Autism spectrum

Short description: Neurodevelopmental disorder

Autism spectrum disorder

Other names|

* Autism spectrum condition (ASC), autism
* Formerly: Kanner syndrome/autistic disorder/childhood autism, Asperger syndrome (AS), childhood disintegrative disorder (CDD), pervasive developmental disorder not otherwise specified (PDD-NOS)

Repetitively stacking or lining up objects is a common trait associated with autism.
Specialty| Psychiatry, clinical psychology, pediatrics, occupational medicine
Symptoms| Difficulties in social interaction, verbal and nonverbal communication, and the presence of repetitive behavior or restricted interests
Complications| Social isolation, educational and employment problems,[1] anxiety,[1] stress,[1] bullying, depression,[1][2] self-harm
Usual onset| Early childhood
Duration| Lifelong
Causes| Multifactorial, with many uncertain factors
Risk factors| Family history, certain genetic conditions, having older parents, certain prescribed drugs, perinatal and neonatal health issues
Diagnostic method| Based on combination of clinical observation of behavior and development and comprehensive diagnostic testing completed by a team of qualified professionals (including psychiatrists, clinical psychologists, neuropsychologists, pediatricians, and speech-language pathologists). For adults, the use of a patient's written and oral history of autistic traits becomes more important
Differential diagnosis| Intellectual disability, anxiety, bipolar disorder, depression, Rett syndrome, attention deficit hyperactivity disorder, schizoid personality disorder, selective mutism, schizophrenia, obsessive–compulsive disorder, social anxiety disorder, Einstein syndrome, PTSD,[3] learning disorders (mainly speech disorders)
Management| Applied behavior analysis, cognitive behavioral therapy, occupational therapy, psychotropic medication,[4] speech–language pathology
Frequency|

* 1 in 100 children (1%) worldwide[5]

Autism, formally called autism spectrum disorder (ASD) or autism spectrum condition (ASC),[6] is a neurodevelopmental disorder marked by impaired social communication and restricted and repetitive patterns of behavior. Other common signs include difficulty with social interaction, verbal and nonverbal communication, along with perseverative interests, stereotypic body movements, rigid routines, and hyper- or hyporeactivity to sensory input. Autism is clinically regarded as a spectrum disorder, meaning that it can manifest very differently in each person. For example, some are nonspeaking, while others have proficient spoken language. Because of this, there is wide variation in the support needs of people across the autism spectrum.

There are many theories about what causes autism; it is highly heritable and mainly genetic, but many genes are involved, and environmental factors may also be relevant.[7] The syndrome frequently co-occurs with other conditions, including attention deficit hyperactivity disorder, epilepsy, and intellectual disability. Disagreements persist about what should be included as part of the diagnosis, whether there are meaningful subtypes of autism,[8] and the significance of autism-associated traits in the wider population.[9][10] The combination of broader criteria, increased awareness, and potentially increasing actual prevalence, has led to a trend of steadily increasing estimates of autism prevalence,[11] perpetuating the disproven myth that it is caused by vaccines.[12]

Psychiatry has traditionally classified autism as a mental disorder, but the autism rights movement and an increasing number of researchers see autism as part of neurodiversity, the natural diversity in human thinking and experience, with strengths, differences, and weaknesses.[13] From this point of view, autistic people often still have a disability, but need to be accommodated rather than cured.[14][15] This perspective has led to significant controversy among those who are autistic and advocates, practitioners, and charities.[16][17] As of 2023, consensus is growing among researchers of various empirical and theoretical positions that the established ASD criteria are ineffective to describe autism as a unitary biological entity, and that alternative research approaches should be encouraged.[18]

There is no cure for autism. Although early intervention services based on applied behavior analysis (ABA) can help children gain self-care, social, and language skills,[19][20][21][22] independent living is unlikely in more severe forms of the condition. Speech and occupational therapy, as well as implementing alternative modes of communication, are effective adjunctive therapies, but some in the autism rights movement consider ABA therapy unethical and unhelpful.[23] Pharmacological treatments also may be useful; the atypical antipsychotics risperidone and aripiprazole are empirically validated for alleviating co-morbid irritability.[24]

## Contents

* 1 Classification
* 1.1 Spectrum model
* 1.2 ICD
* 1.3 DSM
* 2 Common characteristics
* 2.1 Pre-diagnosis
* 2.2 Broader autism phenotype
* 2.3 Social and communication skills
* 2.4 Restricted and repetitive behaviors
* 2.4.1 Self-injury
* 2.5 Other features
* 3 Possible causes
* 3.1 Biological subgroups
* 3.1.1 Syndromic autism and non-syndromic autism
* 3.2 Genetics
* 3.3 Early life
* 3.3.1 Disproven vaccine hypothesis
* 3.4 Etiological hypotheses
* 3.5 Evolutionary hypotheses
* 4 Pathophysiology
* 5 Diagnosis
* 6 Conditions correlated or comorbid to autism
* 6.1 Correlations
* 6.2 Comorbidities
* 7 Management
* 7.1 Non-pharmacological interventions
* 7.1.1 Education
* 7.2 Pharmacological interventions
* 7.3 Alternative medicine
* 7.4 Prevention
* 8 Prognosis
* 9 Epidemiology
* 10 History
* 11 Society and culture
* 11.1 Neurodiversity movement
* 11.2 Symbols and flags
* 11.3 Caregivers
* 11.4 LGBT identity and religious beliefs
* 12 See also
* 13 References
* 13.1 Sources
* 14 Further reading
* 15 External links

## Classification

### Spectrum model

Before the DSM-5 (2013) and ICD-11 (2022) diagnostic manuals were adopted, what is now called ASD was found under the diagnostic category pervasive developmental disorder. The previous system relied on a set of closely related and overlapping diagnoses such as Asperger syndrome and Kanner syndrome. This created unclear boundaries between the terms, so for the DSM-5 and ICD-11, a spectrum approach was taken. The new system is also more restrictive, meaning fewer people now qualify for diagnosis.[25]

The DSM-5 and ICD-11 use different categorization tools to define this spectrum. DSM-5 uses a "level" system, which ranks how in need of support the patient is,[26] while the ICD-11 system has two axes, intellectual impairment and language impairment,[27] as these are seen as the most crucial factors.

Autism is currently defined as a highly variable neurodevelopmental disorder[28] that is generally thought to cover a broad and deep spectrum, manifesting very differently from one person to another. Some have high support needs, may be non-speaking, and experience developmental delays; this is more likely with other co-existing diagnoses. Others have relatively low support needs; they may have more typical speech-language and intellectual skills but atypical social/conversation skills, narrowly focused interests, and wordy, pedantic communication.[29] They may still require significant support in some areas of their lives. The spectrum model should not be understood as a continuum running from mild to severe, but instead means that autism can present very differently in each person.[30] How a person presents can depend on context, and may vary over time.[31]

While the DSM and ICD greatly influence each other, there are also differences. For example, Rett syndrome was included in ASD in the DSM-5, but in the ICD-11 it was excluded and placed in the chapter on Developmental Anomalies. The ICD and the DSM change over time, and there has been collaborative work toward a convergence of the two since 1980 (when DSM-III was published and ICD-9 was current), including more rigorous biological assessment—in place of historical experience—and a simplification of the classification system.[32][33][34][35]

As of 2023, empirical and theoretical research is leading to a growing consensus among researchers that the established ASD criteria are ineffective to describe autism as a unitary biological entity, and that alternative research approaches must be encouraged, such as going back to autism prototypes, exploring new causal models of autism, or developing transdiagnostic endophenotypes.[18] Proposed alternatives to the current disorder-focused spectrum model deconstruct autism into at least two separate phenomena: (1) a non-pathological spectrum of behavioral traits in the population,[36][37] and (2) the neuropathological burden of rare genetic mutations and environmental risk factors potentially leading to neurodevelopmental and psychological disorders,[36][37] (3) governed by an individual's cognitive ability to compensate.[36]

### ICD

The World Health Organization's International Classification of Diseases (11th Revision), ICD-11, was released in June 2018 and came into full effect as of January 2022.[38][32] It describes ASD as follows:[39]

> Autism spectrum disorder is characterised by persistent deficits in the ability to initiate and to sustain reciprocal social interaction and social communication, and by a range of restricted, repetitive, and inflexible patterns of behaviour, interests or activities that are clearly atypical or excessive for the individual's age and sociocultural context. The onset of the disorder occurs during the developmental period, typically in early childhood, but symptoms may not become fully manifest until later, when social demands exceed limited capacities. Deficits are sufficiently severe to cause impairment in personal, family, social, educational, occupational or other important areas of functioning and are usually a pervasive feature of the individual's functioning observable in all settings, although they may vary according to social, educational, or other context. Individuals along the spectrum exhibit a full range of intellectual functioning and language abilities.

— ICD-11, chapter 6, section A02

ICD-11 was produced by professionals from 55 countries out of the 90 involved and is the most widely used reference worldwide.

### DSM

The American Psychiatric Association's Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR), released in 2022, is the current version of the DSM. It is the predominant mental health diagnostic system used in the United States and Canada, and is often used in Anglophone countries.

Its fifth edition, DSM-5, released in May 2013, was the first to define ASD as a single diagnosis,[40] which is still the case in the DSM-5-TR.[41] ASD encompasses previous diagnoses, including the four traditional diagnoses of autism—classic Kanner syndrome, Asperger syndrome, childhood disintegrative disorder, and pervasive developmental disorder not otherwise specified (PDD-NOS)—and the range of diagnoses that included the word "autism".[42] Rather than distinguishing among these diagnoses, the DSM-5 and DSM-5-TR adopt a dimensional approach with one diagnostic category for disorders that fall under the autism spectrum umbrella. Within that category, the DSM-5 and the DSM include a framework that differentiates each person by dimensions of symptom severity, as well as by associated features (i.e., the presence of other disorders or factors that likely contribute to the symptoms, other neurodevelopmental or mental disorders, intellectual disability, or language impairment).[41] The symptom domains are (a) social communication and (b) restricted, repetitive behaviors, and there is the option of specifying a separate severity—the negative effect of the symptoms on the person—for each domain, rather than just overall severity.[43] Before the DSM-5, the DSM separated social deficits and communication deficits into two domains.[44] Further, the DSM-5 changed to an onset age in the early developmental period, with a note that symptoms may manifest later when social demands exceed capabilities, rather than the previous, more restricted three years of age.[45] These changes remain in the DSM-5-TR.[41]

## Common characteristics

### Pre-diagnosis

For many autistic people, characteristics first appear during infancy or childhood and follow a steady course without remission (different developmental timelines are described in more detail below).[46] Autistic people may be severely impaired in some respects but average, or even superior, in others.[47][48][49]

Clinicians consider assessment for ASD when a patient shows:

* regular difficulties in social interaction or communication
* restricted or repetitive behaviors (often called "stimming")
* resistance to changes or restricted interests

These features are typically assessed with the following, when appropriate:

* problems in obtaining or sustaining employment or education
* difficulties in initiating or sustaining social relationships
* connections with mental health or learning disability services
* a history of neurodevelopmental conditions (including learning disabilities and ADHD) or mental health conditions.[50][51]

There are many signs associated with autism; the presentation varies widely:[52][53]

Common signs for autism spectrum disorder

* avoidance of eye-contact
* little or no babbling as an infant
* not showing interest in indicated objects
* delayed language skills (e.g. having a smaller vocabulary than peers or difficulty expressing themselves in words)
* reduced interest in other children or caretakers, possibly with more interest in objects
* difficulty playing reciprocal games (e.g. peek-a-boo)
* hyper- or hypo-sensitivity to or unusual response to the smell, texture, sound, taste, or appearance of things
* resistance to changes in routine
* repetitive, limited, or otherwise unusual usage of toys (e.g. lining up toys)
* repetition of words or phrases (echolalia)
* repetitive motions or movements, including stimming
* self-harming

### Broader autism phenotype

The broader autism phenotype (BAP) describes people who may not have ASD but do have autistic traits, such as avoiding eye contact and stimming.[54]

### Social and communication skills

According to the medical model, autistic people experience social communications impairments. Until 2013, deficits in social function and communication were considered two separate symptom domains.[55] The current social communication domain criteria for autism diagnosis require people to have deficits across three social skills: social-emotional reciprocity, nonverbal communication, and developing and sustaining relationships.[41]

A deficit-based view predicts that autistic–autistic interaction would be less effective than autistic–non-autistic interactions or even non-functional.[56] But recent research has found that autistic–autistic interactions are as effective in information transfer as interactions between non-autistics are, and that communication breaks down only between autistics and non-autistics.[56][57] Also contrary to social cognitive deficit interpretations, recent research recorded similar social cognitive performances in autistic and non-autistic adults, with both of them rating autistic individuals less favorably than non-autistic individuals; however, autistic individuals showed more interest in engaging with autistic people than non-autistic people did, and learning of a person's ASD diagnosis did not influence their interest level.[58]

Thus, there has been a recent shift to acknowledge that autistic people may simply respond and behave differently than people without ASD.[59] So far, research has identified two unconventional features by which autistic people create shared understanding (intersubjectivity): "a generous assumption of common ground that, when understood, led to rapid rapport, and, when not understood, resulted in potentially disruptive utterances; and a low demand for coordination that ameliorated many challenges associated with disruptive turns."[57] Autistic interests, and thus conversational topics, seem to be largely driven by an intense interest in specific topics (monotropism).[60][61]

Historically, autistic children were said to be delayed in developing a theory of mind, and the empathizing–systemizing theory has argued that while autistic people have compassion (affective empathy) for others with similar presentation of symptoms, they have limited, though not necessarily absent, cognitive empathy.[62] This may present as social naïvety,[63] lower than average intuitive perception of the utility or meaning of body language, social reciprocity,[64] and/or social expectations, including the habitus, social cues, and/or some aspects of sarcasm,[65] which to some degree may also be due to comorbid alexithymia.[66] But recent research has increasingly questioned these findings, as the "double empathy problem" theory (2012) argues that there is a lack of mutual understanding and empathy between both neurotypical persons and autistic individuals.[67][68][69][70][71]

As communication is bidirectional,[72] research on communication difficulties has since also begun to study non-autistic behavior, with researcher Catherine Crompton writing in 2020 that non-autistic people "struggle to identify autistic mental states, identify autistic facial expressions, overestimate autistic egocentricity, and are less willing to socially interact with autistic people. Thus, although non-autistic people are generally characterised as socially skilled, these skills may not be functional, or effectively applied, when interacting with autistic people."[56] Any previously observed communication deficits of autistic people may thus have been constructed through a neurotypical bias in autism research, which has come to be scrutinized for "dehumanization, objectification, and stigmatization".[73] Recent research has proposed that autistics' lack of readability and a neurotypical lack of effort to interpret atypical signals may cause a negative interaction loop, increasingly driving both groups apart into two distinct groups with different social interaction styles.[72]

Differences in verbal communication begin to be noticeable in childhood, as many autistic children develop language skills at an uneven pace. Verbal communication may be delayed or never develop (nonverbal autism), while reading ability may be present before school age (hyperlexia).[74][75] Reduced joint attention seem to distinguish autistic from neurotypical infants.[76] Infants may show delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children may have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences and more likely to simply repeat others' words (echolalia).[77] The CDC estimated in 2015 that around 40% of autistic children do not speak at all.[78] Autistic adults' verbal communication skills largely depend on when and how well speech is acquired during childhood.[74]

Temple Grandin in 2011

Autistic people display atypical nonverbal behaviors or show differences in nonverbal communication. They may make infrequent eye contact, even when called by name, or avoid it altogether. Autistic people often recognize fewer emotions and their meaning from others' facial expressions, and may not respond with facial expressions expected by their non-autistic peers.[79][75] Temple Grandin, an autistic woman involved in autism activism, described her inability to understand neurotypicals' social communication as leaving her feeling "like an anthropologist on Mars".[80] Autistic people struggle to understand the social context and subtext of neurotypical conversational or printed situations, and form different conclusions about the content.[81] Autistic people may not control the volume of their voice in different social settings.[82] At least half of autistic children have unusual prosody.[82]

What may look like self-involvement or indifference to non-autistic people stems from autistic differences in recognizing how other people have their own personalities, perspectives, and interests.[81][83] Most published research focuses on the interpersonal relationship difficulties between autistic people and their non-autistic counterparts and how to solve them through teaching neurotypical social skills, but newer research has also evaluated what autistic people want from friendships, such as a sense of belonging and good mental health.[84][85] Children with ASD are more frequently involved in bullying situations than their neurotypical peers, and predominantly experience bullying as victims rather than perpetrators or victim-perpetrators, especially after controlling for comorbid psychopathology.[86] Prioritizing dependability and intimacy in friendships during adolescence, coupled with lowered friendship quantity and quality, often lead to increased loneliness in autistic people.[87] As they progress through life, autistic people observe and form a model of social patterns, and develop coping mechanisms, referred to as "masking",[88][89] which has recently been found to come with psychological costs and a highly increased risk of suicidality.[72]

### Restricted and repetitive behaviors

A young autistic boy who has arranged his toys in a row

ASD includes a wide variety of characteristics. Some of these include behavioral characteristics which widely range from slow development of social and learning skills to difficulties creating connections with other people. Autistic people may experience these challenges with forming connections due to anxiety or depression, which they are more likely to experience, and as a result isolate themselves.[90]

Other behavioral characteristics include abnormal responses to sensations (such as sights, sounds, touch, taste and smell) and problems keeping a consistent speech rhythm. The latter problem influences social skills, leading to potential problems in understanding for interlocutors. Autistic people's behavioral characteristics typically influence development, language, and social competence. Their behavioral characteristics can be observed as perceptual disturbances, disturbances of development rate, relating, speech and language, and motility.[91]

The second core symptom of autism spectrum is a pattern of restricted and repetitive behaviors, activities, and interests. In order to be diagnosed with ASD under the DSM-5-TR, a person must have at least two of the following behaviors:[41][92]

* An older autistic boy arranging brads on a cork coaster. Repetitive behaviors – Repetitive behaviors such as rocking, hand flapping, finger flicking, head banging, or repeating phrases or sounds.[93] These behaviors may occur constantly or only when the person gets stressed, anxious or upset. These behaviors are also known as stimming.
* Resistance to change – A strict adherence to routines such as eating certain foods in a specific order or taking the same path to school every day.[93] The person may become distressed if there is a change or disruption to their routine.
* Restricted interests – An excessive interest in a particular activity, topic, or hobby, and devoting all their attention to it. For example, young children might completely focus on things that spin and ignore everything else. Older children might try to learn everything about a single topic, such as the weather or sports, and perseverate or talk about it constantly.[93]
* Sensory reactivity – An unusual reaction to certain sensory inputs, such as negative reaction to specific sounds or textures, fascination with lights or movements, or apparent indifference to pain or heat.[94]

