WordNet

bring disorder to (同)disarray
a physical condition in which there is a disturbance of normal functioning; "the doctor prescribed some medicine for the disorder"; "everyone gets stomach upsets from time to time" (同)upset
a disturbance of the peace or of public order
characteristic of or affected with autism; "autistic behavior"; "autistic children"
not arranged in order (同)unordered

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〈U〉『無秩序』,混乱,乱雑(confusion) / 《しばしば複数形で》(社会的・政治的な)粉争,騒動 / 〈C〉(肉体的・精神的な)不調,異常,障害 / …‘の'秩序を乱す / 〈心身〉‘に'異常を起こさせる
自閉性(症)の

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出典(authority):フリー百科事典『ウィキペディア（Wikipedia）』「2017/03/19 22:46:51」(JST)

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Autism is a neurodevelopmental disorder characterized by impaired social interaction, verbal and non-verbal communication, and restricted and repetitive behavior. Parents usually notice signs in the first two years of their child's life.^[1] These signs often develop gradually, though some children with autism reach their developmental milestones at a normal pace and then regress.^[2] The diagnostic criteria require that symptoms become apparent in early childhood, typically before age three.^[3]

Autism is due to a combination of genetic and environmental factors.^[4] Some cases are strongly associated with certain infections during pregnancy including rubella and use of alcohol or cocaine.^[5] Controversies surround other proposed environmental causes;^[6] for example, the vaccine hypotheses, which have since been disproven. Autism affects information processing in the brain by altering how nerve cells and their synapses connect and organize; how this occurs is not well understood.^[7] In the DSM V, autism is included within the autism spectrum (ASDs), as is Asperger syndrome, which lacks delays in cognitive development and language, and pervasive developmental disorder, not otherwise specified (commonly abbreviated as PDD-NOS), which was diagnosed when the full set of criteria for autism or Asperger syndrome were not met.^[8]^[3]

Early speech or behavioral interventions can help children with autism gain self-care, social, and communication skills.^[9] Although there is no known cure,^[9] there have been reported cases of children who recovered.^[10] Not many children with autism live independently after reaching adulthood, though some become successful.^[11] An autistic culture has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.^[12]

Globally, autism is estimated to affect 21.7 million people as of 2013.^[13] As of 2010, the number of people affected is estimated at about 1–2 per 1,000 worldwide. It occurs four to five times more often in boys than girls. About 1.5% of children in the United States (one in 68) are diagnosed with ASD as of 2014^[update], a 30% increase from one in 88 in 2012.^[14]^[15]^[16] The rate of autism among adults aged 18 years and over in the United Kingdom is 1.1%.^[17] The number of people diagnosed has been increasing dramatically since the 1980s, partly due to changes in diagnostic practice and government-subsidized financial incentives for named diagnoses;^[16] the question of whether actual rates have increased is unresolved.^[18]

1 Characteristics
- 1.1 Social development
- 1.2 Communication
- 1.3 Repetitive behavior
- 1.4 Other symptoms
2 Causes
3 Mechanism
- 3.1 Pathophysiology
- 3.2 Neuropsychology
4 Diagnosis
- 4.1 Classification
5 Screening
6 Prevention
7 Management
- 7.1 Education
- 7.2 Medication
- 7.3 Alternative medicine
- 7.4 Cost
8 Society and culture
9 Prognosis
10 Epidemiology
11 History
12 References
13 Further reading
14 External links

Characteristics

Play media

Autism spectrum disorder video

Autism is a highly variable neurodevelopmental disorder^[19] that first appears during infancy or childhood, and generally follows a steady course without remission.^[20] People with autism may be severely impaired in some respects but normal, or even superior, in others.^[21] Overt symptoms gradually begin after the age of six months, become established by age two or three years,^[22] and tend to continue through adulthood, although often in more muted form.^[23] It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.^[24] Autism's individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.^[25]

Social development

Social deficits distinguish autism and the related autism spectrum disorders (ASD; see Classification) from other developmental disorders.^[23] People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals, or people with normal neural development, as leaving her feeling "like an anthropologist on Mars".^[26]

Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from social norms; for example, they have less eye contact and turn-taking, and do not have the ability to use simple movements to express themselves, such as pointing at things.^[27] Three- to five-year-old children with autism are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers.^[28] Most children with autism display moderately less attachment security than neurotypical children, although this difference disappears in children with higher mental development or less severe ASD.^[29] Older children and adults with ASD perform worse on tests of face and emotion recognition^[30] although this may be partly due to a lower ability to define a person's own emotions.^[31]

Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel. Functional friendships, such as those resulting in invitations to parties, may affect the quality of life more deeply.^[32]

There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with intellectual disability, autism is associated with aggression, destruction of property, and tantrums.^[33]

Communication

About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.^[34] Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, children with autism have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Children with autism are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia)^[35]^[36] or reverse pronouns.^[37] Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:^[8] for example, they may look at a pointing hand instead of the pointed-at object,^[27]^[36] and they consistently fail to point at objects in order to comment on or share an experience.^[8] Children with autism may have difficulty with imaginative play and with developing symbols into language.^[35]^[36]

In a pair of studies, high-functioning children with autism aged 8–15 performed equally well as, and adults better than, individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.^[38]

Repetitive behavior

A young boy with autism who has arranged his toys in a row

Autistic individuals can display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R) categorizes as follows.^[39]

Stereotyped behaviors: Repetitive movements, such as hand flapping, head rolling, or body rocking.
Compulsive behaviors: Time-consuming behaviors intended to reduce anxiety that an individual feels compelled to perform repeatedly or according to rigid rules, such as placing objects in a specific order, checking things, or hand washing.
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.^[39]
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.^[8]

No single repetitive or self-injurious behavior seems to be specific to autism, but autism appears to have an elevated pattern of occurrence and severity of these behaviors.^[40]

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.^[24] An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants.^[41] Many individuals with ASD show superior skills in perception and attention, relative to the general population.^[42] Sensory abnormalities are found in over 90% of those with autism, and are considered core features by some,^[43] although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.^[44] Differences 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).^[45] An estimated 60%–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking;^[43] deficits in motor coordination are pervasive across ASD and are greater in autism proper.^[46]

Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur;^[47] this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal symptoms, there is a lack of published rigorous data to support the theory that children with autism have more or different gastrointestinal symptoms than usual;^[48] studies report conflicting results, and the relationship between gastrointestinal problems and ASD is unclear.^[49]

Parents of children with ASD have higher levels of stress.^[27] Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children and were similar to siblings of children with Down syndrome in these aspects of the sibling relationship. However, they reported lower levels of closeness and intimacy than siblings of children with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.^[50]

Causes

It has long been presumed that there is a common cause at the genetic, cognitive, and neural levels for autism's characteristic triad of symptoms.^[51] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.^[51]^[52]

Deletion (1), duplication (2) and inversion (3) are all chromosome abnormalities that have been implicated in autism.^[53]

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 multigene interactions of common genetic variants.^[54]^[55] 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.^[23] Many genes have been associated with autism through sequencing the genomes of affected individuals and their parents.^[56]

Studies of twins suggest that heritability is 0.7 for autism and as high as 0.9 for ASD, and siblings of those with autism are about 25 times more likely to be autistic than the general population.^[43] However, 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 ASDs have been shown to selectively cause ASD.^[54] Numerous candidate genes have been located, with only small effects attributable to any particular gene.^[54] Most loci individually explain less than 1% of cases of autism.^[57] The large number of autistic individuals with unaffected family members may result from spontaneous structural variation — such as deletions, duplications or inversions in genetic material during meiosis.^[58]^[59] 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.^[53]

Several lines of evidence point to synaptic dysfunction as a cause of autism.^[7] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.^[60] Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes.^[61] All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, there is strong evidence that autism arises very early in development.^[62]

