essay on autism

Autism Spectrum Disorder (ASD) Essay

Autism is a serious disorder that has the potential to disrupt the success of people living with it. This report shall set out to explore various aspects regarding this disorder. To this end, an overview of the symptoms, causes, diagnosis and treatment shall be offered. This shall aim at expanding our understanding regarding this disorder so as to enable us to be better prepared to handle it whenever the need arises.

Introduction

Autism has been noted to be among the most prevalent childhood psychiatric disorder. Kuder (2003) denotes that in the USA, an estimated 2.1% of the population aged between 8 and 17 is affected by autism in its various forms.

Autism is manifested by varied behavior but it is chiefly characterized by inability to communicate, lingual deficits, lack of a sustained attention, low level of activity, temper tantrums, sleep disturbance, aggression inadequate motor control and other non-compliant behavior. These behaviors are detrimental to the social and educational endeavors of the people involved.

Biological and genetic aspects of autism Spectrum Disorders

Autism spectrum is a medical term that is used to describe children and adults who experience difficulties in motor coordination, socializing, communicating (verbal and non-verbal) and language acquisition (Tager-Flusberg, Paul and Lord, 2005). The authors describe autism as a neurological disorder that stems from the brain’s inability to carryout some functions normally.

The causes of Autism as well as the reasons why it affects lingual and communication skills are not entirely known though there is a close linkage between Autism and genetics.

Studies indicate that Autism Spectrum Disorder (ASD) is inherited between family members. A study conducted by the American Psychiatric Association (2000) indicated that there is a 3-6% chance of getting autism amongst siblings.

However, Korvatska et al (2002) state that the difficulty experienced by scientists in pinpointing the genetic aspects of autism emanates from the lack of extended family histories. In most cases, autistic individual become more detached socially that they rarely marry or have children. As such, finding a family that has detailed genetic information regarding autism is difficult.

On a brighter note, twins have been used to explore the genetics behind autism (Beaudet, 2007). One study indicated an 82% likelihood of an autistic identical twin having the same disorder. This is in contrast to the 10% likelihood indicated by results from fraternal twins. More sophisticated studies have in the recent past concluded that 90% of autism related behavioral phenotypes are as a result of inherited genes (Happé & Ronald, 2008). This shows that there is a strong relationship between autism and genes.

Biologically, the root cause of autism has been difficult due to relative inability to access and study the brain systematically. However, technological innovations and advancements such as MRIs, CT scans and SPECT have made it possible to study the structure and functionality of the brain.

As a result, specialists have been able to deduce that majority of the brain’s structures play a pivotal role in the development of ASD. According to NIMH (2009, p. 1) they include but are not limited to “the cerebellum, cerebral cortex, limbic system, corpus callosum, basal ganglia, and brain stem”.

Similarly, other studies indicate that various neurotransmitters such as serotonin and epinephrine have a strong link to autism. The diagram below shows the biological basis of Autism Spectrum Disorder. It shows various structures of the brain and explains the functions that each play. Various symptoms of ASD are as a result of the structures’ inability to carry out their normal function.

A diagram showing brain structures linked to ASD

ASD Etiology

As mentioned earlier, the causes of ASD are not well known. However, researches conducted in this regard indicate that genetic, nutritional and environmental factors play a pivotal role in the development of the disorders. Results from numerous studies indicate that genetic factors predominate.

Others indicate that certain foods, infectious diseases, plastic and metallic extracts could cause autism. Similarly, smoking, alcohol, illicit drugs and some (mercury-based) childhood vaccines have also been attributed to causing autism. However, none of these causes are conclusive and more research needs to be conducted. This is to mean that the theory of causation regarding autism is not complete as yet.

Prevalence of ASD

The most recent survey conducted by center of disease control (CDC) indicated that autism rates have increased significantly over the past three decades. In most cases, studies indicate that autism is most prevalent among children. According to Rutter (2005), boys are four times more likely to be autistic than their female counterparts.

In addition, the author states that the symptoms of autism exhibit themselves from childbirth until three years of age. Parents are the most likely to discover these symptoms. As a result, they should ensure that they have their children checked at the onset of various abnormal behaviors.

Rutter (2005) asserts that the prevalence of autism disorder has been facilitated by ignorance and assumptions made by caretakers. In some cases, parents assume that their children are ‘slow and that they will develop as they grow up. However, this approach has proven to be costly since autism can best be handled as soon as it is detected.

Delaying makes it difficult to come up with remedies and coping mechanisms for both parents and the individuals having autism disorders. The main symptoms of this disorder include communication (verbal and non-verbal) difficulties, inability to develop and maintain relations with other people, abnormal lingual patterns and repetitive behaviors. Whenever any of these symptoms are discovered, it is highly recommended that medical or psychiatric assistance be sought.

Diagnosis of ASD

An early diagnosis of ASD is important since it enables the people involved to come up with effective interventions before its too late. Recent studies show that intensive interventions administered in a control environment for a minimum of two years during preschool leads to behavioral and social improvements among children with ASD.

Clinicians base their diagnosis depending on the behavioral traits exhibited by a child. For a diagnosis to be made, NIMH (2009) asserts that at least one of the symptoms associated with ASD must be present. This means that a patient must have abnormal patterns of communication, socialization and restrictive behaviors.

In most cases, the diagnosis is made through a two-stage process. The first stage is “a developmental screening normally conducted during the routine childhood check-ups, while the second one involves a more comprehensive behavioral analysis by a team of experts (NIMH, 2009, p. 1).” Below are the stages that are followed to diagnose ASD.

The American Psychiatric Association (2000) recommends that every parent should ensure that a developmental screening test is carried out for his/her child during the “well child” check-up. The author contends that screening plays a pivotal role in the early identification of ASD symptoms.

Due to its importance, there are various screening instruments that have been developed to facilitate the diagnosis process. They include but are not limited to Checklist of Autism in Toddlers (CHAT) and its modified version; M-CHAT. Similarly, the Screening Tool for Autism in Two-Year-Olds (STAT) as well as the Social Communication Questionnaire (SCQ) have proven to be effective in diagnosing ASD in children aged between two years old and above four years old respectively.

According to Tadevosyan-Leyfer et al (2003), questionnaires given to parents provide important information during the diagnosis process. As such, some instruments rely on such responses while others depend on these responses as well as observations made by the caregiver. However, these screening instruments are not as effective as they should be when it comes to identifying mild ASD or Asperger syndrome. As a result, other screening instruments such as the Autism Spectrum Screening Questionnaire (ASSQ) and the Childhood Asperger Syndrome Test (CAST) among others have been developed so as to diagnose these forms of ASD (NIMH, 2009).

Comprehensive Diagnostic Evaluation

This is the second stage of diagnosis and it relies on the skills of a team of different experts such as psychologists, psychiatrists, neurologists, and therapists among others. This evaluation entails a comprehensive analysis of neural, genetic, cognitive and language testing in order to conclude whether a patient is suffering from autism or other behavioral disorders.

Some of the instruments used at this stage include: Autism Diagnosis Interview-Revised (ADI-R), which is a structured interview designed to test a child’s “communication, social interaction, restrictive behaviors and age-of-onset symptoms, and the Autism Diagnosis Observation Scheduling (ADOS-G), which is designed to identify abnormal, missing or delayed communication and social behaviors (NIMH, 2009, p. 1).”

The teams of experts that conduct this diagnosis determine the strengths and weaknesses of the child and recommend various treatment options that should be undertaken.

Treatment of ASD

According to Freitag (2007) there is no one-shoe-fits-all approach to treating ASD. However, specialists in this area seem to agree on the fact that early interventions are of great importance. Arguably, the best treatment is one that considers the interests of the patient, allows the patient to learn in accordance to his/her ability and causes no harm to the overall well being of the patient. With this in mind, there are specialized programs and treatments that have proven to be effective against ASD symptoms.

For starters, Applied Behavioral Analysis (ABA) is among the most used intervention in treating ASD (SAMHSA, 2011). Similarly, there are dietary and medical interventions that help suppress unwanted behaviors among autistic children (NIMH, 2009). In regard to learning, there are specialized educational programs that seek to enhance the socio-communicative, cognitive and language skills of autistic students.

It can be articulated from this report that Autism is a problem that needs to be focused on. With proper understanding as to what the condition entails, parents and practitioners are better armed to assist patients overcome the weaknesses brought about by the condition and therefore achieve successful lives.

From this study, it can be authoritatively stated that early diagnosis and treatment of Autism spectrum is necessary to increase the chances of success in learning for the child suffering from this disease. Whereas Autism is not curable, it can be managed so as to ensure that it is not disruptive to the life of the individual during his/her future endeavors.

American Psychiatric Association. (2000). Diagnostic and statistical manual of mental disorders: DSM-IV-TR (fourth edition, text revision). Washington DC: American Psychiatric Association.

Beaudet, A. L. (2007). Autism: highly heritable but not inherited. Nat Med, 13(5): 534–6.

Freitag, C. M. (2007). The genetics of autistic disorders and its clinical relevance: a review of the literature. Mol Psychiatry. 12(1): 2–22.

Happé, F., & Ronald, A. (2008). The ‘fractionable autism triad’: a review of evidence from behavioral, genetic, cognitive and neural research. Neuropsychol Rev, 18(4): 287–304.

Korvatska, E et al. (2002). Genetic and immunologic considerations in autism. Neurobiology of Disease , 9: 107-125.

Kuder, S. (2003). Teaching Students with Language and Communication Disabilities. USA: Allyn and Bacon.

NIMH. (2009) Autism Spectrum Disorders (Pervasive Developmental Disorders) . Web.

Rutter, M. (2005). Incidence of autism spectrum disorders: changes over time and their meaning. Acta Paediatr. 94(1): 2–15.

SAMHSA. (2011). Autism Spectrum Disorders . Web.

Tadevosyan-Leyfer, O et al. (2003). A principal components analysis of the autism diagnostic interview-revised. Journal of the American Academy of Child and Adolescent Psychiatry, 42(7): 864-872.

Tager-Flusberg, H., & Lord, C. (2005). Language and Communication in Autism. Web.

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Bibliography

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Laboratory Diagnosis of Autism Spectrum Disorders
Teenagers With Autism Disorder
Autism Spectrum Disorder
Autism Spectrum Disorders and Educational Interventions
Autism Spectrum Disorder Features in Children
Autism Spectrum Disorder in Relation to Education
Emerging Adults With ASD and the Importance of Close Relationships
Autism Spectrum Disorder in Children and Its Impact on the Family
Autism Spectrum Disorders: Diagnostic Procedure
Autism Spectrum Disorder: Diagnosis, Impact, Treatment
Mental Illnesses History and Treatment
Psychopathologies: Co-occurring Diagnoses
The Identification of Bipolar Disorders
How Do People Labelled With a Mental Illness Deal With Their Stigmatization?
Attention Deficit Hyperactivity Disorder Causes

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Home — Essay Samples — Nursing & Health — Autism — Why Autism Awareness is Important

Why Autism Awareness is Important

Categories: Autism Psychological Disorders

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CONCEPTUAL ANALYSIS article

Research, clinical, and sociological aspects of autism.

$\nPaul Whiteley$

ESPA Research, Unit 133i Business Innovation Centre, The Robert Luff Laboratory, Education & Services for People With Autism Research, Sunderland, United Kingdom

The concept of autism continues to evolve. Not only have the central diagnostic criteria that define autism evolved but understanding of the label and how autism is viewed in research, clinical and sociological terms has also changed. Several key issues have emerged in relation to research, clinical and sociological aspects of autism. Shifts in research focus to encompass the massive heterogeneity covered under the label and appreciation that autism rarely exists in a diagnostic vacuum have brought about new questions and challenges. Diagnostic changes, increasing moves towards early diagnosis and intervention, and a greater appreciation of autism in girls and women and into adulthood and old age have similarly impacted on autism in the clinic. Discussions about autism in socio-political terms have also increased, as exemplified by the rise of ideas such as neurodiversity and an increasingly vocal dialogue with those diagnosed on the autism spectrum. Such changes are to be welcomed, but at the same time bring with them new challenges. Those changes also offer an insight into what might be further to come for the label of autism.

Introduction

Although there is still debate in some quarters about who first formally defined autism ( 1 ), most people accept that Kanner ( 2 ) should be credited as offering the first recognised description of the condition in the peer-reviewed scientific literature. The core diagnostic features covering issues in areas of social and communicative interaction alongside the presence of restricted and/or repetitive patterns of behaviour ( 3 ) described in his small caseload still remain central parts of the diagnosis today. The core issue of alterations in social cognition affecting emotion recognition and social attention ( 4 ) remain integral to the diagnosis of autism. The additional requirement for such behaviours to significantly impact on various areas of day-to-day functioning completes the diagnostic criteria.

From defining a relatively small group of people, the evolution of the diagnostic criteria for autism has gone hand-in-hand with a corresponding increase in the numbers of people being diagnosed. Prevalence figures that referred to 4.5 per 10,000 ( 5 ) in the 1960s have been replaced by newer estimates suggesting that 1 in 59 children (16 per 1,000) present with an autism spectrum disorder (ASD) in 2014 ( 6 ). The widening of the definition of autism has undoubtedly contributed to the significant increase in the numbers of people being diagnosed. It would be unacceptably speculative however, to define diagnostic changes as being the sole cause of the perceived prevalence increases.

Alongside the growth in numbers of people being diagnosed with autism so there have been changes in other areas related to autism; specifically those related to the research, clinical practice and sociological aspects of autism. Many of the changes have centred on key issues around the acceptance that autism is an extremely heterogeneous condition both in terms of presentation and also in relation to the genetic and biological complexity underlying its existence. That autism rarely exists in some sort of diagnostic vacuum is another part of the changes witnessed over the decades following the description of autism.

In this paper we highlight some of the more widely discussed changes in areas of research, clinical practice and sociological terms in relation to autism. We speculate on how such changes might also further develop the concept of autism in years to come.

Autism Research

As the definition of autism has subtly changed over the years, so ideas and trends in autism research have waxed and waned. The focus on psychology and behaviour as core descriptive features of autism has, in many respects, guided research and clinical views and opinions about the condition. Social cognition, including areas as diverse as social motivation, emotion recognition, social attention and social learning ( 4 ), remains a mainstay of research in this area. The rise of psychoanalysis and related ideas such as attachment theory in the early 20th century for example, played a huge role in the now discredited ideas that maternal bonding or cold parenting were a cause of autism. The seemingly implicit need for psychology to formulate theories has also no doubt played a role in perpetuating all-manner of different grand and unifying reasons on why autism comes about and the core nature of the condition.

As time moved on and science witnessed the rise of psychiatric genetics, where subtle changes to the genetic code were correlated with specific behavioural and psychiatric labels, so autism science also moved in the same direction. Scientific progress allowing the genetic code to be more easily and more cost-effectively read opened up a whole new scientific world in relation to autism and various other labels. It was within this area of genetic science that some particularly important discoveries were made: (a) for the vast majority of people, autism is not a single gene “disorder,” and (b) genetic polymorphisms whilst important, are not the only mechanism that can affect gene expression. Mirroring the role of genetics in other behavioural and psychiatric conditions ( 7 ), the picture that is emerging suggests that yes, there are genetic underpinnings to autism, but identifying such label-specific genetic issues is complicated and indeed, wide-ranging.

What such genetic studies also served to prove is that autism is heterogeneous. They complemented the wide-ranging behavioural profiles that are included under the diagnostic heading of autism. Profiles that ranged from those who are profoundly autistic and who require almost constant attention to meet their daily needs, to those who have jobs, families and are able to navigate the world [seemingly] with little or minimal support for much of the time.

It is this heterogeneity that is perhaps at the core of where autism is now from several different perspectives. A heterogeneity that not only relates to the presentation of the core traits of autism but also to how autism rarely manifests in a diagnostic vacuum ( 8 ). Several authors have talked about autism as part of a wider clinical picture ( 9 , 10 ) and how various behavioural/psychiatric/somatic issues seem to follow the diagnosis. Again, such a shift mirrors what is happening in other areas of science, such as the establishment of the Research Domain Criteria (RDoC) project ( 11 ). RDoC recognised that defining behavioural and psychiatric conditions on the basis of presented signs and symptoms does not necessarily “reflect” the relevant underlying processes and systems that might be important. It recognised that in order to deliver important clinical information about how and why a condition manifests, or the best strategies to intervene, research cannot just singularly start with the label. Science and clinical practice need more information rather than just a blanket descriptive label such as autism.

To talk about autism as a condition that also manifests various over-represented comorbid labels also asks a fundamental question: is the word “comorbidity” entirely accurate when referring to such labels? ( 12 ). Does such comorbidity instead represent something more fundamental to at least some presentations of autism or is it something that should be seen more transiently? Numerous conditions have been detailed to co-occur alongside autism. These include various behavioural and psychiatric diagnoses such as depression, anxiety and attention-deficit hyperactivity disorder (ADHD) ( 13 ). Other more somatic based conditions such as epilepsy ( 14 ), sleep ( 15 ) and various facets of gastrointestinal (GI) functioning ( 16 ) have also been discussed in the peer-reviewed science literature. Some of these co-occurring conditions have been described in the context of specific genetic conditions manifesting autism. Issues with the BCKDK (Branched Chain Ketoacid Dehydrogenase Kinase) gene for example, have been discussed in the context of autism, intellectual (learning) disability and epilepsy appearing together ( 17 ). Such a diagnostic combination is not unusual; autism often being described as the primary diagnosis with epilepsy and learning disability seen as “add-ons.” But should this be the case? Other evidence pointing to the possibility that epilepsy might under some circumstances beget autism ( 18 ) suggests that under some circumstances, such co-occurring conditions are so much more than just co-occurring or comorbid.

Other evidence for questioning the label “comorbid” comes from various animal models of autism. Accepting that one has to be particularly careful about extrapolating from animal models of autism to the more complex presentation of autism in humans ( 19 ), various models have suggested that autism may for some, fundamentally coexist with GI or bowel issues ( 20 , 21 ). Such observations have been noted across different animal models and cover important issues such as gut motility for example, that have been talked about in the context of autism ( 22 ).

Similarly, when one talks about the behavioural and psychiatric comorbidity in the context of autism, an analogous question arises about whether comorbidity is the right term. Anxiety and depression represent important research topics in the context of autism. Both issues have long been talked about in the context of autism ( 1 , 13 , 23 ) but only in recent years have their respective “links” to autism been more closely scrutinised.