Autistic people can display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.[95]

* Stereotyped behaviors: Repetitive movements, such as hand flapping, head rolling, or body rocking.
* Compulsive behaviors: Time-consuming behaviors intended to reduce anxiety, that a person feels compelled to perform repeatedly or according to rigid rules, such as placing objects in a specific order, checking things, or handwashing.
* Sameness: Resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
* Ritualistic behavior: Unvarying pattern of daily activities, such as an unchanging menu or a dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.[95]
* Restricted interests: Interests or fixations that are abnormal in theme or intensity of focus, such as preoccupation with a single television program, toy, or game.
* Self-injury: Behaviors such as eye-poking, skin-picking, hand-biting and head-banging.[76]

#### Self-injury

Self-injurious behaviors (SIB) are relatively common in autistic people, and can include head-banging, self-cutting, self-biting, and hair-pulling.[96] Some of these can result in serious injury or death.[96] Following are theories about the cause of self-injurious behavior in children with developmental delay, including autistic children:[97]

* Frequency and/or continuation of self-injurious behavior can be influenced by environmental factors (e.g. reward in return for halting self-injurious behavior). This theory does not apply to younger children with autism. There is some evidence that frequency of self-injurious behavior can be reduced by removing or modifying environmental factors that reinforce the behavior.[97]: 10–12
* Higher rates of self-injury are also noted in socially isolated people with autism. Studies have shown that socialization skills are related factors to self-injurious behavior for people with autism.[98]
* Self-injury could be a response to modulate pain perception when chronic pain or other health problems that cause pain are present.[97]: 12–13
* An abnormal basal ganglia connectivity may predispose to self-injurious behavior.[97]: 13

The suicide rate for verbal autistics is nine times that of the general population.[99]

### Other features

Autistic people may have symptoms that do not contribute to the official diagnosis, but that can affect the person or the family.[100]

* Some people with ASD show unusual or notable abilities, ranging from splinter skills (such as the memorization of trivia) to rare talents in mathematics, music, or artistic reproduction, which in exceptional cases are considered a part of the savant syndrome.[101][102][103] One study describes how some people with ASD show superior skills in perception and attention relative to the general population.[104] Sensory abnormalities are found in over 90% of autistic people, and are considered core features by some.[105]
* More generally, autistic people tend to show a "spiky skills profile", with strong abilities in some areas contrasting with much weaker abilities in others.[106]
* Differences between the previously recognized disorders under the autism spectrum are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements).[107] An estimated 60–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking;[105][108] deficits in motor coordination are pervasive across ASD and are greater in autism proper.[109][110]
* Pathological demand avoidance can occur. People with this set of autistic symptoms are more likely to refuse to do what is asked or expected of them, even to activities they enjoy.
* Unusual or atypical eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator.[100] Selectivity is the most common problem, although eating rituals and food refusal also occur.[111]

## Possible causes

Main article: Social:Causes of autism

Exactly what causes autism remains unknown.[112][113][114][115] It was long mostly presumed that there is a common cause at the genetic, cognitive, and neural levels for the social and non-social components of ASD's symptoms, described as a triad in the classic autism criteria.[116] But it is increasingly suspected that autism is instead a complex disorder whose core aspects have distinct causes that often cooccur.[116][117] It is unlikely that ASD has a single cause;[117] many risk factors identified in the research literature may contribute to ASD. These include genetics, prenatal and perinatal factors (meaning factors during pregnancy or very early infancy), neuroanatomical abnormalities, and environmental factors. It is possible to identify general factors, but much more difficult to pinpoint specific ones. Given the current state of knowledge, prediction can only be of a global nature and so requires the use of general markers.[118]

### Biological subgroups

Research into causes has been hampered by the inability to identify biologically meaningful subgroups within the autistic population[119] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.[120] Newer technologies such as fMRI and diffusion tensor imaging can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism;[121] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.[122] It has been proposed to classify autism using genetics as well as behavior.[123]

#### Syndromic autism and non-syndromic autism

Main article: Medicine:Syndromic autism

Autism spectrum disorder (ASD) can be classified into two categories: "syndromic autism" and "non-syndromic autism."

Syndromic autism refers to cases where ASD is one of the characteristics associated with a broader medical condition or syndrome, representing about 25% of ASD cases. The causes of syndromic autism are often known, and monogenic disorders account for approximately 5% of these cases.

Non-syndromic autism, also known as classic or idiopathic autism, represents the majority of cases, and its cause is typically polygenic and unknown.

### Genetics

Main article: Medicine:Heritability of autism

Hundreds of different genes are implicated in susceptibility to developing autism,[124] most of which alter the brain structure in a similar way.

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by rare mutations with major effects, or by rare multi-gene interactions of common genetic variants.[125][126] Complexity arises due to interactions among multiple genes, the environment, and epigenetic factors which do not change DNA sequencing but are heritable and influence gene expression.[127] Many genes have been associated with autism through sequencing the genomes of affected people and their parents.[128] But most of the mutations that increase autism risk have not been identified. Typically, autism cannot be traced to a Mendelian (single-gene) mutation or to a single chromosome abnormality, and none of the genetic syndromes associated with ASD have been shown to selectively cause ASD.[125] Numerous genes have been found, with only small effects attributable to any particular gene.[125] Most loci individually explain less than 1% of cases of autism.[129] As of 2018[update], it appeared that between 74% and 93% of ASD risk is heritable.[92] After an older child is diagnosed with ASD, 7% to 20% of subsequent children are likely to be as well.[92] If parents have one autistic child, they have a 2% to 8% chance of having a second child who is autistic. If the autistic child is an identical twin, the other will be affected 36% to 95% of the time. A fraternal twin is affected up to 31% of the time. The large number of autistic people with unaffected family members may result from spontaneous structural variation, such as deletions, duplications or inversions in genetic material during meiosis.[130][131] Hence, a substantial fraction of autism cases may be traceable to genetic causes that are highly heritable but not inherited: that is, the mutation that causes the autism is not present in the parental genome.[132][verification needed]

As of 2018[update], understanding of genetic risk factors had shifted from a focus on a few alleles to an understanding that genetic involvement in ASD is probably diffuse, depending on a large number of variants, some of which are common and have a small effect, and some of which are rare and have a large effect. The most common gene disrupted with large effect rare variants appeared to be CHD8, but less than 0.5% of autistic people have such a mutation. The gene CHD8 encodes the protein chromodomain helicase DNA binding protein 8, which is a chromatin regulator enzyme that is essential during fetal development, CHD8 is an ATP dependent enzyme.[133][134][135] The protein contains an Snf2 helicase domain that is responsible for the hydrolysis of ATP to ADP.[135] CHD8 encodes for a DNA helicase that function as a transcription repressor by remodeling chromatin structure by altering the position of nucleosomes. CHD8 negatively regulates Wnt signaling. Wnt signaling is important in the vertebrate early development and morphogenesis. It is believed that CHD8 also recruits the linker histone H1 and causes the repression of β-catenin and p53 target genes.[133] The importance of CHD8 can be observed in studies where CHD8-knockout mice died after 5.5 embryonic days because of widespread p53 induced apoptosis. Some studies have determined the role of CHD8 in autism spectrum disorder (ASD). CHD8 expression significantly increases during human mid-fetal development.[133] The chromatin remodeling activity and its interaction with transcriptional regulators have shown to play an important role in ASD aetiology.[134] The developing mammalian brain has a conserved CHD8 target regions that are associated with ASD risk genes.[136] The knockdown of CHD8 in human neural stem cells results in dysregulation of ASD risk genes that are targeted by CHD8.[137] Recently CD8 has been associated to the regulation of long non-coding RNAs (lncRNAs),[138] and the regulation of X chromosome inactivation (XCI) initiation, via regulation of Xist long non-coding RNA,[ambiguous] the master regulator of XCI,[ambiguous] though competitive binding to Xist regulatory regions.[139]

Some ASD is associated with clearly genetic conditions, like fragile X syndrome, but only around 2% of autistic people have fragile X.[92] Hypotheses from evolutionary psychiatry suggest that these genes persist because they are linked to human inventiveness, intelligence or systemising.[140][141]

Current research suggests that genes that increase susceptibility to ASD are ones that control protein synthesis in neuronal cells in response to cell needs, activity and adhesion of neuronal cells, synapse formation and remodeling, and excitatory to inhibitory neurotransmitter balance. Therefore, although up to 1,000 different genes are thought to increase the risk of ASD, all of them eventually affect normal neural development and connectivity between different functional areas of the brain in a similar manner that is characteristic of an ASD brain. Some of these genes are known to modulate production of the GABA neurotransmitter, the nervous system's main inhibitory neurotransmitter. These GABA-related genes are under-expressed in an ASD brain. On the other hand, genes controlling expression of glial and immune cells in the brain, e.g. astrocytes and microglia, respectively, are over-expressed, which correlates with increased number of glial and immune cells found in postmortem ASD brains. Some genes under investigation in ASD pathophysiology are those that affect the mTOR signaling pathway, which supports cell growth and survival.[142]

All these genetic variants contribute to the development of the autism spectrum, but it cannot be guaranteed that they are determinants for the development.[143]

ASD may be under-diagnosed in women and girls due to an assumption that it is primarily a male condition,[144] but genetic phenomena such as imprinting and X linkage have the ability to raise the frequency and severity of conditions in males, and theories have been put forward for a genetic reason why males are diagnosed more often, such as the imprinted brain hypothesis and the extreme male brain theory.[145][146][147]

### Early life

Several prenatal and perinatal complications have been reported as possible risk factors for autism. These risk factors include maternal gestational diabetes, maternal and paternal age over 30, bleeding during pregnancy after the first trimester, use of certain prescription medication (e.g. valproate) during pregnancy, and meconium in the amniotic fluid. Research is not conclusive on the relation of these factors to autism, but each of them has been identified more frequently in children with autism compared to their siblings who do not have autism and other typically developing youth.[148] While it is unclear if any single factors during the prenatal phase affect the risk of autism,[149] complications during pregnancy may be a risk.[149]

There are also studies being done to test whether certain types of regressive autism have an autoimmune basis.[150]

Maternal nutrition and inflammation during preconception and pregnancy influences fetal neurodevelopment. Intrauterine growth restriction is associated with ASD, in both term and preterm infants.[151] Maternal inflammatory and autoimmune diseases may damage fetal tissues, aggravating a genetic problem or damaging the nervous system.[152]

Exposure to air pollution during child pregnancy, especially heavy metals and particulates, may increase the risk of autism.[153][154] Environmental factors that have been claimed without evidence to contribute to or exacerbate autism include certain foods, infectious diseases, solvents, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,[155] and prenatal stress. Some, such as the MMR vaccine, have been completely disproven.[156][157][158][159]

#### Disproven vaccine hypothesis

Main articles: Unsolved:Vaccines and autism and Social:MMR vaccine and autism

Parents may first become aware of ASD symptoms in their child around the time of a routine vaccination. This has led to unsupported and disproven theories blaming vaccine "overload", the vaccine preservative thiomersal, or the MMR vaccine for causing autism spectrum disorder.[160] In 1998, British physician and academic Andrew Wakefield led a fraudulent, litigation-funded study that suggested that the MMR vaccine may cause autism.[161][162][163][164][165]

Two versions of the vaccine causation hypothesis were that autism results from brain damage caused by either the MMR vaccine itself, or by mercury used as a vaccine preservative.[166] No convincing scientific evidence supports these claims.[12] They are biologically implausible,[160] and further evidence continues to refute them, including the observation that the rate of autism continues to climb despite elimination of thimerosal from most routine vaccines given to children from birth to 6 years of age.[167][168][169][170][171]

A 2014 meta-analysis examined ten major studies on autism and vaccines involving 1.25 million children worldwide; it concluded that neither the vaccine preservative thimerosal (mercury), nor the MMR vaccine, which has never contained thimerosal,[172] lead to the development of ASDs.[173] Despite this, misplaced parental concern has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.[174][175]

### Etiological hypotheses

Several hypotheses have been presented that try to explain how and why autism develops by integrating known causes (genetic and environmental effects) and findings (neurobiological and somatic). Some are more comprehensive, such as the Pathogenetic Triad, which proposes and operationalizes three core features (an autistic personality, cognitive compensation, neuropathological burden) that interact to cause autism,[176] and the Intense World Theory, which explains autism through a hyper-active neurobiology that leads to an increased perception, attention, memory, and emotionality.[177] There are also simpler hypotheses that explain only individual parts of the neurobiology or phenotype of autism, such as mind-blindness (a decreased ability for theory of mind), the weak central coherence theory, or the extreme male brain and empathising–systemising theory.

### Evolutionary hypotheses

Research exploring the evolutionary benefits of autism and associated genes has suggested that autistic people may have played a "unique role in technological spheres and understanding of natural systems" in the course of human development.[178][179] It has been suggested that it may have arisen as "a slight trade off for other traits that are seen as highly advantageous", providing "advantages in tool making and mechanical thinking", with speculation that the condition may "reveal itself to be the result of a balanced polymorphism, like sickle cell anemia, that is advantageous in a certain mixture of genes and disadvantageous in specific combinations".[180]

In 2011, a paper in Evolutionary Psychology proposed that autistic traits, including increased abilities for spatial intelligence, concentration and memory, could have been naturally selected to enable self-sufficient foraging in a more (although not completely) solitary environment, referred to as the "Solitary Forager Hypothesis".[181][182][183] A 2016 paper examines Asperger syndrome as "an alternative prosocial adaptive strategy" which may have developed as a result of the emergence of "collaborative morality" in the context of small-scale hunter-gathering, i.e. where "a positive social reputation for making a contribution to group wellbeing and survival" becomes more important than complex social understanding.[184]

Conversely, some multidisciplinary research suggests that recent human evolution may be a driving force in the rise of a number of medical conditions in recent human populations, including autism. Studies in evolutionary medicine indicate that as biological evolution becomes outpaced by cultural evolution, disorders linked to bodily dysfunction increase in prevalence due to a lack of contact with pathogens and negative environmental conditions that once widely affected ancestral populations. Because natural selection primarily favors reproduction over health and longevity, the lack of this impetus to adapt to certain harmful circumstances creates a tendency for genes in descendant populations to over-express themselves, which may cause a wide array of maladies, ranging from mental disorders to autoimmune diseases.[185]

## Pathophysiology

Main articles: Biology:Mechanism of autism and Biology:Pathophysiology of autism

## Diagnosis

Main article: Biology:Diagnosis of autism

## Conditions correlated or comorbid to autism

Main article: Medicine:Conditions comorbid to autism spectrum disorders

Autism is correlated or comorbid with several personality traits/disorders.[122] Comorbidity may increase with age and may worsen the course of youth with ASDs and make intervention and treatment more difficult. Distinguishing between ASDs and other diagnoses can be challenging because the traits of ASDs often overlap with symptoms of other disorders, and the characteristics of ASDs make traditional diagnostic procedures difficult.[186][187]

### Correlations

Research indicates that autistic people are significantly more likely to be LGBT than the general population.[188] There is tentative evidence that gender dysphoria occurs more frequently in autistic people.[189][190] A 2021 anonymized online survey of 16- to 90-year-olds revealed that autistic males are more likely to identify as bisexual than their non-autistic peers, while autistic females are more likely to identify as homosexual than non-autistic females do.[191]

People on the autism spectrum are significantly more likely to be non-theistic than members of the general population.[192]

### Comorbidities

* The most common medical condition occurring in people with ASDs is seizure disorder or epilepsy, which occurs in 11–39% of autistic people.[193] The risk varies with age, cognitive level, and type of language disorder.[194]
* Tuberous sclerosis, an autosomal dominant genetic condition in which non-malignant tumors grow in the brain and on other vital organs, is present in 1–4% of people with ASDs.[195]
* Intellectual disabilities are some of the most common comorbid disorders with ASDs. As diagnosis is increasingly being given to people with higher functioning autism, there is a tendency for the proportion with comorbid intellectual disability to decrease over time. In a 2019 study, it was estimated that approximately 30-40% of people diagnosed with ASD also have intellectual disability.[196] Recent research has suggested that autistic people with intellectual disability tend to have rarer, more harmful, genetic mutations than those found in people solely diagnosed with autism.[197] A number of genetic syndromes causing intellectual disability may also be comorbid with ASD, including fragile X, Down, Prader-Willi, Angelman, Williams syndrome,[198] branched-chain keto acid dehydrogenase kinase deficiency,[199][200] and SYNGAP1-related intellectual disability.[201][202]
* Learning disabilities are also highly comorbid in people with an ASD. Approximately 25–75% of people with an ASD also have some degree of a learning disability.[203]
* Various anxiety disorders tend to co-occur with ASDs, with overall comorbidity rates of 7–84%.[204] They are common among children with ASD; there are no firm data, but studies have reported prevalences ranging from 11% to 84%. Many anxiety disorders have symptoms that are better explained by ASD itself, or are hard to distinguish from ASD's symptoms.[205]
* Rates of comorbid depression in people with an ASD range from 4–58%.[206]
* The relationship between ASD and schizophrenia remains a controversial subject under continued investigation, and recent meta-analyses have examined genetic, environmental, infectious, and immune risk factors that may be shared between the two conditions.[207][208][209] Oxidative stress, DNA damage and DNA repair have been postulated to play a role in the aetiopathology of both ASD and schizophrenia.[210]
* Deficits in ASD are often linked to behavior problems, such as difficulties following directions, being cooperative, and doing things on other people's terms.[211] Symptoms similar to those of attention deficit hyperactivity disorder (ADHD) can be part of an ASD diagnosis.[212]
* Sensory processing disorder is also comorbid with ASD, with comorbidity rates of 42–88%.[213]
* Starting in adolescence, some people with Asperger syndrome (26% in one sample)[214] fall under the criteria for the similar condition schizoid personality disorder, which is characterized by a lack of interest in social relationships, a tendency towards a solitary or sheltered lifestyle, secretiveness, emotional coldness, detachment and apathy.[214][215][216] Asperger syndrome was traditionally called "schizoid disorder of childhood."
* Genetic disorders \- about 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndromes.[217]
* Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms.[218][verification needed]
* Gastrointestinal problems are one of the most commonly co-occurring medical conditions in autistic people.[219] These are linked to greater social impairment, irritability, language impairments, mood changes, and behavior and sleep problems.[219][220][221] A 2015 review proposed that immune, gastrointestinal inflammation, malfunction of the autonomic nervous system, gut flora alterations, and food metabolites may cause brain neuroinflammation and dysfunction.[220] A 2016 review concludes that enteric nervous system abnormalities might play a role in neurological disorders such as autism. Neural connections and the immune system are a pathway that may allow diseases originated in the intestine to spread to the brain.[221]
* Sleep problems affect about two-thirds of people with ASD at some point in childhood. These most commonly include symptoms of insomnia, such as difficulty falling asleep, frequent nocturnal awakenings, and early morning awakenings. Sleep problems are associated with difficult behaviors and family stress, and are often a focus of clinical attention over and above the primary ASD diagnosis.[222]
* Dysautonomia is common in ASD, affecting heart rate and blood pressure and causing symptoms such as brain fog, blurry vision, and bowel dysfunction.[223] It can be diagnosed through a Tilt table test.[224]
* The frequency of ASD is 10 times higher in Mast cell activation syndrome patients than in the general population. This immunological condition causes cardiovascular, dermatological, gastrointestinal, neurological, and respiratory problems.[225]

