What is Autism Spectrum Disorder?

Feb 18, 2021 | ABA and Autism

By Meagan Harder, M.A. & Jessica Juanico, PhD, BCBA-D, Department of Applied Behavioral Science, University of Kansas

Meagan M. Harder, MA, BCBA

Meagan M. Harder, MA, BCBA

Meagan Harder graduated with her Master’s in Applied Behavioral Science from the University of Kansas in 2020. She is currently working in Madison Metropolitan School District coaching teachers and training paraprofessionals using behavior analytic principles.

Jessica F. Juanico, PhD, BCBA-D

Jessica F. Juanico, PhD, BCBA-D

Jessica Juanico is the Assistant Director for the online Applied Behavior Analysis Programs at the University of Kansas within the Department of Applied Behavioral Science. She is also an Assistant Professor of Practice for the programs.

Autism spectrum disorder (ASD) is a developmental disability that may affect many aspects of an individual’s day-to-day functioning (National Institute of Neurological Disorders and Stroke, 2020). Although prevalence of ASD varies depending on the source and sample, a recent study by the Center for Disease Control and Prevention estimated ASD affects 1 in 54 individuals and is more four times more common in males than females (Center for Disease Control and Prevention, 2019; Fombonne, 2005). ASD is characterized by persistent deficits in social communication and interactions (e.g., abnormal social approach, lack of conversing back-and-forth, poorly integrated verbal skills, lack of developing and maintaining relationships) and restricted, repetitive patterns of behavior (e.g., repetitive motor movements or speech, insistence on sameness, inflexible adherence to routines, highly fixed interests, and hyper- or hypo- reactivity to sensory input). The characteristics of ASD can range in severity, appearance, frequency, and level of support required for daily functioning (American Psychiatric Association, 2013; Pratt et al., 2017).  

In addition to the characteristics above, individuals with ASD may experience difficulties with social awareness, effective communication, flexibility, and emotion regulation. Some individuals may engage in behaviors such as aggression, self-injurious behavior, property destruction, elopement, and tantrums. Although there is no cure for ASD, there are many learning opportunities for individuals with ASD to become more independent in their day-to-day functioning (National Institute of Neurological Disorders and Stroke, 2020). Additionally, many individuals with ASD are independent, functioning members of society.  

The history of ASD is unique in that our understanding of ASD has changed across time. Likely, our understanding of ASD will continue to evolve as more research is conducted. Therefore, it is important to review the history of ASD to fully understand ASD today. 

History of ASD 

The first recognized description of ASD was written by German psychiatrist, Eugene Blueler, in 1911. He considered ASD to be a facet of schizophrenia in which thought processes were characterized as “infantile wishes to avoid unsatisfying realities and replace them with fantasies and hallucinations” (Evans, 2013).   

In 1943, Dr. Leo Kanner, coined the term “early infantile autism” to describe children who lacked interest in other people. He further characterized his patients as having “extreme autistic aloneness,” “delayed echolalia,” and an “anxiously obsessive desire for the maintenance of sameness” (Chaste & Leboyer, 2012). Additionally, Dr. Kanner noted that some children were of average intelligence and had extraordinary memory. Based on these findings, Dr. Kanner viewed ASD as a profound emotional disturbance that did not affect intellectual abilities. As a result of Dr. Kanner’s work, the second edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM) defined “autism as a psychiatric condition — a form of childhood schizophrenia removed from reality” (American Psychiatric Association, 1968; Chaster & Leboyer, 2010).   

In the 1950s and 1960s, the perceived origin of ASD was environmental factors resulting from “cold and unemotional mothers,” often referred to as “refrigerator mothers.” This myth was dispelled by a growing body of research in the 1970s that demonstrated that ASD had a basis in biology and genetic causes (Flostein & Rutter, 1977).  

With a new understanding of the causes of ASD, diagnostic criteria were updated in the DSM-III in the 1980s and included six diagnostic criteria: onset before 30 months of age, pervasive lack of interest in people, severe impairments in communication, peculiar patters in speech (e.g., echolalia), bizarre responses to the environment, and absence of delusions or hallucinations that would be better characterized as schizophrenia (American Psychiatric Association, 1978, 1994).  Furthermore, the updated diagnostic criteria established ASD as its own diagnosis separate from schizophrenia and classified ASD as a pervasive developmental disorder (Volkmar et al., 1986). In 1987, the DSM-III was revised yet again and resulted in 16 criteria – eight of which had to be met for a diagnosis of ASD to be made (e.g., markedly lack of awareness, no communication, lack of ability for imitation or play).  