Depression covers various different types of clinical presentations. Some research has suggested that in the context of autism, depressive illnesses such as bipolar disorder can present atypically ( 24 ). Combined with other study ( 25 ) suggesting that interventions targeting depressive symptoms might also impact on core autistic features, the possibility that autism and depression or depressive symptoms might be more closely linked than hitherto appreciated arises. Likewise with anxiety in mind, similar conclusions could be drawn from the existing research literature that anxiety may be a more central feature of autism. This on the basis of connections observed between traits of the two conditions ( 26 ) alongside shared features such as an intolerance of uncertainty ( 27 ) exerting an important effect.

A greater appreciation of the heterogeneity of autism and consideration of the myriad of other conditions that seem to be over-represented alongside autism pose serious problems to autism research. The use of “autism pure” where research participants are only included into studies on the basis of not having epilepsy or not possessing a diagnosis of ADHD or related condition pose a serious problem when it comes to the generalisation of research results to the wider population. Indeed, with the vast heterogeneity that encompasses autism, one has to question how, in the context of the current blanket diagnosis of autism or ASD, one could ever provide any universal answers about autism.

Autism in the Clinic

As mentioned previously, various subtle shifts in the criteria governing the diagnosis of autism have been witnessed down the years. Such changes have led to increased challenges for clinicians diagnosing autism from several different perspectives. One of the key challenges has come about as a function of the various expansions and contractions of what constitutes autism from a diagnostic point of view. This includes the adoption of autism as a spectrum disorder in more recent diagnostic texts.

The inclusion of Asperger syndrome in the DSM-IV and ICD-10 diagnostic schedules represented an expansion of the diagnostic criteria covering autism. Asperger syndrome defined by Hans Asperger ( 28 ) as autistic features without significant language impairment and with intelligence in the typical range, was included in the text for various different reasons. Allen Frances, one of the architects of the DSM-IV schedule, mentioned the importance of having a “ specific category to cover the substantial group of patients who failed to meet the stringent criteria for autistic disorder, but nonetheless had substantial distress or impairment from their stereotyped interests, eccentric behaviors, and interpersonal problems ” ( 29 ). It is now widely accepted that the inclusion of Asperger syndrome in diagnostic texts led to an increase in the number of autism diagnoses being given.

More recent revisions to the DSM criteria covering autism—DSM-5—included the removal of Asperger syndrome as a discrete diagnosis on the autism spectrum ( 30 ). Instead, a broader categorisation of autism spectrum disorder (ASD) was adopted. The reasons for the removal of Asperger syndrome from DSM-5 are complex. The removal has however generally been positively greeted as a function of on-going debates about whether there are/were important differences between autism and Asperger syndrome to require a distinction ( 31 ) alongside more recent revelations about the actions of Asperger during World War II ( 32 ). Studies comparing DSM-IV (and its smaller revisions) with DSM-5 have also hinted that the diagnostic differences between the schedules may well-impact on the numbers of people in receipt of a diagnosis ( 33 ).

Shifts in the diagnostic text covering autism represent only one challenge to autism in the clinical sense. Other important factors continue to complicate the practice of diagnosing autism. Another important issue is a greater realisation that although the presence of observable autistic features are a necessary requirement for a diagnosis of autism, such features are also apparent in various other clinical labels. Autistic features have been noted in a range of other conditions including schizophrenia ( 34 ), personality disorders ( 35 ) and eating disorders ( 36 ) for examples. Coupled with the increasingly important observation that autism rarely exists in a diagnostic vacuum, the clinical challenges to accurately diagnosing autism multiply as a result.

The additional suggestion of “behavioural profiles” within the autism spectrum adds to the complexity. Terms such as pathological demand avoidance (PDA) coined by Newson and colleagues ( 37 ) have started to enter some diagnostic processes, despite not yet being formally recognised in diagnostic texts. Including various autistic traits alongside features such as “resisting and avoiding the ordinary demands of life” and the “active use of various strategies to resist demands via social manipulation,” debate continues about the nature of PDA and its diagnostic value ( 38 ).

Early diagnosis and intervention for autism have also witnessed some important clinical changes over the years. Driven by an acceptance of the idea that earlier diagnosis means that early intervention can be put in place to “ameliorate” some of the more life-changing effects of autism, there has been a sharp focus on the ways and means of identifying autism early and/or highlighting those most at risk of a diagnosis. It's long been known that there is a heritable aspect to autism, whether in terms of traits or diagnosis ( 39 ). In this respect, preferential screening for autism in younger siblings when an older child has been diagnosed is not an uncommon clinical sentiment ( 40 ). Other work looking at possible “red flags” for autism, whether in behaviour ( 41 ) or in more physiological terms still continue to find popularity in both research and clinical terms.

But still however, autism continues to confound. As of yet, there are only limited reliable red flags to determine or preclude the future presence of autism ( 42 ). Early behavioural interventions for autism have not yet fulfilled the promise they are said to hold ( 43 ) and autism is not seemingly present in the earliest days of development for all ( 44 , 45 ). There is still a way to go.

Autism in a modern clinical sense is also witnessing change in several other quarters. The traditional focus of autism on children, particularly boys, is being replaced by a wider acceptance that (a) autism can and does manifest in girls and women, and (b) children with autism age and mature to become adults with autism. Even the psychological mainstay of autism—issues with social cognition—is undergoing discussion and revision.

On the issue of autism presentation in females, several important themes are becoming more evident. Discussions about whether there may be subtle differences in the presentation of autism in females compared to males are being voiced, pertinent to the idea that there may be one or more specific female phenotypes of autism ( 46 ). Further characterisation has hinted that sex differences in the core domain of repetitive stereotyped behaviours ( 47 ) for example, may be something important when it comes to assessing autism in females.

Allied to the idea of sex differences in autism presentation, is an increasing emphasis on the notion of camouflaging or masking ( 48 ). This masking assumes that there may active or adaptive processes on-going that allow females to hide some of their core autistic features and which potentially contributes to the under-identification of autism. Although some authors have talked about the potentially negative aspects of masking in terms of the use of cognitive resources to “maintain the mask,” one could also view such as adaptation in a more positive light relating to the learning of such a strategy as a coping mechanism. Both the themes of possible sex differences in presentation and masking add to the clinical complexity of reliably assessing for autism.

Insofar as the growing interest in the presentation of autism in adulthood, there are various other clinical considerations. Alongside the idea that the presentation of autism in childhood might not be the same as autism in adulthood ( 49 ), the increasing number of people receiving a diagnosis in adulthood is a worthy reminder that autism is very much a lifelong condition for many, but not necessarily all ( 50 ). The available research literature also highlights how autism in older adults carries some unique issues ( 51 ) some of which will require clinical attention.

Insofar as the issue of social cognition and autism, previous sweeping generalisations about a deficit in empathy for example, embodying all autism are also being questioned. Discussions are beginning debating issues such as how empathy is measured and whether such measurements in the context of autism are as accurate as once believed ( 52 ). Whether too, the concept of social cognition and all the aspects it encompasses is too generalised in its portrayal of autism, including the notion of the “double empathy problem” ( 53 ) where reciprocity and mutual understanding during interaction are not solely down to the person with autism. Rather, they come about because experiences and understanding differ from an autistic and non-autistic point of view. Such discussions are beginning to have a real impact on the way that autism is perceived.

Autism in Sociological Terms

To talk about autism purely through a research or clinical practice lens does not do justice to the existing peer-reviewed literature in its entirety. Where once autism was the sole domain of medical or academic professionals, so now there is a growing appreciation of autism in socio-political terms too, with numerous voices from the autism spectrum being heard in the scientific literature and beyond.

There are various factors that have contributed to the increased visibility of those diagnosed with autism contributing to the narrative about autism. As mentioned, the fact that children with autism become autistic adults is starting to become more widely appreciated in various circles. The expansion of the diagnostic criteria has also played a strong role too, as the diagnostic boundaries of the autism spectrum were widened to include those with sometimes good vocal communicative abilities. The growth in social media and related communication forms likewise provided a platform for many people to voice their own opinions about what autism means to them and further influence discussions about autism. The idea that autistic people are experts on autism continues to grow ( 54 ).

For some people with autism, the existing narrative about autism based on a deficit model (deficits in socio-communicative abilities for example) is seemingly over-emphasised. The existing medical model of autism focusing such deficits as being centred on the person does not offer a completely satisfying explanation for autism and how its features can disable a person. Autism does not solely exist in a sociological as well as diagnostic vacuum. In this context, the rise and rise of the concept of neurodiversity offered an important alternative to the existing viewpoint.

Although still the topic of some discussion, neurodiversity applied to autism is based on several key tenets: (a) all minds are different, and (b) “ neurodiversity is the idea that neurological differences like autism and ADHD are the result of normal, natural variation in the human genome ” ( 55 ). The adoption of the social model of disability by neurodiversity proponents moves the emphasis on the person as the epicentre of disability to that where societal structures and functions tend to be “ physically, socially and emotionally inhospitable towards autistic people ” ( 56 ). The message is that subtle changes to the social environment could make quite a lot of difference to the disabling features of autism.

Although a popular idea in many quarters, the concept of neurodiversity is not without its critics both from a scientific and sociological point of view ( 57 ). Certain key terms often mentioned alongside neurodiversity (e.g., neurotypical) are not well-defined or are incompatible with the existing research literature ( 58 ). The idea that societal organisation is a primary cause of the disability experienced by those with the most profound types of autism is also problematic in the context of current scientific knowledge and understanding. Other issues such as the increasing use of self-diagnosis ( 59 ) and the seeming under-representation of those with the most profound forms of autism in relation to neurodiversity further complicate the movement and its aims.

The challenges that face the evolving concept of neurodiversity when applied to autism should not however detract from the important effects that it has had and continues to have. Moving away from the idea that autistic people are broken or somehow incomplete as a function of their disability is an important part of the evolution of autism. The idea that autism is something to be researched as stand-alone issue separate from the person is something else that is being slowly being eroded by such a theory.

The concept of autism continues to evolve in relation to research, clinical practice and sociological domains. Such changes offer clues as to the future directions that autism may take and the challenges that lie ahead.

The continuing focus on the huge heterogeneity and comorbidity clusters that define autism are ripe for the introduction of a new taxonomy for describing the condition. A more plural definition—the autisms—could represent one starting position ( 60 ) encompassing a greater appreciation that (a) there is variety in the presentation of the core features of autism, (b) there are seemingly several different genetic and biological pathways that bring someone to a diagnosis of autism, (c) different developmental trajectories are an important facet of the autism spectrum, and (d) the various “comorbidities” that variably present alongside autism may offer important clues about the classification of autism. Some authors have stressed that a multi-dimensional conceptualisation may be more appropriate than a categorical concept ( 61 ) but further investigations are required.

In relation to the proposed pluralisation of the label, several long held “beliefs” about autism are also ripe for further investigation. The idea that autism is innate and presents in the earliest days in all does not universally hold ( 45 ). The finding that some children experience a period of typical development and then regress into autism ( 62 ) is becoming more readily discussed in research and clinical circles, albeit not universally so. Similarly, the belief that autism is a lifelong condition for all is also not borne out by the peer-reviewed literature ( 63 ). Terms such as optimal outcome ( 64 ) might not be wholly appropriate, but do nonetheless, shed light on an important phenomenon noted in at least some cases of autism where diagnostic cut-off points are reached at one point but not another. These and other important areas provide initial support for the adoption of the idea of the plural autisms.

Allied to the notion of “the autisms” is the requirement to overhaul the terminology around the use of the “level of functioning” phrase ( 65 ). “High functioning” is typically used to describe those people on the spectrum who present with some degree of communicative language, possess typical or above-average intelligence and who can seemingly traverse the world with only minimal levels of support. “Low functioning”, conversely, is used to describe those with significant support needs who may also be non-communicative. Aside from the societal implications of labelling someone “low functioning” and the possible connotations stemming from such a label, such functioning categorisation do not seemingly offer as accurate a representation as many people might think. The high-functioning autistic child who for example, has been excluded from school on the basis of their behaviour, cannot be readily labelled “high-functioning” if the presentation of their autistic behaviours has led to such a serious outcome. This on the basis that part of the diagnostic decision to diagnose autism is taken by appreciation of whether or not presented behaviours significantly interfere with day-to-day living ( 3 ). What might replace functioning labels is still a matter for debate. The use of “levels of support requirement” utilised in current diagnostic criteria offer a template for further discussions. Such discussions may also need to recognise that the traits of autism are not static over a lifetime ( 51 ) and support levels may vary as a result.

Whatever terminology is put forward to replace functioning labels, there is a need to address some very apparent differences in the way that parts of the autism spectrum are viewed, represented and included in research. Described as the “understudied populations” by some authors ( 66 ) those with limited verbal communicative language and learning disability have long been disadvantaged in research terms and also in more general depictions of autism. In more recent times, there has been a subtle shift to acknowledge the bias that exists against those with a more profound presentation of autism ( 67 ). Further developments are however required to ensure that such groups are not excluded; not least also to guarantee the generalisability of autism research to the entire spectrum and not just one portion of it.

On the topic of generalisability to the entire autism spectrum, the moves to further involve those diagnosed with autism in research, clinical and sociological discussions presents opportunities and obstacles in equal measure. The application of the International Classification of Functioning, Disability and Health (ICF) to autism ( 68 ) to measure “health-related functioning” represented a key moment in autism participatory research. Taking on board various views and opinions about autism, the development of the ICF core autism sets has allowed those with autism and their significant others to voice their opinions about autism ( 69 ).

Such joint initiatives are to be welcomed on the basis of the multiple perspectives they offer including lived experience of autism. But with such participation, so questions are also raised about how representative such opinions are to the entire autism spectrum ( 70 ). Questions on whether those who are able to participate in such initiatives “can ever truly speak for the entire autism spectrum?” are bound to follow. Questions also about whether such first-hand reports are more important than parental or caregiver input when it comes to individuals on the autism spectrum are likewise important to ask. This bearing in mind that those with autism participating in such initiatives bring with them the same potential biases as researchers and clinicians carry with them about the nature of autism, albeit not necessarily in total agreement.

The translation of research findings into clinical practice represents another important issue that has yet to be suitably addressed. Although covering a sizeable area, several important stumbling blocks have prohibited the move from “bench to bedside” when it comes to autism research. The focus for example, on the overt behavioural presentation of autism, has in some senses continued to hinder the translational progress of more biological-based findings into autism practice. Nowhere is this seemingly more evident than when it comes to the over-representation of gastrointestinal (GI) issues in relation to autism and their management or treatment. Despite multiple findings of such issues being present ( 16 ), very little is seemingly offered despite autism-specific screening and management guidance being in place for nearly a decade at the time of writing ( 71 ). Other quite consistently reported research findings in relation to low functional levels of vitamin D ( 72 ) for example, have similarly not sparked massive shifts in clinical practices. Ignoring such potentially important clinical features contributes to a state of relative health inequality that is experienced by many on the autism spectrum.

Without trying to prioritise some areas over others, there are some important topics in relation to autism that are becoming important to autism research and clinical practice. Many of these topics are more “real life” focused; taking into account the impact of autism or autistic traits on daily living skills and functioning. These include issues such as the truly shocking early mortality statistics around autism ( 73 ) and the need for more detailed inquiry into the factors around such risks such as suicide ( 74 ) and self-injury ( 75 ) and wandering/elopement ( 76 ) alongside the considerable influence of conditions such as epilepsy.

Although already previously hinted at in this paper, the nature of the relationship between autism and various “comorbid” conditions observed to be over-represented alongside is starting to become more widely discussed in scientific circles. Whether for example, moves to intervene to mitigate issues such as depression in relation to autism might also have knock-on effects on the presentation of core autistic features is something being considered. Interest in other topics such as employment, ageing, parenting and the worrying issue of contact with law enforcement or criminal justice systems ( 77 ) are also in the ascendancy.

Conclusions

Autism as a diagnostic label continues to evolve in research, clinical practice and sociological terms. Although the core features described by Kanner and others have weathered such evolution, important shifts in knowledge, views and opinions have influenced many important issues around those core behaviours. As well as increasing understanding of autism, many of the changes, past and present, have brought about challenges too.

Author Contributions

All authors contributed equally to the writing and review of this manuscript.

This paper was fully funded by ESPA Research using part of a donation from the Robert Luff Foundation (charity number: 273810). The Foundation played no role in the content, formulation or conclusions reached in this manuscript.

Conflict of Interest

The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.