## Management

Main article: Medicine:Autism therapies

There is no treatment as such for autism,[226] and many sources advise that this is not an appropriate goal,[227][228] although treatment of co-occurring conditions remains an important goal.[229] There is no cure for autism as of 2023, nor can any of the known treatments significantly reduce brain mutations caused by autism, although those who require little to no support are more likely to experience a lessening of symptoms over time.[230][231][232] Several interventions can help children with autism,[233] and no single treatment is best, with treatment typically tailored to the child's needs.[234] Studies of interventions have methodological problems that prevent definitive conclusions about efficacy,[235] but the development of evidence-based interventions has advanced.[236]

The main goals of treatment are to lessen associated deficits and family distress, and to increase quality of life and functional independence. In general, higher IQs are correlated with greater responsiveness to treatment and improved treatment outcomes.[237][19] Behavioral, psychological, education, and/or skill-building interventions may be used to assist autistic people to learn life skills necessary for living independently,[238] as well as other social, communication, and language skills. Therapy also aims to reduce challenging behaviors and build upon strengths.[239]

Intensive, sustained special education programs and behavior therapy early in life may help children acquire self-care, language, and job skills.[234] Although evidence-based interventions for autistic children vary in their methods, many adopt a psychoeducational approach to enhancing cognitive, communication, and social skills while minimizing problem behaviors. While medications have not been found to help with core symptoms, they may be used for associated symptoms, such as irritability, inattention, or repetitive behavior patterns.[240]

### Non-pharmacological interventions

Intensive, sustained special education or remedial education programs and behavior therapy early in life may help children acquire self-care, social, and job skills. Available approaches include applied behavior analysis, developmental models, structured teaching, speech and language therapy, cognitive behavioral therapy,[241] social skills therapy, and occupational therapy.[242] Among these approaches, interventions either treat autistic features comprehensively, or focus treatment on a specific area of deficit.[19] Generally, when educating those with autism, specific tactics may be used to effectively relay information to these people. Using as much social interaction as possible is key in targeting the inhibition autistic people experience concerning person-to-person contact. Additionally, research has shown that employing semantic groupings, which involves assigning words to typical conceptual categories, can be beneficial in fostering learning.[243]

There has been increasing attention to the development of evidence-based interventions for autistic young children. Three theoretical frameworks outlined for early childhood intervention include applied behavior analysis (ABA), the developmental social-pragmatic model (DSP) and cognitive behavioral therapy (CBT).[241][19] Although ABA therapy has a strong evidence base, particularly in regard to early intensive home-based therapy, ABA's effectiveness may be limited by diagnostic severity and IQ of the person affected by ASD.[244] The Journal of Clinical Child and Adolescent Psychology has published a paper deeming two early childhood interventions "well-established": individual comprehensive ABA, and focused teacher-implemented ABA combined with DSP.[19]

Another evidence-based intervention that has demonstrated efficacy is a parent training model, which teaches parents how to implement various ABA and DSP techniques themselves.[19] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation.

In October 2015, the American Academy of Pediatrics (AAP) proposed new evidence-based recommendations for early interventions in ASD for children under 3.[245] These recommendations emphasize early involvement with both developmental and behavioral methods, support by and for parents and caregivers, and a focus on both the core and associated symptoms of ASD.[245] But a Cochrane review found no evidence that early intensive behavioral intervention (EIBI) is effective in reducing behavioral problems associated with autism in most autistic children, though it did improve IQ and language skills.[246] The Cochrane review acknowledged that this may be due to the low quality of studies available on EIBI and therefore providers should recommend EIBI based on their clinical judgment and the family's preferences.[246] No adverse effects of EIBI treatment were found.[246] A meta-analysis in that same database indicates that due to the degrees of severity in ASD, there is variable responses to differing early ABA interventions.[20]

ASD treatment generally focuses on behavioral and educational interventions to target its two core symptoms: social communication deficits and restricted, repetitive behaviors.[247] If symptoms continue after behavioral strategies have been implemented, some medications can be recommended to target specific symptoms or co-existing problems such as restricted and repetitive behaviors (RRBs), anxiety, depression, hyperactivity/inattention and sleep disturbance.[247] Melatonin, for example, can be used for sleep problems.[248]

Several parent-mediated behavioral therapies target social communication deficits in children with autism, but their efficacy in treating RRBs is uncertain.[249]

#### Education

An autistic three-year-old points to fish in an aquarium, as part of an experiment on the effect of intensive shared-attention training on language development.[250]

Educational interventions often used include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy and social skills therapy.[234] Among these approaches, interventions either treat autistic features comprehensively, or focalize treatment on a specific area of deficit.[236]

The quality of research for early intensive behavioral intervention (EIBI)—a treatment procedure incorporating over thirty hours per week of the structured type of ABA that is carried out with very young children—is low; more vigorous research designs with larger sample sizes are needed.[246] Two theoretical frameworks outlined for early childhood intervention include structured and naturalistic ABA interventions, and developmental social pragmatic models (DSP).[236] One interventional strategy utilizes a parent training model, which teaches parents how to implement various ABA and DSP techniques, allowing for parents to disseminate interventions themselves.[236] Various DSP programs have been developed to explicitly deliver intervention systems through at-home parent implementation. Despite the recent development of parent training models, these interventions have demonstrated effectiveness in numerous studies, being evaluated as a probable efficacious mode of treatment.[236] Early, intensive ABA therapy has demonstrated effectiveness in enhancing communication and adaptive functioning in preschool children;[234][251] it is also well-established for improving the intellectual performance of that age group.[234]

In 2018, a Cochrane meta-analysis database concluded that some recent research is beginning to suggest that because of the heterology of ASD, there are two different ABA teaching approaches to acquiring spoken language: children with more general expressive language delays respond sufficiently to the naturalistic approach, whereas children with significant receptive language delays require discrete trial training—the structured and intensive form of ABA.[20] A 2023 semi-randomized control trial study of 168 participants showed similar findings.[21]

Similarly, a teacher-implemented intervention that utilizes a more naturalistic form of ABA combined with a developmental social pragmatic approach has been found to be beneficial in improving social-communication skills in young children, although there is less evidence in its treatment of global symptoms.[236] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.[252] The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.[253]

### Pharmacological interventions

Medications may be used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.[254] They may also be used for associated health problems, such as ADHD, anxiety, or if the person is hurting themself or aggressive with others,[254][255] but their routine prescription for ASD's core features is not recommended.[256] More than half of US children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.[257][258] The atypical antipsychotic drugs risperidone and aripiprazole are FDA-approved for treating associated aggressive and self-injurious behaviors.[240][259] But their side effects must be weighed against their potential benefits, and autistic people may respond atypically.[240] Side effects may include weight gain, tiredness, drooling, and aggression.[240] Some emerging data show positive effects of aripiprazole and risperidone on restricted and repetitive behaviors (i.e., stimming; e.g., flapping, twisting, complex whole-body movements),[256] but due to the small sample size and different focus of these studies and the concerns about its side effects, antipsychotics are not recommended as primary treatment of RRBs.[260] SSRI antidepressants, such as fluoxetine and fluvoxamine, have been shown to be effective in reducing repetitive and ritualistic behaviors, while the stimulant medication methylphenidate is beneficial for some children with co-morbid inattentiveness or hyperactivity.[234] There is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[261] No known medication relieves autism's core symptoms of social and communication impairments.[240]

### Alternative medicine

A multitude of alternative therapies have been researched and implemented. Many have resulted in harm to autistic people.[242] A 2020 systematic review on adults with autism provided evidence that mindfulness-based interventions may decrease stress, anxiety, ruminating thoughts, anger, and aggression and improve mental health.[262]

Although popularly used as an alternative treatment for autistic people, as of 2018[update] there is no good evidence to recommend a gluten- and casein-free diet as a standard treatment.[263][264][265] A 2018 review concluded that it may be a therapeutic option for specific groups of children with autism, such as those with known food intolerances or allergies, or with food intolerance markers. The authors analyzed the prospective trials conducted to date that studied the efficacy of the gluten- and casein-free diet in children with ASD (4 in total). All of them compared gluten- and casein-free diet versus normal diet with a control group (2 double-blind randomized controlled trials, 1 double-blind crossover trial, 1 single-blind trial). In two of the studies, whose duration was 12 and 24 months, a significant improvement in ASD symptoms (efficacy rate 50%) was identified. In the other two studies, whose duration was 3 months, no significant effect was observed.[263] The authors concluded that a longer duration of the diet may be necessary to achieve the improvement of the ASD symptoms.[263] Other problems documented in the trials carried out include transgressions of the diet, small sample size, the heterogeneity of the participants and the possibility of a placebo effect.[265][266][267] In the subset of people who have gluten sensitivity there is limited evidence that suggests that a gluten-free diet may improve some autistic behaviors.[268][269][270]

The preference that autistic children have for unconventional foods can lead to reduction in bone cortical thickness with this risk being greater in those on casein-free diets, as a consequence of the low intake of calcium and vitamin D; however, suboptimal bone development in ASD has also been associated with lack of exercise and gastrointestinal disorders.[271] In 2005, botched chelation therapy killed a five-year-old child with autism.[272][273] Chelation is not recommended for autistic people since the associated risks outweigh any potential benefits.[274] Another alternative medicine practice with no evidence is CEASE therapy, a pseudoscientific mixture of homeopathy, supplements, and "vaccine detoxing".[275]

Results of a systematic review on interventions to address health outcomes among autistic adults found emerging evidence to support mindfulness-based interventions for improving mental health. This includes decreasing stress, anxiety, ruminating thoughts, anger, and aggression.[276] An updated Cochrane review (2022) found evidence that music therapy likely improves social interactions, verbal communication, and nonverbal communication skills.[277] There has been early research on hyperbaric treatments in children with autism.[278] Studies on pet therapy have shown positive effects.[279]

### Prevention

While infection with rubella during pregnancy causes fewer than 1% of cases of autism,[280] vaccination against rubella can prevent many of those cases.[281]

## Prognosis

Main article: Biology:Prognosis of autism

There is no evidence of a cure for autism.[234][122] The degree of symptoms can decrease, occasionally to the extent that people lose their diagnosis of ASD;[282][283] this occurs sometimes after intensive treatment[284] and sometimes not. It is not known how often this outcome happens,[285] with reported rates in unselected samples ranging from 3% to 25%.[282][283] Although core difficulties tend to persist, symptoms often become less severe with age.[127] Acquiring language before age six, having an IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely in autistic people with higher support needs.[286]

The prognosis of autism describes the developmental course, gradual autism development, regressive autism development, differential outcomes, academic performance and employment.

## Epidemiology

Main article: Medicine:Epidemiology of autism

Reports of autism cases per 1,000 children rose considerably in the US from 1996 to 2007. It is unknown how much growth came from changes in rates of autism.

The World Health Organization (WHO) estimates about 1 in 100 children had autism during the period from 2012 to 2021 as that was the average estimate in studies published during that period with a trend of increasing prevalence over time. However, the study's 1% figure may reflect an underestimate of prevalence in low- and middle-income countries.[5][287] The number of people diagnosed has increased considerably since the 1990s, which may be partly due to increased recognition of the condition.[288]

While rates of ASD are consistent across cultures, they vary greatly by gender, with boys diagnosed far more frequently than girls: 1 in 70 boys, but only 1 in 315 girls at eight years of age.[289] Girls, however, are more likely to have associated cognitive impairment, suggesting that less severe forms of ASD are likely being missed in girls and women.[290] Prevalence differences may be a result of gender differences in expression of clinical symptoms, with women and girls with autism showing less atypical behaviors and, therefore, less likely to receive an ASD diagnosis.[291]

Using DSM-5 criteria, 92% of the children diagnosed per DSM-IV with one of the disorders which is now considered part of ASD will still meet the diagnostic criteria of ASD. However, if both ASD and the social (pragmatic) communication disorder categories of DSM-5 are combined, the prevalence of autism is mostly unchanged from the prevalence per the DSM-IV criteria. The best estimate for prevalence of ASD is 0.7% or 1 child in 143 children.[292] Relatively mild forms of autism, such as Asperger's as well as other developmental disorders, are included in the DSM-5 diagnostic criteria.[293] ASD rates were constant between 2014 and 2016 but twice the rate compared to the time period between 2011 and 2014 (1.25 vs 2.47%). A Canadian meta-analysis from 2019 confirmed these effects as the profiles of people diagnosed with autism became less and less different from the profiles of the general population.[294] In the US, the rates for diagnosed ASD have been steadily increasing since 2000 when records began being kept.[295] While it remains unclear whether this trend represents a true rise in incidence, it likely reflects changes in ASD diagnostic criteria, improved detection, and increased public awareness of autism.[296] In 2012, the NHS estimated that the overall prevalence of autism among adults aged 18 years and over in the UK was 1.1%.[297] A 2016 survey in the United States reported a rate of 25 per 1,000 children for ASD.[298] Rates of autism are poorly understood in many low- and middle-income countries, which affects the accuracy of global ASD prevalence estimates,[299] but it is thought that most autistic people live in low- and middle-income countries.[300]

In 2020, the Centers for Disease Control's Autism and Developmental Disabilities Monitoring (ADDM) Network reported that approximately 1 in 54 children in the United States (1 in 34 boys, and 1 in 144 girls) is diagnosed with an autism spectrum disorder (ASD), based on data collected in 2016.[301][302] This estimate is a 10% increase from the 1 in 59 rate in 2014, a 105% increase from the 1 in 110 rate in 2006, and a 176% increase from the 1 in 150 rate in 2000.[301] Diagnostic criteria for ASD have changed significantly since the 1980s; for example, U.S. special-education autism classification was introduced in 1994.[155]

In the UK, from 1998 to 2018, the autism diagnoses increased by 787%.[288] This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness[303][304][305] (particularly among women),[288] though unidentified environmental risk factors cannot be ruled out.[306] The available evidence does not rule out the possibility that autism's true prevalence has increased;[303] a real increase would suggest directing more attention and funding toward psychosocial factors and changing environmental factors instead of continuing to focus on genetics.[307] It has been established that vaccination is not a risk factor for autism and is not a cause of any increase in autism prevalence rates, if any change in the rate of autism exists at all.[173]

Males have higher likelihood of being diagnosed with ASD than females. The sex ratio averages 4.3:1 and is greatly modified by cognitive impairment: it may be close to 2:1 with intellectual disability and more than 5.5:1 without.[155] Several theories about the higher prevalence in males have been investigated, but the cause of the difference is unconfirmed;[308] one theory is that females are underdiagnosed.[309]

The risk of developing autism is greater with older fathers than with older mothers; two potential explanations are the known increase in mutation burden in older sperm, and the hypothesis that men marry later if they carry genetic liability and show some signs of autism.[28] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.[310]

## History

Main article: Medicine:History of autism

## Society and culture

An autistic culture has emerged, accompanied by the autistic rights and neurodiversity movements, that argues autism should be accepted as a difference to be accommodated instead of cured,[311][312][313][314][315] although a minority of autistic people might still accept a cure.[316] Worldwide, events related to autism include World Autism Awareness Day, Autism Sunday, Autistic Pride Day, Autreat, and others.[317][318][319][320]

Social-science scholars study those with autism in hopes to learn more about "autism as a culture, transcultural comparisons ... and research on social movements."[321] Many autistic people have been successful in their fields.[322]

### Neurodiversity movement

Some autistic people, as well as a growing number of researchers,[13] have advocated a shift in attitudes toward the view that autism spectrum disorder is a difference, rather than a disease that must be treated or cured.[323][324] Critics have bemoaned the entrenchment of some of these groups' opinions.[325][326][327][328]

The neurodiversity movement and the autism rights movement are social movements within the context of disability rights, emphasizing the concept of neurodiversity, which describes the autism spectrum as a result of natural variations in the human brain rather than a disorder to be cured.[313][99] The autism rights movement advocates for including greater acceptance of autistic behaviors; therapies that focus on coping skills rather than imitating the behaviors of those without autism;[329] and the recognition of the autistic community as a minority group.[329][330]

Autism rights or neurodiversity advocates believe that the autism spectrum is genetic and should be accepted as a natural variation in the human genome.[313] These movements are not without detractors; a common argument against neurodiversity activists is that most of them have relatively low support needs, or are self-diagnosed, and do not represent the views of autistic people with higher support needs.[330][331][332] Jacquiline den Houting explores this critique, determining that the voices of low-support needs autistics are "some of the most influential within the neurodiversity movement, although admittedly these voices are a minority within the advocacy community"; she suggests this is in part a shortcoming of the wider neurotypical community, referencing non-speaking self-advocate Amy Sequenzia's writing.[333][334][undue weight? - discuss] Pier Jaarsma and Stellan Welin make the argument that only high-functioning autistic people should be included under the neurodiversity banner, as low-functioning autists' condition may rightfully be viewed as a disability.[335] The concept of neurodiversity is contentious in autism advocacy and research groups and has led to infighting.[336][337]

### Symbols and flags

Over the years, multiple organizations have tried to capture the essence of autism in symbols. In 1963, the board for the National Autistic Society, led by Gerald Gasson, proposed the "puzzle piece" as a symbol for autism, because it fit their view of autism as a "puzzling condition".[338] In 1999, the Autism Society adopted the puzzle ribbon as the universal sign of autism awareness.[338] In 2004, neurodiversity advocates Amy and Gwen Nelson conjured the "rainbow infinity symbol". It was initially the logo for their website, Aspies for Freedom. Nowadays, the prismatic colors are often associated with the neurodiversity movement in general.[339] The autism spectrum has also been symbolized by the infinity symbol itself.[340] In 2018, Julian Morgan wrote the article "Light It Up Gold", a response to Autism Speaks's "Light It Up Blue" campaign, launched in 2007.[341][342] Aurum is Latin for gold,[339] and gold has been used to symbolize autism, since both words start with "Au". Though a consensus for a flag to unite autism and neurodiversity has not yet been established, one has gained traction on Reddit.[343] The flag implements a gradient to represent the Pride Movement and incorporates a golden infinity symbol as its focal point.[344] While flags are symbols of solidarity, they may trigger negative associations, such as apparent rivalry among two or more flags.[345] For this reason, flags are sought that can be tailored to the personal preferences of any neurotype.[346][347]

* Autism infinity symbol

* Autistic pride flag

* The puzzle piece symbol as used in the autism awareness ribbon used by Autism Speaks

* An Autistic Pride flag at a "Pride is a Protest" march in June 2021.

