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History of autism.

Autism is the most prolifically researched of all the child psychiatric disorders. This brief history of autism demonstrates that the concept and definition of the disorder has changed over the years along with socio-political shifts in beliefs about the treatments and services provided to those with autism.

Autism Spectrum Disorders (ASD) are a group of developmental disabilities characterized by impairment in reciprocal social interactions, abnormal development and use of language, and monotonously repetitive behaviors. ASDs take diverse forms, ranging from profound communication and behavioral problems to social difficulties with normal language and in some cases special talents in the areas of in math and natural sciences. ASDs are usually apparent before 3 years of age and may be diagnosed as young as 18 months. Because no biologic marker exists and the specific cause of ASD is unknown, the diagnosis is made by professionals who evaluate the child's developmental progress to identify the presence of developmental disorders. It is estimated that between 1 in 80 and 1 in 240 with an average of 1 in 110 children in the United States have ASDs. ASDs are reported in all racial, ethnic and socioeconomic groups, and is, on average, 4 to 5 times more common in boys than girls (Rice, 2009).


The first recorded reference to autistic symptoms was made by Gaspard Itard a French physician describing Victor "the wild boy of Aveyron" found naked in the woods in 1798. Victor was described as expressionless, insensitive to loud or pleasing noise, indifferent to smells, and attending only to objects he wanted. Itard worked with him for years and Victor learned to speak a few words, carry out simple commands, and to form attachments to his caregivers. Wing (1997) and Firth (2003) have no doubt that Victor was autistic.

Early History

The term "autism" was coined by Eugen Bleuler, a Swiss psychiatrist and psychologist, around 1912 and originally referred to "an escape from reality." Autism and autistic come from the Greek word "autos" meaning self. The term originally referred to a basic disturbance in schizophrenia, referring to an extreme withdrawal of oneself from social life (Firth, 2003).

In the first half of the 20th century, physicians, psychiatrists and psychologists working in the field of abnormal child development began studying and trying to define sub-groups of children diagnosed with childhood psychoses. Leo Kanner was among this group and in 1943 provided the first formal documentation of autism. Kanner (1943) described cases of children he believed to be afflicted with a syndrome not previously described. He noted these children "have come into the world with innate inability to form the usual biologically provided affected contact with people" (p. 217). He noted language delays, literalness, inability to use language for communication, a desire for "aloneness," and an ability to relate to objects in their environment only when they wanted to and it did not interfere with their self-imposed isolation. This was unlike children with schizophrenia who do not have this level of control over their perception of reality. Kanner also noted that the parents of these children showed a degree of rigidity and social difficulty themselves. Kanner (1949) was influenced by psychoanalytic theories, and suggested that the children's condition might be due to being raised by cold, detached, rigid parents who were perfectionists. He used the term "refrigerator mothers." Kanner also believed that there was no physical pathology in the brain.

Kanner's ideas about the parents of autistic children were accepted by psychiatrists and psychologists. The results were that many parents were overwhelmed by guilt, and families were spilt by attempts to blame one of the parents. Some families spent large sums of money on psychoanalytic treatment for their children.

During this same period, Hans Asperger a Viennese psychiatrist, was documenting similar behaviors in children in Austria. He described four cases of "autistic psychopathy of childhood" and called it Asperger's Syndrome (Wing, 1981). He also noted the children's poor social and emotional relationships, idiosyncratic language use, and lack of feelings for others. However, he noted that some had extraordinary gifts in mathematics and natural sciences (Firth, 2003). He noted that some of the parents had similar personality traits or were eccentric, but his approach to the parents was to consider their potential in helping their children. He also stressed the "constitutional basis" of these characteristics and considered the possibility of a genetic link to autism. The overall tone of Asperger's work is more positive than Kanner's. Asperger's approach to the syndrome was to offer treatment and education. Asperger's work was not well known in the United States until Wing (1981) introduced it.

Dr. Bruno Bettelheim (1967), who headed the University of Chicago's Orthogenic School, supported the psychoanalytic dissection of the parent-child relationship resulting in the blamethe-parent mentality which carried over into the speculation about the cause of autism. He claimed his program was a haven for children who had been forced to withdraw into themselves as a result of their mother's cruelty and neglect. Bettelheim's 1956 grant from the Ford Foundation supported 11 years of work which he claimed to have had significant results in his treatment of autistic children at his school. Meanwhile he continued to confront parents whom he claimed harmed their children as a result of their frigid neglect (Pollak, 1998).