1. Evans B. How autism became autism: the radical transformation of a central concept of child development in Britain. Hist Human Sci. (2013) 26:3–31. doi: 10.1177/0952695113484320

PubMed Abstract | CrossRef Full Text | Google Scholar

2. Kanner L. Autistic disturbances of affective contact. Nervous Child. (1943) 2:217–50.

Google Scholar

3. Diagnostic and Statistical Manual (DSM) version 5 . Washington, DC: American Psychiatric Association (2013).

4. Happé F, Cook JL, Bird G. The structure of social cognition: In(ter)dependence of sociocognitive processes. Ann Rev Psychol. (2017) 68:243–67. doi: 10.1146/annurev-psych-010416-044046

5. Lotter V. Epidemiology of autistic conditions in young children. Soc Psychiatry. (1966) 1:124–3. doi: 10.1007/BF00584048

CrossRef Full Text | Google Scholar

6. Baio J, Wiggins L, Christensen DL, Maenner MJ, Daniels J, Warren Z, et al. Prevalence of autism spectrum disorder among children aged 8 years - autism and developmental disabilities monitoring network, 11 sites, United States, 2014. MMWR Surveill Summ. (2018) 67:1–23. doi: 10.15585/mmwr.ss6706a1

7. Border R, Johnson EC, Evans LM, Smolen A, Berley N, Sullivan PF, et al. No support for historical candidate gene or candidate gene-by-interaction hypotheses for major depression across multiple large samples. Am J Psychiatry. (2019) 176:376–87. doi: 10.1176/appi.ajp.2018.18070881

8. Salazar F, Baird G, Chandler S, Tseng E, O'Sullivan T, Howlin P, et al. Co-occurring psychiatric disorders in preschool and elementary school-aged children with autism spectrum disorder. J Autism Dev Disord. (2015) 45:2283–94. doi: 10.1007/s10803-015-2361-5

9. Gillberg C, Fernell E. Autism plus versus autism pure. J Autism Dev Disord. (2014) 44:3274–6. doi: 10.1007/s10803-014-2163-1

10. Gillberg C. The ESSENCE in child psychiatry: early symptomatic syndromes eliciting neurodevelopmental clinical examinations. Res Dev Disabil. (2010) 31:1543–51. doi: 10.1016/j.ridd.2010.06.002

11. Cuthbert BN, Insel TR. Toward the future of psychiatric diagnosis: the seven pillars of RDoC. BMC Med. (2013) 11:126. doi: 10.1186/1741-7015-11-126

12. Rubenstein E, Bishop-Fitzpatrick L. A matter of time: the necessity of temporal language in research on health conditions that present with autism spectrum disorder. Autism Res. (2019) 12:20–5. doi: 10.1002/aur.2010

13. Underwood JFG, Kendall KM, Berrett J, Lewis C, Anney R, van den Bree MBM, et al. Autism spectrum disorder diagnosis in adults: phenotype and genotype findings from a clinically derived cohort. Br J Psychiatry. (2019) 26:1–7. doi: 10.1192/bjp.2019.30

14. Strasser L, Downes M, Kung J, Cross JH, De Haan M, et al. Prevalence and risk factors for autism spectrum disorder in epilepsy: a systematic review and meta-analysis. Dev Med Child Neurol. (2018) 60:19–29. doi: 10.1111/dmcn.13598

15. Souders MC, Zavodny S, Eriksen W, Sinko R, Connell J, Kerns C, et al. Sleep in children with autism spectrum disorder. Curr Psychiatry Rep. (2017) 19:34. doi: 10.1007/s11920-017-0782-x

16. Holingue C, Newill C, Lee LC, Pasricha PJ, Daniele Fallin M, et al. Gastrointestinal symptoms in autism spectrum disorder: a review of the literature on ascertainment and prevalence. Autism Res. (2018) 11:24–36. doi: 10.1002/aur.1854

17. Novarino G, El-Fishawy P, Kayserili H, Meguid NA, Scott EM, Schroth J, et al. Mutations in BCKD-kinase lead to a potentially treatable form of autism with epilepsy. Science. (2012) 338:394–7. doi: 10.1126/science.1224631

18. Sundelin HE, Larsson H, Lichtenstein P, Almqvist C, Hultman CM, Tomson T, et al. Autism and epilepsy: a population-based nationwide cohort study. Neurology. (2016) 87:192–7. doi: 10.1212/WNL.0000000000002836

19. Sjoberg EA. Logical fallacies in animal model research. Behav Brain Funct. (2017) 13:3. doi: 10.1186/s12993-017-0121-8

20. Wei SC, Yang-Yen HF, Tsao PN, Weng MT, Tung CC, Yu LCH, et al. SHANK3 regulates intestinal barrier function through modulating ZO-1 expression through the PKCε-dependent Pathway. Inflamm Bowel Dis. (2017) 23:1730–40. doi: 10.1097/MIB.0000000000001250

21. James DM, Kozol RA, Kajiwara Y, Wahl AL, Storrs EC, Buxbaum JD, et al. Intestinal dysmotility in a zebrafish (Danio rerio) shank3a;shank3b mutant model of autism. Mol Autism. (2019) 10:3. doi: 10.1186/s13229-018-0250-4

22. Ridha Z, Quinn R, Croaker GD. Predictors of slow colonic transit in children. Pediatr Surg Int. (2015) 31:137–42. doi: 10.1007/s00383-014-3651-2

23. Hollocks MJ, Lerh JW, Magiati I, Meiser-Stedman R, Brugha TS. Anxiety and depression in adults with autism spectrum disorder: a systematic review and meta-analysis. Psychol Med. (2019) 49:559–72. doi: 10.1017/S0033291718002283

24. Vannucchi G, Masi G, Toni C, Dell'Osso L, Erfurth A, Perugi G. Bipolar disorder in adults with Asperger?s syndrome: a systematic review. J Affect Disord. (2014) 168:151–60. doi: 10.1016/j.jad.2014.06.042

25. Andersen PN, Skogli EW, Hovik KT, Egeland J, Øie M. Associations among symptoms of autism, symptoms of depression and executive functions in children with high-functioning autism: a 2 year follow-up study. J Autism Dev Disord. (2015) 45:2497–507. doi: 10.1007/s10803-015-2415-8

26. van Steensel FJ, Bögels SM, Wood JJ. Autism spectrum traits in children with anxiety disorders. J Autism Dev Disord. (2013) 43:361–70. doi: 10.1007/s10803-012-1575-z

27. Vasa RA, Kreiser NL, Keefer A, Singh V, Mostofsky SH. Relationships between autism spectrum disorder and intolerance of uncertainty. Autism Res. (2018) 11:636–44. doi: 10.1002/aur.1916

28. Barahona-Corrêa JB, Filipe CN. A concise history of asperger syndrome: the short reign of a troublesome diagnosis. Front Psychol. (2016) 6: 2024. doi: 10.3389/fpsyg.2015.02024

29. Frances A. Will DSM5 contain or worsen the “epidemic” of autism? Psychol Today . (2010). Available online at: https://www.psychologytoday.com/us/blog/dsm5-in-distress/201003/will-dsm5-contain-or-worsen-the-epidemic-autism (accessed June 11, 2019).

30. Gamlin C. When asperger's disorder came out. Psychiatr Danub . (2017) 29(Suppl 3):214–8. Available online at: http://www.psychiatria-danubina.com/UserDocsImages/pdf/dnb_vol29_noSuppl%203/dnb_vol29_noSuppl%203_214.pdf

PubMed Abstract | Google Scholar

31. Macintosh KE, Dissanayake C. Annotation: the similarities and differences between autistic disorder and Asperger's disorder: a review of the empirical evidence. J Child Psychol Psychiatry. (2004) 45:421–34. doi: 10.1111/j.1469-7610.2004.00234.x

32. Czech H. Hans Asperger, National Socialism, and “race hygiene” in Nazi-era Vienna. Mol Autism. (2018) 9:29. doi: 10.1186/s13229-018-0208-6

33. Peters WJ, Matson JL. Comparing rates of diagnosis using DSM-IV-TR versus DSM-5 criteria for autism spectrum disorder. J Autism Dev Disord. (2019) 50:1898–906. doi: 10.1007/s10803-019-03941-1

34. De Crescenzo F, Postorino V, Siracusano M, Riccioni A, Armando M, Curatolo P, et al. Autistic symptoms in schizophrenia spectrum disorders: a systematic review and meta-analysis. Front Psychiatry. (2019) 10:78. doi: 10.3389/fpsyt.2019.00078

35. Dell'Osso L, Cremone IM, Carpita B, Fagiolini A, Massimetti G, Bossini L, et al. Correlates of autistic traits among patients with borderline personality disorder. Compr Psychiatry. (2018) 83:7–11. doi: 10.1016/j.comppsych.2018.01.002

36. Baron-Cohen S, Jaffa T, Davies S, Auyeung B, Allison C, Wheelwright S. Do girls with anorexia nervosa have elevated autistic traits?. Mol Autism. (2013) 4:24. 36. doi: 10.1186/2040-2392-4-24

37. Newson E, Le Maréchal K, David C. Pathological demand avoidance syndrome: a necessary distinction within the pervasive developmental disorders. Arch Dis Child. (2003) 88:595–600. doi: 10.1136/adc.88.7.595

38. Green J, Absoud M, Grahame V, Malik O, Simonoff E, Le Couteur A, et al. Pathological demand avoidance: symptoms but not a syndrome. Lancet Child Adolesc Health. (2018) 2:455–64. doi: 10.1016/S2352-4642(18)30044-0

39. Palmer N, Beam A, Agniel D, Eran A, Manrai A, Spettell C, et al. Association of sex with recurrence of autism spectrum disorder among siblings. JAMA Pediatr. (2017) 171:1107–12. doi: 10.1001/jamapediatrics.2017.2832

40. Deconinck N, Soncarrieu M, Dan B. Toward better recognition of early predictors for autism spectrum disorders. Pediatr Neurol. (2013) 49:225–31. doi: 10.1016/j.pediatrneurol.2013.05.012

41. Barbaro J, Dissanayake C. Early markers of autism spectrum disorders in infants and toddlers prospectively identified in the Social Attention and Communication Study. Autism. (2013) 17:64–86. doi: 10.1177/1362361312442597

42. Ozonoff S, Heung K, Byrd R, Hansen R, Hertz-Picciotto I. The onset of autism: patterns of symptom emergence in the first years of life. Autism Res. (2008) 1:320–8. doi: 10.1002/aur.53

43. Reichow B, Hume K, Barton EE, Boyd BA. Early intensive behavioral intervention (EIBI) for young children with autism spectrum disorders (ASD). Cochrane Database Syst Rev. (2018) 5:CD009260. doi: 10.1002/14651858.CD009260.pub3

44. Ozonoff S, Young GS, Brian J, Charman T, Shephard E, Solish A, et al. Diagnosis of autism spectrum disorder after age 5 in children evaluated longitudinally since infancy. J Am Acad Child Adolesc Psychiatry. (2018) 57:849–57.e2. doi: 10.1016/j.jaac.2018.06.022

45. Whiteley P, Carr K, Shattock P. Is autism inborn and lifelong for everyone? Neuropsychiatr Dis Treat. (2019) 15:2885–91. doi: 10.2147/NDT.S221901

46. Frazier TW, Georgiades S, Bishop SL, Hardan AY. Behavioral and cognitive characteristics of females and males with autism in the Simons Simplex Collection. J Am Acad Child Adolesc Psychiatry. (2014) 53:329–40.e1–3. doi: 10.1016/j.jaac.2013.12.004

47. Mandy W, Chilvers R, Chowdhury U, Salter G, Seigal A, Skuse D. Sex differences in autism spectrum disorder: evidence from a large sample of children and adolescents. J Autism Dev Disord. (2012) 42:1304–13. doi: 10.1007/s10803-011-1356-0

48. Rynkiewicz A, Schuller B, Marchi E, Piana S, Camurri A, Lassalle A, et al. An investigation of the 'female camouflage effect' in autism using a computerized ADOS-2 and a test of sex/gender differences. Mol Autism. (2016) 7:10. doi: 10.1186/s13229-016-0073-0

49. Happé FG, Mansour H, Barrett P, Brown T, Abbott P, Charlton RA. Demographic and cognitive profile of individuals seeking a diagnosis of autism spectrum disorder in adulthood. J Autism Dev Disord. (2016) 46:3469–80. doi: 10.1007/s10803-016-2886-2

50. Lord C, Elsabbagh M, Baird G, Veenstra-Vanderweele J. Autism spectrum disorder. Lancet. (2018) 392:508–20. doi: 10.1016/S0140-6736(18)31129-2

51. Roestorf A, Bowler DM, Deserno MK, Howlin P, Klinger L, McConachie H, et al. “Older adults with asd: the consequences of aging.” Insights from a series of special interest group meetings held at the International Society for Autism Research 2016–2017. Res Autism Spectr Disord. (2019) 63: 3–12. doi: 10.1016/j.rasd.2018.08.007

52. Fletcher-Watson S, Bird G. Autism and empathy: what are the real links? Autism. (2019) 24:3–6. doi: 10.1177/1362361319883506

53. Milton D. On the ontological status of autism: the “double empathy problem.” Disabil Soc . (2012) 27:883–7. doi: 10.1080/09687599.2012.710008

54. Gillespie-Lynch K, Kapp SK, Brooks PJ, Pickens J, Schwartzman B. Whose expertise is it? Evidence for autistic adults as critical autism experts. Front Psychol. (2017) 8:438. doi: 10.3389/fpsyg.2017.00438

55. Elder Robison J. What is Neurodiversity? Psychology Today . (2013). Available online at: https://www.psychologytoday.com/gb/blog/my-life-aspergers/201310/what-is-neurodiversity (accessed on June 12, 2019).

56. den Houting J. Neurodiversity: an insider's perspective. Autism. (2019) 23:271–3. doi: 10.1177/1362361318820762

57. Clements T. The Problem with the Neurodiversity Movement. Quilette . (2017). Available online at: https://quillette.com/2017/10/15/problem-neurodiversity-movement/ (accessed June 12, 2019).

58. Baron-Cohen S. Editorial perspective: neurodiversity—a revolutionary concept for autism and psychiatry. J Child Psychol Psychiatry. (2017) 58:744–7. doi: 10.1111/jcpp.12703

59. Lewis LF. Exploring the experience of self-diagnosis of autism spectrum disorder in adults. Arch Psychiatr Nurs. (2016) 30:575–80. doi: 10.1016/j.apnu.2016.03.009

60. Whiteley P. Nutritional management of (some) autism: a case for gluten- and casein-free diets? Proc Nutr Soc. (2015) 74:202–7. doi: 10.1017/S0029665114001475

61. Kim H, Keifer C, Rodriguez-Seijas C, Eaton N, Lerner M, Gadow K. Quantifying the optimal structure of the autism phenotype: a comprehensive comparison of dimensional, categorical, and hybrid models. J Am Acad Child Adolesc Psychiatry. (2018) 58:876–86.e2. doi: 10.1016/j.jaac.2018.09.431

62. Landa RJ, Holman KC, Garrett-Mayer E. Social and communication development in toddlers with early and later diagnosis of autism spectrum disorders. Arch Gen Psychiatry. (2007) 64:853–64. doi: 10.1001/archpsyc.64.7.853

63. Baghdadli A, Michelon C, Pernon E, Picot MC, Miot S, Sonié S, et al. Adaptive trajectories and early risk factors in the autism spectrum: a 15-year prospective study. Autism Res. (2018) 11:1455–67. doi: 10.1002/aur.2022

64. Fein D, Barton M, Eigsti IM, Kelley E, Naigles L, Schultz RT, et al. Optimal outcome in individuals with a history of autism. J Child Psychol Psychiatry. (2013) 54:195–205. doi: 10.1111/jcpp.12037

65. Alvares GA, Bebbington K, Cleary D, Evans K, Glasson EJ, Maybery MT, et al. The misnomer of 'high functioning autism': intelligence is an imprecise predictor of functional abilities at diagnosis. Autism. (2019) 24:221–32. doi: 10.1177/1362361319852831

66. Chakrabarti B. Commentary: critical considerations for studying low-functioning autism. J Child Psychol Psychiatry. (2017) 58:436–8. doi: 10.1111/jcpp.12720

67. Russell G, Mandy W, Elliott D, White R, Pittwood T, Ford T. Selection bias on intellectual ability in autism research: a cross-sectional review and meta-analysis. Mol Autism. (2019) 10:9 doi: 10.1186/s13229-019-0260-x

68. Bölte S, de Schipper E, Robison JE, Wong VC, Selb M, Singhal N, et al. Classification of functioning and impairment: the development of ICF core sets for autism spectrum disorder. Autism Res. (2014) 7:167–72. doi: 10.1002/aur.1335

69. Mahdi S, Viljoen M, Yee T, Selb M, Singhal N, Almodayfer O, et al. An international qualitative study of functioning in autism spectrum disorder using the World Health Organization international classification of functioning, disability and health framework. Autism Res. (2018) 11:463–75. doi: 10.1002/aur.1905

70. Hollin G, Pearce W. Autism scientists' reflections on the opportunities and challenges of public engagement: a qualitative analysis. J Autism Dev Disord. (2019) 49:809–18. doi: 10.1007/s10803-018-3783-7

71. Buie T, Campbell DB, Fuchs GJ 3rd, Furuta GT, Levy J, Vandewater J, et al. Evaluation, diagnosis, and treatment of gastrointestinal disorders in individuals with ASDs: a consensus report. Pediatrics. (2010) (125 Suppl 1):S1–18. doi: 10.1542/peds.2009-1878C

72. Bener A, Khattab AO, Al-Dabbagh MM. Is high prevalence of Vitamin D deficiency evidence for autism disorder? In a highly endogamous population. J Pediatr Neurosci. (2014) 9:227–33. doi: 10.4103/1817-1745.147574

73. Hwang YIJ, Srasuebkul P, Foley KR, Arnold S, Trollor JN. Mortality and cause of death of Australians on the autism spectrum. Autism Res. (2019) 12:806–15. doi: 10.1002/aur.2086

74. Chen MH, Pan TL, Lan WH, Hsu JW, Huang KL, Su TP, et al. Risk of suicide attempts among adolescents and young adults with autism spectrum disorder: a nationwide longitudinal follow-up study. J Clin Psychiatry. (2017) 78:e1174–9. doi: 10.4088/JCP.16m11100

75. Moseley RL, Gregory NJ, Smith P, Allison C, Baron-Cohen S. A 'choice', an 'addiction', a way 'out of the lost': exploring self-injury in autistic people without intellectual disability. Mol Autism. (2019) 10:18. doi: 10.1186/s13229-019-0267-3

76. Rice CE, Zablotsky B, Avila RM, Colpe LJ, Schieve LA, Pringle B, et al. Reported wandering behavior among children with autism spectrum disorder and/or intellectual disability. J Pediatr. (2016) 174:232–9.e2. doi: 10.1016/j.jpeds.2016.03.047

77. Cheely CA, Carpenter LA, Letourneau EJ, Nicholas JS, Charles J, King LB. The prevalence of youth with autism spectrum disorders in the criminal justice system. J Autism Dev Disord. (2012) 42:1856–62. doi: 10.1007/s10803-011-1427-2

Keywords: autism, research, clinical, sociological, knowledge, future

Citation: Whiteley P, Carr K and Shattock P (2021) Research, Clinical, and Sociological Aspects of Autism. Front. Psychiatry 12:481546. doi: 10.3389/fpsyt.2021.481546

Received: 28 June 2019; Accepted: 30 March 2021; Published: 29 April 2021.

Reviewed by:

Copyright © 2021 Whiteley, Carr and Shattock. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY) . The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

*Correspondence: Paul Whiteley, paul.whiteley@espa-research.org.uk

Disclaimer: All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers. Any product that may be evaluated in this article or claim that may be made by its manufacturer is not guaranteed or endorsed by the publisher.

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v.25(1); 2016 Feb

A Short Review on the Current Understanding of Autism Spectrum Disorders

Hye ran park.

1 Department of Neurosurgery, Seoul National University Hospital, Seoul 03080, Korea.

Jae Meen Lee

Hyo eun moon, dong soo lee.

2 Department of Nuclear Medicine, Seoul National University College of Medicine, Seoul 03080, Korea.

Bung-Nyun Kim

3 Division of Child and Adolescent Psychiatry, Department of Psychiatry, Seoul National University College of Medicine, Seoul 03080, Korea.

Jinhyun Kim

4 Center for Functional Connectomics, Korea Institute of Science and Technology (KIST), Seoul 02792, Korea.

Dong Gyu Kim

Sun ha paek.

Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterized by a deficit in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures in the first 3 years of life. It is not a single disorder, and it is broadly considered to be a multi-factorial disorder resulting from genetic and non-genetic risk factors and their interaction. Genetic studies of ASD have identified mutations that interfere with typical neurodevelopment in utero through childhood. These complexes of genes have been involved in synaptogenesis and axon motility. Recent developments in neuroimaging studies have provided many important insights into the pathological changes that occur in the brain of patients with ASD in vivo. Especially, the role of amygdala, a major component of the limbic system and the affective loop of the cortico-striatothalamo-cortical circuit, in cognition and ASD has been proved in numerous neuropathological and neuroimaging studies. Besides the amygdala, the nucleus accumbens is also considered as the key structure which is related with the social reward response in ASD. Although educational and behavioral treatments have been the mainstay of the management of ASD, pharmacological and interventional treatments have also shown some benefit in subjects with ASD. Also, there have been reports about few patients who experienced improvement after deep brain stimulation, one of the interventional treatments. The key architecture of ASD development which could be a target for treatment is still an uncharted territory. Further work is needed to broaden the horizons on the understanding of ASD.

INTRODUCTION

Autism spectrum disorder (ASD) is a set of neurodevelopmental disorders characterized by a lack of social interaction, verbal and nonverbal communication in the first 3 years of life. The distinctive social behaviors include an avoidance of eye contact, problems with emotional control or understanding the emotions of others, and a markedly restricted range of activities and interests [ 1 ]. The current prevalence of ASD in the latest large-scale surveys is about 1%~2% [ 2 , 3 ]. The prevalence of ASD has increased in the past two decades [ 4 ]. Although the increase in prevalence is partially the result of changes in DSM diagnostic criteria and younger age of diagnosis, an increase in risk factors cannot be ruled out [ 5 , 6 ]. Studies have shown a male predominance; ASD affects 2~3 times more males than females [ 2 , 3 , 7 ]. This diagnostic bias towards males might result from under-recognition of females with ASD [ 8 ]. Also, some researchers have suggested the possibility that the female-specific protective effects against ASD might exist [ 9 ].

A Swiss psychiatrist, Paul Eugen Bleuler used the term "autism" to define the symptoms of schizophrenia for the first time in 1912 [ 10 ]. He derived it from the Greek word αὐτὀς (autos), which means self. Hans Asperger adopted Bleuler's terminology "autistic" in its modern sense to describe child psychology in 1938. Afterwards, he reported about four boys who did not mix with their peer group and did not understand the meaning of the terms 'respect' and 'polite', and regard for the authority of an adult. The boys also showed specific unnatural stereotypic movement and habits. Asperger describe this pattern of behaviors as "autistic psychopathy", which is now called as Asperger's Syndrome [ 11 ]. The person who first used autism in its modern sense is Leo Kanner. In 1943, he reported about 8 boys and 3 girls who had "an innate inability to form the usual, biologically provided affective contact with people", and introduced the label early infantile autism [ 12 ]. Hans Asperger and Leo Kanner have been considered as those who designed the basis of the modern study of autism.

Most recently, the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5) adopted the term ASD with a dyadic definition of core symptoms: early-onset of difficulties in social interaction and communication, and repetitive, restricted behaviors, interests, or activities [ 13 ]. Atypical language development, which had been included into the triad of ASD, is now regarded as a co-occurring condition.

As stated earlier, the development of the brain in individuals with ASD is complex and is mediated by many genetic and environmental factors, and their interactions. Genetic studies of ASD have identified mutations that interfere with typical neurodevelopment in utero through childhood. These complexes of genes have been involved in synaptogenesis and axon motility. Also, the resultant microstructural, macrostructural, and functional abnormalities that emerge during brain development create a pattern of dysfunctional neural networks involved in socioemotional processing. Microstructurally, an altered ratio of short- to long-diameter axons and disorganization of cortical layers are observed. Macrostructurally, MRI studies assessing brain volume in individuals with ASD have consistently shown cortical and subcortical gray matter overgrowth in early brain development. Functionally, resting-state fMRI studies show a narrative of widespread global underconnectivity in socioemotional networks, and task-based fMRI studies show decreased activation of networks involved in socioemotional processing. Moreover, electrophysiological studies demonstrate alterations in both resting-state and stimulus-induced oscillatory activities in patients with ASD [ 14 ].

The well-conserved sets of genes and genetic pathways were implicated in ASD, many of which contribute toward the formation, stabilization, and maintenance of functional synapses. Therefore, these genetic aspects coupled with an in-depth phenotypic analysis of the cellular and behavioral characteristics are essential to unraveling the pathogenesis of ASD. The number of genes already discovered in ASD holds the promise to translate the knowledge into designing new therapeutic interventions. Also, the fundamental research using animal models is providing key insights into the various facets of human ASD. However, a better understanding of the genetic, molecular, and circuit level aberrations in ASD is still needed [ 15 ].

Neuroimaging studies have provided many important insights into the pathological changes that occur in the brain of patients with ASD in vivo. Importantly, ASD is accompanied by an atypical path of brain maturation, which gives rise to differences in neuroanatomy, functioning, and connectivity. Although considerable progress has been made in the development of animal models and cellular assays, neuroimaging approaches allow us to directly examine the brain in vivo, and to probably facilitate the development of a more personalized approach to the treatment of ASD [ 16 ].

ASD is not a single disorder. It is now broadly considered to be a multi-factorial disorder resulting from genetic and non-genetic risk factors and their interaction.

Genetic causes including gene defects and chromosomal anomalies have been found in 10%~20% of individuals with ASD [ 17 , 18 ]. Siblings born in families with an ASD subject have a 50 times greater risk of ASD, with a recurrence rate of 5%~8% [ 19 ]. The concordance rate reaches up to 82%~92% in monozygotic twins, compared with 1%~10% in dizygotic twins. Genetic studies suggested that single gene mutations alter developmental pathways of neuronal and axonal structures involved in synaptogenesis [ 20 , 21 , 22 ]. In the cases of related with fragile X syndrome and tuberous sclerosis, hyperexcitability of neocortical circuits caused by alterations in the neocortical excitatory/inhibitory balance and abnormal neural synchronization is thought to be the most probable mechanisms [ 23 , 24 ]. Genome-wide linkage studies suggested linkages on chromosomes 2q, 7q, 15q, and 16p as the location of susceptibility genes, although it has not been fully elucidated [ 25 , 26 ]. These chromosomal abnormalities have been implicated in the disruption of neural connections, brain growth, and synaptic/dendritic morphology [ 27 , 28 , 29 ]. Metabolic errors including phenylketonuria, creatine deficiency syndromes, adenylosuccinate lyase deficiency, and metabolic purine disorders are also account for less than 5% of individuals with ASD [ 30 ]. Recently, the correlation between cerebellar developmental patterning gene ENGRAILED 2 and autism was reported [ 31 ]. It is the first genetic allele that contributes to ASD susceptibility in as many as 40% of ASD cases. Other genes such as UBE3A locus, GABA system genes, and serotonin transporter genes have also been considered as the genetic factors for ASD [ 18 ].

Diverse environmental causative elements including pre-natal, peri-natal, and post-natal factors also contribute to ASD [ 32 ]. Prenatal factors related with ASD include exposure to teratogens such as thalidomide, certain viral infections (congenital rubella syndrome), and maternal anticonvulsants such as valproic acid [ 33 , 34 ]. Low birth weight, abnormally short gestation length, and birth asphyxia are the peri-natal factors [ 34 ]. Reported post-natal factors associated with ASD include autoimmune disease, viral infection, hypoxia, mercury toxicity, and others [ 33 , 35 , 36 ]. Table 1 summarizes the known and putative ASD-related genes and environmental factors contributing to the ASD.

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In recent years, some researchers suggest that ASD is the result of complex interactions between genetic and environmental risk factors [ 37 ]. Understanding the interaction between genetic and environmental factors in the pathogenesis of ASD will lead to optimal treatment strategy.

Clinical features and Diagnosis

ASD is typically noticed in the first 3 years of life, with deficits in social behaviors and nonverbal interactions such as reduced eye contact, facial expression, and body gestures [ 1 ]. Children also manifest with non-specific symptoms such as unusual sensory perception skills and experiences, motor clumsiness, and insomnia. Associated phenomena include mental retardation, emotional indifference, hyperactivity, aggression, self-injury, and repetitive behaviors such as body rocking or hand flapping. Repetitive, stereotyped behaviors are often accompanied by cognitive impairment, seizures or epilepsy, gastrointestinal complaints, disturbedd sleep, and other problems. Differential diagnosis includes childhood schizophrenia, learning disability, and deafness [ 38 , 39 ].

ASD is diagnosed clinically based on the presence of core symptoms. However, caution is required when diagnosing ASD because of non-specific manifestations in different age groups and individual abilities in intelligence and verbal domains. The earliest nonspecific signs recognized in infancy or toddlers include irritability, passivity, and difficulties with sleeping and eating, followed by delays in language and social engagement. In the first year of age, infants later diagnosed with ASD cannot be easily distinguished from control infants. However, some authors report that about 50% of infants show behavioral abnormalities including extremes of temperament, poor eye contact, and lack of response to parental voices or interaction. At 12 months of age, individuals with ASD show atypical behaviors, across the domains of visual attention, imitation, social responses, motor control, and reactivity [ 40 ]. There is also report about atypical language trajectories, with mild delays at 12 months progressing to more severe delays by 24 months [ 40 ]. By 3 years of age, the typical core symptoms such as lack of social communication and restricted/repetitive behaviors and interests are manifested. ASD can be easily differentiated from other psychosocial disorders in late preschool and early school years.

Amygdala and ASD

The frontal and temporal lobes are the markedly affected brain areas in the individuals with ASD. In particular, the role of amygdala in cognition and ASD has been proved in numerous neuropathological and neuroimaging studies. The amygdala located the medial temporal lobe anterior to the hippocampal formation has been thought to have a strong association with social and aggressive behaviors in patients with ASD [ 41 , 42 ]. The amygdala is a major component of the limbic system and affective loop of the cortico-striato-thalamo-cortical circuit [ 43 ].

The amygdala has 2 specific functions including eye gaze and face processing [ 44 ]. The lesion of the amygdala results in fear-processing, modulation of memory with emotional content, and eye gaze when looking at human face [ 45 , 46 , 47 ]. The findings in individuals with amygdala lesion are similar to the phenomena in ASD. The amygdala receives highly processed somatosensory, visual, auditory, and all types of visceral inputs. It sends efferents through two major pathways, the stria terminalis and the ventral amygdalofugal pathway.

The amygdala comprises a collection of 13 nuclei. Based on histochemical analyses, these 13 nuclei are divided into three primary subgroups: the basolateral (BL), centromedial (CM), and superficial groups [ 42 ]. The BL group attributes amygdala to have a role as a node connecting sensory stimuli to higher social cognition level. It links the CM and superficial groups, and it has reciprocal connection with the orbitofrontal cortex, anterior cingulate cortex (ACC), and the medial prefrontal cortex (mPFC) [ 48 ]. The BL group contains neurons responsive to faces and actions of others, which is not found in the other two groups of amygdala [ 49 , 50 ]. The CM group consists of the central, medial, cortical nuclei, and the periamygdaloid complex. It innervates many of the visceral and autonomic effector regions of the brain stem, and provides a major output to the hypothalamus, thalamus, ventral tegmental area, and reticular formation [ 51 ]. The superficial group includes the nucleus of the lateral olfactory tract [ 42 ].

Neurochemistrial studies revealed high density of benzodiazepine/GABAa receptors and a substantial set of opiate receptors in the amygdala. It also includes serotonergic, dopaminergic, cholinergic, and noradrenergic cell bodies and pathways [ 52 ]. Since some patients with temporal epilepsy and aggressive behavior experienced improvement in aggressiveness after bilateral stereotactic ablation of basal and corticomedial amygdaloid nuclei, the role of amygdala in emotional processing, especially rage processing has been investigated [ 53 , 54 , 55 , 56 ]. Some evidences for the amygdala deficit in patients with ASD have been suggested. Post-mortem studies found the pathology in the amygdala of individuals with ASD compared to age- and sex-matched controls [ 57 , 58 , 59 ]. Small neuronal size and increased cell density in the cortical, medial, and central nuclei of the amygdala were detected in ASD patients.

Several studies proposed the use of an animal model to confirm the evidence for the association between amygdala and ASD [ 60 , 61 ]. Despite the limitation which stems from the need to prove higher order cognitive disorder, the studies suggested that disease-associated alterations in the temporal lobes during experimental manipulations of the amygdala in animals have produced some symptoms of ASD [ 62 ]. Especially, the Kluver-Bucy syndrome, which is caused by bilateral damage to the anterior temporal lobes in monkeys, has characteristic manifestations similar to ASD [ 63 , 64 ]. Monkeys with the Kluver-Bucy syndrome shows absence of social chattering, lack of facial expression, absence of emotional reactions, repetitive abnormal movement patterns, and increased aggression. Sajdyk et al. performed experiments on rats and discovered that physiological activation of the BL nucleus of the amygdala by blocking tonic GABAergic inhibition or enhancing glutamate or the stress-associated peptide corticotropin-releasing factor (CRF)-mediated excitation caused reduction in social behaviors [ 65 ]. On the contrary, lesioning of the amygdala or blocking amygdala excitability with glutamate antagonist increased dyadic social interactions [ 60 ]. Besides animals, humans who underwent lesioning of the amygdala showed impairments in social judgment. This phenomenon is called acquired ASD [ 66 , 67 , 68 ]. The pattern of social deficits was similar in idiopathic and acquired ASD [ 69 ]. Felix-Ortiz and Tye sought to understand the role of projections from the BL amygdala to the ventral hippocampus in relation to behavior. Their study using mice showed that the BLS-ventral hippocampus pathway involved in anxiety plays a role in the mediation of social behavior as well [ 70 ].

The individuals with temporal lobe tumors involving the amygdala and hippocampus provide another evidence of the correlation between the amygdala and ASD. Some authors reported that patients experienced autistic symptoms after temporal lobe was damaged by a tumor [ 71 , 72 ]. Also, individuals with tuberous sclerosis experienced similar symptoms including facial expression due to a temporal lobe hamartoma [ 73 ].

Although other researchers failed to find structural abnormalities in the mesial temporal lobe of autistic subjects by performing magnetic resonance imaging (MRI) studies [ 74 , 75 , 76 ], recent development in neuroimaging has facilitated the investigation of amygdala pathology in ASD. Studies using structural MRI estimated volumes of the amygdala and related structures in individuals with ASD and age-, gender, and verbal IQ-matched healthy controls [ 77 ]. Increase in bilateral amygdala volume and reduction in hippocampal and parahippocampal gyrus volumes were noted in individuals with ASD. Also, the lateral ventricles and intracranial volumes were significantly increased in the autistic subjects; however, overall temporal lobe volumes were similar between the ASD and control groups.

There was a significant difference in the whole brain voxel-based scans of individuals with ASD and control groups [ 78 ]. Individuals with ASD showed decreased gray matter volume in the right paracingulate sulcus, the left occipito-temporal cortex, and the left inferior frontal sulcus. On the contrary, the gray matter volume in the bilateral cerebellum was increased. Otherwise, they showed increased volume in the left amygdala/periamygdaloid cortex, the right inferior temporal gyrus, and the middle temporal gyrus.

Recently, the development of functional neuroimaging also provided some evidence for the correlation between amygdala deficit and ASD. A study using Technetium-99m (Tc-99m) single-photon emission computed tomography (SPECT) found that regional cerebral blood flow (rCBF) was decreased in the bilateral insula, superior temporal gyri, and left prefrontal cortices in individuals with ASD compared to age- and gender-matched controls with mental retardation [ 79 ]. Also, the authors found that rCBF in both the right hippocampus and amygdala was correlated with a behavioral rating subscale.

On proton magnetic resonance spectroscopy (MRS) in the right hippocampal-amygdala region and the left cerebellar hemisphere, autistic subjects showed decreased level of N-acetyl aspartate (NAA) in both areas [ 80 ]. There was no difference in the level of the other metabolites, such as creatine and choline. This study implies that a decreased level of NAA might be associated with neuronal hypofunction or immature neurons.

These findings support the claim that amygdala might be a key structure in the development of ASD and a target for the management of the disease.

Prefrontal cortex and ASD

Frontal lobe has been considered as playing an important role in higher-level control and a key structure associated with autism. Individuals with frontal lobe deficit demonstrate higher-order cognitive, language, social, and emotion dysfunction, which is deficient in autism [ 81 ]. Recently, neuroimaging and neuropsychological studies have attempted to delineate distinct regions of prefrontal cortex supporting different aspects of executive function. Some authors have reported that the excessive rates of brain growth in infants with ASD, which is mainly contributed by the increase of frontal cortex volume [ 82 , 83 ]. Especially, the PFC including Brodmann areas 8, 9, 10, 11, 44, 45, 46, and 47 has been noted for the structure related with ASD [ 84 ]. The PFC is cytoarchitectonically defined as the presence of a cortical granular layer IV [ 85 ], and anatomically refers to the regions of the cerebral cortex that are anterior to premotor cortex and the supplementary motor area [ 86 ]. The PFC has extensive connections with other cortical, subcortical and brain stem sites [ 87 ]. It receives inputs from the brainstem arousal systems, and its function is particularly dependent on its neurochemical environment [ 88 ].

The PFC is broadly divided into the medial PFC (mPFC) and the lateral PFC (lPFC). The mPFC is further divided into four distinct regions: medial precentral cortex, anterior cingulate cortex, prelimbic and infralimbic prefrontal cortex [ 89 ]. While the lPFC is thought to support cognitive control process [ 90 ], the mPFC has reciprocal connections with brain regions involved in emotional processing (amygdala), memory (hippocampus) and higher-order sensory regions (within temporal cortex) [ 91 ]. This involvement of mPFC in social cognition and interaction implies that mPFC might be a key region in understanding self and others [ 92 ].

The mPFC involves in fear learning and extinction by reciprocal synaptic connections with the basolateral amygdala [ 93 , 94 ]. It is believed that the mPFC regulates and controls amygdala output and the accompanying behavioral phenomena [ 95 , 96 ]. Previous authors investigated how memory processing is regulated by interactions between BLA and mPFC by means of functional disconnection [ 97 , 98 ]. Disturbed communication within amygdala-mPFC circuitry caused deficits in memory processing. These informations provide support for a role of the mPFC in the development of ASD.

Nucleus Accumbens and ASD

Besides amygdala, nucleus accumbens (NAc) is also considered as the key structure which is related with the social reward response in ASD. NAc borders ventrally on the anterior limb of the internal capsule, and the lateral subventricular fundus of the NAc is permeated in rostral sections by internal capsule fiber bundles. The rationale for NAc to be considered as the potential target of DBS for ASD is its predominant role in modulating the processing of reward and pleasure [ 99 ]. Anticipation of rewarding stimuli recruits the NAc as well as other limbic structures, and the experience of pleasure activates the NAc as well as the caudate, putamen, amygdala, and VMPFC [ 100 , 101 , 102 ]. It is well known that dysfunction of NAc regarding rewarding stimuli in subjects with depression. Bewernick et al. demonstrated antidepressant effects of NAc-DBS in 5 of the 10 patients suffering from severe treatment-resistant depression [ 103 ].