Exposure to air pollution during pregnancy, especially heavy metals and particulates, may increase the risk of autism.^[63] Environmental factors that have been claimed without evidence to contribute to or exacerbate autism include certain foods, infectious diseases, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,^[18] and prenatal stress. No evidence has been found for these claims, and some such as the MMR vaccine have been completely disproven.^[64]

Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to unsupported theories blaming vaccine "overload", a vaccine preservative, or the MMR vaccine for causing autism.^[65] The latter theory was supported by a litigation-funded study that has since been shown to have been "an elaborate fraud".^[66] Although these theories lack convincing scientific evidence and are biologically implausible,^[65] parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously controlled childhood diseases in some countries, and the preventable deaths of several children.^[67]^[68]

Mechanism

Autism's symptoms result from maturation-related changes in various systems of the brain. How autism occurs is not well understood. Its mechanism can be divided into two areas: the pathophysiology of brain structures and processes associated with autism, and the neuropsychological linkages between brain structures and behaviors.^[69] The behaviors appear to have multiple pathophysiologies.^[25]

Pathophysiology

Autism affects the amygdala, cerebellum, and many other parts of the brain.^[70]

Unlike many other brain disorders, such as Parkinson's, autism does not have a clear unifying mechanism at either the molecular, cellular, or systems level; it is not known whether autism is a few disorders caused by mutations converging on a few common molecular pathways, or is (like intellectual disability) a large set of disorders with diverse mechanisms.^[19] Autism appears to result from developmental factors that affect many or all functional brain systems,^[71] and to disturb the timing of brain development more than the final product.^[70] Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.^[62] This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.^[72] Just after birth, the brains of children with autism tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether early overgrowth occurs in all children with autism. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization.^[43] Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:

An excess of neurons that causes local overconnectivity in key brain regions.^[73]
Disturbed neuronal migration during early gestation.^[74]^[75]
Unbalanced excitatory–inhibitory networks.^[75]
Abnormal formation of synapses and dendritic spines,^[75] for example, by modulation of the neurexin–neuroligin cell-adhesion system,^[76] or by poorly regulated synthesis of synaptic proteins.^[77]^[78] Disrupted synaptic development may also contribute to epilepsy, which may explain why the two conditions are associated.^[79]

The immune system is thought to play an important role in autism. Children with autism have been found by researchers to have inflammation of both the peripheral and central immune systems as indicated by increased levels of pro-inflammatory cytokines and significant activation of microglia.^[80]^[81]^[82] Biomarkers of abnormal immune function have also been associated with increased impairments in behaviors that are characteristic of the core features of autism such as deficits in social interactions and communication.^[81] Interactions between the immune system and the nervous system begin early during the embryonic stage of life, and successful neurodevelopment depends on a balanced immune response. It is thought that activation of a pregnant mother's immune system such as from environmental toxicants or infection can contribute to causing autism through causing a disruption of brain development.^[83]^[84]^[85] This is supported by recent studies that have found that infection during pregnancy is associated with an increased risk of autism.^[86]^[87]

The relationship of neurochemicals to autism is not well understood; several have been investigated, with the most evidence for the role of serotonin and of genetic differences in its transport.^[7] The role of group I metabotropic glutamate receptors (mGluR) in the pathogenesis of fragile X syndrome, the most common identified genetic cause of autism, has led to interest in the possible implications for future autism research into this pathway.^[88] Some data suggests neuronal overgrowth potentially related to an increase in several growth hormones^[89] or to impaired regulation of growth factor receptors. Also, some inborn errors of metabolism are associated with autism, but probably account for less than 5% of cases.^[90]

The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties. The MNS operates when an animal performs an action or observes another animal perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions.^[91] Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger syndrome, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.^[92] However, individuals with autism also have abnormal brain activation in many circuits outside the MNS^[93] and the MNS theory does not explain the normal performance of children with autism on imitation tasks that involve a goal or object.^[94]

Autistic individuals tend to use different areas of the brain (yellow) for a movement task compared to a control group (blue).^[95]