A Period of Change

The 1960s brought the introduction of the scientific method into the study of autism, the development of parent groups, and federal support to improve the education of disabled and retarded children. Prior to the 1960s papers on autism were either clinical case descriptions or theory presentations. The 1960s brought carefully designed studies.

Dr. Bernard Rimland (1964), also a parent of a child with autism, challenged the theory that cold, rigid and neglectful parents were the cause of children withdrawing into an autistic world. Dr. Rimland presented evidence that autism had a biological basis, and that autism was not caused by frigid mothers. While the general public paid little attention to his book, parents who felt like victims embraced Rimland's book. Parents of autistic children also organized and founded the National Society for Autistic Children in 1965 (now the Autism Society of America) which currently has over 200 chapters.

The first epidemiological study of autism was conducted by Lotter (1966). He screened the entire population of 8 to 10 year olds, 78,000 children, in Middlesex country for indicators of autism. He found that 4.5 in 10,000 children had this syndrome with a higher incidence in boys. Rutter's (1968, 1971) comparative studies validated the syndrome and features of autism, and in a study with Bartak (1973) found behavioral approaches were the best teaching methods. His twin and family studies found that autism has a genetic basis (Folstein & Rutter, 1977). Hermelin and O'Connor (1970) studied the psychological features of children with autism as well as the "savant" phenomenon. Firth's (1991, 2003) research identified the neurological basis of the psychological deficits, and Wing's (1981, 1997) research aided in changing the concept of autism to include the viewpoint of the "autistic spectrum."

In 1975 the government enacted PL94-142, the Education for the Handicapped Act to ensure free appropriate public education for children with disabilities ages 3-21 years. An important concept of PL 94-142 was the "least restrictive environment." This meant that a child was placed in the most normalized educational setting that he or she could handle and still have success. Children with disabilities could no longer be isolated in special classroom. This meant that appropriate educational services for children with autism would be provided by the state's school system. In addition, once it was determined that a child had a disability that would interfere with their educational achievement, the law required the development of an IEP (Individualized Educational Plan). In 1990 the Education for the Handicapped Act was changed to IDEA (Individuals with Disabilities Education Act). One of the important changes for children with autistic disorders was that for the first time they would be eligible for educational services that included the use of assistive technology. This was especially important to the children with communication problems.

The diagnosis of autism became easier in 1980 when autism was added to the DSM-III (Diagnostic and Statistical Manual, 3rd Ed.) under the category of Pervasive Developmental Disorders. There it was listed as "infantile autism." The revised edition (DSM-IIIR) released in 1987 dropped the word "infantile" and infantile autism became "autistic disorder." The required age of onset was also dropped. The DSM-III and DSM-IIIR were formatted into a series of criteria or symptoms that were associated with each of the disorders such as "autistic disorder." This method of diagnosis, focusing on symptoms rather than causative factors, was different from the psychoanalytic approach the psychiatrists had used in the past.

1990s to Present

In 1994 the DSM-IV was released. For the first time clinicians input was used and as a result the category of Pervasive Developmental Disorders was now a spectrum, as proposed by Wing in 1981. The five points on the autism spectrum included: autistic disorder, Rett disorder, childhood disintegrative disorder, Asperger's disorder and pervasive developmental disorder-not otherwise specified. The use of research results also lead to the reintroduction of the age of onset for autism disorders. Clinicians in the field had confirmed that the onset of symptoms could be consistently demonstrated at 18 months. The language criteria became more specific so that "markedly abnormal nonverbal communication" became "marked impairments in the use of multiple nonverbal behaviors such as eye-to-eye gaze, facial expression, body posture, and gestures to regulate social interaction" (Grinker, 2007, p.139). It is unclear if these changes helped to clarify the diagnosis of autistic disorders or if there was only more confusion (Grinker, 2007). This dilemma was important because the prevalence of autism has continued to rise.