### Caregivers

Families who care for an autistic child face added stress from a number of different causes.[348][349] Parents may struggle to understand the diagnosis and to find appropriate care options. They often take a negative view of the diagnosis, and may struggle emotionally.[350] More than half of parents over age 50 are still living with their child, as about 85% of autistic people have difficulties living independently.[351] Some studies also find decreased earnings among parents who care for autistic children.[352][353] Siblings of children with ASD report greater admiration and less conflict with the affected sibling than siblings of unaffected children, like siblings of children with Down syndrome. But they reported lower levels of closeness and intimacy than siblings of children with Down syndrome; siblings of people with ASD have a greater risk of negative well-being and poorer sibling relationships as adults.[354]

### LGBT identity and religious beliefs

Research indicates that autistic people are substantially more likely to be LGBT--particularly transgender or non-binary--than the general population.[188]

They are also significantly more likely to be non-theistic.[192]

## See also

* Outline of autism
* Animal model of autism
* Autism and memory
* Autism spectrum disorders in the media
* Autistic art
* Controversies in autism
* Global perceptions of autism
* List of autistic fictional characters
* List of films about autism
* Sex and gender differences in autism
* Violence and autism

## References

1. ↑ 1.0 1.1 1.2 1.3 "Still too much delay in recognition of autism spectrum disorder". Epidemiology and Psychiatric Sciences (Cambridge University Press) 31 (e1): e1. January 2022. doi:10.1017/S2045796021000822. OCLC 727338545. PMID 35012703.
2. ↑ Pezzimenti, F.; Han, G. T.; Vasa, R. A.; Gotham, K. (2019). "Depression in Youth with Autism Spectrum Disorder". Child and Adolescent Psychiatric Clinics of North America 28 (3): 397–409. doi:10.1016/j.chc.2019.02.009. PMID 31076116.
3. ↑ "At the intersection of autism and trauma". 26 September 2018. https://www.spectrumnews.org/features/deep-dive/intersection-autism-trauma/#:~:text=And people with more autistic,in other forms of PTSD.
4. ↑ "Autism's drug problem". 19 April 2017. https://www.spectrumnews.org/features/deep-dive/autisms-drug-problem/.
5. ↑ 5.0 5.1 Zeidan, Jinan; Fombonne, Eric; Scorah, Julie; Ibrahim, Alaa; Durkin, Maureen S.; Saxena, Shekhar; Yusuf, Afiqah; Shih, Andy et al. (2022-05-15). "Global prevalence of autism: A systematic review update". Autism Research 15 (5): 778–790. doi:10.1002/aur.2696. ISSN 1939-3806. PMID 35238171.
6. ↑ "COVID-19 guide – Autism Spectrum Condition (ASC)". National Health Service, United Kingdom. 7 June 2020. https://www.england.nhs.uk/coronavirus/documents/covid-19-guide-autism-spectrum-condition-asc/. "ASC is a 'spectrum condition' meaning that, while all people with autism share certain difficulties, their condition affects them in different ways."
7. ↑ "Annual Research Review: The role of the environment in the developmental psychopathology of autism spectrum condition". Journal of Child Psychology and Psychiatry, and Allied Disciplines 57 (3): 271–292. March 2016. doi:10.1111/jcpp.12501. ISSN 0021-9630. OCLC 01307942. PMID 26782158.
8. ↑ "The Diagnosis of Autism: From Kanner to DSM-III to DSM-5 and Beyond". Journal of Autism and Developmental Disorders 51 (12): 4253–4270. December 2021. doi:10.1007/s10803-021-04904-1. PMID 33624215.
9. ↑ "The Broad Autism Phenotype" (in en-US). Autism Spectrum Disorders. Oxford University Press. 2011. pp. 457–476. doi:10.1093/med/9780195371826.003.0031. ISBN 978-0-19-996521-2.
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14. ↑ "Welcome to the Autistic Community" (in en-US). Autistic Self Advocacy Network. https://autismacceptance.com/.
15. ↑ "Clearing Up Some Misconceptions about Neurodiversity" (in en). Nature America, Inc.. 6 June 2019. https://blogs.scientificamerican.com/observations/clearing-up-some-misconceptions-about-neurodiversity/.
16. ↑ "My Time with Autism Speaks". Autistic Community and the Neurodiversity Movement: Stories from the Frontline. Singapore: Springer. 2020. pp. 221–232. doi:10.1007/978-981-13-8437-0_16. ISBN 978-981-13-8437-0.
17. ↑ Opar, Alisa (2019-04-24). "In search of truce in the autism wars". Spectrum (Simons Foundation). doi:10.53053/VRKL4748. https://www.spectrumnews.org/features/deep-dive/search-truce-autism-wars. Retrieved 9 July 2022.
18. ↑ 18.0 18.1 Waterhouse, Lynn; Mottron, Laurent (2 May 2023). "Editorial: Is autism a biological entity?". Frontiers in Psychiatry 14. doi:10.3389/fpsyt.2023.1180981. PMID 37200904.
19. ↑ 19.0 19.1 19.2 19.3 19.4 19.5 "Evidence Base Update for Autism Spectrum Disorder". Journal of Clinical Child and Adolescent Psychology (Taylor & Francis) 44 (6): 897–922. 2015. doi:10.1080/15374416.2015.1077448. ISSN 1537-4416. PMID 26430947.
20. ↑ 20.0 20.1 20.2 "Communication interventions for autism spectrum disorder in minimally verbal children". The Cochrane Database of Systematic Reviews 2018 (11): CD012324. November 2018. doi:10.1002/14651858.CD012324.pub2. PMID 30395694.
21. ↑ 21.0 21.1 Kasari C, Shire S, Shih W, Landa R, Levato L, Smith T (June 2023). "Spoken language outcomes in limited language preschoolers with autism and global developmental delay: RCT of early intervention approaches". Autism Research 16 (6): 1236–1246. doi:10.1002/aur.2932. PMID 37070270.
22. ↑ Yu, Qian; Li, Enyao; Li, Liguo; Liang, Weiyi (May 2020). "Efficacy of Interventions Based on Applied Behavior Analysis for Autism Spectrum Disorder: A Meta-Analysis" (in en). Psychiatry Investigation 17 (5): 432–443. doi:10.30773/pi.2019.0229. PMID 32375461.
23. ↑ "'The line between intervention and abuse' – autism and applied behaviour analysis" (in en). History of the Human Sciences 30 (2): 107–126. 2017-04-01. doi:10.1177/0952695117702571. ISSN 0952-6951.
24. ↑ "Medication Treatment for Autism" (in en). 19 April 2021. https://www.nichd.nih.gov/health/topics/autism/conditioninfo/treatments/medication-treatment.
25. ↑ "Why Asperger's Syndrome is no longer listed in the DSM". https://www.parents.com/health/autism/what-happened-to-aspergers/.
26. ↑ "Diagnostic Criteria | Autism Spectrum Disorder (ASD) | NCBDDD | CDC". 2 November 2022. https://www.cdc.gov/ncbddd/autism/hcp-dsm.html.
27. ↑ "ICD-11 for Mortality and Morbidity Statistics". https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/437815624.
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30. ↑ "The autistic spectrum" (in English). The Lancet 350 (9093): 1761–1766. December 1997. doi:10.1016/S0140-6736(97)09218-0. PMID 9413479.
31. ↑ "Diagnostic criteria – a guide for all audiences" (in en). https://www.autism.org.uk/advice-and-guidance/topics/diagnosis/diagnostic-criteria/all-audiences.
32. ↑ 32.0 32.1 ﻿Status on ICD-11: The WHO Launch﻿ (Report). CDC/NCHS. 18 July 2018. https://ncvhs.hhs.gov/wp-content/uploads/2018/08/ICD-11_WHO-v_7-17-2018.pdf. Retrieved 22 October 2021.
33. ↑ "ICD vs. DSM". APA Monitor (American Psychological Association) 40 (9): p. 63. 2009. https://www.apa.org/monitor/2009/10/icd-dsm.
34. ↑ "International surveys on the use of ICD-10 and related diagnostic systems". Psychopathology 35 (2–3): 72–75. 2002. doi:10.1159/000065122. PMID 12145487.
35. ↑ "The classification of mental disorder: a simpler system for DSM–V and ICD–11". Advances in Psychiatric Treatment 16 (1): 14–19. January 2010. doi:10.1192/apt.bp.109.007120.
36. ↑ 36.0 36.1 36.2 Sarovic, Darko (16 November 2021). "A Unifying Theory for Autism: The Pathogenetic Triad as a Theoretical Framework". Frontiers in Psychiatry 12. doi:10.3389/fpsyt.2021.767075. PMID 34867553.
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38. ↑ "WHO releases new International Classification of Diseases (ICD 11)". https://www.who.int/news/item/18-06-2018-who-releases-new-international-classification-of-diseases-(icd-11).
39. ↑ ICD-11.
40. ↑ , Wikidata Q3064664
41. ↑ 41.0 41.1 41.2 41.3 41.4 DSM-5-TR.
42. ↑ DSM-5-TR, "Autism spectrum disorder encompasses disorders previously referred to as early infantile autism, childhood autism, Kanner's autism, high-functioning autism, atypical autism, pervasive developmental disorder not otherwise specified, childhood disintegrative disorder, and Asperger's disorder".
43. ↑ DSM-5-TR, "It may be helpful to note level of support needed for each of the two core psychopathological domains in Table 2 (e.g., 'requiring very substantial support for deficits in social communication and requiring substantial support for restricted, repetitive behaviors')".
44. ↑ "How will DSM-5 affect autism diagnosis? A systematic literature review and meta-analysis". Journal of Autism and Developmental Disorders 44 (8): 1918–1932. August 2014. doi:10.1007/s10803-014-2065-2. PMID 24531932.
45. ↑ "DSM-5 Diagnostic Criteria". U.S. Department of Health & Human Services Interagency Autism Coordinating Committee. https://iacc.hhs.gov/about-iacc/subcommittees/resources/dsm5-diagnostic-criteria.shtml#autism-spectrum-disorder.
46. ↑ "F84. Pervasive developmental disorders". World Health Organization. 2007. http://apps.who.int/classifications/apps/icd/icd10online/?gf80.htm+f84.
47. ↑ "Autism Spectrum Disorder". Handbook of Pragmatic Language Disorders. Cham, Switzerland: Springer. 2021. pp. 45–78. doi:10.1007/978-3-030-74985-9_3. ISBN 978-3-030-74984-2. OCLC 1269056169.
48. ↑ Biopsychology (8th ed.). Boston, Massachusetts: Pearson. 2011. p. 235. ISBN 978-0-205-03099-6. OCLC 1085798897.
49. ↑ "Cognitive Assessment". Autism Spectrum Disorders. American Psychiatric Association. 2018. doi:10.1176/appi.books.9781615371921. ISBN 978-1-61537-192-1.
50. ↑ Autism spectrum disorder in adults: diagnosis and management, NICE, 14 June 2021, CG142, https://www.nice.org.uk/guidance/cg142, retrieved 24 October 2021
51. ↑ "About autism spectrum disorder (ASD)" (in en). 18 January 2016. https://www.canada.ca/en/public-health/services/diseases/autism-spectrum-disorder-asd/about-autism-spectrum-disorder-asd.html.
52. ↑ "What are the signs and symptoms of ASD?" (in en). 18 January 2016. https://www.canada.ca/en/public-health/services/diseases/autism-spectrum-disorder-asd/signs-symptoms-autism-spectrum-disorder-asd.html.
53. ↑ National Center on Birth Defects and Developmental Disabilities (25 March 2020). "What is Autism Spectrum Disorder?". https://www.cdc.gov/ncbddd/autism/facts.html.
54. ↑ "Broader autism phenotype: evidence from a family history study of multiple-incidence autism families". The American Journal of Psychiatry 154 (2): 185–190. February 1997. doi:10.1176/ajp.154.2.185. PMID 9016266.
55. ↑ "Social Skills Deficits in Autism Spectrum Disorder: Potential Biological Origins and Progress in Developing Therapeutic Agents". CNS Drugs 32 (8): 713–734. August 2018. doi:10.1007/s40263-018-0556-y. PMID 30105528.
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58. ↑ DeBrabander, Kilee M.; Morrison, Kerrianne E.; Jones, Desiree R.; Faso, Daniel J.; Chmielewski, Mike; Sasson, Noah J. (13 December 2019). "Do First Impressions of Autistic Adults Differ Between Autistic and Nonautistic Observers?" (in en). Autism in Adulthood 1 (4): 250–257. doi:10.1089/aut.2019.0018. PMID 36601322.
59. ↑ "Basics About Autism Spectrum Disorder (ASD)" (in en-us). 31 March 2022. https://www.cdc.gov/ncbddd/autism/facts.html.
60. ↑ Grove, Rachel; Hoekstra, Rosa A; Wierda, Marlies; Begeer, Sander (May 20, 2020). "Special interests and subjective wellbeing in autistic adults" (in en). Autism Research 11 (5): 766–775. doi:10.1002/aur.1931. PMID 29427546. https://pubmed.ncbi.nlm.nih.gov/29427546/.
61. ↑ Murray, Dinah; Lesser, Mike; Lawson, Wendy (May 2005). "Attention, monotropism and the diagnostic criteria for autism" (in en). Autism Research 9 (2): 139–156. doi:10.1177/1362361305051398. PMID 15857859.
62. ↑ Baron-Cohen, Simon; Knickmeyer, Rebecca C.; Belmonte, Matthew K. (4 November 2005). "Sex differences in the brain: implications for explaining autism". Science 310 (5749): 819–823. doi:10.1126/science.1115455. PMID 16272115. Bibcode: 2005Sci...310..819B. http://docs.autismresearchcentre.com/papers/2005_BC_etal_Science.pdf. Retrieved 10 September 2023.
63. ↑ "Introduction". Asperger syndrome. New York: Guilford Press. 2000. pp. 1–24. ISBN 1-57230-534-7.
64. ↑ Gernsbacher, Morton Ann (2017-08-06). "Editorial Perspective: The use of person-first language in scholarly writing may accentuate stigma" (in en). Journal of Child Psychology and Psychiatry 58 (7): 859–861. doi:10.1111/jcpp.12706. PMID 28621486.
65. ↑ "DSM-5 Full Text Online". http://repository.poltekkes-kaltim.ac.id/657/1/Diagnostic and statistical manual of mental disorders _ DSM-5 ( PDFDrive.com ).pdf.
66. ↑ "Alexithymia". Disorders of Emotion in Neurologic Disease. Handbook of Clinical Neurology. 183. Elsevier. 2021. pp. 47–62. doi:10.1016/b978-0-12-822290-4.00004-9. ISBN 978-0-12-822290-4.
67. ↑ Milton, Damian E. M. (October 2012). "On the ontological status of autism: the 'double empathy problem'" (in en). Disability & Society 27 (6): 883–887. doi:10.1080/09687599.2012.710008. ISSN 0968-7599. http://www.tandfonline.com/doi/abs/10.1080/09687599.2012.710008.
68. ↑ Milton, Damian; Gurbuz, Emine; López, Beatriz (November 2022). "The 'double empathy problem': Ten years on" (in en). Autism 26 (8): 1901–1903. doi:10.1177/13623613221129123. ISSN 1362-3613. PMID 36263746. http://journals.sagepub.com/doi/10.1177/13623613221129123. Retrieved 25 February 2023.
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70. ↑ Sasson, Noah J.; Faso, Daniel J.; Nugent, Jack; Lovell, Sarah; Kennedy, Daniel P.; Grossman, Ruth B. (2017-02-01). "Neurotypical Peers are Less Willing to Interact with Those with Autism based on Thin Slice Judgments" (in en). Scientific Reports 7 (1): 40700. doi:10.1038/srep40700. ISSN 2045-2322. PMID 28145411. Bibcode: 2017NatSR...740700S.
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73. ↑ Bothan, Monique; Cage, Eilidh (24 November 2022). ""Autism research is in crisis": A mixed method study of researcher's constructions of autistic people and autism research" (in en). Frontiers in Psychology 13. doi:10.3389/fpsyg.2022.1050897. PMID 36506950.
74. ↑ 74.0 74.1 Bal, Vanessa H.; Kim, So-Hyun; Fok, Megan; Lord, Catherine (12 August 2018). "Autism Spectrum Disorder symptoms from 2 to 19: Implications for diagnosing adolescents and young adults" (in en). Autism Research 12 (1): 89–99. doi:10.1002/aur.2004. PMID 30101492.
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76. ↑ 76.0 76.1 "Identification and evaluation of children with autism spectrum disorders". Pediatrics 120 (5): 1183–1215. November 2007. doi:10.1542/peds.2007-2361. PMID 17967920. http://pediatrics.aappublications.org/cgi/content/full/120/5/1183.
77. ↑ "Language disorders: autism and other pervasive developmental disorders". Pediatric Clinics of North America 54 (3): 469–81, vi. June 2007. doi:10.1016/j.pcl.2007.02.011. PMID 17543905.
78. ↑ National Center on Birth Defects and Developmental Disabilities (26 February 2015). "Signs & Symptoms: Autism Spectrum Disorder". https://www.cdc.gov/ncbddd/autism/signs.html. (Also available in Spanish.)
79. ↑ "Autism: Overview". American Speech-Language-Hearing Association. https://www.asha.org/Practice-Portal/Clinical-Topics/Autism/.
80. ↑ Cohen, David; Grandin, Temple (25 October 2005). "Temple Grandin: 'I'm an anthropologist from Mars'". The Guardian (Kings Place, London: Scott Trust). ISSN 0261-3077. OCLC 60623878. https://www.theguardian.com/education/2005/oct/25/highereducationprofile.academicexperts.
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82. ↑ 82.0 82.1 "Is voice a marker for Autism spectrum disorder? A systematic review and meta-analysis". Autism Research 10 (3): 384–407. March 2017. doi:10.1002/aur.1678. PMID 27501063. https://pure.au.dk/ws/files/101709535/046565.full.pdf. Retrieved 27 March 2020.
83. ↑ Understanding and Working With the Spectrum of Autism: An Insider's View. London UK, & Philadelphia PA: Jessica Kingsley Publishers. 2001. pp. 33. ISBN 978-1853029714. https://archive.org/details/understandingwor00laws_352.
84. ↑ Finke, Erinn (16 May 2022). "The Kind of Friend I Think I Am: Perceptions of Autistic and Non‑autistic Young Adults" (in en). Journal of Autism and Developmental Disorders 53 (8): 3047–3064. doi:10.1007/s10803-022-05573-4. PMID 35570241. https://www.researchgate.net/publication/360622541.
85. ↑ O'Connor, Rachel A G; van den Bedem, Neeltje; Blijd-Hoogewys, Els M A; Stockmann, Lex; Rieffe, Carolien (22 January 2022). "Friendship quality among autistic and non-autistic (pre-) adolescents: Protective or risk factor for mental health?" (in en). Autism 26 (8): 2041–2051. doi:10.1177/13623613211073448. PMID 35068188.
86. ↑ van Roekel, Eeske; Scholte, Ron H. J.; Didden, Robert (2010). "Bullying Among Adolescents With Autism Spectrum Disorders: Prevalence and Perception". Journal of Autism and Developmental Disorders 40 (1): 63–73. doi:10.1007/s10803-009-0832-2. PMID 17543905.
87. ↑ O'Connor, Rachel A G; van den Bedem, Neeltje; Blijd-Hoogewys, Els M A; Stockmann, Lex; Rieffe, Carolien (November 2022). "Sex differences in friendships and loneliness in autistic and non-autistic children across development" (in en). Molecular Autism 4 (9): 9. doi:10.1186/s13229-023-00542-9. PMID 36829214.
88. ↑ Pearson, Amy; Rose, Kieran (2021-03-01). "A Conceptual Analysis of Autistic Masking: Understanding the Narrative of Stigma and the Illusion of Choice". Autism in Adulthood 3 (1): 52–60. doi:10.1089/aut.2020.0043. ISSN 2573-9581. PMID 36601266.
89. ↑ Petrolini, Valentina; Rodríguez-Armendariz, Ekaine; Vicente, Agustín (2023). "Autistic camouflaging across the spectrum" (in en). New Ideas in Psychology 68: 100992. doi:10.1016/j.newideapsych.2022.100992.
90. ↑ "Engaging people on the autism spectrum". Autism Spectrum Australia. 7 October 2013. https://www.autismspectrum.org.au/about-aspect/diversity-inclusion/engaging-people-on-the-autism-spectrum.
91. ↑ Teaching Autistic Children to Communicate. Rockville, Maryland: Aspens System Corporation. 1983. p. 180. ISBN 978-0-89443-884-4.
92. ↑ 92.0 92.1 92.2 92.3 "Autism spectrum disorder". The Lancet 392 (10146): 508–520. August 2018. doi:10.1016/S0140-6736(18)31129-2. PMID 30078460.