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.^[96] In autism there is evidence for reduced functional connectivity of the default network, a large-scale brain network involved in social and emotional processing, with intact connectivity of the task-positive network, used in sustained attention and goal-directed thinking^{[clarification needed]}. In people with autism the two networks are not negatively correlated in time, suggesting an imbalance in toggling between the two networks, possibly reflecting a disturbance of self-referential thought.^[97]

The underconnectivity theory of autism hypothesizes that autism is marked by underfunctioning high-level neural connections and synchronization, along with an excess of low-level processes.^[98] Evidence for this theory has been found in functional neuroimaging studies on autistic individuals^[38] and by a brainwave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex.^[99] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.^[100]

From studies based on event-related potentials, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for nonsocial stimuli.^[101] For example, magnetoencephalography studies have found evidence in children with autism of delayed responses in the brain's processing of auditory signals.^[102]

In the genetic area, relations have been found between autism and schizophrenia based on duplications and deletions of chromosomes; research showed that schizophrenia and autism are significantly more common in combination with 1q21.1 deletion syndrome. Research on autism/schizophrenia relations for chromosome 15 (15q13.3), chromosome 16 (16p13.1) and chromosome 17 (17p12) are inconclusive.^[103]

Functional connectivity studies have found both hypo- and hyper-connectivity in brains of people with autism. Hypo-connectivity seems to dominate, especially for interhemispheric and cortico-cortical functional connectivity.^[104]

Neuropsychology

Two major categories of cognitive theories have been proposed about the links between autistic brains and behavior.

The first category focuses on deficits in social cognition. Simon Baron-Cohen's empathizing–systemizing theory postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing.^[105] These theories are somewhat related to Baron-Cohen's earlier theory of mind approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by the atypical responses of children with autism to the Sally–Anne test for reasoning about others' motivations,^[105] and the mirror neuron system theory of autism described in Pathophysiology maps well to the hypothesis.^[92] However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic intentions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.^[106]

The second category focuses on nonsocial or general processing: the executive functions such as working memory, planning, inhibition. In his review, Kenworthy states that "the claim of executive dysfunction as a causal factor in autism is controversial", however, "it is clear that executive dysfunction plays a role in the social and cognitive deficits observed in individuals with autism".^[107] Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.^[108] A strength of the theory is predicting stereotyped behavior and narrow interests;^[109] two weaknesses are that executive function is hard to measure^[107] and that executive function deficits have not been found in young children with autism.^[30]

Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people.^[110] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.^[111] These theories map well from the underconnectivity theory of autism.

Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties.^[52] A combined theory based on multiple deficits may prove to be more useful.^[112]

Diagnosis

Diagnosis is based on behavior, not cause or mechanism.^[25]^[113] Under the DSM-5, autism is characterized by persistent deficits in social communication and interaction across multiple contexts, as well as restricted, repetitive patterns of behavior, interests, or activities. These deficits are present in early childhood, typically before age three, and lead to clinically significant functional impairment. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with unusual objects. The disturbance must not be better accounted for by Rett syndrome, intellectual disability or global developmental delay.^[3] ICD-10 uses essentially the same definition.^[20]

Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semistructured parent interview, and the Autism Diagnostic Observation Schedule (ADOS)^[114] uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.^[27] The Diagnostic interview for social and communication disorders (DISCO) may also be used.^[115]

A pediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions.^[116] A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.^[117] A differential diagnosis for ASD at this stage might also consider intellectual disability, hearing impairment, and a specific language impairment^[116] such as Landau–Kleffner syndrome.^[118] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.^[119]

Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.^[120] Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,^[121] consensus guidelines in the US and UK are limited to high-resolution chromosome and fragile X testing.^[120] A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations.^[122] As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics.^[123] Metabolic and neuroimaging tests are sometimes helpful, but are not routine.^[120]

ASD can sometimes be diagnosed by age 14 months, although diagnosis becomes increasingly stable over the first three years of life: for example, a one-year-old who meets diagnostic criteria for ASD is less likely than a three-year-old to continue to do so a few years later.^[1] In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice.^[116] Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.