In the mid-1990s key events in the United States and Britain led parents in both countries to embrace an unproven hypothesis that vaccines caused autism. One group of researchers in the UK, lead by Andrew Wakefield proposed that the measles virus caused a leaky gut, sending toxic substances into the bloodstream and ultimately the brain. Separating the MMR into three individual vaccines would be safer. Wakefield's idea expanded on a finding of intestinal disease in children with autism (Wakefield, Murch, Anthony, et al., 1998). Parents, in large numbers, began to refuse to have their children vaccinated. Some parents accepted Wakefield's hypothesis, others believed that the triple vaccine overtaxed the immune system of susceptible children, or that the preservative thimerasol, which contained mercury, was somehow responsible for the onset of autism in affected children (Gross, 2009). Researchers conducted numerous studies to determine if there was a link. In 2004 the Institute of Medicine's Immunization Safety Review Committee released a report of their analysis of all published and unpublished epidemiological studies regarding the hypothesis that vaccines, specifically the measles-mumps-rubella (MMR) vaccine and thimerasol-containing vaccines were causally associated with autism. The committee concluded that the body of evidence favored rejection of a causal relationship between the MMR vaccine and autism. In 2010, The Lancet, the medical journal that published Wakefield's paper, retracted it. In the original paper Wakefield claimed to have investigated "a consecutive series" of 12 children referred to the Royal Free Hospital and School of Medicine with a regressive developmental disorder. However, Britain's General Medical Council found that Wakefield carefully selected the children in the study, and that some of Wakefield's research was funded by lawyers acting for parents who were involved in lawsuits against vaccine manufacturers. The Council found Wakefield had acted unethically and had shown "callous disregard" for the children in the study by subjecting them to invasive tests. The vaccine-autism theory persists despite the abundance of evidence that no causal link exists. Some fault the media, some well-organized groups that exploit parents' hopes and fears, and others information technology which has transformed the way trust and knowledge are produced (Gross, 2009).

In 2001 George W. Bush signed the No Child Left Behind Act (NCLB). The NCLB was written to improve school accountability. Benefits to parents and their children with ASD included an emphasis on early intervention services, increased communication between parents and schools, and assurances that teachers were highly trained in the areas needed to provide a quality education to all children.

There has been long-standing support from twin and family studies of a genetic component in the etiology of autism. Twin studies have shown a 60% to 90% concordance rate for classic autism among monozygotic twins depending on the use of narrow or broad diagnostic criteria. Dizygotic twins, in contrast, show a 0 to 10% concordance under the same models (Folstein & Rutter, 1977; Folstein & Rosen-Sheidley, 2001). Researchers are constantly identifying new gene associations and are gaining a better understanding of the role and function of mitrochondrial DNA (mtDNA) in the etiology of ASD. It is clear autism is not a single-gene disorder, but it is unknown if it is associated with 10 genes or 100 genes. In addition, scientists do not understand how these genes function or interact with environmental factors (Dhillon, Hellings & Butler, 2011; El-Fishawy & State, 2010).

Advanced neuropathologic research has identified morphological and neurochemical changes in the autistic brain (Polsek, Jagatic, Cepanec, et al., 2011). Early brain overgrowth is one of the most important morphological abnormalities of the autistic brain. There is also evidence of abnormal minicolumnar structure in the frontal, temporal and anterior cingulate cortices. Minicolumns are the basic units of cortical information processing. Neurochemical research is focused on the study of neurotransmitters, particularly in the glutamate and GABA-related abnormalities found in the autistic brain.

The most recent controversy surrounding autism is the proposed new definition of autism. A panel of experts appointed by the American Psychiatric Association, which is completing work on the fifth edition of the DSM, is considering a new definition of autism which will narrow the criteria for a diagnosis of autism (Jabr, 2012). What is in question is how many of the DSM-5 criteria a patient must meet to be diagnosed with autism. Since the 1980s the prevalence of autism has increased dramatically worldwide, and many psychiatrists agree that the increase is at least partially explained by the loose criteria in the DSM-IV (Jabr, 2012). Many parents fear their children will be left out with the new diagnostic criteria, and will not have access to needed health services or to school and other state-based services. The DSM-5 is scheduled for release in May 2013.


Since its discovery 60 years ago ASDs remain puzzling and difficult to understand. People with autism may be severely impaired and low-functioning or may be mildly affected with Asberger's syndrome. There have also been changes in the concept and definition of the disorder over the years. Sociopolitical shifts and research findings have also significantly changed the understanding of autism and improved the care and treatment offered to affected people.


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Bonnie Holaday, RN, DNS, FAAN Professor, School of Nursing, Clemson University
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Title Annotation:Chapters
Author:Holaday, Bonnie
Publication:South Carolina Nurse
Article Type:Disease/Disorder overview
Geographic Code:1USA
Date:Apr 1, 2012
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