93. ↑ 93.0 93.1 93.2 "Autism spectrum disorder: Clinical features". https://www.uptodate.com/contents/autism-spectrum-disorder-clinical-features.
94. ↑ DSM-5-TR, "Hyper- or hyporeactivity to sensory input or unusual interest in sensory aspects of the environment (e.g., apparent indifference to pain/temperature, adverse response to specific sounds or textures, excessive smelling or touching of objects, visual fascination with lights or movement)".
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107. ↑ "A meta-analysis of sensory modulation symptoms in individuals with autism spectrum disorders". Journal of Autism and Developmental Disorders 39 (1): 1–11. January 2009. doi:10.1007/s10803-008-0593-3. PMID 18512135.
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110. ↑ Wang, Leah A. L.; Petrulla, Victoria; Zampella, Casey J.; Waller, Rebecca; Schultz, Robert T. (2022). "Gross motor impairment and its relation to social skills in autism spectrum disorder: A systematic review and two meta-analyses." (in en). Psychological Bulletin 148 (3–4): 273–300. doi:10.1037/bul0000358. ISSN 1939-1455. PMID 35511567.
111. ↑ "Atypical behaviors in children with autism and children with a history of language impairment". Research in Developmental Disabilities (Elsevier) 28 (2): 145–162. 2007. doi:10.1016/j.ridd.2006.02.003. ISSN 0891-4222. PMID 16581226.
112. ↑ Matson, Johnny L.; Sturmey, Peter, eds (2022) (in en). Handbook of autism and pervasive developmental disorder: assessment, diagnosis, and treatment. Autism and Child Psychopathology Series. Cham: Springer Nature. p. 18. doi:10.1007/978-3-030-88538-0. ISBN 978-3-030-88538-0. OCLC 1341298051. "To date no one genetic feature or environmental cause has proven etiological in explaining most cases autism or has been able to account for rising rates of autism."
113. ↑ Sauer, Ann Katrin; Stanton, Janelle E.; Hans, Sakshi; Grabrucker, Andreas M. (2021). "Autism Spectrum Disorders: Etiology and Pathology". written at Brisbane, Australia. in Grabrucker, Andreas M. (in en). Autism spectrum disorders. Andreas M. Grabrucker. Brisbane: Exon Publications. August 20, 2021. pp. 1–16. doi:10.36255/exonpublications.autismspectrumdisorders.2021.etiology. ISBN 978-0-6450017-8-5. OCLC 1280592589. "The cause of ASD is unknown, but several genetic and non-genetic risk factors have been characterized that, alone or in combination, are implicated in the development of ASD."
114. ↑ Kałużna-Czaplińska, Joanna; Żurawicz, Ewa; Jóźwik-Pruska, Jagoda (2018). "Focus on the Social Aspect of Autism" (in en). Journal of Autism and Developmental Disorders (Springer Nature) 48 (5): 1861–1867. November 29, 2017. doi:10.1007/s10803-017-3407-7. ISSN 1573-3432. PMID 29188587. "Despite extensive ASD research lasting more than 60 years, its causes are still unknown.".
115. ↑ Medavarapu, Srinivas; Marella, Lakshmi Lavanya; Sangem, Aneela; Kairam, Ram (2019). "Where is the Evidence? A Narrative Literature Review of the Treatment Modalities for Autism Spectrum Disorders" (in en). Cureus (Springer Nature) 11 (1): e3901. January 16, 2019. doi:10.7759/cureus.3901. ISSN 2168-8184. PMID 30911457. "It is important to realize that the etiology of autism is unknown and at present, there is no cure, although there are interventions that may be effective in alleviating some symptoms and improving skills that may help autistic persons lead more productive lives.".
116. ↑ 116.0 116.1 "The 'fractionable autism triad': a review of evidence from behavioural, genetic, cognitive and neural research". Neuropsychology Review 18 (4): 287–304. December 2008. doi:10.1007/s11065-008-9076-8. PMID 18956240.
117. ↑ 117.0 117.1 "Time to give up on a single explanation for autism". Nature Neuroscience 9 (10): 1218–1220. October 2006. doi:10.1038/nn1770. PMID 17001340.
118. ↑ "The origins of social impairments in autism spectrum disorder: studies of infants at risk". Neural Networks 23 (8–9): 1072–6. 2010. doi:10.1016/j.neunet.2010.07.008. PMID 20800990.
119. ↑ "Autism and the environment: challenges and opportunities for research". Pediatrics 121 (6): 1225–1229. June 2008. doi:10.1542/peds.2007-3000. PMID 18519493. http://pediatrics.aappublications.org/cgi/content/full/121/6/1225.
120. ↑ "Childhood developmental disorders: an academic and clinical convergence point for psychiatry, neurology, psychology and pediatrics". Journal of Child Psychology and Psychiatry, and Allied Disciplines 50 (1–2): 87–98. January 2009. doi:10.1111/j.1469-7610.2008.02046.x. ISSN 0021-9630. OCLC 01307942. PMID 19220592.
121. ↑ "Neural systems approaches to the neurogenetics of autism spectrum disorders". Neuroscience 164 (1): 247–256. November 2009. doi:10.1016/j.neuroscience.2009.05.054. PMID 19482063.
122. ↑ 122.0 122.1 122.2 "Autism". The Lancet 374 (9701): 1627–1638. November 2009. doi:10.1016/S0140-6736(09)61376-3. PMID 19819542. (Erratum: doi:10.1016/S0140-6736(11)61666-8, [1])
123. ↑ "Unraveling autism". American Journal of Human Genetics 82 (1): 7–9. January 2008. doi:10.1016/j.ajhg.2007.12.003. PMID 18179879.
124. ↑ "Clustering the autisms using glutamate synapse protein interaction networks from cortical and hippocampal tissue of seven mouse models". Molecular Autism 9 (48): 48. 2018. doi:10.1186/s13229-018-0229-1. PMID 30237867.
125. ↑ 125.0 125.1 125.2 "Advances in autism genetics: on the threshold of a new neurobiology". Nature Reviews. Genetics 9 (5): 341–355. May 2008. doi:10.1038/nrg2346. PMID 18414403.
126. ↑ "Multiple rare variants in the etiology of autism spectrum disorders". Dialogues in Clinical Neuroscience 11 (1): 35–43. 2009. doi:10.31887/DCNS.2009.11.1/jdbuxbaum. PMID 19432386.
127. ↑ 127.0 127.1 "Autism: definition, neurobiology, screening, diagnosis". Pediatric Clinics of North America 55 (5): 1129–46, viii. October 2008. doi:10.1016/j.pcl.2008.07.005. PMID 18929056.
128. ↑ "Insights into Autism Spectrum Disorder Genomic Architecture and Biology from 71 Risk Loci". Neuron 87 (6): 1215–1233. September 2015. doi:10.1016/j.neuron.2015.09.016. PMID 26402605.
129. ↑ "Autism genetics". Behavioural Brain Research 251: 95–112. August 2013. doi:10.1016/j.bbr.2013.06.012. PMID 23769996.
130. ↑ "Copy-number variations associated with neuropsychiatric conditions". Nature 455 (7215): 919–923. October 2008. doi:10.1038/nature07458. PMID 18923514. Bibcode: 2008Natur.455..919C.
131. ↑ "Frequency and Complexity of De Novo Structural Mutation in Autism". American Journal of Human Genetics 98 (4): 667–679. April 2016. doi:10.1016/j.ajhg.2016.02.018. PMID 27018473.
132. ↑ "Autism: highly heritable but not inherited". Nature Medicine 13 (5): 534–536. May 2007. doi:10.1038/nm0507-534. PMID 17479094.
133. ↑ 133.0 133.1 133.2 "CHD8 suppresses p53-mediated apoptosis through histone H1 recruitment during early embryogenesis". Nature Cell Biology 11 (2): 172–182. February 2009. doi:10.1038/ncb1831. PMID 19151705.
134. ↑ 134.0 134.1 "From neural development to cognition: unexpected roles for chromatin". Nature Reviews Genetics 14 (5): 347–359. May 2013. doi:10.1038/nrg3413. PMID 23568486.
135. ↑ 135.0 135.1 "CHD8 is an ATP-dependent chromatin remodeling factor that regulates beta-catenin target genes". Molecular and Cellular Biology 28 (12): 3894–3904. June 2008. doi:10.1128/mcb.00322-08. PMID 18378692.
136. ↑ "CHD8 regulates neurodevelopmental pathways associated with autism spectrum disorder in neural progenitors". Proceedings of the National Academy of Sciences of the United States of America 111 (42): E4468–E4477. October 2014. doi:10.1073/pnas.1405266111. PMID 25294932. Bibcode: 2014PNAS..111E4468S.
137. ↑ "The autism-associated chromatin modifier CHD8 regulates other autism risk genes during human neurodevelopment". Nature Communications 6 (1): 6404. March 2015. doi:10.1038/ncomms7404. PMID 25752243. Bibcode: 2015NatCo...6.6404C.
138. ↑ "The autism-associated gene chromodomain helicase DNA-binding protein 8 (CHD8) regulates noncoding RNAs and autism-related genes". Translational Psychiatry 5 (5): e568. May 2015. doi:10.1038/tp.2015.62. PMID 25989142.
139. ↑ "Chd8 regulates X chromosome inactivation in mouse through fine-tuning control of Xist expression". Communications Biology 4 (1): 485. April 2021. doi:10.1038/s42003-021-01945-1. PMID 33859315.
140. ↑ "Autism As a Disorder of High Intelligence". Frontiers in Neuroscience 10: 300. 30 June 2016. doi:10.3389/fnins.2016.00300. PMID 27445671.
141. ↑ The pattern seekers: how autism drives human invention. Basic Books. 10 November 2020. ISBN 978-1-5416-4713-8. OCLC 1204602315.
142. ↑ "The emerging picture of autism spectrum disorder: genetics and pathology". Annual Review of Pathology: Mechanisms of Disease 10: 111–44. 2015. doi:10.1146/annurev-pathol-012414-040405. PMID 25621659.
143. ↑ "An analytical framework for whole-genome sequence association studies and its implications for autism spectrum disorder". Nature Genetics 50 (5): 727–736. April 2018. doi:10.1038/s41588-018-0107-y. PMID 29700473.
144. ↑ "Thousands of autistic girls and women 'going undiagnosed' due to gender bias". The Guardian. 14 September 2018. https://www.theguardian.com/society/2018/sep/14/thousands-of-autistic-girls-and-women-going-undiagnosed-due-to-gender-bias.
145. ↑ "Psychosis and autism as diametrical disorders of the social brain". The Behavioral and Brain Sciences 31 (3): 241–61; discussion 261–320. June 2008. doi:10.1017/S0140525X08004214. PMID 18578904. http://eprints.lse.ac.uk/21571/1/Psychosis and autism as diametrical disorders of the social brain (LSERO).pdf. Retrieved 10 June 2022.
146. ↑ "Evolution in health and medicine Sackler colloquium: Comparative genomics of autism and schizophrenia". Proceedings of the National Academy of Sciences of the United States of America 107 (Suppl 1): 1736–1741. January 2010. doi:10.1073/pnas.0906080106. PMID 19955444. Bibcode: 2010PNAS..107.1736C.
147. ↑ "Sex differences in the brain: implications for explaining autism". Science 310 (5749): 819–823. November 2005. doi:10.1126/science.1115455. PMID 16272115. Bibcode: 2005Sci...310..819B. http://irep.ntu.ac.uk/id/eprint/2710/1/219535_PubSub1971_Belmonte.pdf. Retrieved 15 May 2022.
148. ↑ "Perinatal and neonatal risk factors for autism: a comprehensive meta-analysis". Pediatrics 128 (2): 344–55. August 2011. doi:10.1542/peds.2010-1036. PMID 21746727.
149. ↑ 149.0 149.1 "Prenatal risk factors for autism: comprehensive meta-analysis". The British Journal of Psychiatry 195 (1): 7–14. July 2009. doi:10.1192/bjp.bp.108.051672. PMID 19567888.
150. ↑ "Regression in autistic spectrum disorders". Neuropsychology Review 18 (4): 305–319. December 2008. doi:10.1007/s11065-008-9073-y. PMID 18956241.
151. ↑ "Neurodevelopment: The Impact of Nutrition and Inflammation During Preconception and Pregnancy in Low-Resource Settings". Pediatrics 139 (Suppl 1): S38–S49. April 2017. doi:10.1542/peds.2016-2828F. PMID 28562247.
152. ↑ "Pathophysiology of autism spectrum disorders: revisiting gastrointestinal involvement and immune imbalance". World Journal of Gastroenterology 20 (29): 9942–9951. August 2014. doi:10.3748/wjg.v20.i29.9942. PMID 25110424.
153. ↑ "Maternal lifestyle and environmental risk factors for autism spectrum disorders". International Journal of Epidemiology 43 (2): 443–464. April 2014. doi:10.1093/ije/dyt282. PMID 24518932.
154. ↑ "A Systematic Review and Meta-Analysis of Multiple Airborne Pollutants and Autism Spectrum Disorder". PLOS ONE 11 (9): e0161851. 2016. doi:10.1371/journal.pone.0161851. PMID 27653281. Bibcode: 2016PLoSO..1161851L.
155. ↑ 155.0 155.1 155.2 "The epidemiology of autism spectrum disorders". Annual Review of Public Health 28: 235–58. 2007. doi:10.1146/annurev.publhealth.28.021406.144007. PMID 17367287.
156. ↑ "Prenatal stress and risk for autism". Neuroscience and Biobehavioral Reviews 32 (8): 1519–1532. October 2008. doi:10.1016/j.neubiorev.2008.06.004. PMID 18598714.
157. ↑ "The Anti-vaccination Movement: A Regression in Modern Medicine". Cureus 10 (7): e2919. July 2018. doi:10.7759/cureus.2919. PMID 30186724.
158. ↑ "Vaccine Adverse Events: Separating Myth from Reality". American Family Physician 95 (12): 786–794. June 2017. PMID 28671426.
159. ↑ "Vaccines for measles, mumps, rubella, and varicella in children". The Cochrane Database of Systematic Reviews 2021 (11): CD004407. November 2021. doi:10.1002/14651858.CD004407.pub5. PMID 34806766.
160. ↑ 160.0 160.1 "Vaccines and autism: a tale of shifting hypotheses". Clinical Infectious Diseases 48 (4): 456–461. February 2009. doi:10.1086/596476. PMID 19128068.
161. ↑ "MMR doctor Andrew Wakefield fixed data on autism". The Sunday Times. 8 February 2009. https://www.thetimes.co.uk/article/mmr-doctor-andrew-wakefield-fixed-data-on-autism-mgj82qsk50g.
162. ↑ "Lancet retracts 'utterly false' MMR paper". The Guardian. 2 February 2010. https://www.theguardian.com/society/2010/feb/02/lancet-retracts-mmr-paper.
163. ↑ "Influenza Vaccine". Adverse Effects of Vaccines: Evidence and Causality. Committee to Review Adverse Effects of Vaccines, Board on Population Health and Public Health Practice. Washington, D.C.: Institute of Medicine/National Academies Press. August 2011. doi:10.17226/13164. ISBN 978-0-309-21435-3. https://nap.nationalacademies.org/read/13164/chapter/8. Retrieved 19 January 2019.
164. ↑ "The vaccine-autism connection: a public health crisis caused by unethical medical practices and fraudulent science". The Annals of Pharmacotherapy 45 (10): 1302–1304. October 2011. doi:10.1345/aph.1Q318. PMID 21917556.
165. ↑ "Wakefield's article linking MMR vaccine and autism was fraudulent". British Medical Journal 342: c7452. January 2011. doi:10.1136/bmj.c7452. PMID 21209060.
166. ↑ "Route of decomposition of thiomersal (thimerosal)". International Journal of Pharmaceutics 208 (1–2): 23–34. November 2000. doi:10.1016/S0378-5173(00)00514-7. PMID 11064208.
167. ↑ "Understanding Vaccines, Mercury and Thimerosal". https://www.fda.gov/media/83535/download.
168. ↑ Dona, Asif (2006). "Immunizations and Autism: A Review of the Literature". Canadian Journal of Neurological Sciences 33 (4): 341–346. doi:10.1017/S031716710000528X. PMID 17168158. https://www.cambridge.org/core/services/aop-cambridge-core/content/view/16B999364BFFD9F0DA3B09F25C1DE28C/S031716710000528Xa.pdf/immunizations-and-autism-a-review-of-the-literature.pdf. Retrieved 6 July 2023.
169. ↑ "Thimerosal questions and answers". 18 February 2021. https://www.fda.gov/vaccines-blood-biologics/vaccines/thimerosal-vaccines-questions-and-answers.
170. ↑ "Autism overflows: increasing prevalence and proliferating theories". Neuropsychology Review 18 (4): 273–286. December 2008. doi:10.1007/s11065-008-9074-x. PMID 19015994.
171. ↑ "87% of Flu Vaccine Doses have Reduced or "no" (only trace amounts of) Thimerosal". 16 September 2022. https://www.cdc.gov/flu/prevent/vaxsupply.htm.
172. ↑ "Frequently Asked Questions about Thimerosal". Centers for Disease Control and Prevention. https://www.cdc.gov/vaccinesafety/concerns/thimerosal/faqs.html.
173. ↑ 173.0 173.1 "Vaccines are not associated with autism: an evidence-based meta-analysis of case-control and cohort studies". Vaccine 32 (29): 3623–3629. June 2014. doi:10.1016/j.vaccine.2014.04.085. PMID 24814559.
174. ↑ Vaccines and autism:
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175. ↑ "Measles outbreak in Dublin, 2000". The Pediatric Infectious Disease Journal 22 (7): 580–584. July 2003. doi:10.1097/00006454-200307000-00002. PMID 12867830.
176. ↑ "A Unifying Theory for Autism: The Pathogenetic Triad as a Theoretical Framework". Frontiers in Psychiatry 12: 767075. November 2021. doi:10.3389/fpsyt.2021.767075. PMID 34867553.
177. ↑ "The intense world theory - a unifying theory of the neurobiology of autism". Frontiers in Human Neuroscience 4: 224. 21 December 2010. doi:10.3389/fnhum.2010.00224. PMID 21191475. "The proposed neuropathology is hyper-functioning of local neural microcircuits, best characterized by hyper-reactivity and hyper-plasticity. Such hyper-functional microcircuits are speculated to become autonomous and memory trapped leading to the core cognitive consequences of hyper-perception, hyper-attention, hyper-memory and hyper-emotionality. The theory is centered on the neocortex and the amygdala, but could potentially be applied to all brain regions. (...) This may lead to obsessively detailed information processing of fragments of the world and an involuntarily and systematic decoupling of the autist from what becomes a painfully intense world.".
178. ↑ "How our autistic ancestors played an important role in human evolution" (in en). 27 March 2017. https://theconversation.com/how-our-autistic-ancestors-played-an-important-role-in-human-evolution-73477.
179. ↑ "The Stone Age Origins of Autism" (in en). Recent Advances in Autism Spectrum Disorders. II. 6 March 2013.
180. ↑ "An Examination of Autism Spectrum Disorders in Relation to Human Evolution and Life History Theory". Nebraska Anthropologist 57. 2010. https://digitalcommons.unl.edu/nebanthro/57/. Retrieved 28 June 2022.
181. ↑ "Conceptualizing the autism spectrum in terms of natural selection and behavioral ecology: the solitary forager hypothesis". Evolutionary Psychology 9 (2): 207–238. May 2011. doi:10.1177/147470491100900209. PMID 22947969.
182. ↑ "Autism may have had advantages in humans' hunter-gatherer past, researcher believes" (in en). University of Southern California. 3 June 2011. https://www.sciencedaily.com/releases/2011/06/110603122849.htm.
183. ↑ "Lonely hunters". 8 July 2011. https://www.spectrumnews.org/opinion/lonely-hunters/.
184. ↑ "Are there alternative adaptive strategies to human pro-sociality? The role of collaborative morality in the emergence of personality variation and autistic traits". Time and Mind 9 (4): 289–313. 1 October 2016. doi:10.1080/1751696X.2016.1244949. ISSN 1751-696X.
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186. ↑ "Psychiatric Disorders in People with Autism Spectrum Disorders: Phenomenology and Recognition". International handbook of autism and pervasive developmental disorders. New York: Springer. 2011. pp. 53–74. ISBN 978-1-4419-8064-9. OCLC 746203105.
187. ↑ "Mental health of adults with autism spectrum disorders and intellectual disability". Current Opinion in Psychiatry 23 (5): 421–6. September 2010. doi:10.1097/YCO.0b013e32833cfc18. PMID 20613532.