Underdiagnosis and overdiagnosis are problems in marginal cases, and much of the recent increase in the number of reported ASD cases is likely due to changes in diagnostic practices. The increasing popularity of drug treatment options and the expansion of benefits has given providers incentives to diagnose ASD, resulting in some overdiagnosis of children with uncertain symptoms. Conversely, the cost of screening and diagnosis and the challenge of obtaining payment can inhibit or delay diagnosis.^[124] It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes or blindisms.^[125]

Classification

Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior.^[20] These symptoms do not imply sickness, fragility, or emotional disturbance.^[23]

Of the five PDD forms, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical autism) is diagnosed when the criteria are not met for a more specific disorder.^[126] Unlike with autism, people with Asperger syndrome have no substantial delay in language development.^[127] The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the autism spectrum disorders (ASD)^[9] or sometimes the autistic disorders,^[128] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder; in clinical practice, though, autism, ASD, and PDD are often used interchangeably.^[120] ASD, in turn, is a subset of the broader autism phenotype, which describes individuals who may not have ASD but do have autistic-like traits, such as avoiding eye contact.^[129]

The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, developmentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication.^[130] Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary.^[43] Sometimes the syndrome is divided into low-, medium- or high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds,^[131] or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided into syndromal and non-syndromal autism; the syndromal autism is associated with severe or profound intellectual disability or a congenital syndrome with physical symptoms, such as tuberous sclerosis.^[132] Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.^[133]

Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype,^[2]^[35]^[1]^[134] or that there is a continuum of behaviors between autism with and without regression.^[135]

Research into causes has been hampered by the inability to identify biologically meaningful subgroups within the autistic population^[136] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.^[137] 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;^[138] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.^[7] It has been proposed to classify autism using genetics as well as behavior.^[139]

Screening

About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months.^[1] According to an article failure to meet any of the following milestones "is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome".^[24]

No babbling by 12 months.
No gesturing (pointing, waving, etc.) by 12 months.
No single words by 16 months.
No two-word (spontaneous, not just echolalic) phrases by 24 months.
Any loss of any language or social skills, at any age.

The United States Preventive Services Task Force in 2016 found it was unclear if screening was beneficial or harmful among children in whom there is no concerns.^[140] The Japanese practice is to screen all children for ASD at 18 and 24 months, using autism-specific formal screening tests. In contrast, in the UK, children whose families or doctors recognize possible signs of autism are screened. It is not known which approach is more effective.^[7] Screening tools include the Modified Checklist for Autism in Toddlers (M-CHAT), the Early Screening of Autistic Traits Questionnaire, and the First Year Inventory; initial data on M-CHAT and its predecessor, the Checklist for Autism in Toddlers (CHAT), on children aged 18–30 months suggests that it is best used in a clinical setting and that it has low sensitivity (many false-negatives) but good specificity (few false-positives).^[1] It may be more accurate to precede these tests with a broadband screener that does not distinguish ASD from other developmental disorders.^[141] Screening tools designed for one culture's norms for behaviors like eye contact may be inappropriate for a different culture.^[142] Although genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.^[143]

Prevention

Infection with rubella during pregnancy causes fewer than 1% of cases of autism;^[144] vaccination against rubella can prevent many of those cases.^[145]

Management

A three-year-old with autism points to fish in an aquarium, as part of an experiment on the effect of intensive shared-attention training on language development.^[95]