Two groups reported about the neural basis of social reward processing in ASD. Schmitz et al. examined responses to a task that involved monetary reward. They investigated the neural substrates of reward feedback in the context of a sustained attention task, and found increased activation in the left anterior cingulate gyrus and left mid-frontal gyrus on rewarded trials in ASD [ 104 ]. Scott-Van Zeeland et al. investigated the neural correlates of rewarded implicit learning in children with ASD using both social and monetary rewards. They found diminished ventral striatal response during social, but not monetary, rewarded learning [ 105 ]. According to them, activity within the ventral striatum predicted social reciprocity within the control group, but not within the ASD group.

Anticipation of pleasurable stimuli recruits the NAc, whereas the experience of pleasure activates VMPFC [ 106 ]. NAc is activated by incentive motivation to reach salient goals [ 106 ]. Increased activation in the left anterior cingulate gyrus and left mid-frontal gyrus was noted during both the anticipatory and consummatory phase of the reward response [ 104 , 107 , 108 ]. However, the activity within the ventral striatum was decreased in autistic subjects, which caused impairment in social reciprocity [ 105 ].

These findings indicate that reward network function in ASD is contingent on both the temporal phase of the response and the type of reward processed, suggesting that it is critical to assess the temporal chronometry of responses in a study of reward processing in ASD. NAc might be one of the candidates as a target of DBS which is introduced as below.

Various educational and behavioral treatments have been the mainstay of the management of ASD. Most experts agree that the treatment for ASD should be individualized. Treatment of disabling symptoms such as aggression, agitation, hyperactivity, inattention, irritability, repetitive and self-injurious behavior may allow educational and behavioral interventions to proceed more effectively [ 109 ].

Increasing interest is being shown in the role of various pharmacological treatments. Medical management includes typical antipsychotics, atypical antipsychotics, antidepressants, selective serotonin reuptake inhibitors, α2-adrenergic agonists, β-adrenergic antagonist, mood stabilizers, and anticonvulsants [ 110 , 111 ]. So far, there has been no agent which has been proved effective in social communication [ 112 ]. A major factor in the choice of pharmacologic treatment is awareness of specific individual physical, behavioral or psychiatric conditions comorbid with ASD, such as obsessive-compulsive disorder, schizophrenia, mood disorder, and intellectual disability [ 113 ]. Antidepressants were the most commonly used agents followed by stimulants and antipsychotics. The high prevalence of comorbidities is reflected in the rates of psychotropic medication use in people with ASD. Antipsychotics were effective in treating the repetitive behaviors in children with ASD; however, there was not sufficient evidence on the efficacy and safety in adolescents and adults [ 114 ]. There are also alternative options including opiate antagonist, immunotherapy, hormonal agents, megavitamins and other dietary supplements [ 109 , 113 ].

However, the autistic symptoms remain refractory to medication therapy in some patients [ 115 ]. These individuals have severely progressed disease and multiple comorbidities causing decreased quality of life [ 44 , 110 ]. Interventional therapy such as deep brain stimulation (DBS) may be an alternative therapeutic option for these patients.

Two kinds of interventions have been used for treating ASD; focused intervention practices and comprehensive treatments [ 116 ]. The focused intervention practices include prompting, reinforcement, discrete trial teaching, social stories, or peer-mediated interventions. These are designed to produce specific behavioral or developmental outcomes for individual children with ASD, and used for a limited time period with the intent of demonstrating a change in the targeted behaviors. The comprehensive treatment models are a set of practices performed over an extended period of time and are intense in their application, and usually have multiple components [ 116 ].

Since it was approved by the FDA in 1997, DBS has been used to send electrical impulses to specific parts of the brain [ 117 , 118 ]. In recent years, the spectrum for which therapeutic benefit is provided by DBS has widely been expanded from movement disorders such as Parkinson's disease, essential tremor, and dystonia to psychiatric disorders. Some authors have demonstrated the efficacy of DBS for psychiatric disorders including refractory obsessive-compulsive disorder, depression, Tourette syndrome, and others for the past few years [ 119 , 120 , 121 ].

To the best of our knowledge, there have been 2 published articles of 3 patients who underwent DBS for ASD accompanied by life-threatening self-injurious behaviors not alleviated by antipsychotic medication [ 122 , 123 ]. The targets were anterior limb of the internal capsule and globus pallidus internus, only globus pallidus, and BL nucleus of the amygdala, respectively. All patients obtained some benefit from DBS. Although the first patient showed gradual re-deterioration after temporary improvement, the patient who underwent DBS of the BL nucleus experienced substantial improvement in self-injurious behavior and social communication. These experiences suggested the possibility of DBS for the treatment of ASD. For patients who did not obtain benefit from other treatments, DBS may be a viable therapeutic option. Understanding the structures which contribute to the occurrence of ASD might open a new horizon for management of ASD, particularly DBS. Accompanying development of neuroimaging technique enables more accurate targeting and heightens the efficacy of DBS. However, the optimal DBS target and stimulation parameters are still unknown, and prospective controlled trials of DBS for various possible targets are required to determine optimal target and stimulation parameters for the safety and efficacy of DBS.

ASD should be considered as a complex disorder. It has many etiologies involving genetic and environmental factors, and further evidence for the role of amygdala and NA in the pathophysiology of ASD has been obtained from numerous studies. However, the key architecture of ASD development which could be a target for treatment is still an uncharted territory. Further work is needed to broaden the horizons on the understanding of ASD.

Acknowledgements

This study was partly supported by the Korea Institute of Planning & Evaluation for Technology in Food, Agriculture, Forestry, and Fisheries, Republic of Korea (311011-05-3-SB020), by the Korea Healthcare Technology R&D Project (HI11C21100200) funded by Ministry of Health & Welfare, Republic of Korea, by the Technology Innovation Program (10050154, Business Model Development for Personalized Medicine Based on Integrated Genome and Clinical Information) funded by the Ministry of Trade, Industry & Energy (MI, Korea), and by the Bio & Medical Technology Development Program of the NRF funded by the Korean government, MSIP (2015M3C7A1028926).

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Jackie Schuld Art Therapy Blog

Feb 17, 2023

The Great List of Autistic Essays

I’m a late-identified autistic who loves writing about autism. How much do I love it? I’ve written over 150 essays on it in the past six months alone.

How do I think of so many autistic topics to write about? I’m an art therapist who specializes in late-identified autistic adults. That means I not only have my personal experience to draw from, but also the hundreds of hours spent listening to my clients.

I share most of my essays here on Medium, which means it has now become quite the library. In an effort to make my essays more accessible to those wanting clear, relatable information about late-identified autism in adults, I’ve sorted my essays into topics below. While I wish I could provide a link to each of them for you… I’ve got to prioritize my time and energy. So if a specific essay interests you, just pop it into the search and it’ll come up

Autism in a Neurotypical World

What Would a World Designed by Autistic People Be Like

The Harm in "They're a Little Autistic"

Autism Does Not Directly Cause Socializing Problems

Please Trust My Lived Autistic Experience

Can Someone Please Create a Neurodivergent Intentional Living Community

What if I Accept that Most Neurotypicals Won't Like Me

How Neuro-Bias Shows Up in Professional Testing

Your Autistic Experience Sounds Just LIke my Neurotypical One

Neurotypical Words that Don't Work for Autistics: Overachiever

But Neurotypicals Experience That, Too!

Neurotypical Norms That Don’t Work for Autistics: Hustle Goals

The Fear of Being a Hypocritical Autistic

Neurodiversity: Us vs Them?

How to Meet an Autistic Adult Exactly Where They're At

Autism Characteristics

The Autistic Mind Loves to Take Detours

4 Reasons Why Autism Symptoms Lists are Confusing

My Autistic Brain: Sunshine and Detours

The Joys of Being Autistic: Part 1

Stop Saying Autistic People Can't Empathize

Redefining Fun for Autistic Adults

9 Reasons Why Autism Looks So Similar to CPTSD

We Need More Depictions of the Interior Experience of Autism

Clarity is What my Autistic Mind Craves

How Trauma and Autism Can be a Confusing Mix to Decipher

Why am I like This? Understanding the Autistic Brain

My Autistic Mind Does What it Wants

The Dissociated Autistic Performance State

The Joys of Being Autistic: Increased Creativity and Innovation

My Autistic Memory Is Not the Same as Others

The Firehouse Dilemma: Autism and Infodumping

The Variability of the Autistic Sensory System

5 Reasons Autistics are Especially Hard on Themselves

The Shame That Often Accompanies Autism

Knowing You’re Different as an Autistic Adult

3 Reasons Autism is Worse After You Learn You're Autistic

Disability and Internalized Ableism

I Had to Dismantle My Fear of Autistic People

Is Autism a Disability?

I’m Ok With Saying I have a Disability, Right?

Dog Training

The Difficulties of Adjusting to a New Dog When You're Autistic

Tips for Adjusting to a New Dog When You're Autistic

5 Tips to Integrate a Dog into Your Autistic Life

Defining and Explaining Autism

What I Wish Others Knew About Autism

Let’s Drop the “Disorder” From Autism Spectrum Disorder

How Low and High Autism Labels are Misleading

We Need All the Autism Theories and Models

Autism Can Be a Murky Thing To Understand

How I Explain Autism to Someone Unfamiliar With It

What is Late Identified Autism

Autistic Statistics are Not Accurate for Late-Identified Autistics

I'm Here for the Autistic Awakening

How It Helps to Know You’re Autistic

Why It Matters to Know You're Neurodivergent

What is Neurodiversity and Why Does it Matter

How Neurodivergent Acceptance Can Improve Our Lived Experiences

How Unidentified Autistics are Taught to Socially Camouflage and Mask

Is There a World Where I can Be Unmasked?

The False Dichotomy of Masked and Unmasked Autism

6 Reasons Why UnMasking Is Harder Than it Sounds

What if You have to Mask Everywhere?

My Personal Experience as an Autistic

Hating Cooking as an Autistic Adult

I Make Giant Lists About Autism for Fun

The Challenges of Writing Publically About Autism

The Risk of Sharing my Autistic Passions with Others

I'm Reclaiming Weird for My Autistic Self

I Expand and Then I Contract

I Stopped Seeing Myself As Broken When I learned I was Autistic

Respecting my Limits as an Autistic Business Owner

I Need to Lessen the Pressure on my Autistic Self

My Autistic Brain Doesn’t Want to Watch TV Right Now

Embracing Who I am as an Autistic Adult

I Used to be a Very Judgemental When I Didn’t Know I was Autistic

A Letter from An Autistic Adult to Trust

Don’t Get So Upset: A Line that Doesn’t Work for This Autist

Why This Autistic Writer Didn't Respond to Your Comment

Relationships

Is Dating Worth it as an Autistic Adult?

Is it Possible to be Happily Partnered as an Autistic Adult?

Not Liking People as an Autistic Adult

Self-Identification

So You Think You Might Be Autistic

Dearly Newly Identified Autistic Person

Am I Actually Autistic?

Dearest Smart, Weird, and Caring Autistic

I Am Deeply Unsure About Autism

How to Self Identify Autism as an Adult

When the Past Makes Sense after a Late-Identification of Autism

Where to Start When You First Learn You’re Autistic

6 Strategies to Harness the Hyperfocus Power of an Autistic Mind

Leave the Gremlin In the Cave: Self-Isolation as a Necessary Autistic Tool

No Plans Days as an Autistic Tool

Making Accommodations for Myself as an Autistic Adult

How Many Accommodations Can We Ask for as Autistic Adults?

Using Art to Help Your Autistic Mind

Dissociation as an Autistic Tool

The Power of the Home Environment for Autistics

Is It Ok to Honor My Autistic Needs?

Recognizing When It's Not Time to Make Decisions as an Autistic

Therapy for Autistics

Dearest Autistic Client of Mine

8 Ways Therapy Can Help With Late Identified Autism

Gaslighting the Autistic Experience

Dearest Therapist Who Knows Barely Anything About Autism

I'm an Autistic Therapist: Sometimes It's Easier Than Everyday Life

Does Your Therapist Know Enough About Autism to Help You?

Questions to Ask a Potential Therapist When You're Autistic

How I Work with Newly Identified Autistic People

What to Ask When You're Seeking Therapy for Late-Identified Autism

12 Ways Therapy Can Enhance Life for Late Identified Autistic Adults

Therapy is Not for Fixing Autism

The Harm I Caused When I Didn't Know about Autism

A Newly Identified Autistic Therapist Working with Newly Identified Autistics

Common Therapy Advice That is Counterproductive for Autistics

A Therapist Told Me Treating Autism is Like Treating Depression

Who Can Diagnose Autism in Adults?

Autistic Adults Deserve Better from the Mental Health Field

Undiagnosed Autism

The Correlation Between Intelligence and Undiagnosed Autism

10 Consequences of a Life with Unidentified Autism

The Gap Between “Diagnosable Autism” and a Lifetime of Unidentified Autism

Autism Diagnosis Criteria are Limiting for Men Too

No Autistic Should Receive a Diagnosis Letter Like Mine

Identifying Autism in Undiagnosed Women Abstract

How I Identify Autism in Undiagnosed Women

Autistic Stereotypes Block People From Knowing They're Autistic

Thank you for reading. If you’d like to read more, sign up for my FUNletter . If you would like to explore your autistic identity with an autistic therapist, you can learn more about my therapy services here .

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Published: 28 May 2021

Advances in autism research, 2021: continuing to decipher the secrets of autism

Julio Licinio ORCID: orcid.org/0000-0001-6905-5884 1 &
Ma-Li Wong 1

Molecular Psychiatry volume 26 , pages 1426–1428 ( 2021 ) Cite this article

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Autism spectrum disorders
Neuroscience

We are proud to publish this Special Issue focused on autism, a topic that has been exceedingly important for Molecular Psychiatry since our inception. It is not too bold a statement to say that we were a fundamental contributor to bringing autism to the forefront of the national discourse. A Pubmed search reveals 403 articles published in Molecular Psychiatry since our founding in 1996. Our first autism article by Vincent et al., published in July 1996, examined the fragile X syndrome gene (FMR1) for mutations in autistic individuals, using single-stranded conformational polymorphism analysis; those authors identified three new FMR1 polymorphisms and identified specific and significant association findings with autism [ 1 ].

In late 2001–early 2002 we received four exciting papers with findings on the genetics of autism that were published together in our March 2002 issue, with an accompanying editorial [ 2 , 3 , 4 , 5 , 6 ]. We issued then a press release that was picked up by Time magazine and served as the basis for their unprecedented May 6, 2002 cover story on autism, featuring as that iconic magazine’s cover a young boy who was visibly autistic [ 7 ]. That was the first time that a person with autism was the cover of a national magazine. The magazine’s cover displayed in big yellow letters “Inside the world of autism” and it had a subtitle stating “More than one million Americans may have it, and the number of new cases is exploding. What scientists have discovered. What families should know.” The full story, by Nash [ 8 ], was entitled: “The Secrets of Autism,” with the following subtitle: “The number of children diagnosed with autism and Asperger’s in the U.S. is exploding. Why?” Time ’s cover article was so successful that their editors expanded that from a single issue into an entire series on autism over multiple issues. That Time series effectively made autism emerge as a mainstream topic of kitchen table conversations across America. As that effort was triggered by our press release and four articles on autism, it is reasonable to boast that Molecular Psychiatry launched the national conversation on autism.

The four papers highlighted in our March 2002 issue were within the first 20 articles that we published on this topic. Now, 383 papers later, we have a much more substantial body of work that further unravels the secrets of autism, the culmination of which is this autism Special Issue, with 26 truly superb papers on autism [ 9 , 10 , 11 , 12 , 13 , 14 , 15 , 16 , 17 , 18 , 19 , 20 , 21 , 22 , 23 , 24 , 25 , 26 , 27 , 28 , 29 , 30 , 31 , 32 , 33 , 34 ]. These extraordinary articles cover essentially all aspects of this disorder, from the training of specialists, to the interface with other disorders, such as polycystic ovarian syndrome and Alzheimer’s disease, and in-depth analyses of genetics, structural and functional imaging, as well as neuroscience, including postmortem brain studies, transcriptome of induced pluripotent stem cell models, assessments of the role of vitamin D, and studies highlighting the contributions of inflammatory mediators to autism.

We have had for over three decades a particular interest on the interface of immune mediators and psychiatric disorders [ 35 ]. It is very rewarding to see the interface of immune mediators and psychiatry evolve from a hypothesis, that we and others explored decades ago, into a broad and established area within psychiatric neuroscience. As we have developed a new model of analysis of the simultaneous contributions of multiple genes and environmental factors to a psychiatric phenotype [ 36 ], were also encouraged to see studies looking at the polygenic risk for autism in the context of childhood trauma, life-time self-harm, and suicidal behavior and ideation [ 30 ], as well in comparison to several other psychiatric disorders [ 32 ].

One paper in this issue, by Frye et al., is highly usual, and particularly intriguing: it investigates the role of the mitochondrion, in the influence of prenatal air pollution exposure on neurodevelopment and behavior in 96 children with autism spectrum disorder [ 22 ]. Second and third trimester average and maximal daily exposure to fine air particulate matter of diameter ≤2.5 µm (PM 2.5 ) was obtained from the Environmental Protection Agency’s Air Quality System. Mediation analysis found that mitochondrial respiration linked to energy production accounted for 25% and 10% of the effect of average prenatal PM 2.5 exposure on neurodevelopment and behavioral symptoms, respectively. Those results suggest that prenatal exposure to PM 2.5 disrupts neurodevelopment and behavior through complex mechanisms, including long-term changes in mitochondrial respiration and that patterns of early development need to be considered when studying the influence of environmental agents on neurodevelopmental outcomes.

We are honored to have initiated the national conversation on autism twenty years ago and we believe that the 403 autism papers published to date in Molecular Psychiatry , including, but not limited to those highlighted in this Special Issue, report major advances in a key area of molecular psychiatry. It is particularly rewarding to see that these articles cover the full spectrum of research translation [ 37 ], from molecules to society.

In future issues, Molecular Psychiatry will continue to publish outstanding advances in autism research.

Vincent JB, Konecki DS, Munstermann E, Bolton P, Poustka A, Poustka F, et al. Point mutation analysis of the FMR-1 gene in autism. Mol Psychiatry. 1996;1:227–31.

CAS PubMed Google Scholar

Licinio J, Alvarado II. Progress in the genetics of autism. Mol Psychiatry. 2002;7:229.