188. ↑ 188.0 188.1 Graham Holmes, Laura; Ames, Jennifer L.; Massolo, Maria L.; Nunez, Denise M.; Croen, Lisa A. (2022-04-01). "Improving the Sexual and Reproductive Health and Health Care of Autistic People". Pediatrics (American Academy of Pediatrics) 149 (Supplement 4): e2020049437J. doi:10.1542/peds.2020-049437J. ISSN 0031-4005. PMID 35363286. "A substantial proportion of autistic adolescents and adults are LGBTQIA+. Autistic people are more likely to be transgender or gender nonconforming compared with non-autistic people, and findings from a recent autism registry study suggest that among autistic people able to self-report on a survey, up to 18% of men and 43% of women may be sexual minorities.".
189. ↑ "Gender dysphoria and autism spectrum disorder: A narrative review". International Review of Psychiatry 28 (1): 70–80. 2016. doi:10.3109/09540261.2015.1111199. PMID 26753812.
190. ↑ "Gender Dysphoria and Autism Spectrum Disorder: A Systematic Review of the Literature". Sexual Medicine Reviews 4 (1): 3–14. January 2016. doi:10.1016/j.sxmr.2015.10.003. PMID 27872002. https://figshare.com/articles/journal_contribution/9620366. Retrieved 19 June 2023.
191. ↑ "The sexual health, orientation, and activity of autistic adolescents and adults". Autism Research 14 (11): 2342–2354. November 2021. doi:10.17863/CAM.74771. PMID 34536071.
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193. ↑ "Epilepsy and epileptiform EEG: association with autism and language disorders". Developmental Disabilities Research Reviews 6 (4): 300–8. 2000. doi:10.1002/1098-2779(2000)6:4<300::AID-MRDD9>3.0.CO;2-R. PMID 11107195.
194. ↑ "The role of epilepsy and epileptiform EEGs in autism spectrum disorders". Pediatric Research 65 (6): 599–606. June 2009. doi:10.1203/PDR.0b013e31819e7168. PMID 19454962.
195. ↑ "Autism and tuberous sclerosis". Journal of Child Neurology 19 (9): 675–9. September 2004. doi:10.1177/08830738040190090701. PMID 15563013.
196. ↑ Sala, G.; Hooley, M.; Attwood, T. (2019). "Autism and Intellectual Disability: A Systematic Review of Sexuality and Relationship Education". Sexuality and Disability 37 (3): 353–382. doi:10.1007/s11195-019-09577-4.
197. ↑ Jensen, M.; Smolen, C.; Girirajan, S. (2020). "Gene discoveries in autism are biased towards comorbidity with intellectual disability". Journal of Medical Genetics 57 (9): 647–652. doi:10.1136/jmedgenet-2019-106476. PMID 32152248.
198. ↑ "Childhood autism and associated comorbidities". Brain & Development 29 (5): 257–272. June 2007. doi:10.1016/j.braindev.2006.09.003. PMID 17084999.
199. ↑ Schenkman, Lauren (2023-02-21). "Dietary changes ease traits in rare autism-linked condition" (in en-US). https://www.spectrumnews.org/news/dietary-changes-ease-traits-in-rare-autism-linked-condition/.
200. ↑ "BCKDK deficiency: a treatable neurodevelopmental disease amenable to newborn screening". Brain 146 (7): 3003–3013. 2023-02-02. doi:10.1093/brain/awad010. PMID 36729635.
201. ↑ "Large-Scale Exome Sequencing Study Implicates Both Developmental and Functional Changes in the Neurobiology of Autism". Cell 180 (3): 568–584.e23. February 2020. doi:10.1016/j.cell.2019.12.036. PMID 31981491.
202. ↑ "SYNGAP1-Related Intellectual Disability". Gene Reviews. 2019. PMID 30789692. https://www.ncbi.nlm.nih.gov/books/NBK537721/. Retrieved 25 July 2020.
203. ↑ "Autism and learning disability". Autism 8 (2): 125–40. June 2004. doi:10.1177/1362361304042718. PMID 15165430.
204. ↑ Child Psychopathology. New York: The Guilford Press. 2003. pp. 409–454. ISBN 978-1-57230-609-7. https://archive.org/details/childpsychopatho00mash_735.
205. ↑ "Anxiety in children and adolescents with autism spectrum disorders". Clinical Psychology Review 29 (3): 216–229. April 2009. doi:10.1016/j.cpr.2009.01.003. PMID 19223098.
206. ↑ "Psychiatric problems in individuals with autism, their parents and siblings". International Review of Psychiatry 11 (4): 278–298. 1999. doi:10.1080/09540269974177.
207. ↑ "The association between autism and schizophrenia spectrum disorders: A review of eight alternate models of co-occurrence". Neuroscience and Biobehavioral Reviews 55: 173–83. August 2015. doi:10.1016/j.neubiorev.2015.04.012. PMID 25956249. http://pure-oai.bham.ac.uk/ws/files/22611324/Chisholm_et_al_Association_between_autism_and_schizophrenia_2015_Post_Print.pdf. Retrieved 20 August 2019.
208. ↑ "Modifiable risk factors for schizophrenia and autism—shared risk factors impacting on brain development". Neurobiology of Disease 53: 3–9. May 2013. doi:10.1016/j.nbd.2012.10.023. PMID 23123588.
209. ↑ "Comparative immunogenetics of autism and schizophrenia". Genes, Brain and Behavior 10 (7): 689–701. October 2011. doi:10.1111/j.1601-183X.2011.00710.x. PMID 21649858.
210. ↑ "DNA Damage and Repair in Schizophrenia and Autism: Implications for Cancer Comorbidity and Beyond". International Journal of Molecular Sciences 17 (6): 856. June 2016. doi:10.3390/ijms17060856. PMID 27258260.
211. ↑ "Behaviour management problems as predictors of psychotropic medication and use of psychiatric services in adults with autism". Journal of Autism and Developmental Disorders 37 (6): 1080–5. July 2007. doi:10.1007/s10803-006-0248-1. PMID 17053989. http://cogprints.org/6268/2/JADD_2007.pdf. Retrieved 23 March 2012.
212. ↑ "Shared heritability of attention-deficit/hyperactivity disorder and autism spectrum disorder". European Child & Adolescent Psychiatry 19 (3): 281–95. March 2010. doi:10.1007/s00787-010-0092-x. PMID 20148275.
213. ↑ "Efficacy of sensory and motor interventions for children with autism". Journal of Autism and Developmental Disorders 32 (5): 397–422. October 2002. doi:10.1023/A:1020541906063. PMID 12463517.
214. ↑ 214.0 214.1 "Personality disorders and autism spectrum disorders: what are the connections?". Comprehensive Psychiatry 53 (4): 333–40. May 2012. doi:10.1016/j.comppsych.2011.05.014. PMID 21821235.
215. ↑ "Lifelong eccentricity and social isolation. II: Asperger's syndrome or schizoid personality disorder?". The British Journal of Psychiatry 153: 783–91. December 1988. doi:10.1192/bjp.153.6.783. PMID 3256377.
216. ↑ "Cluster A - Schizoid Personality Disorder and Substance Use Disorders". Integrated Treatment for Co-Occurring Disorders: Personality Disorders and Addiction. Routledge. 2008. pp. 31–32. ISBN 978-0-7890-3693-3. https://books.google.com/books?id=O5HY1xcfjEcC&pg=PA31.
217. ↑ "Genetics of autism: complex aetiology for a heterogeneous disorder". Nature Reviews Genetics 2 (12): 943–955. December 2001. doi:10.1038/35103559. PMID 11733747.
218. ↑ "Autism and metabolic diseases". Journal of Child Neurology 23 (3): 307–314. March 2008. doi:10.1177/0883073807308698. PMID 18079313.
219. ↑ 219.0 219.1 "Serotonin as a link between the gut-brain-microbiome axis in autism spectrum disorders". Pharmacological Research 132: 1–6. June 2018. doi:10.1016/j.phrs.2018.03.020. PMID 29614380.
220. ↑ 220.0 220.1 "Gastrointestinal symptoms and autism spectrum disorder: links and risks - a possible new overlap syndrome". Pediatric Health, Medicine and Therapeutics 6: 153–166. 2015. doi:10.2147/PHMT.S85717. PMID 29388597.
221. ↑ 221.0 221.1 "The bowel and beyond: the enteric nervous system in neurological disorders". Nature Reviews. Gastroenterology & Hepatology 13 (9): 517–528. September 2016. doi:10.1038/nrgastro.2016.107. PMID 27435372. "immune dysregulation, GI inflammation, malfunction of the ANS, genetic and metabolic activity of the microbiome, and dietary metabolites may contribute to brain dysfunction and neuroinflammation depending upon individual genetic vulnerability".
222. ↑ "Sleep problems in autism spectrum disorders: prevalence, nature, & possible biopsychosocial aetiologies". Sleep Medicine Reviews 13 (6): 403–411. December 2009. doi:10.1016/j.smrv.2009.02.003. PMID 19398354.
223. ↑ "Autism medical comorbidities". World Journal of Clinical Pediatrics 10 (3): 15–28. May 2021. doi:10.5409/wjcp.v10.i3.15. PMID 33972922.
224. ↑ "Dysautonomia: Perioperative Implications". Anesthesiology 116 (1): 205–215. January 2012. doi:10.1097/ALN.0b013e31823db712. PMID 22143168.
225. ↑ "Mast cell activation and autism". Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease 1822 (1): 34–41. January 2022. doi:10.1016/j.bbadis.2010.12.017. PMID 21193035.
226. ↑ "Fake and harmful autism 'treatments'" (in en). 2 May 2019. https://www.nhs.uk/conditions/autism/autism-and-everyday-life/fake-and-harmful-treatments/.
227. ↑ "Making information and the words we use accessible". https://www.england.nhs.uk/learning-disabilities/about/get-involved/involving-people/making-information-and-the-words-we-use-accessible/.
228. ↑ "How to talk about autism" (in en). https://www.autism.org.uk/what-we-do/help-and-support/how-to-talk-about-autism.
229. ↑ "The psychiatric management of autism in adults (CR228)" (in en). https://www.rcpsych.ac.uk/improving-care/campaigning-for-better-mental-health-policy/college-reports/2020-college-reports/cr228.
230. ↑ "Asperger's syndrome". Adolescent Medicine Clinics 17 (3): 771–88; abstract xiii. October 2006. doi:10.1016/j.admecli.2006.06.010. PMID 17030291.
231. ↑ "Asperger syndrome". European Child & Adolescent Psychiatry 18 (1): 2–11. June 2008. doi:10.1007/s00787-008-0701-0. PMID 18563474. http://www.ssoar.info/ssoar/handle/document/12424. Retrieved 21 September 2018.
232. ↑ "Modeling clinical outcome of children with autistic spectrum disorders". Pediatrics 116 (1): 117–22. July 2005. doi:10.1542/peds.2004-1118. PMID 15995041.
233. ↑ "10 Facts about Autism Spectrum Disorder (ASD)" (in en). https://www.acf.hhs.gov/ecd/10-facts-about-asd.
234. ↑ 234.0 234.1 234.2 234.3 234.4 234.5 234.6 "Management of children with autism spectrum disorders". Pediatrics 120 (5): 1162–1182. November 2007. doi:10.1542/peds.2007-2362. PMID 17967921.
235. ↑ "Behavioural and developmental interventions for autism spectrum disorder: a clinical systematic review". PLOS ONE 3 (11): e3755. 2008. doi:10.1371/journal.pone.0003755. PMID 19015734. Bibcode: 2008PLoSO...3.3755O.
236. ↑ 236.0 236.1 236.2 236.3 236.4 236.5 "Evidence Base Update for Autism Spectrum Disorder". Journal of Clinical Child and Adolescent Psychology (Taylor & Francis) 44 (6): 897–922. 2 November 2015. doi:10.1080/15374416.2015.1077448. ISSN 1537-4416. PMID 26430947.
237. ↑ "Meta-analysis of Early Intensive Behavioral Intervention for children with autism". Journal of Clinical Child and Adolescent Psychology (Taylor & Francis) 38 (3): 439–450. May 2009. doi:10.1080/15374410902851739. PMID 19437303.
238. ↑ "The effect of Autism Spectrum Disorders on adaptive independent living skills in adults with severe intellectual disability". Research in Developmental Disabilities (Elsevier) 30 (6): 1203–1211. November 2009. doi:10.1016/j.ridd.2009.04.001. PMID 19450950.
239. ↑ "NIMH » Autism Spectrum Disorder". National Institutes of Health (US). https://www.nimh.nih.gov/health/publications/autism-spectrum-disorder/index.shtml.
240. ↑ 240.0 240.1 240.2 240.3 240.4 "An update on pharmacotherapy for autism spectrum disorder in children and adolescents". Current Opinion in Psychiatry 28 (2): 91–101. March 2015. doi:10.1097/YCO.0000000000000132. PMID 25602248.
241. ↑ 241.0 241.1 "Cognitive Behavioral Therapy for Autism Spectrum Disorders: A Systematic Review". Pediatrics (American Academy of Pediatrics (AAP)) 147 (5). May 2021. doi:10.1542/peds.2020-049880. PMID 33888566.
242. ↑ 242.0 242.1 "Management of children with autism spectrum disorders". Pediatrics 120 (5): 1162–1182. November 2007. doi:10.1542/peds.2007-2362. PMID 17967921. http://pediatrics.aappublications.org/cgi/content/full/120/5/1162.
243. ↑ Children with Autism: A Developmental Perspective. Cambridge: Harvard University Press. 2002. pp. 178–179. ISBN 978-0-674-05313-7.
244. ↑ "Evidence-based comprehensive treatments for early autism". Journal of Clinical Child and Adolescent Psychology (Taylor & Francis) 37 (1): 8–38. January 2008. doi:10.1080/15374410701817808. ISSN 1537-4416. PMID 18444052.
245. ↑ 245.0 245.1 "Early Intervention for Children With Autism Spectrum Disorder Under 3 Years of Age: Recommendations for Practice and Research". Pediatrics 136 (Supplement 1): S60-81. October 2015. doi:10.1542/peds.2014-3667E. PMID 26430170.
246. ↑ 246.0 246.1 246.2 246.3 "Early intensive behavioral intervention (EIBI) for young children with autism spectrum disorders (ASD)". The Cochrane Database of Systematic Reviews 5 (10): CD009260. May 2018. doi:10.1002/14651858.CD009260.pub3. PMID 29742275.
247. ↑ 247.0 247.1 "Autism spectrum disorder in children and adolescents: Pharmacologic interventions". March 2020. https://www.uptodate.com/contents/autism-spectrum-disorder-in-children-and-adolescents-pharmacologic-interventions.
248. ↑ "Practice guideline: Treatment for insomnia and disrupted sleep behavior in children and adolescents with autism spectrum disorder: Report of the Guideline Development, Dissemination, and Implementation Subcommittee of the American Academy of Neurology". Neurology 94 (9): 392–404. March 2020. doi:10.1212/WNL.0000000000009033. PMID 32051244.
249. ↑ "Evidence-based, parent-mediated interventions for young children with autism spectrum disorder: The case of restricted and repetitive behaviors" (in en-US). Autism 19 (6): 662–72. August 2015. doi:10.1177/1362361314545685. PMID 25186943.
250. ↑ "Opening a window to the autistic brain". PLOS Biology 2 (8): E267. August 2004. doi:10.1371/journal.pbio.0020267. PMID 15314667.
251. ↑ Virués-Ortega, Javier (1 June 2010). "Applied behavior analytic intervention for autism in early childhood: Meta-analysis, meta-regression and dose–response meta-analysis of multiple outcomes" (in en). Clinical Psychology Review 30 (4): 387–399. doi:10.1016/j.cpr.2010.01.008. ISSN 0272-7358. PMID 20223569. https://www.sciencedirect.com/science/article/pii/S0272735810000218. Retrieved 17 June 2023.
252. ↑ "Diagnostic and assessment findings: a bridge to academic planning for children with autism spectrum disorders". Neuropsychology Review 18 (4): 367–384. December 2008. doi:10.1007/s11065-008-9072-z. PMID 18855144.
253. ↑ "Inclusion of Learners with Autism Spectrum Disorders in General Education Settings". Topics in Language Disorders 23 (2): 116–133. 2003. doi:10.1097/00011363-200304000-00005. http://www.nursingcenter.com/pdf.asp?AID=520301.
254. ↑ 254.0 254.1 "Autism Spectrum Disorder: Primary Care Principles". American Family Physician 94 (12): 972–979. December 2016. PMID 28075089.
255. ↑ Iffland, Michelle; Livingstone, Nuala; Jorgensen, Mikaela; Hazell, Philip; Gillies, Donna (2023-10-09). Cochrane Developmental, Psychosocial and Learning Problems Group. ed. "Pharmacological intervention for irritability, aggression, and self-injury in autism spectrum disorder (ASD)" (in en). The Cochrane Database of Systematic Reviews 2023 (10): CD011769. doi:10.1002/14651858.CD011769.pub2. PMID 37811711.
256. ↑ 256.0 256.1 "Pharmacological and dietary-supplement treatments for autism spectrum disorder: a systematic review and network meta-analysis". Molecular Autism 13 (1): 10. 2022. doi:10.1186/s13229-022-00488-4. PMID 35246237.
257. ↑ "Medication use among children with autism spectrum disorders". Journal of Child and Adolescent Psychopharmacology 17 (3): 348–355. June 2007. doi:10.1089/cap.2006.17303. PMID 17630868.
258. ↑ "Pharmacologic treatments for the behavioral symptoms associated with autism spectrum disorders across the lifespan". Dialogues in Clinical Neuroscience 14 (3): 263–279. September 2012. doi:10.31887/DCNS.2012.14.3/cdoyle. PMID 23226952.
259. ↑ "Pharmacological treatment options for autism spectrum disorders in children and adolescents". Harvard Review of Psychiatry 16 (2): 97–112. 2008. doi:10.1080/10673220802075852. PMID 18415882.
260. ↑ "Systematic review and guide to management of core and psychiatric symptoms in youth with autism". Acta Psychiatrica Scandinavica 138 (5): 379–400. November 2018. doi:10.1111/acps.12918. PMID 29904907.
261. ↑ Broadstock, Marita; Doughty, Carolyn; Eggleston, Matt (2007). "Systematic review of the effectiveness of pharmacological treatments for adolescents and adults with autism spectrum disorder". Autism 11 (4): 335–348. doi:10.1177/1362361307078132. ISSN 1362-3613. PMID 17656398.
262. ↑ "Interventions to address health outcomes among autistic adults: A systematic review". Autism 24 (6): 1345–1359. August 2020. doi:10.1177/1362361320913664. PMID 32390461.
263. ↑ 263.0 263.1 263.2 "Are therapeutic diets an emerging additional choice in autism spectrum disorder management?". World Journal of Pediatrics 14 (3): 215–223. June 2018. doi:10.1007/s12519-018-0164-4. PMID 29846886. "Current literature knowledge provides evidence that ketogenic and casein/gluten-free diet may have their own place in our reserve for the therapeutic management of specific subsets of children with autism. ... More clinical studies about the effect of gluten/caseinfree diet in these patients are available. However, available data arise from studies with small sample size and are still controversial. In general, despite encouraging data, no definite proof still exists. Under this view, the use of therapeutic diets in children with autism should be restricted to specific subgroups, such as children with autism and epilepsy or specific inborn errors of metabolism (ketogenic diet), children with known food intolerance/allergy or even children with food intolerance markers (gluten- and casein-free diet). Their implementation should always be guided by health care practitioners.".
264. ↑ "Evidence of the gluten-free and casein-free diet in autism spectrum disorders: a systematic review". Journal of Child Neurology 29 (12): 1718–1727. December 2014. doi:10.1177/0883073814531330. PMID 24789114.
265. ↑ 265.0 265.1 "Gluten- and casein-free diets for autistic spectrum disorder". The Cochrane Database of Systematic Reviews (2): CD003498. April 2008. doi:10.1002/14651858.CD003498.pub3. PMID 18425890. "Knivsberg 2002 "monitoring of the compliance with diet was not carried out" ... "several reports of children 'sneaking food' from siblings or classmates"".