The main goals when treating children with autism 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.^[146]^[147] No single treatment is best and treatment is typically tailored to the child's needs.^[9] Families and the educational system are the main resources for treatment.^[7] Studies of interventions have methodological problems that prevent definitive conclusions about efficacy,^[148] however the development of evidence-based interventions has advanced in recent years.^[146] Although many psychosocial interventions have some positive evidence, suggesting that some form of treatment is preferable to no treatment, the methodological quality of systematic reviews of these studies has generally been poor, their clinical results are mostly tentative, and there is little evidence for the relative effectiveness of treatment options.^[149] Intensive, sustained special education programs and behavior therapy early in life can help children acquire self-care, social, and job skills,^[9] and often improve functioning and decrease symptom severity and maladaptive behaviors;^[150] claims that intervention by around age three years is crucial are not substantiated.^[151] Available approaches include applied behavior analysis (ABA), developmental models, structured teaching, speech and language therapy, social skills therapy, and occupational therapy.^[9] Among these approaches, interventions either treat autistic features comprehensively, or focalize treatment on a specific area of deficit.^[146] There is some evidence that early intensive behavioral intervention (EIBI), an early intervention model based on ABA for 20 to 40 hours a week for multiple years, is an effective treatment for some children with ASD.^[152] Two theoretical frameworks outlined for early childhood intervention include applied behavioral analysis (ABA) and developmental social pragmatic models (DSP).^[146] 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.^[146] 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.^[146]

Education

Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children^[153] and is well-established for improving intellectual performance of young children.^[150] Similarly, teacher-implemented intervention that utilizes an ABA combined with a developmental social pragmatic approach has been found to be a well-established treatment in improving social-communication skills in young children, although there is less evidence in its treatment of global symptoms.^[146] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.^[117] It is not known whether treatment programs for children lead to significant improvements after the children grow up,^[150] and the limited research on the effectiveness of adult residential programs shows mixed results.^[154] 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.^[155]

Medication

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.^[23]^[156] 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.^[157] Antipsychotics, such as risperidone and aripiprazole, have been found to be useful for treating irritability, repetitive behavior, and sleeplessness that often occurs with autism, however their side effects must be weighed against their potential benefits, and people with autism may respond atypically.^[158] There is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.^[159] No known medication relieves autism's core symptoms of social and communication impairments.^[160] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function,^[61]^[88] suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.^[60]^[161]

Alternative medicine

Although many alternative therapies and interventions are available, few are supported by scientific studies.^[30]^[162] Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.^[32] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.^[163] Some alternative treatments may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets;^[164] in 2005, botched chelation therapy killed a five-year-old child with autism.^[165] There has been early research looking at hyperbaric treatments in children with autism.^[166]

Although popularly used as an alternative treatment for people with autism, there is no good evidence that a gluten-free diet is of benefit.^[167]^[168]^[169] 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.^[167]^[170]^[171]^[172]

Cost

Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of $4.11 million (net present value in 2017 dollars, inflation-adjusted from 2003 estimate),^[173] with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity.^[174] Publicly supported programs are often inadequate or inappropriate for a given child, and unreimbursed out-of-pocket medical or therapy expenses are associated with likelihood of family financial problems;^[175] one 2008 US study found a 14% average loss of annual income in families of children with ASD,^[176] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.^[177] US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.^[178] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.^[179]

Society and culture

The rainbow-colored infinity is often used as a symbol for the diversity of the autism spectrum as well as neurodiversity in general.

The emergence of the autism rights movement has served as an attempt to encourage people to be more tolerant of those with autism.^[180] Through this movement, people hope to cause others to think of autism as a difference instead of a disease. Proponents of this movement wish to seek "acceptance, not cures."^[181] There have also been many worldwide events promoting autism awareness such as World Autism Awareness Day, Light It Up Blue, Autism Sunday, Autistic Pride Day, Autreat, and others.^[182]^[183]^[184]^[185]^[186] There have also been many organizations dedicated to increasing the awareness of autism and the effects that autism has on someone’s life. These organizations include Autism Speaks, Autism National Committee, Autism Society of America, and many others.^[187] Social-science scholars have had an increased focused on studying those with autism in hopes to learn more about "autism as a culture, transcultural comparisons... and research on social movements."^[188] Media has had an influence on how the public perceives those with autism. Rain Man, a film that won 4 Oscars including Best Picture, depicts a character with autism who has incredible talents and abilities.^[189] While many autistics don't have these special abilities, there are some autistic individuals who have been successful in their fields.^[190]^[191]^[192]