In 1994, the DSM-IV first categorized ASD as a spectrum in which an individual could be diagnosed with one of five separate disorders (American Psychiatric Association, 1994). These disorders included autistic disorder, Asperger’s disorder, childhood disintegrative disorder, Rett’s Disorder, and pervasive developmental disorder not otherwise specified. Additionally, there were 16 diagnostic criteria across three different categories of symptoms – 1. impairment in social interactions, 2. communication impairments, and 3. restricted, repetitive, and stereotyped behaviors or interests (Herman, 2019). This array of disorders may have resulted in inconsistent application of diagnoses across diagnosticians (American Psychiatric Association, 2013). 

Understanding of ASD Today 

In the most recent update to the DSM (i.e., DSM-5), the five separate disorders that fell under Autistic Disorder (i.e., autistic disorder, Asperger’s disorder, childhood disintegrative disorder, and pervasive developmental disorder not otherwise specified) were removed. Additionally, the three categories of symptoms were decreased to two – 1. impairments in social communication/interaction and 2. restricted and repetitive behaviors. Those who previously met the criteria for a diagnosis under the DSM-IV should still meet the criteria for ASD in the DSM-5. Researchers believe the new diagnostic criteria better reflect our understanding of ASD today and allows for greater consistency in diagnoses (American Psychiatric Association, 2013).  

As scientists understand ASD today, ASD may be caused by a mixture of environmental and genetic factors. Environmental factors may range from events during development, bacteria in the gut, or other complications with pregnancy (Chaste & Leboyer, 2012). Although the Human Genome Project (Venter et al., 2001) identified hundreds of genetic markers, they were unable to link any genes exclusively to autism (Chaste & Leboyer, 2012; Lictenstein et al., 2010; Muhle et al., 2004). Recent studies reveal that ASD affects males four times more than females (Fombonne, 2005); however, it is unclear why. Several theories have been proposed including the role of the sex chromosome and hormonal influences in utero. However, none of these theories have been confirmed (Fombonne, 2005).  

Although there is no cure for ASD and it remains unclear as to what causes ASD, scientists continue to work effortlessly to improve the lives of all individuals who are affected by a diagnosis of ASD. 

References

American Psychiatric Association. (1968). Diagnostic and statistical manual of mental disorders (2nd ed.).

American Psychiatric Association. (1978). Diagnostic and statistical manual of mental disorders (3rd ed.).

American Psychiatric Association. (1994). Diagnostic and statistical manual of mental disorders (4th ed.).

American Psychiatric Association. (2013). Diagnostic and statistical manual of mental disorders (5th ed.). https://doi.org/10.1176/appi.books.9780890425596

Center for Disease Control and Prevention. (2019, August 27). New data on autism. https://www.cdc.gov/ncbddd/autism/new-data.html

Chaste, P., & Leboyer, M. (2012). Autism risk factors: genes, environment, and gene-environment interactions. Dialogues in Clinical Neuroscience, 14(3), 281–292. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3513682/

Evans, B. (2013). How autism became autism: The radical transformation of a central concept of child development in Britain. History of the Human Science, 26(3), 3-31. https://doi.org/10.1177/0952695113484320

Folstein, S., & Rutter, M. (1977). Infantile autism: A genetic study of 21 twin pairs. The Journal of Child Psychology and Psychiatry, 18(4), 297-321. https://doi.org/10.1111.j.1469-7610.1977.tb00443.x

Fombonne, E. (2005). Epidemiology of autistic disorder and other pervasive developmental disorders. Journal of Clinical Psychiatry, 66(10), 3-8. https://www.psychiatrist.com/jcp/article/pages/2005/v66s10/v66s1001.aspx

Herman, E. (2019). Autism in the DSM. https://blogs.uoregon.edu/autismhistoryproject/topics/autism-in-the-dsm/

Lichtenstein, P., Carlström, E., Råstam, M., Gillberg, C., & Anckarsäter, H. (2010). The genetics of autism spectrum disorders and related neuropsychiatric disorders in childhood. The American Journal of Psychiatry, 167(11), 1357–1363. https://doi.org/10.1176/appi.ajp.2010.10020223

Muhle, R., Trentacoste, S. V., & Rapin, I. (2004) The genetics of autism. Pediatrics, 113(5), 472-486. https://doi.org/10.1542/peds.113.5.e472

National Institute of Neurological Disorders and Stroke (2020). Autism spectrum disorder fact sheet. https://www.ninds.nih.gov/Disorders/Patient-Caregiver-Education/Fact-Sheets/Autism-Spectrum-Disorder-Fact-Sheet

Pratt, C., Hopf, R., & Larriba-Quest, K. (2017). Characteristics of individuals with an autism spectrum disorder (ASD). The Reporter, 21(17). https://www.iidc.indiana.edu/irca/articles/characteristics-of-individuals-with-an-asd.html

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