266. ↑ "The Gluten-Free/Casein-Free Diet: A Double-Blind Challenge Trial in Children with Autism". Journal of Autism and Developmental Disorders 46 (1): 205–220. January 2016. doi:10.1007/s10803-015-2564-9. PMID 26343026. "20 natural challenges when parents reported that children by mistake consumed foods containing gluten or casein.".
267. ↑ "Placebo response in pharmacological and dietary supplement trials of autism spectrum disorder (ASD): systematic review and meta-regression analysis". Molecular Autism 11 (1): 66. 2020. doi:10.1186/s13229-020-00372-z. PMID 32847616.
268. ↑ "The relationship of autism and gluten". Clinical Therapeutics 35 (5): 578–583. May 2013. doi:10.1016/j.clinthera.2013.04.011. PMID 23688532. "At this time, the studies attempting to treat symptoms of autism with diet have not been sufficient to support the general institution of a gluten-free or other diet for all children with autism. There may be a subgroup of patients who might benefit from a gluten-free diet, but the symptom or testing profile of these candidates remains unclear.".
269. ↑ "Non-celiac gluten sensitivity: a work-in-progress entity in the spectrum of wheat-related disorders". Best Practice & Research. Clinical Gastroenterology 29 (3): 477–491. June 2015. doi:10.1016/j.bpg.2015.04.006. PMID 26060112. "autism spectrum disorders (ASD) have been hypothesized to be associated with NCGS [47,48]. Notably, a gluten- and casein-free diet might have a positive effect in improving hyperactivity and mental confusion in some patients with ASD. This very exciting association between NCGS and ASD deserves further study before conclusions can be firmly drawn".
270. ↑ "[Is gluten the great etiopathogenic agent of disease in the XXI century?]" (in es). Nutricion Hospitalaria 30 (6): 1203–1210. December 2014. doi:10.3305/nh.2014.30.6.7866. PMID 25433099.
271. ↑ "Characterizing the Interplay Between Autism Spectrum Disorder and Comorbid Medical Conditions: An Integrative Review". Frontiers in Psychiatry 9: 751. 2019. doi:10.3389/fpsyt.2018.00751. PMID 30733689.
272. ↑ "Complementary and alternative medicine treatments for children with autism spectrum disorders". Child and Adolescent Psychiatric Clinics of North America 17 (4): 803–20, ix. October 2008. doi:10.1016/j.chc.2008.06.004. PMID 18775371.
273. ↑ "Deaths resulting from hypocalcemia after administration of edetate disodium: 2003-2005". Pediatrics 118 (2): e534–e536. August 2006. doi:10.1542/peds.2006-0858. PMID 16882789. http://pediatrics.aappublications.org/cgi/content/full/118/2/e534.
274. ↑ "Chelation for autism spectrum disorder (ASD)". The Cochrane Database of Systematic Reviews (5): CD010766. May 2015. doi:10.1002/14651858.CD010766. PMID 26106752.
275. ↑ "CEASE Therapy for Autism: the Controversy of a "Cure"". 24 November 2021. https://www.autismparentingmagazine.com/cease-therapy-controversy-cure/.
276. ↑ "Interventions to address health outcomes among autistic adults: A systematic review". Autism 24 (6): 1345–1359. August 2020. doi:10.1177/1362361320913664. PMID 32390461.
277. ↑ "Music therapy for autistic people". The Cochrane Database of Systematic Reviews 2022 (5): CD004381. May 2022. doi:10.1002/14651858.CD004381.pub4. PMID 35532041.
278. ↑ ﻿Therapies for Children With Autism Spectrum Disorders﻿ (Report No. 11-EHC029-EF). Agency for Healthcare Research and Quality (US). April 2011. p. 8. PMID 21834171. https://www.ncbi.nlm.nih.gov/books/NBK56343/. Retrieved 15 May 2022. "Hyperbaric therapy, in which oxygen is administered in special chambers that maintain a higher air pressure, has shown possible effects in other chronic neurologic conditions and has also undergone preliminary exploration in ASDs." [needs update]
279. ↑ "Reflections on Recent Research Into Animal-Assisted Interventions in the Military and Beyond". Current Psychiatry Reports 19 (12): 110. November 2017. doi:10.1007/s11920-017-0861-z. PMID 29177710.
280. ↑ "Epidemiology of autism spectrum disorders". Pediatric Clinics of North America 59 (1): 27–43, ix–x. February 2012. doi:10.1016/j.pcl.2011.10.003. PMID 22284791.
281. ↑ "Rubella". Lancet 385 (9984): 2297–2307. June 2015. doi:10.1016/S0140-6736(14)60539-0. PMID 25576992.
282. ↑ 282.0 282.1 "Can children with autism recover? If so, how?". Neuropsychology Review 18 (4): 339–366. December 2008. doi:10.1007/s11065-008-9075-9. PMID 19009353.
283. ↑ 283.0 283.1 "Optimal outcome in individuals with a history of autism". Journal of Child Psychology and Psychiatry, and Allied Disciplines 54 (2): 195–205. February 2013. doi:10.1111/jcpp.12037. PMID 23320807.
284. ↑ "Intervention for optimal outcome in children and adolescents with a history of autism". Journal of Developmental and Behavioral Pediatrics 35 (4): 247–256. May 2014. doi:10.1097/DBP.0000000000000037. PMID 24799263.
285. ↑ "Evidence-based comprehensive treatments for early autism". Journal of Clinical Child and Adolescent Psychology (Taylor & Francis) 37 (1): 8–38. January 2008. doi:10.1080/15374410701817808. PMID 18444052.
286. ↑ "Diagnosis and epidemiology of autism spectrum disorders". Canadian Journal of Psychiatry 48 (8): 517–525. September 2003. doi:10.1177/070674370304800803. PMID 14574827.
287. ↑ "Autism" (in en). 30 March 2022. https://www.who.int/news-room/fact-sheets/detail/autism-spectrum-disorders.
288. ↑ 288.0 288.1 288.2 "Time trends in autism diagnosis over 20 years: a UK population-based cohort study". Journal of Child Psychology and Psychiatry, and Allied Disciplines 63 (6): 674–682. August 2021. doi:10.1111/jcpp.13505. ISSN 0021-9630. OCLC 01307942. PMID 34414570. "The figure starkly illustrates an overall 787% increase in recorded incidence of autism diagnosis over 20 years.".
289. ↑ "Prevalence of Autism Spectrum Disorder Among Children Aged 8 Years - Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2016" (in en-us). MMWR. Surveillance Summaries 69 (4): 1–12. March 2020. doi:10.15585/mmwr.ss6904a1. PMID 32214087.
290. ↑ ICD-11, "Females diagnosed with autism spectrum disorder are more frequently diagnosed with co-occurring disorders of intellectual development, suggesting that less severe presentations may go undetected as compared to males".
291. ↑ "Gender differences in co-morbid psychopathology and clinical management in adults with autism spectrum disorders". Research in Autism Spectrum Disorders 5 (2): 803–808. 2011. doi:10.1016/j.rasd.2010.09.009. ISSN 1750-9467.
292. ↑ Autism spectrum disorders (First ed.). Washington, DC: American Psychiatric Association Publishing. 30 April 2018. ISBN 978-1-61537-192-1. OCLC 1022084798.
293. ↑ "Prevalence of Autism Spectrum Disorder Among Children Aged 8 Years – Autism and Developmental Disabilities Monitoring Network, 11 Sites, United States, 2014". MMWR. Surveillance Summaries 67 (6): 1–23. April 2018. doi:10.15585/mmwr.ss6706a1. PMID 29701730.
294. ↑ "Temporal Changes in Effect Sizes of Studies Comparing Individuals With and Without Autism: A Meta-analysis". JAMA Psychiatry 76 (11): 1124–1132. August 2019. doi:10.1001/jamapsychiatry.2019.1956. PMID 31433441.
295. ↑ "CDC estimates 1 in 68 school-aged children have autism; no change from previous estimate" (in en-us). CDC. 31 March 2016. https://www.cdc.gov/media/releases/2016/p0331-children-autism.html.
296. ↑ "Epidemiology of autism spectrum disorders". Handbook of Autism and Pervasive Developmental Disorders. Diagnosis, Development, and Brain Mechanisms. 1. New York: Wiley. 2014. pp. 57–96. doi:10.1002/9781118911389. ISBN 978-1-118-91138-9.
297. ↑ "Estimating the prevalence of autism spectrum conditions in adults: extending the 2007 Adult Psychiatric Morbidity Survey". National Health Service, UK. 31 January 2012. http://www.hscic.gov.uk/catalogue/PUB05061/esti-prev-auti-ext-07-psyc-morb-surv-rep.pdf.
298. ↑ "Report: Autism Rate Rises to 1 in 40 Children". 26 November 2018. https://www.webmd.com/brain/autism/news/20181126/report-autism-rate-rises-to-1-in-40-children.
299. ↑ "Autism" (in en). https://www.who.int/news-room/fact-sheets/detail/autism-spectrum-disorders.
300. ↑ "Autism: A Global Perspective" (in en). Current Developmental Disorders Reports 2 (1): 58–64. 1 March 2015. doi:10.1007/s40474-014-0033-3. ISSN 2196-2987.
301. ↑ 301.0 301.1 CDC (27 March 2020). "Data and Statistics on Autism Spectrum Disorder | CDC" (in en-us). https://www.cdc.gov/ncbddd/autism/data.html.
302. ↑ Maenner, Matthew J.; Warren, Zachary; Williams, Ashley Robinson et al. (2023). "Prevalence and characteristics of autism spectrum disorder among children aged 8 years—Autism and Developmental Disabilities Monitoring Network, 11 sites, United States, 2020" (in en-us). MMWR. Surveillance Summaries 72 (2): 1–14. doi:10.15585/mmwr.ss7202a1. ISSN 1546-0738. PMID 34855725.
303. ↑ 303.0 303.1 "Epidemiology of pervasive developmental disorders". Pediatric Research 65 (6): 591–598. June 2009. doi:10.1203/PDR.0b013e31819e7203. PMID 19218885.
304. ↑ "The epidemiology of autistic spectrum disorders: is the prevalence rising?". Developmental Disabilities Research Reviews 8 (3): 151–161. 2002. doi:10.1002/mrdd.10029. PMID 12216059.
305. ↑ "Three Reasons Not to Believe in an Autism Epidemic". Current Directions in Psychological Science 14 (2): 55–58. April 2005. doi:10.1111/j.0963-7214.2005.00334.x. PMID 25404790.
306. ↑ "Incidence of autism spectrum disorders: changes over time and their meaning". Acta Paediatrica 94 (1): 2–15. January 2005. doi:10.1111/j.1651-2227.2005.tb01779.x. PMID 15858952.
307. ↑ "Tracing the origins of autism: a spectrum of new studies". Environmental Health Perspectives 114 (7): A412–A418. July 2006. doi:10.1289/ehp.114-a412. PMID 16835042.
308. ↑ "Autism risk factors: genes, environment, and gene-environment interactions". Dialogues in Clinical Neuroscience 14 (3): 281–292. September 2012. doi:10.31887/DCNS.2012.14.3/pchaste. PMID 23226953.
309. ↑ "Etiologies underlying sex differences in Autism Spectrum Disorders". Frontiers in Neuroendocrinology 35 (3): 255–71. August 2014. doi:10.1016/j.yfrne.2014.03.006. PMID 24705124.
310. ↑ "New developments in autism". Psychiatric Clinics of North America 32 (1): 1–14. March 2009. doi:10.1016/j.psc.2008.10.004. PMID 19248913.
311. ↑ "Autism Movement Seeks Acceptance, Not Cures". NPR. 26 June 2006. https://www.npr.org/templates/story/story.php?storyId=5488463.
312. ↑ "Autistic and proud of it". New Scientist (Reed Elsevier). ISSN 0262-4079. https://www.newscientist.com/article/mg18625041-500-autistic-and-proud-of-it/. Retrieved 10 November 2015.
313. ↑ 313.0 313.1 313.2 "The autism rights movement". New York Magazine. 25 May 2008. ISSN 0028-7369. https://nymag.com/news/features/47225/.
314. ↑ The Economic World. New York city: Chronicle Publishing Company. 1917. p. 366.
315. ↑ "Fieldwork on another planet: social science perspectives on the autism spectrum". BioSocieties 3 (3): 325–341. 2008. doi:10.1017/S1745855208006236.
316. ↑ "Results and Analysis of the Autistic Not Weird 2022 Autism Survey - Autistic Not Weird" (in en-GB). 23 March 2022. https://autisticnotweird.com/autismsurvey/.
317. ↑ "World Autism Awareness Day, 2 April". United Nations. https://www.un.org/en/events/autismday/.
318. ↑ "Autistic Pride Day 2015: A Message to the Autistic Community". 18 June 2015. http://autisticadvocacy.org/2015/06/autistic-pride-day-2015-a-message-to-the-autistic-community/.
319. ↑ "Autism Sunday – Home". 2010. http://www.autismsunday.co.uk/.
320. ↑ "About Autreat". Autreat.com. 2013. http://www.autreat.com/autreat.html.
321. ↑ "Fieldwork on Another Planet: Social Science Perspectives on the Autism Spectrum". BioSocieties 3 (3): 325–341. 2008. doi:10.1017/S1745855208006236. ISSN 1745-8552.
322. ↑ "Mapping the Autistic Advantage from the Accounts of Adults Diagnosed with Autism: A Qualitative Study". Autism in Adulthood 1 (2): 124–133. 13 April 2019. doi:10.1089/aut.2018.0035. PMID 31058260.
323. ↑ "'Surplus suffering': differences between organizational understandings of Asperger's syndrome and those people who claim the 'disorder'". Disability & Society 22 (7): 761–76. 2007. doi:10.1080/09687590701659618.
324. ↑ "Is Asperger syndrome necessarily viewed as a disability?". Focus Autism Other Dev Disabl 17 (3): 186–91. 2002. doi:10.1177/10883576020170030801. A preliminary, freely readable draft, with slightly different wording in the quoted text, is in: "Is Asperger's syndrome necessarily a disability?". Cambridge: Autism Research Centre. 2002. http://autismresearchcentre.com/docs/papers/2002_BC_ASDisability.pdf.
325. ↑ "The Autism Rights Movement". 23 May 2008. https://nymag.com/news/features/47225/.
326. ↑ "Autism spectrum disorder: difference or disability?" (in en). The Lancet Neurology 15 (11): 1126. 1 October 2016. doi:10.1016/S1474-4422(16)30002-3. ISSN 1474-4422. https://www.thelancet.com/journals/laneur/article/PIIS1474-4422(16)30002-3/abstract.
327. ↑ "Fieldwork on Another Planet: Social Science Perspectives on the Autism Spectrum". BioSocieties 3 (3): 325–341. 1 September 2008. doi:10.1017/S1745855208006236. ISSN 1745-8560.
328. ↑ "A medical condition or just a difference? The question roils autism community." (in en-US). The Washington Post. ISSN 0190-8286. https://www.washingtonpost.com/national/health-science/a-medical-condition-or-just-a-difference-the-question-roils-autism-community/2019/05/03/87e26f7e-6845-11e9-8985-4cf30147bdca_story.html.
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332. ↑ "Biocertification and Neurodiversity the Role and Implications of Self-Diagnosis in Autistic Communities". April 2016. https://www.researchgate.net/publication/291949788.
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338. ↑ 338.0 338.1 Solomon, Debra (2 May 2018). "The History of the Autism Puzzle Piece Ribbon | Autism Career Coach Queens" (in en-US). https://spectrumroadmap.com/the-history-of-the-autism-puzzle-piece-ribbon/.
339. ↑ 339.0 339.1 Morgan, Julian (11 March 2018). "Going Gold For Autism Acceptance" (in en). https://www.autisticuk.org/post/going-gold-for-autism-acceptance.
340. ↑ Muzikar, Debra (20 April 2019). "The Autism Puzzle Piece: A symbol that's going to stay or go?" (in en-US). https://the-art-of-autism.com/the-autism-puzzle-piece-a-symbol-of-what/.
341. ↑ Willingham, Emily. "No Foolin': Forget About Autism Awareness And Lighting Up Blue" (in en). Forbes. https://www.forbes.com/sites/emilywillingham/2017/04/01/no-foolin-forget-about-autism-awareness-and-lighting-up-blue/. Retrieved 10 October 2023.
342. ↑ Franco, Janelle (2014). "Puzzle Piece Project and Autism Awareness Month". Autism Speaks. https://campussuite-storage.s3.amazonaws.com/prod/1558550/996e2c54-539e-11e8-b9a1-0a0344361b00/1954741/f51bb58c-a4c7-11e9-8c86-121ab0aa6810/file/puzzlepieceproject_educational_tool_kit.pdf.
343. ↑ There have been multiple conversations about the flag on Reddit. Take for example: Reddit (2019). "I tried creating an autism/neurodiversity flag. It's a work in progress"" Reddit (2022). "Autism pride flag goes hard". Reddit (2022). "where did this flag even come from? first time i ever saw it was during r/place, now i see it everywhere".
344. ↑ AU-TI (2021). "A New Autistic Pride Flag Has Suddenly Appeared & It's Amazing". https://au-ti.com/2021/12/23/a-new-autistic-pride-flag-has-suddenly-appeared-its-amazing/.
345. ↑ Shanafelt, Robert (September 2008). "The nature of flag power: How flags entail dominance, subordination, and social solidarity" (in en). Politics and the Life Sciences 27 (2): 13–27. doi:10.2990/27_2_13. ISSN 0730-9384. PMID 19267587. https://www.cambridge.org/core/journals/politics-and-the-life-sciences/article/abs/nature-of-flag-power-how-flags-entail-dominance-subordination-and-social-solidarity/DB73F478AC2B16D4AFF64A10F85581FC.
346. ↑ Du, Xuehong; Jiao, Jianxin; Tseng, Mitchell M. (2003). "Identifying customer need patterns for customization and personalization". Integrated Manufacturing Systems 14 (5): 387–396. doi:10.1108/09576060310477799. https://www.emerald.com/insight/content/doi/10.1108/09576060310477799/full/html.
347. ↑ Kalyanaraman, Sriram; Sundar, S. Shyam (1 March 2006). "The Psychological Appeal of Personalized Content in Web Portals: Does Customization Affect Attitudes and Behavior?" (in en). Journal of Communication 56 (1): 110–132. doi:10.1111/j.1460-2466.2006.00006.x. ISSN 0021-9916. https://academic.oup.com/joc/article/56/1/110-132/4102581.
348. ↑ Handbook of Autism and Pervasive Developmental Disorders: Volume Two: Assessment, Interventions, and Policy. 2 (4th ed.). Hoboken, New Jersey: John Wiley & Sons. 2014. p. 301. ISBN 978-1-118-28220-5. OCLC 946133861. https://books.google.com/books?id=4yzqAgAAQBAJ&pg=PA301. Retrieved 1 March 2019.
349. ↑ "Parenting a child with autism" (in en). Jornal Brasileiro de Psiquiatria 68 (1): 42–47. March 2019. doi:10.1590/0047-2085000000223. ISSN 0047-2085.
350. ↑ "An Alternative-Medicine Believer's Journey Back to Science". WIRED. 29 April 2015. https://www.wired.com/2015/04/alternative-medicine-believers-journey-back-science/. "The entire diagnosis and explanation took no more than 45 minutes. 'In the moment of diagnosis, it feels like the death of your hopes and dreams,' Louise [Laidler] says. There's a quiet grief in her voice, even though two decades have passed. 'In a way, it's even harder than a death, because you can't mourn and go on,' she says. 'You have to figure out how to care for your new child.'"
351. ↑ "Parent and family impact of autism spectrum disorders: a review and proposed model for intervention evaluation". Clinical Child and Family Psychology Review 15 (3): 247–77. September 2012. doi:10.1007/s10567-012-0119-6. PMID 22869324.
352. ↑ "Association of childhood autism spectrum disorders and loss of family income". Pediatrics 121 (4): e821–e826. April 2008. doi:10.1542/peds.2007-1594. PMID 18381511. http://pediatrics.aappublications.org/cgi/content/full/121/4/e821.
353. ↑ "Child care problems and employment among families with preschool-aged children with autism in the United States". Pediatrics 122 (1): e202–e208. July 2008. doi:10.1542/peds.2007-3037. PMID 18595965. http://pediatrics.aappublications.org/cgi/content/full/122/1/e202.
354. ↑ "Siblings of individuals with autism spectrum disorders across the life course". Developmental Disabilities Research Reviews 13 (4): 313–320. 2007. doi:10.1002/mrdd.20171. PMID 17979200. http://www.waisman.wisc.edu/family/pubs/Autism/2007 siblings_autism_life-course.pdf.