Prognosis

There is no known cure.^[9]^[7] Children recover occasionally, so that they lose their diagnosis of ASD;^[10] this occurs sometimes after intensive treatment and sometimes not. It is not known how often recovery happens;^[150] reported rates in unselected samples of children with ASD have ranged from 3% to 25%.^[10] Most children with autism acquire language by age five or younger, though a few have developed communication skills in later years.^[193] Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination.^[32] Although core difficulties tend to persist, symptoms often become less severe with age.^[23]

Few high-quality studies address long-term prognosis. Some adults show modest improvement in communication skills, but a few decline; no study has focused on autism after midlife.^[194] Acquiring language before age six, having an IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism.^[195] Most people with autism face significant obstacles in transitioning to adulthood.^[196]

Epidemiology

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

Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD,^[18] and 11 per 1,000 children in the United States for ASD as of 2008;^[15]^[144] because of inadequate data, these numbers may underestimate ASD's true rate.^[120] Globally, autism affects an estimated 21.7 million people as of 2013, while Asperger syndrome affects a further 31.1 million.^[13] In 2012, the NHS estimated that the overall prevalence of autism among adults aged 18 years and over in the UK was 1.1%.^[17] Rates of PDD-NOS's has been estimated at 3.7 per 1,000, Asperger syndrome at roughly 0.6 per 1,000, and childhood disintegrative disorder at 0.02 per 1,000.^[197] CDC's most recent estimate is that 1 out of every 68 children, or 14.7 per 1,000, has an ASD as of 2010.^[198]

The number of reported cases of autism increased dramatically in the 1990s and early 2000s. This increase is largely attributable to changes in diagnostic practices, referral patterns, availability of services, age at diagnosis, and public awareness,^[197]^[199] though unidentified environmental risk factors cannot be ruled out.^[6] The available evidence does not rule out the possibility that autism's true prevalence has increased;^[197] a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.^[200]

Boys are at higher risk for ASD than girls. 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.^[18] Several theories about the higher prevalence in males have been investigated, but the cause of the difference is unconfirmed;^[84] one theory is that females are underdiagnosed.^[201]

Although the evidence does not implicate any single pregnancy-related risk factor as a cause of autism, the risk of autism is associated with advanced age in either parent, and with diabetes, bleeding, and use of psychiatric drugs in the mother during pregnancy.^[84]^[202] The risk 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.^[43] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.^[203]

Several other conditions are common in children with autism.^[7] They include:

Genetic disorders. About 10–15% of autism cases have an identifiable Mendelian (single-gene) condition, chromosome abnormality, or other genetic syndrome,^[204] and ASD is associated with several genetic disorders.^[205]
Intellectual disability. The percentage of autistic individuals who also meet criteria for intellectual disability has been reported as anywhere from 25% to 70%, a wide variation illustrating the difficulty of assessing autistic intelligence.^[206] In comparison, for PDD-NOS the association with intellectual disability is much weaker,^[207] and by definition, the diagnosis of Asperger's excludes intellectual disability.^[208]
Anxiety disorders 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.^[209]
Epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.^[210]
Several metabolic defects, such as phenylketonuria, are associated with autistic symptoms.^[90]
Minor physical anomalies are significantly increased in the autistic population.^[211]
Preempted diagnoses. Although the DSM-IV rules out concurrent diagnosis of many other conditions along with autism, the full criteria for Attention deficit hyperactivity disorder (ADHD), Tourette syndrome, and other of these conditions are often present and these comorbid diagnoses are increasingly accepted.^[212]
Sleep problems affect about two-thirds of individuals with ASD at some point in childhood. These most commonly include symptoms of insomnia such as difficulty in 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.^[213]

History

Leo Kanner introduced the label early infantile autism in 1943.