Article CAS Google Scholar

Jamain S, Betancur C, Quach H, Philippe A, Fellous M, Giros B, et al. Linkage and association of the glutamate receptor 6 gene with autism. Mol Psychiatry. 2002;7:302–10.

Kim SJ, Cox N, Courchesne R, Lord C, Corsello C, Akshoomoff N, et al. Transmission disequilibrium mapping at the serotonin transporter gene (SLC6A4) region in autistic disorder. Mol Psychiatry. 2002;7:278–88.

Bonora E, Bacchelli E, Levy ER, Blasi F, Marlow A, Monaco AP, et al. Mutation screening and imprinting analysis of four candidate genes for autism in the 7q32 region. Mol Psychiatry. 2002;7:289–301.

Buxbaum JD, Silverman JM, Smith CJ, Greenberg DA, Kilifarski M, Reichert J, et al. Association between a GABRB3 polymorphism and autism. Mol Psychiatry. 2002;7:311–6.

Time Magazine. Inside the world of autism. More than one million Americans may have it, and the number of new cases is exploding. What scientists have discovered. What families should know. Time. 2002. http://content.time.com/time/covers/0,16641,20020506,00.html .

Nash M. The Secrets of Autism: The number of children diagnosed with autism and Asperger’s in the U.S. is exploding. Why?” Time. 2002. http://content.time.com/time/subscriber/article/0,33009,1002364,00.html .

Pasca SP, Veenstra-VanderWeele J, McPartland JC. Research and training in autism spectrum disorder to catalyze the next genomic and neuroscience revolutions. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0830-5 . [Epub ahead of print].

Lombardo MV. Ribosomal protein genes in post-mortem cortical tissue and iPSC-derived neural progenitor cells are commonly upregulated in expression in autism. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0773-x . [Epub ahead of print].

Griesi-Oliveira K, Passos-Bueno MR. Reply to Lombardo, 2020: An additional route of investigation: what are the mechanisms controlling ribosomal protein genes dysregulation in autistic neuronal cells? Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0792-7 . [Epub ahead of print].

Menon V, Andrade C, Thennarasu K. Polycystic ovarian syndrome and autism spectrum disorder in the offspring: Should the primary outcome have been different? Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0571-5 . [Epub ahead of print].

Chapman R, Veit W. The essence of autism: fact or artefact? Mol Psychiatry 2020. https://doi.org/10.1038/s41380-020-00959-1 . [Epub ahead of print].

Niesler B, Rappold GA. Emerging evidence for gene mutations driving both brain and gut dysfunction in autism spectrum disorder. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0778-5 . [Epub ahead of print].

Antunes C, Da Silva JD, Guerra-Gomes S, Alves ND, Ferreira F, Loureiro-Campos E, et al. Tet3 ablation in adult brain neurons increases anxiety-like behavior and regulates cognitive function in mice. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0695-7 . [Epub ahead of print].

Xiong GJ, Cheng XT, Sun T, Xie Y, Huang N, Li S, et al. Defects in syntabulin-mediated synaptic cargo transport associate with autism-like synaptic dysfunction and social behavioral traits. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0713-9 .

Rapanelli M, Tan T, Wang W, Wang X, Wang ZJ, Zhong P, et al. Behavioral, circuitry, and molecular aberrations by region-specific deficiency of the high-risk autism gene Cul3. Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0498-x . [Epub ahead of print].

Guo D, Peng Y, Wang L, Sun X, Wang X, Liang C, et al. Autism-like social deficit generated by Dock4 deficiency is rescued by restoration of Rac1 activity and NMDA receptor function. Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0472-7 . [Epub ahead of print].

Gordon A, Forsingdal A, Klewe IV, Nielsen J, Didriksen M, Werge T, et al. Transcriptomic networks implicate neuronal energetic abnormalities in three mouse models harboring autism and schizophrenia-associated mutations. Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0576-0 . [Epub ahead of print].

Ben-Reuven L, Reiner O. Dynamics of cortical progenitors and production of subcerebral neurons are altered in embryos of a maternal inflammation model for autism. Mol Psychiatry. 2019 Nov 18. https://doi.org/10.1038/s41380-019-0594-y . [Epub ahead of print].

Ramirez-Celis A, Becker M, Nuno M, Schauer J, Aghaeepour N, Van de Water J. Risk assessment analysis for maternal autoantibody-related autism (MAR-ASD): a subtype of autism. Mol Psychiatry. 2021. https://doi.org/10.1038/s41380-020-00998-8 . [Epub ahead of print].

Frye RE, Cakir J, Rose S, Delhey L, Bennuri SC, Tippett M, et al. Prenatal air pollution influences neurodevelopment and behavior in autism spectrum disorder by modulating mitochondrial physiology. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-00885-2 . [Epub ahead of print].

Lee BK, Eyles DW, Magnusson C, Newschaffer CJ, McGrath JJ, Kvaskoff D, et al. Developmental vitamin D and autism spectrum disorders: findings from the Stockholm Youth Cohort. Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0578-y .

Griesi-Oliveira K, Fogo MS, Pinto BGG, Alves AY, Suzuki AM, Morales AG, et al. Transcriptome of iPSC-derived neuronal cells reveals a module of co-expressed genes consistently associated with autism spectrum disorder. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0669-9 . [Epub ahead of print].

Rontani P, Perche O, Greetham L, Jullien N, Gepner B, Feron F, et al. Impaired expression of the COSMOC/MOCOS gene unit in ASD patient stem cells. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0728-2 . [Epub ahead of print].

Ivashko-Pachima Y, Hadar A, Grigg I, Korenkova V, Kapitansky O, Karmon G, et al. Discovery of autism/intellectual disability somatic mutations in Alzheimer’s brains: mutated ADNP cytoskeletal impairments and repair as a case study. Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0563-5 . [Epub ahead of print].

Fung LK, Flores RE, Gu M, Sun KL, James D, Schuck RK, et al. Thalamic and prefrontal GABA concentrations but not GABAA receptor densities are altered in high-functioning adults with autism spectrum disorder. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0756-y .

Andersson M, Tangen A, Farde L, Bolte S, Halldin C, Borg J, et al. Serotonin transporter availability in adults with autism-a positron emission tomography study. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-00868-3 . [Epub ahead of print].

Zurcher NR, Loggia ML, Mullett JE, Tseng C, Bhanot A, Richey L, et al. [(11)C]PBR28 MR-PET imaging reveals lower regional brain expression of translocator protein (TSPO) in young adult males with autism spectrum disorder. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0682-z . [Epub ahead of print].

Warrier V, Baron-Cohen S. Childhood trauma, life-time self-harm, and suicidal behaviour and ideation are associated with polygenic scores for autism. Mol Psychiatry. 2019. https://doi.org/10.1038/s41380-019-0550-x . [Epub ahead of print].

Chiang AH, Chang J, Wang J, Vitkup D. Exons as units of phenotypic impact for truncating mutations in autism. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-00876-3 . [Epub ahead of print].

Ratanatharathorn A, Koenen KC, Chibnik LB, Weisskopf MG, Rich-Edwards JW, Roberts AL. Polygenic risk for autism, attention-deficit hyperactivity disorder, schizophrenia, major depressive disorder, and neuroticism is associated with the experience of childhood abuse. Mol Psychiatry. 2021. https://doi.org/10.1038/s41380-020-00996-w . [Epub ahead of print].

Brownstein CA, Smith RS, Rodan LH, Gorman MP, Hojlo MA, Garvey EA, et al. RCL1 copy number variants are associated with a range of neuropsychiatric phenotypes. Mol Psychiatry. 2021. https://doi.org/10.1038/s41380-021-01035-y . [Epub ahead of print].

Sarn N, Jaini R, Thacker S, Lee H, Dutta R, Eng C. Cytoplasmic-predominant Pten increases microglial activation and synaptic pruning in a murine model with autism-like phenotype. Mol Psychiatry. 2020. https://doi.org/10.1038/s41380-020-0681-0 . [Epub ahead of print].

Sternberg EM, Licinio J. Overview of neuroimmune stress interactions. Implications for susceptibility to inflammatory disease. Ann N. Y Acad Sci. 1995;771:364–71.

Wong ML, Dong C, Andreev V, Arcos-Burgos M, Licinio J. Prediction of susceptibility to major depression by a model of interactions of multiple functional genetic variants and environmental factors. Mol Psychiatry. 2012;17:624–33.

Bornstein SR, Licinio J. Improving the efficacy of translational medicine by optimally integrating health care, academia and industry. Nat Med. 2011;17:1567–9.

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Licinio, J., Wong, ML. Advances in autism research, 2021: continuing to decipher the secrets of autism. Mol Psychiatry 26 , 1426–1428 (2021). https://doi.org/10.1038/s41380-021-01168-0

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Mindblindness : An Essay on Autism and Theory of Mind

Simon Baron-Cohen, Professor in Developmental Psychopathology and Director of the Autism Research Centre at the University of Cambridge, is the author of Mindblindness (MIT Press, 1997) and The Essential Difference: The Truth about the Male and Female Mind .

In Mindblindness , Simon Baron-Cohen presents a model of the evolution and development of "mindreading." He argues that we mindread all the time, effortlessly, automatically, and mostly unconsciously. It is the natural way in which we interpret, predict, and participate in social behavior and communication. We ascribe mental states to people: states such as thoughts, desires, knowledge, and intentions.

Building on many years of research, Baron-Cohen concludes that children with autism, suffer from "mindblindness" as a result of a selective impairment in mindreading. For these children, the world is essentially devoid of mental things.

Baron-Cohen develops a theory that draws on data from comparative psychology, from developmental, and from neuropsychology. He argues that specific neurocognitive mechanisms have evolved that allow us to mindread, to make sense of actions, to interpret gazes as meaningful, and to decode "the language of the eyes."

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Mindblindness : An Essay on Autism and Theory of Mind By: Simon Baron-Cohen https://doi.org/10.7551/mitpress/4635.001.0001 ISBN (electronic): 9780262267731 Publisher: The MIT Press Published: 1995

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Educating Children with Autism (2001)

Chapter: 16 conclusions and recommendations.

Below is the uncorrected machine-read text of this chapter, intended to provide our own search engines and external engines with highly rich, chapter-representative searchable text of each book. Because it is UNCORRECTED material, please consider the following text as a useful but insufficient proxy for the authoritative book pages.

16 Conclusions and Recommendations This chapter summarizes the committeeâs conclusions about the state of the science in early intervention for children with autistic spectrum disorders and its recommendations for future intervention strategies, pro- grams, policy, and research. The chapter is organized around seven key areas pertaining to educational interventions for young children with autistic spectrum disorders: how the disorders are diagnosed and as- sessed and how prevalent they are; the effect on and role of families; appropriate goals for educational services; characteristics of effective in- terventions and educational programs; public policy approaches to en- suring access to appropriate education; the preparation of educational personnel; and needs for future research. DIAGNOSIS, ASSESSMENT, AND PREVALENCE Conclusions Autism is a developmental disorder of neurobiologic origin that is defined on the basis of behavioral and developmental features. Autism is best characterized as a spectrum of disorders that vary in severity of symptoms, age of onset, and association with other disorders (e.g., mental retardation, specific language delay, epilepsy). The manifestations of au- tism vary considerably across children and within an individual child over time. There is no single behavior that is always typical of autism and no behavior that would automatically exclude an individual child from a 211

212 EDUCATING CHILDREN WITH AUTISM diagnosis of autism, even though there are strong and consistent com- monalities, especially relative to social deficits. The large constellation of behaviors that define autistic spectrum dis- ordersâgenerally representing deficits in social interaction, verbal and nonverbal communication, and restricted patterns of interest or behav- iorsâare clearly and reliably identifiable in very young children to expe- rienced clinicians and educators. However, distinctions among classical autism and atypical autism, pervasive developmental disorder-not other- wise specified (PDD-NOS), and Aspergerâs disorder can be arbitrary and are often associated with the presence or severity of handicaps, such as mental retardation and severe language impairment. Identifying narrow categories within autism is necessary for some research purposes; however, the clinical or educational benefit to subclas- sifying autistic spectrum disorders purely by diagnosis is debated. In contrast, individual differences in language development, verbal and non- verbal communication, sensory or motor skills, adaptive behavior, and cognitive abilities have significant effects on behavioral presentation and outcome, and, consequently, have specific implications for educational goals and strategies. Thus, the most important considerations in pro- gramming have to do with the strengths and weaknesses of the indi- vidual child, the age at diagnosis, and early intervention. With adequate time and training, the diagnosis of autistic spectrum disorders can be made reliably in 2-year-olds by professionals experi- enced in the diagnostic assessment of young children with autistic spec- trum disorders. Many families report becoming concerned about their childrenâs behavior and expressing this concern, usually to health profes- sionals, even before this time. Research is under way to develop reliable methods of identification for even younger ages. Children with autistic spectrum disorders, like children with vision or hearing problems, re- quire early identification and diagnosis to equip them with the skills (e.g., imitation, communication) to benefit from educational services, with some evidence that earlier initiation of specific services for autistic spectrum disorders is associated with greater response to treatment. Thus, well meaning attempts not to label children with formal diagnoses can deprive children of specialized services. There are clear reasons for early identifi- cation of children, even as young as two years of age, within the autism spectrum. Epidemiological studies and service-based reports indicate that the prevalence of autistic spectrum disorders has increased in the last 10 years, in part due to better identification and broader categorization by educators, physicians, and other professionals. There is little doubt that more children are being identified as requiring specific educational inter- ventions for autistic spectrum disorders. This has implications for the provision of services at many levels. Analysis of data from the Office of

CONCLUSIONS AND RECOMMENDATIONS 213 Special Education Programs, gathered for school-age children since the autism category was recognized in 1991, would support investigation of whether the dramatic increases in the numbers of children served with autistic spectrum disorders are offset by commensurate decreases in other categories in which children with autistic spectrum disorders might have previously been misclassified or whether these dramatic increases have come about for other reasons. Although children with autistic spectrum disorders share some char- acteristics with children who have other developmental disorders and may benefit from many of the same educational techniques, they offer unique challenges to families, teachers, and others who work with them. Their deficits in nonverbal and verbal communication require intense effort and skill even in the teaching of basic information. The unique difficulties in social interaction (e.g., in joint attention) may require more individual guidance than for other children in order to attract and sustain their childrenâs attention. Moreover, ordinary social exchanges between peers do not usually occur without deliberate planning and ongoing struc- turing by the adults in the childâs environment. The absence of typical friendships and peer relationships affects childrenâs motivation systems and the meaning of experiences. Appropriate social interactions may be some of the most difficult and important lessons a child with autistic spectrum disorders will learn. In addition, the frequency of behavior problems, such as tantrums and self-stimulatory and aggressive behavior, is high. The need for sys- tematic selection of rewards for many children with autistic spectrum disorders, whose motivation or interests can be limited, requires creativ- ity and continued effort from teachers and parents to maximize the childâs potential. Although general principles of learning and behavior analysis apply to autistic spectrum disorders, familiarity with the specific nature of the disorder should contribute to analysis of the contexts (e.g., commu- nicative and social) of behaviors for individual children and result in more effective programming. For example, conducting a functional as- sessment that considers contexts, and then replacing problem behaviors with more appropriate ways to communicate can be an effective method for reducing problem behaviors. Recommendations 1-1 Because of their shared continuities and their unique social diffi- culties, children with any autistic spectrum disorder (autistic disorder, Aspergerâs disorder, atypical autism, PDD-NOS, child- hood disintegrative disorder), regardless of level of severity or function, should be eligible for special educational services within the category of autistic spectrum disorders, as opposed to other

214 EDUCATING CHILDREN WITH AUTISM terminology used by school systems, such as other health im- paired, social emotionally maladjusted, significantly developmen- tally delayed, or neurologically impaired. 1-2 Identification of autistic spectrum disorders should include a for- mal multidisciplinary evaluation of social behavior, language and nonverbal communication, adaptive behavior, motor skills, atypi- cal behaviors, and cognitive status by a team of professionals experienced with autistic spectrum disorders. An essential part of this evaluation is the systematic gathering of information from parents on their observations and concerns. If the school system cannot carry out such an assessment, the local education author- ity should fund the assessment through external sources. Early diagnosis should be emphasized. Because of variability in early development, younger children with autistic spectrum disorders should receive a follow-up diagnostic and educational assess- ment within one to two years of initial evaluation. 1-3 Professional organizations, with the support of the National Insti- tutes of Health (NIH) and the Department of Educationâs Office of Special Education Programs (OSEP), should disseminate infor- mation concerning the nature and range of autistic spectrum dis- orders in young children to all professionals who have contact with children, particularly those who work with infants, toddlers, and preschool children. This information should include the vari- able presentations and patterns of behavior seen in autistic spec- trum disorders from toddlers to school age children. Members of âchild findâ teams within the early intervention systems, as well as primary care providers, should be trained in identifying the âred flags of autistic spectrum disordersâ and the importance and means of early referral for comprehensive diagnostic evaluation. Advocacy groups and relevant federal agencies, as well as profes- sional organizations, should use effective media resources, in- cluding the Internet, to provide information concerning the range of behaviors in autistic spectrum disorders. ROLE OF FAMILIES Conclusions Having a child with an autistic spectrum disorder is a challenge for any family. Involvement of families in the education of young children with autistic spectrum disorders can occur at multiple levels, including advocacy, parents as participating partners in and agents of education or

CONCLUSIONS AND RECOMMENDATIONS 215 behavior change, and family-centered consideration of the needs and strengths of the family as a unit. Nearly all empirically supported treat- ments reviewed by the committee included a parent component, and most research programs used a parent-training approach. More informa- tion is needed about the benefits of a family-centered orientation or com- bined family-centered and formalized parent training in helping parents. It is well established that parents can learn and successfully apply skills to changing the behavior of their children with autistic spectrum disorders, though little is known about the effects of cultural differences, such as race, ethnicity, and social class, nor about the interactions among family factors, child characteristics, and features of educational interven- tion. For most families, having a child with an autistic spectrum disorder creates added stress. Parentsâ use of effective teaching methods can have a significant effect on that stress, as can support from within the family and the community. Parents need access to balanced information about autistic spectrum disorders and the range of appropriate services and technologies in order to carry out their responsibilities. They also need timely information about assessments, educational plans, and the avail- able resources for their children. This information needs to be conveyed to them in a meaningful way that gives them time to prepare to fulfill their roles and responsibilities. In the last ten years the widespread availability of the Internet and media attention to autistic spectrum disorders have increased parentsâ knowledge but often conveyed perspectives that were not balanced nor well-supported scientifically. Of crucial importance is the question of how to make information available to parents and to ensure their active role in advocacy for their childrenâs education. Recommendations 2-1 Parentsâ concerns and perspectives should actively help to shape educational planning. Specifically: a. In order for a family to be effective members of the Indi- vidualized Education Plan (IEP) team that plans a childâs educa- tion, the local school system should provide to the parents, at the beginning of the assessment process, written information con- cerning the nature of autistic spectrum disorders and eligibility categories, the range of alternatives within best practices in early education of autistic spectrum disorders, sources of funding and support (e.g., a support guide and bibliography), and their childâs rights. b. Prior to the IEP meeting, the local school system should provide to each family the written results of their childâs assess-