### Sources

* "Neurodevelopmental Disorders". Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR). Washington, DC: American Psychiatric Association. 18 March 2022. ISBN 978-0-89042-577-0.
* "6A02 Autism spectrum disorder". International Classification of Diseases 11th Revision (ICD-11). World Health Organisation. February 2022. 6A02. https://icd.who.int/browse11/l-m/en#/http://id.who.int/icd/entity/437815624. Retrieved 14 May 2022.

## Further reading

Library resources about
Autism spectrum

* * *

* Online books
* Resources in your library
* Resources in other libraries

* Gabovitch, Elaine; Dutra, Courtney; Lauer, Emily. (2016). The Healthy People 2020 Roadmap for Massachusetts Children & Youth with ASD/DD: Understanding Needs and Measuring Outcomes (Report). Worcester: UMass Chan Medical School. Retrieved 30 June 2022.
* "Stereotypy in Adults with Autism Spectrum Disorders: Relationship and Diagnostic Fidelity". Journal of Developmental and Physical Disabilities 20 (2): 155–165. 2008. doi:10.1007/s10882-007-9086-0.
* , Wikidata Q28240738
* , Wikidata Q37552242 eISSN 1873-3379
* "DSM Criteria that Best Differentiate Intellectual Disability from Autism Spectrum Disorder". Child Psychiatry and Human Development 48 (4): 537–545. August 2017. doi:10.1007/s10578-016-0681-0. PMID 27558812.
* A practical guide to autism: what every parent, family member, and teacher needs to know. Hoboken: Wiley. 2009. ISBN 978-0-470-39473-1. OCLC 748908084. https://archive.org/details/practicalguideto0000volk. Retrieved 12 July 2022.

## External links

* WHO fact sheet on autism

Classification|

* ICD-11: 6A02
* ICD-10: F84.0
* ICD-9-CM: 299.00
* OMIM: 209850

|

External resources|

* Medicine:Curlie: Autism spectrum
* MedlinePlus: 001526
* Patient UK: Autism spectrum

* v
* t
* e

Pervasive developmental disorders and autism spectrum (F84, 299)

Main|

* Causes
* Comorbid conditions
* Epidemiology
* Heritability
* Societal and cultural aspects
* Medical model
* Therapies

Diagnoses|

* Autism spectrum (High-functioning autism
* Classic Autism
* Asperger syndrome
* Pervasive developmental disorder not otherwise specified
* Childhood disintegrative disorder
* Rett syndrome)

Related conditions|

* Alexithymia
* Attention deficit hyperactivity disorder
* Anxiety disorder (obsessive–compulsive disorder)
* Late talker
* Epilepsy
* Fragile X syndrome
* Hyperlexia
* Savant syndrome
* Sensory processing disorder
* Intellectual disability
* Developmental coordination disorder
* Multiple complex developmental disorder

Controversies|

* Autism rights movement
* Autistic enterocolitis
* Facilitated communication
* MMR vaccine
* Rapid prompting method
* Thiomersal (Chelation)

Diagnostic scales|

* Gilliam Asperger's disorder scale
* Autism Diagnostic Observation Schedule
* Autism Diagnostic Interview
* Autism-spectrum quotient
* Childhood Autism Rating Scale

Lists|

* Autism-related topics
* Fictional characters
* Schools

* v
* t
* e

Mental and behavioral disorders (F00–F99 & 290–319)

Adult personality and behavior

| Gender dysphoria|

* Ego-dystonic sexual orientation
* Paraphilia
* Fetishism
* Voyeurism
* Sexual maturation disorder
* Sexual relationship disorder

|

Other|

* Factitious disorder
* Munchausen syndrome
* Impulse control disorder
* Dermatillomania
* Kleptomania
* Pyromania
* Trichotillomania
* Personality disorder

Childhood and learning

| Emotional and behavioral|

* ADHD
* Conduct disorder
* ODD
* Emotional and behavioral disorders
* Separation anxiety disorder
* Movement disorders
* Stereotypic
* Social functioning
* DAD
* RAD
* Selective mutism
* Speech
* Stuttering
* Cluttering
* Tic disorder
* Tourette syndrome

|

Intellectual disability|

* X-linked intellectual disability
* Lujan–Fryns syndrome

Psychological development
(developmental disabilities)|

* Pervasive
* Specific

Mood (affective)

* Bipolar
* Bipolar I
* Bipolar II
* Bipolar NOS
* Cyclothymia
* Depression
* Atypical depression
* Dysthymia
* Major depressive disorder
* Melancholic depression
* Seasonal affective disorder
* Mania

Neurological and symptomatic

| Autism spectrum|

* Autism
* Asperger syndrome
* High-functioning autism
* PDD-NOS
* Savant syndrome

|

Dementia|

* AIDS dementia complex
* Alzheimer's disease
* Creutzfeldt–Jakob disease
* Frontotemporal dementia
* Huntington's disease
* Mild cognitive impairment
* Parkinson's disease
* Pick's disease
* Sundowning
* Vascular dementia
* Wandering

Other|

* Delirium
* Organic brain syndrome
* Post-concussion syndrome

Neurotic, stress-related and somatoform

| Adjustment|

* Adjustment disorder with depressed mood

|

Anxiety|

| Phobia|

* Agoraphobia
* Social anxiety
* Social phobia
* Anthropophobia
* Specific social phobia
* Specific phobia
* Claustrophobia

|

Other|

* Generalized anxiety disorder
* OCD
* Panic attack
* Panic disorder
* Stress
* Acute stress reaction
* PTSD

Dissociative|

* Depersonalization disorder
* Dissociative identity disorder
* Fugue state
* Psychogenic amnesia

Somatic symptom|

* Body dysmorphic disorder
* Conversion disorder
* Ganser syndrome
* Globus pharyngis
* Da Costa's syndrome
* Hypochondriasis
* Mass psychogenic illness
* Neurasthenia
* Nosophobia
* Psychalgia
* Somatization disorder

Physiological and physical behavior

| Eating|

* Anorexia nervosa
* Bulimia nervosa
* Rumination syndrome
* Other specified feeding or eating disorder

|

Nonorganic
sleep|

* Hypersomnia
* Insomnia
* Parasomnia
* Night terror
* Nightmare
* REM sleep behavior disorder

Postnatal|

* Postpartum depression
* Postpartum psychosis

Sexual dysfunction|

| Arousal|

* Erectile dysfunction
* Female sexual arousal disorder

|

Desire|

* Hypersexuality
* Hypoactive sexual desire disorder

Orgasm|

* Anorgasmia
* Delayed ejaculation
* Premature ejaculation
* Sexual anhedonia

Pain|

* Nonorganic dyspareunia
* Nonorganic vaginismus

Psychoactive substances, substance abuse and substance-related

* Drug overdose
* Intoxication
* Physical dependence
* Rebound effect
* Stimulant psychosis
* Substance dependence
* Withdrawal

Schizophrenia, schizotypal and delusional

| Delusional|

* Delusional disorder
* Folie à deux

|

Psychosis and
schizophrenia-like|

* Brief reactive psychosis
* Schizoaffective disorder
* Schizophreniform disorder

Schizophrenia|

* Childhood schizophrenia
* Disorganized (hebephrenic) schizophrenia
* Paranoid schizophrenia
* Pseudoneurotic schizophrenia
* Simple-type schizophrenia

Symptoms and uncategorized

* Catatonia
* False pregnancy
* Intermittent explosive disorder
* Klüver–Bucy syndrome
* Psychogenic non-epileptic seizures
* Psychomotor agitation
* Stereotypy

* v
* t
* e

Digital media use and mental health

Proposed or recognised diagnostic categories|

* Gaming disorder (Video game addiction)
* Problematic social media use
* Internet addiction disorder
* Problematic smartphone use
* Nomophobia
* Computer addiction
* Television addiction
* Internet sex addiction

Disciplines involved|

* Digital sociology
* Digital anthropology
* Psychiatry
* Psychology
* Neuroscience

Associated psychiatric conditions|

* Depression
* Anxiety
* Attention deficit hyperactivity disorder
* Bipolar disorder

Related concepts|

* Electronic media and sleep
* Screen time
* Digital detox
* Smartphone zombie
* Cyberbullying
* Media multitasking
* Online problem gambling
* Technostress
* Computer rage

Find out more on Wikipedia's
Sister projects|

* News stories
from Wikinews
* Definitions
from Wiktionary
* Textbooks
from Wikibooks
* Quotations
from Wikiquote
* Data
from Wikidata

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