laws guaranteed people with disabilities free and appropriate public education in the least restrictive environment. Autism was added as an eligibility category in 1997, ensuring adequate and directed services for children in need.

The next significant change occurred in 1994, when three disorders—Rett's disorder, childhood disintegrative disorder, and Asperger's disorder—were included in DSM-IV.38 Pervasive developmental disorders in this edition of DSM-IV were the results of extensive literature review and large multisite field trials to improve the sensitivity and specificity of diagnosis across different IQ.39 Another major achievement was the alignment of diagnosis among DSM-IV and the International Classification of Mental and Behavioral Disorders (ICD-10).40 This led to the development of internationally recognized research and diagnostic instruments including the Autism Diagnostic Observation Scale, the Autism Diagnostic Interview, and the Childhood Autism Rating Scale.

DSM-5,41 which published in 2013, took a more restrictive approach, and numerous changes in the criteria were made. First, a dimensional approach to the diagnosis was chosen over the categorical approach. Second, the name of the class of disorders was changed from PDD to ASD. Third, multiple disorders in DSM-IV under PDD were removed in favor of a single term “autism spectrum.” A controversial move was to remove the diagnosis of Asperger's disorder. Fourth, a new disorder, social communication disorder, was added, although its clinical significance and utility in education service eligibility remains unclear. Fifth, after reviewing the research data, a decision was made to collapse the social and communication symptom clusters into one category and add symptoms of sensory sensitives. In addition, diagnosis of attention-deficit/hyperactivity disorder can be made with ASD in DSM-5, which was not allowed in DSM-IV. Although ASD is now a single spectrum, DSM allows for diagnostic specifiers that include the severity of symptoms, clinical course, pattern of onset, etiological factors, cognitive abilities, and comorbid conditions.42

Conclusion

DSM-5 presents a narrower construct of autism than its predecessor; hence, raising the possibility that some people with higher IQ as well as those with a previous diagnosis of PDD NOS will be excluded from ASD under the new criteria. Researchers have also assessed the agreement between autism criteria in DSM-IV with DSM-5 and have noted that ASD criteria in DSM-5 are more specific but less sensitive than those in DSM-IV. Removal of subcategories including Asperger's disorder in DSM-5 has also remained controversial. DSM-5 is also not aligned with ICD-11,43 which potentially can affect research and international collaborations. Additionally, there are limitations in its clinical utility because of its focus on standardized instruments, which will improve the reliability of DSM diagnostic assignment when used by researchers or those with specific training, but most community clinicians will not have the opportunity to undergo extensive training.44 With prospective studies, some of these issues will be clarified, and we will see more revisions in future editions.

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Comparison of Leo Kanner's and Hans Asperger's Accounts on Autism

Characteristic Leo Kanner Hans Asperger
Sex Males > females Symptoms do not occur in prepubertal girls
Social impairment Egocentricity and lack of interest in the feelings of others Similar to Kanner
Speech and language Pronoun reversal, repetitive questioning, tendency to invent words Long-winded pedantic speech; developed speech before school; large vocabularies and some “talking like grown-ups”; unusual grasp of highly technical language
Nonverbal communication Impaired, poor eye contact, and other aspects of nonverbal communication Similar to Kanner; poverty of expressive gestures; lack of flexibility in imaginative play
Repetitive behaviors Difficulty in transitions, stereotypic play, and stereotypic body movements Similar to Kanner
Sensory sensitivities Odd responses to sensory stimuli Similar to Kanner
Authors

Ahsan Nazeer, MD, is the Division Chief, Child and Adolescent Psychiatry, Sidra Medicine. Nehdia Hashemi, MD, is a Lecturer in Clinical Medicine, Qatar University School of Medicine. Nazish Imran, FRCPsych, is an Associate Professor, Child & Family Psychiatry Department, King Edward Medical University. Muhammad Waqar Azeem, MD, is the Chair, Department of Psychiatry, Sidra Medicine.

Address correspondence to Ahsan Nazeer, MD, Sidra Medicine, PO Box 26999, Al Luqta Street, Education City North Campus, 2nd Mezzanine, OPC, Office C2M 224, Qatar Foundation, Doha, Qatar; email: anazeer@sidra.org.

Disclosure: The authors have no relevant financial relationships to disclose.

10.3928/00485713-20190207-01

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