216 EDUCATING CHILDREN WITH AUTISM ment, and a contact person to explain the findings if they wish, and should indicate that they will have the opportunity to present their concerns. Early during the IEP meeting, parents should be given an opportunity to voice their questions, concerns, and per- spectives about their childâs development and educational pro- gramming. 2-2 As part of local educational programs and intervention programs for children from birth to age 3, families of children with autistic spectrum disorders should be provided the opportunity to learn techniques for teaching their child new skills and reducing prob- lem behaviors. These opportunities should include not only di- dactic sessions, but also ongoing consultation in which individu- alized problem-solving, including in-home observations or training, occur for a family, as needed, to support improvements at home as well as at school. 2-3 Families that are experiencing stress in raising their children with an autistic spectrum disorder should be provided with mental health support services. Under Part C of the Individuals with Disabilities Education Act (IDEA), which addresses family sup- port and service coordination, including private service provid- ers, services should be extended to include families of children at least up to age 8 years. GOALS FOR EDUCATIONAL SERVICES Conclusions At the root of questions about the most appropriate educational inter- ventions lie differences in assumptions about what is possible and what is important to give students with autistic spectrum disorders through edu- cation. The appropriate goals for educational services are the same as those for other children: personal independence and social responsibility. These goals imply continuous progress in social and cognitive abilities, verbal and nonverbal communication skills, adaptive skills, amelioration of behavioral difficulties, and generalization of abilities across multiple environments. In some cases, reports have suggested that particular treat- ments can foster permanent ârecoveryâ. However, as with other develop- mental disabilities, the core deficits of autistic spectrum disorders have generally been found to persist, to some degree, in most individuals. Research concerning outcomes can be characterized by whether the goal of intervention is broadly defined (e.g., ârecoveryâ or âbest out-

CONCLUSIONS AND RECOMMENDATIONS 217 comeâ) or more specifically defined (e.g., increasing vocabulary or peer- directed social behavior); whether the design involves reporting results in terms of group or individual changes; and whether the goals are short term (i.e., to be achieved in a few weeks or months) or longer term (i.e., over years). A large body of single-subject research has demonstrated substantial progress in individual responses to specific intervention tech- niques in relatively short periods of times (e.g., several months) in many specific areas, including gains in social skills, language acquisition, non- verbal communication, and reductions in challenging behaviors. Studies over longer periods of time have documented joint attention, symbolic play, early language skills, and imitation as core deficits and hallmarks of the disorder that are predictive of longer term outcome in the domains of language, adaptive behaviors, and academic skills. Many treatment studies report postintervention placement as an out- come measure. While successful participation in regular classrooms is an important goal for some children with autistic spectrum disorders, the usefulness of placement in regular education classes as an outcome mea- sure is limited, because placement may be related to many variables other than the characteristics of the child (e.g., prevailing trends in inclusion, availability of other services). The most commonly reported outcome measure in group treatment studies of children with autistic spectrum disorders has been changes in IQ scores, which also have many limita- tions. Studies have reported substantial changes in large numbers of chil- dren in intervention studies and longitudinal studies in which children received a variety of interventions. Even in the treatment studies that have shown the strongest gains, childrenâs outcomes are variable, with some children making substantial progress and others showing very slow gains. The needs and strengths of young children with autistic spectrum disorders are very heterogeneous. Although there is evidence that many interventions lead to improvements and that some children shift in spe- cific diagnosis along the autism spectrum during the preschool years, there does not appear to be a simple relationship between any particular intervention and ârecoveryâ from autistic spectrum disorders. Thus, while substantial evidence exists that treatments can reach short-term specific goals in many areas, gaps remain in addressing larger questions of the relationships between particular techniques, child characteristics, and outcomes. Recommendations The IEP and Individual Family Service Plan (IFSP) should be the vehicles for planning and implementing educational objectives.

218 EDUCATING CHILDREN WITH AUTISM 3-1 Appropriate educational objectives for children with autistic spec- trum disorders should be observable, measurable behaviors and skills. These objectives should be able to be accomplished within 1 year and expected to affect a childâs participation in education, the community, and family life. They should include the devel- opment of: a. Social skills to enhance participation in family, school, and community activities (e.g., imitation, social initiations and re- sponse to adults and peers, parallel and interactive play with peers and siblings); b. Expressive verbal language, receptive language, and non- verbal communication skills; c. A functional symbolic communication system; d. Increased engagement and flexibility in developmentally appropriate tasks and play, including the ability to attend to the environment and respond to an appropriate motivational system; e. Fine and gross motor skills used for age appropriate func- tional activities, as needed; f. Cognitive skills, including symbolic play and basic con- cepts, as well as academic skills; g. Replacement of problem behaviors with more conven- tional and appropriate behaviors; and h. Independent organizational skills and other behaviors that underlie success in regular education classrooms (e.g., complet- ing a task independently, following instructions in a group, ask- ing for help). 3-2 Ongoing measurement of educational objectives must be docu- mented in order to determine whether a child is benefiting from a particular intervention. Every childâs response to the educational program should be assessed after a short period of time. Progress should be monitored frequently and objectives adjusted accord- ingly. CHARACTERISTICS OF EFFECTIVE INTERVENTIONS Conclusions In general, there is consistent agreement across comprehensive inter- vention programs about a number of features, though practical and, some- times, ethical considerations have made well-controlled studies with ran- dom assignment very difficult to conduct without direct evaluation. Characteristics of the most appropriate intervention for a given child must

CONCLUSIONS AND RECOMMENDATIONS 219 be tied to that childâs and familyâs needs. However, without direct evalu- ation, it is difficult to know which features are of greatest importance in a program. Across primarily preschool programs, there is a very strong consensus that the following features are critical: â¢ entry into intervention programs as soon as an autism spectrum diagnosis is seriously considered; â¢ active engagement in intensive instructional programming for a minimum of the equivalent of a full school day, 5 days (at least 25 hours) a week, with full year programming varied according to the childâs choronological age and developmental level; â¢ repeated, planned teaching opportunities generally organized around relatively brief periods of time for the youngest children (e.g., 15- 20 minute intervals), including sufficient amounts of adult attention in one-to-one and very small group instruction to meet individualized goals; â¢ inclusion of a family component, including parent training; â¢ low student/teacher ratios (no more than two young children with autistic spectrum disorders per adult in the classroom); and â¢ mechanisms for ongoing program evaluation and assessments of individual childrenâs progress, with results translated into adjustments in programming. Curricula across different programs differ in a number of ways. They include the ways in which goals are prioritized, affecting the relative time spent on verbal and nonverbal communication, social activities, behav- ioral, academic, motor, and other domains. Strategies from various pro- grams represent a range of techniques, including discrete trials, incidental teaching, structured teaching, âfloor timeâ, and individualized modifica- tions of the environment, including schedules. Some programs adopt a unilateral use of one set of procedures, and others use a combination of approaches. Programs also differ in the relative amount of time spent in homes, centers, or schools, when children are considered ready for inclu- sion into regular classrooms, how the role of peers as intervention agents is supported, and in the use of distraction-free or natural environments. Programs also differ in the credentials that are required of direct support and supervisory staff and the formal and informal roles of collateral staff, such as speech language pathologists and occupational therapists. Overall, many of the programs are more similar than different in terms of levels of organization, staffing, ongoing monitoring, and the use of certain techniques, such as discrete trials, incidental learning, and struc- tured teaching. However, there are real differences in philosophy and practice that provide a range of alternatives for parents and school sys- tems considering various approaches. The key to any childâs educational program lies in the objectives specified in the IEP and the ways they are

220 EDUCATING CHILDREN WITH AUTISM addressed. Much more important than the name of the program attended is how the environment and educational strategies allow implementation of the goals for a child and family. Thus, effective services will and should vary considerably across individual children, depending on a childâs age, cognitive and language levels, behavioral needs, and family priorities. Recommendations The committeeâs recommendations for effective treatment are made on the basis of empirical findings, information from selected representa- tive programs, and findings in the general education and developmental literature. In particular, it is well established that children with autism spend much less time in focused and socially directed activity when in unstructured situations than do other children. Therefore, it becomes crucial to specify time engaged in social and focused activity as part of a program for children with autistic spectrum disorders. 4-1 Based on a set of individualized, specialized objectives and plans that are systematically implemented, educational services should begin as soon as a child is suspected of having an autistic spec- trum disorder. Taking into account the needs and strengths of an individual child and family, the childâs schedule and educational environment, in and out of the classroom, should be adapted as needed in order to implement the IEP. Educational services should include a minimum of 25 hours a week, 12 months a year, in which the child is engaged in systematically planned, develop- mentally appropriate educational activity aimed toward identi- fied objectives. Where this activity takes place and the content of the activity should be determined on an individual basis, de- pending on characteristics of both the child and the family. 4-2 A child must receive sufficient individualized attention on a daily basis so that individual objectives can be effectively implemented; individualized attention should include individual therapies, de- velopmentally appropriate small group instruction, and direct one-to-one contact with teaching staff. 4-3 Assessment of a childâs progress in meeting objectives should be used on an ongoing basis to further refine the IEP. Lack of objec- tively documentable progress over a 3 month period should be taken to indicate a need to increase intensity by lowering stu-

CONCLUSIONS AND RECOMMENDATIONS 221 dent/teacher ratios, increasing programming time, reformulat- ing curricula, or providing additional training and consultation. 4-4 To the extent that it leads to the specified educational goals (e.g., peer interaction skills, independent participation in regular edu- cation), children should receive specialized instruction in settings in which ongoing interactions occur with typically developing children. 4-5 Six kinds of interventions should have priority: a. Functional, spontaneous communication should be the pri- mary focus of early education. For very young children, pro- gramming should be based on the assumption that most children can learn to speak. Effective teaching techniques for both verbal language and alternative modes of functional communication, drawn from the empirical and theoretical literature, should be vigorously applied across settings. b. Social instruction should be delivered throughout the day in various settings, using specific activities and interventions planned to meet age-appropriate, individualized social goals (e.g., with very young children, response to maternal imitation; with preschool children, cooperative activities with peers). c. The teaching of play skills should focus on play with peers, with additional instruction in appropriate use of toys and other materials. d. Other instruction aimed at goals for cognitive develop- ment should also be carried out in the context in which the skills are expected to be used, with generalization and maintenance in natural contexts as important as the acquisition of new skills. Because new skills have to be learned before they can be general- ized, the documentation of rates of acquisition is an important first step. Methods of introduction of new skills may differ from teaching strategies to support generalization and maintenance. e. Intervention strategies that address problem behaviors should incorporate information about the contexts in which the behaviors occur; positive, proactive approaches; and the range of techniques that have empirical support (e.g., functional assess- ment, functional communication training, reinforcement of alter- native behaviors). f. Functional academic skills should be taught when appro- priate to the skills and needs of a child.

222 EDUCATING CHILDREN WITH AUTISM PUBLIC POLICIES Conclusions The Individuals with Disabilities Education Act (IDEA) contains the necessary provisions for ensuring rights to appropriate education for chil- dren with autistic spectrum disorders. However, the implementation and specification of these services are variable. Early intervention for young children with autistic spectrum disorders is expensive, and most local schools need financial help from the state and federal programs to pro- vide appropriate services. The large number of court cases is a symptom of the tension between families and school systems. Case law has yielded an inconsistent pattern of findings that vary according to the characteristics of the individual cases. The number of challenges to decision-making for programming within school systems reflects parentsâ concerns about the adequacy of knowledge and the expertise of school systems in determining their childrenâs education and implementing appropriate techniques. The treatment of autistic spectrum disorders often involves many disciplines and agencies. This confuses lines of financial and intellectual responsibility and complicates assessment and educational planning. When communication between families and school systems goes awry, it can directly affect childrenâs programming and the energy and financial resources that are put into education rather than litigation. Support sys- tems are not generally adequate in undergirding local service delivery programs and maximizing the usefulness of different disciplines and agencies, and transitions between service delivery agencies are often prob- lematic. A number of states have successful models for providing services to children with autism, and mechanisms are becoming increasingly effi- cient and flexible in some states. In most cases, existing agencies at state and federal levels can develop appropriate programs without restructur- ingâwith the possible addition of special task forces or committees de- signed to deal with issues particular to children with autistic spectrum disorders. Recommendations The committee recommends that a variety of steps be taken to ensure that policies are effectively carried out at the state and local levels. 5-1 At the federal level, the National Institutes of Healthâs Autism Coordinating Committee and the Federal Interagency Coordinat- ing Council should jointly appoint a clinical research oversight

CONCLUSIONS AND RECOMMENDATIONS 223 task force of professionals knowledgeable in the field of autistic spectrum disorders, to review and periodically report on basic and applied research programs to the parent agencies and to track program implementation through the State Interagency Coordi- nating Councils or relevant state agencies. Administrative sup- port for these efforts should be provided by the appropriate de- partment of the Secretaryâs office. 5-2 States should have regional resource and training centers with expertise in autistic spectrum disorders to provide training and technical support to local schools. States should also have a mechanism to evaluate the adequacy of current support systems to local schools and recommend ways for improvement. One such mechanism could be an autistic spectrum disorders support systems task force that would examine the relevant provisions for personnel preparation, technical assistance, and demonstration of exemplary programs and would make recommendations as to what would be needed to bring a stateâs support systems into alignment with quality education for children with autistic spec- trum disorders. States should monitor coordination among and transitions between service delivery systems and should develop ways to facilitate these processes. 5-3 Families should have access to consultation and legal knowledge such as provided by an ombudsman who is independent of the school system and who could be a standard part of Individual- ized Educational Plan planning and meetings. The ombudsman should be knowledgeable about autistic spectrum disorders and about relevant law and court decisions. The ombudsmanâs role should include attending IEP meetings, interpreting the school systemâs communications about a child to parents, and propos- ing, at the parentsâ request, alternatives to those presented by the school system. Professional and advocacy groups should work together to provide this service, with the Governorâs Council for Developmental Disabilities or the Autistic Spectrum Disorders Support Systems Task Force responsible for ensuring funding for training and support of this service. 5-4 State and federal agencies should consider ways to work with and support professional and advocacy groups to provide up-to- date, practical, scientifically valid information to parents and practitioners.

224 EDUCATING CHILDREN WITH AUTISM 5-5 States should have clearly defined minimum standards for per- sonnel in educational settings for children with autistic spectrum disorders. For example, at a minimum, teachers should have some special preparation (e.g., preservice course work, equiva- lent inservice training, workshops, and supervised practice in re- search-based practices in autistic spectrum disorders) and should have well-trained, experienced support personnel available to provide ongoing training and additional consultation. 5-6 States should develop a systematic strategy to fund the interven- tions that are necessary for children with autistic spectrum disor- ders in local schools, so that this cost is not borne primarily by the parents or local school systems. State education departments should develop interagency collaborations to pool support for local systems. A state fund for intensive intervention, or more systematic use of Medicaid waivers or other patterns of funding currently in place in some states, should be considered. Families should not be expected to fund or provide the majority of educa- tional programming for their children. 5-7 An updated, accurate summary of case law, consultation services, and mediation mechanisms in autistic spectrum disorders should be made accessible by the Office of Special Education Programs so that schools and parents can understand the options available to them when conflicts arise. 5-8 Since levels of information about autistic spectrum disorders vary greatly within the groups and agencies that make funding and policy decisions about autistic spectrum disorders, including state task forces in education and review panels in federal agencies, it is crucial that persons knowledgeable in the range of needs and interventions associated with autistic spectrum disorders be in- cluded in those decision-making activities. PERSONNEL PREPARATION Conclusions The nature of autistic spectrum disorders and other disabilities that frequently accompany them has significant implications for approaches to education and intervention at school, in the home, and in the commu- nity. Approaches that emphasize the use of specific âpackagesâ of mate- rials and methods associated with comprehensive intervention programs

CONCLUSIONS AND RECOMMENDATIONS 225 may understate the multiple immediate and long-term needs of children for behavior support and for instruction across areas. Teachers are faced with a huge task. They must be familiar with theory and research concerning best practices for children with autistic spectrum disorders, including methods of applied behavior analysis, naturalistic learning, assistive technology, socialization, communication, inclusion, adaptation of the environment, language interventions, assess- ment, and the effective use of data collection systems. Specific problems in generalization and maintenance of behaviors also affect the need for training in methods of teaching children with autistic spectrum disorders. The wide range of IQ scores and verbal skills associated with autistic spectrum disorders, from profound mental retardation and severe lan- guage impairments to superior intelligence, intensify the need for person- nel training. To enable teachers to adequately work with parents and with other professionals to set appropriate goals, teachers need familiar- ity with the course of autistic spectrum disorders and the range of pos- sible outcomes. Teachers learn according to the same principles as their students. Multiple exposures, opportunities to practice, and active involvement in learning are all important aspects of learning for teachers, as well as stu- dents. Many states and community organizations have invested substan- tial funds in teacher preparation through workshops and large-audience lectures by well-known speakers. While such presentations can stimulate enthusiasm, they do not substitute for ongoing consultation and hands- on opportunities to observe and practice skills working with children with autistic spectrum disorders. Personnel preparation remains one of the weakest elements of effec- tive programming for children with autistic spectrum disorders and their families. Ways of building on the knowledge of teachers as they acquire experience with children with autistic spectrum disorders, and ways of keeping skilled personnel within the field, are critical. This is particularly true given recent trends for dependence on relatively inexperienced assis- tants for in-home programs. Providing knowledge about autistic spec- trum disorders to special education and regular education administra- tors, as well as to specialized providers with major roles in early intervention (e.g., speech language pathologists) will be critical in effect- ing change that is proactive. Findings concerning change in educational and other opportunities suggest that administrative attitudes and sup- port are critical in improving schools. Recommendations The committee recommends that relevant state and federal agencies institute an agenda for upgrading personnel preparation for those who

226 EDUCATING CHILDREN WITH AUTISM work with, and are responsible for, children with autistic spectrum disor- ders and their families. These efforts should be part of a larger effort to coordinate and collaborate with the already established infrastructure of special education, regional resource centers, technical assistance pro- grams, personnel preparation, communication sharing, and other relevant aspects of the existing infrastructure. Professionals aware of the special nature of these children are already carrying out many of these recom- mendations in a limited fashion. The committee urges agencies to pro- vide the personnel preparation resources needed for intensified efforts to build a viable support structure for educating children with autistic spec- trum disorders. 6-1 The Office of Special Education Programs should establish a 5- year plan to provide priority funds for preservice and inservice preparation for teachers, paraprofessionals, and other personnel providing services for children with autistic spectrum disorders, including children under age 3 years. 6-2 The need for a team approach involving many professions should be addressed by personnel preparation and practicum work within multidisciplined organizations and teams. 6-3 A special emphasis should be placed on training of trainers. There is a short supply of expertise and experience in the field of educa- tion for children with autistic spectrum disorders, and special attention should be paid to rapidly increase the capabilities of the trainers, who may have experience in special education or related fields, but not in the special skills and practices for children with autistic spectrum disorders. 6-4 The existing support systems that provide short-term training (e.g., technical assistance systems, resource centers, etc.) should include people with special expertise in autistic spectrum disor- ders on their staff. 6-5 The content of the curriculum for children with autistic spectrum disorders should be based on sound research. A continuing pro- gram should be established from such agencies as the National Institute of Mental Health and the National Institute of Child Health and Human Development to translate their research into usable information for practitioners. Work on family research is particularly relevant.

CONCLUSIONS AND RECOMMENDATIONS 227 NEEDED RESEARCH Conclusions There are several distinct and substantial bodies of research relevant to young children with autistic spectrum disorders. One body identifies neurological, behavioral, and developmental characteristics. Another body of research addresses diagnostic practices and related issues of prevalence. Another has examined the effects of comprehensive early treatment programs on the immediate and long-term outcomes of chil- dren and their families. These treatment studies tended to use some form of group experimental design. An additional body of research has ad- dressed individual instructional or intervention approaches, with many studies in this literature using single-subject experimental methodology. Altogether, a large research base exists, but with relatively little integra- tion across bodies of literature. Highly knowledgeable researchers in one area of autistic spectrum disorders may have minimal information from other perspectives, even about studies with direct bearing on their find- ings. Most researchers have not used randomized group comparison de- signs because of the practical and ethical difficulties in randomly assign- ing children and families to treatment groups. In addition, there have been significant controversies over the type of control or contrast group to use and the conditions necessary for demonstrating effectiveness. Al- though a number of comprehensive programs have provided data on their effectiveness, and, in some cases, claims have been made that certain treatments are superior to others, there have been virtually no compari- sons of different comprehensive interventions of equal intensity. Across several of the bodies of literature, the children and families who have participated in studies are often inadequately described. Stan- dardized diagnoses, descriptions of ethnicity, the social class, and associ- ated features of the children (such as mental retardation and language level) are often not specified. Fidelity of treatment implementation has not been consistently assessed. Generalization, particularly across set- tings, and maintenance of treatment effects are not always measured. Though there is little evidence concerning the effectiveness of discipline- specific therapies, there is substantial research supporting the effective- ness of many specific therapeutic techniques. Recommendations 7-1 Funding agencies and professional journals should require minimium standards in design and description of intervention projects. All intervention studies should provide the following information:

228 EDUCATING CHILDREN WITH AUTISM a. Adequate information concerning the children and fami- lies who participated, and who chose not to participate or with- drew from participation, including chronological age, develop- mental assessment data (including verbal and nonverbal IQ levels), standardized diagnoses, gender, race, family characteris- tics, socioeconomic status, and relevant health or other biological impairments; b. description of the intervention in sufficient detail so that an external group could replicate it; detailed documentation is crucial especially if no treatment manual is available; c. fidelity of treatment and degree of implementation; d. specific objective measures of expected outcomes, assessed at regular intervals; and e. measures of outcome that are independent of the interven- tion, in terms of both the evaluators and the measures, and in- clude broad immediate and long-term effects on children and families, particularly generalization and maintenance effects. 7-2 Funders and performers of research should recognize that valu- able information can be provided by a variety of approaches to research in intervention, including group experimental and single-subject designs. 7-3 In order to help educators and consumers make informed deci- sions about appropriate methods of intervention for particular children, federal agencies involved in autistic spectrum disorders initiatives (including the Office of Special Education Programs, the Office of Educational Research and Improvement, the Na- tional Institute of Child Health and Human Development, the National Institute of Mental Health, the National Institute of Neu- rological Disorders and Stroke, and the National Institute on Deaf- ness and Other Communication Disorders) and nonprofit agen- cies with similar national missions (such as Autism Society of America Foundation, Cure Autism Now, and National Alliance for Autism Research) should form a research task force and spe- cifically allocate federal responsibilites for recruiting and funding a comprehensive program of research related to intervention and treatment. This program should include: a. development of more specific, precise measures of impor- tant areas of outcome, such as social functioning, peer relation- ships, spontaneous communication and language, and the acqui- sition of competence in natural contexts (e.g., classroom, home);

CONCLUSIONS AND RECOMMENDATIONS 229 b. definition of appropriate educational skills and sequences in social and cognitive development, informed by normal devel- opmental literature; c. measurement of the effects of the interactions between fam- ily variables (e.g., family structure, family supports, socioeco- nomic status), child factors (such as degree of language impair- ment), and responses to educational interventions (including family-centered, parent training, and other approaches) on out- comes. d. longitudinal treatment studies, where feasible, built on a clinical model with randomly assigned samples of sufficient size to assess the effectiveness of differing modes of treatment. 7-4 Treatment studies should recognize the common components of many comprehensive programs (e.g., standardized curriculum, family training, presence of typically developing peers) and should target and measure, longitudinally when feasible, âactive ingredientsâ and mediating variables that influence the effects of intervention (e.g., communication and interaction opportunities for engagement, levels of interaction and initiation, specific teach- ing techniques, proportion of time in close proximity of peers). The concomitant development of innovative treatments building on these âactive ingredientsâ should be supported. 7-5 In response to amendments in IDEA to make education more outcome oriented, a federal initiative should solicit and fund stud- ies in the following areas, not easily supported under the current review system: a. the development of instruments for measurement of diag- nosis and critical aspects of development, particularly tools for early screening of autistic spectrum disorders and for measure- ment of response to interventions; b. the development and application of sophisticated statisti- cal methods of analysis of change and growth, particularly multi- variate designs and those applicable to small samples; and c. the development and dissemination of novel research de- signs that combine individual and group approaches in ways that minimize biases and maximize the power of small samples. 7-6 Competitively funded initiatives in early education in autistic spectrum disorders should require plans and contain sufficient funding for short- and long-term assessment of child outcomes and measures of program efficacy.

Autism is a word most of us are familiar with. But do we really know what it means?

Children with autism are challenged by the most essential human behaviors. They have difficulty interacting with other people—often failing to see people as people rather than simply objects in their environment. They cannot easily communicate ideas and feelings, have great trouble imagining what others think or feel, and in some cases spend their lives speechless. They frequently find it hard to make friends or even bond with family members. Their behavior can seem bizarre.

Education is the primary form of treatment for this mysterious condition. This means that we place important responsibilities on schools, teachers and children's parents, as well as the other professionals who work with children with autism. With the passage of the Individuals with Disabilities Education Act of 1975, we accepted responsibility for educating children who face special challenges like autism. While we have since amassed a substantial body of research, researchers have not adequately communicated with one another, and their findings have not been integrated into a proven curriculum.

Educating Children with Autism outlines an interdisciplinary approach to education for children with autism. The committee explores what makes education effective for the child with autism and identifies specific characteristics of programs that work. Recommendations are offered for choosing educational content and strategies, introducing interaction with other children, and other key areas.

This book examines some fundamental issues, including:

How children's specific diagnoses should affect educational assessment and planning
How we can support the families of children with autism
Features of effective instructional and comprehensive programs and strategies
How we can better prepare teachers, school staffs, professionals, and parents to educate children with autism
What policies at the federal, state, and local levels will best ensure appropriate education, examining strategies and resources needed to address the rights of children with autism to appropriate education.

Children with autism present educators with one of their most difficult challenges. Through a comprehensive examination of the scientific knowledge underlying educational practices, programs, and strategies, Educating Children with Autism presents valuable information for parents, administrators, advocates, researchers, and policy makers.

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The Portrayal of Autism in ‘Rain Man’: Insights and Impacts

This essay about the portrayal of autism in ‘Rain Man’ explores the film’s nuanced depiction of autism through the character of Raymond Babbitt, portrayed by Dustin Hoffman. It examines the film’s impact on raising awareness and fostering understanding of neurodiversity, while also critically analyzing its strengths and shortcomings in representing the lived experiences of individuals on the autism spectrum. Despite its achievements in humanizing autism, ‘Rain Man’ is scrutinized for potentially sensationalizing the condition and overlooking the everyday challenges faced by those on the spectrum. Ultimately, the essay emphasizes the importance of engaging thoughtfully with representations of autism in popular culture to promote empathy and inclusivity.

How it works

The cinematic landscape often serves as a mirror reflecting society’s perception of diverse experiences, including those of individuals on the autism spectrum. Among the notable portrayals in cinema history, ‘Rain Man’ stands as a landmark, etching the complexities of autism through the character of Raymond Babbitt. Directed by Barry Levinson and starring Dustin Hoffman as Raymond alongside Tom Cruise, the film embarks on a journey that intertwines familial bonds with the intricacies of neurodiversity.

Central to the allure of ‘Rain Man’ is the nuanced portrayal of Raymond’s autism.

Hoffman’s portrayal offers a glimpse beyond the surface, delving into the intricate patterns of behavior and cognition characteristic of autism spectrum disorder. Through Raymond’s idiosyncrasies and remarkable abilities, the film provides viewers with a window into the multifaceted nature of autism, challenging preconceived notions and fostering empathy.

However, amidst the accolades lie nuanced critiques of the film’s representation. While ‘Rain Man’ succeeds in humanizing autism, some argue it falls prey to sensationalism, emphasizing Raymond’s exceptional abilities at the expense of depicting the everyday struggles faced by individuals on the spectrum. The danger of reducing autism to a mere spectacle looms large, overshadowing the lived experiences and diversity within the autistic community.

Yet, ‘Rain Man’ undeniably catalyzed a seismic shift in public perception and discourse surrounding autism. Beyond the silver screen, the film ignited conversations, prompting society to confront its biases and misconceptions. In its wake, advocacy efforts gained momentum, paving the way for greater inclusivity and understanding of neurodiversity. The legacy of ‘Rain Man’ extends far beyond its runtime, leaving an indelible mark on the fabric of cultural consciousness.

In the final analysis, ‘Rain Man’ serves as both a prism and a mirror, refracting the myriad facets of autism while reflecting society’s evolving understanding of difference and acceptance. As we navigate the cinematic landscape, it is imperative to engage critically with representations of autism, acknowledging their power to shape perceptions and narratives. Ultimately, the true measure of progress lies not in mere representation but in the depth of empathy and understanding we extend to one another.

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What is autism spectrum disorder? How to support the community this Autism Acceptance Month

April marks Autism Acceptance Month with World Autism Day occurring on April 2 every year. The month is meant to be a time for uplifting autistic voices and sharing in the community's joy. But for Samantha Edwards, an autistic content creator and neurodivergent life coach, the month also signifies an influx of harmful myths about autistic people.

"April is a wonderful month to crack down on that and listen to autistic voices and their stories and listen to their struggles," she says. "Acceptance, at the end of the day, is going to promote more inclusivity."

Here’s how you can uplift the neurodivergent community this April and all year long.

What is autism?

Autism is a developmental disability that affects the way people experience the world . This may include differences in processing senses, thinking, physically moving, communicating, socializing and going about daily living.

“We’re born autistic and we’re autistic our whole lives,” says Zoe Gross, the director of advocacy at Autistic Self Advocacy Network . “It affects everything about the way we interact with and perceive the world.”

Autism affects every autistic person differently, and there isn’t one way to be autistic. Gross describes it as an ice cream sundae bar: The traits of autism can be mixed and matched from person to person.

Here’s what autism isn’t, Gross says – something to be scared of or pity.

“In truth, autism is just a neutral fact about us, it’s not necessarily a good or a bad thing,” she says. “It’s just the way our brains are.”

Another misconception is that autistic people don’t have empathy. Gross recalled a time when a teacher asked her if she loved her parents. Of course she loves them, she responded, but the question itself was a symptom of a larger myth about autistic people and emotions.

“Where that comes from is that we may not know what other people are feeling if they don’t tell us because autistic people may not be good at reading body language or other kinds of subtle social cues,” Gross says. “But that doesn’t mean we don’t care what people are feeling.”

World Autism Day: A love letter to parents of a newly-diagnosed child

How common is autism?

About one in 36 children have autism spectrum disorder, the Centers for Disease Control and Prevention states. This number is on the rise, especially as children of color receive more diagnoses after being largely overlooked throughout history.

Edwards started her online autism advocacy journey to combat the misconceptions about autism. As an autistic person and a parent of two autistic children, she says she wants to make the world a more accessible place for future generations.

A large part of her work is advocating for the self-diagnosed community, which she says “are very welcome and included in the autistic community.”

One of the more harmful narratives is that people, especially teenagers, are self-diagnosing after watching a handful of TikTok videos with captions like “Signs you may be autistic” or “10 things that are actually traits of autism.” But that’s “really not the case,” says Edwards. Online platforms like TikTok give the autistic community, like other marginalized communities, more visibility than ever before.

“It is harmful for all of these self-diagnosed autistics that really did put in the research – some have years, even a lifetime of research – to be told, ‘Oh, you watched a couple TikTok videos so you’re not valid,'” Edwards says.

Some medical professionals push back against self-diagnosing, especially when it comes to social media. But there’s also the nuanced issue of access to healthcare services that may lead to a professional diagnosis, which can be limited for some autistic individuals .

What is Autism Acceptance Month?

April is Autism Acceptance Month but many, especially those outside of the autism community, used to refer to the month as " Autism Awareness Month." Autistic advocacy organizations have been using “acceptance” rather than “awareness” for over a decade, and the Autism Society of America shifted the terminology in 2021.

According to ASAN, Autism Acceptance Month was created by and for autistic people to respect the rights and humanity of all autistic people and center “the perspectives and needs of autistic people with intellectual disabilities, nonspeaking autistic people, and autistic people with the highest support needs.”

Using “acceptance” instead of “awareness” is an intentional choice because, as Edwards says, “we’re just moving on.”

“It’s 2023, I do believe most people are aware of what autism is,” she says. “We’ve got the awareness and now we need the resources, we need the advocacy.”

Awareness campaigns have historically focused on how many people have autism or a search for a “cure.” A now-removed 2009 campaign from advocacy organization Autism Speaks opened by saying “I am autism. I’m visible in your children, but if I can help it, I am invisible to you until it’s too late.”

The “awareness” approach, Gross says, further stigmatizes autism as something scary.

“That’s not the way we want to approach giving people information about autism, we want people to view autism as a part of human diversity and autistic people as part of their community,” Gross says.

How to support the autistic community

Don’t speak over autistic voices

“ Nothing about us without us ” is a disability rights slogan that’s top of mind during Autism Acceptance Month.

When it comes to research, policy and advocacy, the most important thing is that autistic people are “in the driver’s seat,” Gross says. It means that decisions about autism need to be made by or with autistic people. It also means centering the stories and experiences of autistic people.

Avoid harmful labels and language

“Low-functioning” and “high-functioning” are labels often ascribed to autistic people. These are harmful , ASAN says, because “we all have things we are good at and things we need help with.”

“People will say, ‘How can I do without the terms low-functioning and high-functioning?’ And what I want to ask is like ‘What are you doing with them now?’” Gross says. “What I encourage people to do is just say what they mean. If they mean this person can’t speak, (say) ‘I’m talking about someone who can’t speak.’ If they mean this person has a job, just say ‘I’m talking about an autistic person who has a job.’”

Neurotypical people may also wonder what’s more appropriate to say – person with autism or autistic person?

Many self-advocates prefer identity first language because it works against the stigma that being autistic is something bad or something that makes you less than. Identity first language (“autistic person”) recognizes and validates that identity.

“Autism is something that you are and not something that you have, you’re not carrying autism around in a bag,” Edwards says. “It’s something that makes your brain different.”

But it’s a personal preference . For example, Gross says people with intellectual disabilities may use person-first language ("person with autism") because “they feel they’ve been so dehumanized and people only see their disability and don’t see them.”

The bottom line: How someone refers to their autism is personal based on what makes them feel the most affirmed and validated.

Support autistic-run organizations and businesses

Edwards recommends supporting organizations that center autistic voices and are run by autistic people, like ASAN and the Autistic Women and Nonbinary Network.

This month, Edwards says she’ll be using her platform to uplift other autistic and disabled creators.

“There’s so many of us that are … trying to make a really big difference in this movement, so I’m really proud of everyone this past year,” she says. “I just want to uplift each other and get the right message out.”

Organizations with primarily neurotypical leadership have led autistic advocates to move away from their symbols (like Autism Speaks’ signature blue color and puzzle piece) in favor of new ones created by autistic self-advocates. The first puzzle piece logo in 1963 featured a crying child in the center and was designed to show autism as a “puzzling condition.” A 2018 study found the general public has a negative implicit bias against the imagery of a puzzle piece, which participants associated with “imperfection, incompletion, uncertainty, difficulty, the state of being unsolved, and, most poignantly, being missing.”

“We recognize discord within the community, including those who dislike the puzzle piece symbol or prefer a different symbol, but there are also many who embrace it and want to continue to see it associated with autism,” Autism Speaks told USA TODAY in a statement.

The organization says it is regularly seeking feedback from those within the autistic community on whether or not to continue its use and encouraged feedback at [email protected] .

Many favor a rainbow or gold infinity symbol and use “ Red Instead ,” which Edwards says symbolizes the passion autistic people have.

Don’t perpetuate myths about autism

Edwards recommends neurotypical people support the neurodiverse community by staying up to date on current research and taking a second glance before sharing something that furthers stereotypes about autistic people.

“We all deserve our human rights, and we all deserve respect,” Gross says. “We all deserve to be able to make choices in our lives, we deserve to live free from neglect and abuse, we deserve to have services that are truly person-centered and individualized for us and that meet our needs. Those aren’t optional, fancy things that you get by being mildly impacted.”

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Autism Spectrum Disorder (ASD) Essay

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What is autism spectrum disorder? How to support the community this Autism Acceptance Month

​​​What is autism?

How common is autism?

What is Autism Acceptance Month?

How to support the autistic community

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What is autism?