A few examples of autistic symptoms and treatments were described long before autism was named. The Table Talk of Martin Luther, compiled by his notetaker, Mathesius, contains the story of a 12-year-old boy who may have been severely autistic.^[214] Luther reportedly thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated, although a later critic has cast doubt on the veracity of this report.^[215] The earliest well-documented case of autism is that of Hugh Blair of Borgue, as detailed in a 1747 court case in which his brother successfully petitioned to annul Blair's marriage to gain Blair's inheritance.^[216] The Wild Boy of Aveyron, a feral child caught in 1798, showed several signs of autism; the medical student Jean Itard treated him with a behavioral program designed to help him form social attachments and to induce speech via imitation.^[217]

The New Latin word autismus (English translation autism) was coined by the Swiss psychiatrist Eugen Bleuler in 1910 as he was defining symptoms of schizophrenia. He derived it from the Greek word autós (αὐτός, meaning "self"), and used it to mean morbid self-admiration, referring to "autistic withdrawal of the patient to his fantasies, against which any influence from outside becomes an intolerable disturbance".^[218]

The word autism first took its modern sense in 1938 when Hans Asperger of the Vienna University Hospital adopted Bleuler's terminology autistic psychopaths in a lecture in German about child psychology.^[219] Asperger was investigating an ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate diagnosis until 1981.^[217] Leo Kanner of the Johns Hopkins Hospital first used autism in its modern sense in English when he introduced the label early infantile autism in a 1943 report of 11 children with striking behavioral similarities.^[37] Almost all the characteristics described in Kanner's first paper on the subject, notably "autistic aloneness" and "insistence on sameness", are still regarded as typical of the autistic spectrum of disorders.^[52] It is not known whether Kanner derived the term independently of Asperger.^[220]

Kanner's reuse of autism led to decades of confused terminology like infantile schizophrenia, and child psychiatry's focus on maternal deprivation led to misconceptions of autism as an infant's response to "refrigerator mothers". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from intellectual disability and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy.^[221] As late as the mid-1970s there was little evidence of a genetic role in autism; now it is thought to be one of the most heritable of all psychiatric conditions.^[222] Although the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD,^[217] parents continue to feel social stigma in situations where their child's autistic behavior is perceived negatively by others,^[223] and many primary care physicians and medical specialists still express some beliefs consistent with outdated autism research.^[224]

The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely.^[225] Sociological and cultural aspects of autism have developed: some in the community seek a cure, while others believe that autism is simply another way of being.^[12]^[226]

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^ ^a ^b ^c ^d Rogers SJ, Vismara LA (2008). "Evidence-based comprehensive treatments for early autism". J Clin Child Adolesc Psychol. 37 (1): 8–38. doi:10.1080/15374410701817808. PMC 2943764. PMID 18444052.
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^ Lack of research on drug treatments:
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^ Hediger ML, England LJ, Molloy CA, Yu KF, Manning-Courtney P, Mills JL (2008). "Archived copy". J Autism Dev Disord. pp. 848–56. doi:10.1007/s10803-007-0453-6. PMID 17879151. Archived from the original on 1 October 2013. Retrieved 2008-04-17. Lay summary – NIH News (29 January 2008).
^ Brown MJ, Willis T, Omalu B, Leiker R (2006). "Deaths resulting from hypocalcemia after administration of edetate disodium: 2003–2005". Pediatrics. 118 (2): e534–6. doi:10.1542/peds.2006-0858. PMID 16882789. Archived from the original on 27 July 2009.
^ Warren Z, Veenstra-VanderWeele J, Stone W, et al. (April 2011). "Therapies for Children With Autism Spectrum Disorders": 8. PMID 21834171. 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.
^ ^a ^b Buie T (2013). "The relationship of autism and gluten". Clin Ther (Review). 35 (5): 578–83. 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.
^ Marí-Bauset S, Zazpe I, Mari-Sanchis A, Llopis-González A, Morales-Suárez-Varela M (Dec 2014). "Evidence of the gluten-free and casein-free diet in autism spectrum disorders: a systematic review". J Child Neurol. 29 (12): 1718–27. doi:10.1177/0883073814531330. hdl:10171/37087. PMID 24789114.
^ Millward C, Ferriter M, Calver S, Connell-Jones G (2008). Ferriter M, ed. "Gluten- and casein-free diets for autistic spectrum disorder". Cochrane Database Syst Rev (2): CD003498. doi:10.1002/14651858.CD003498.pub3. PMC 4164915. PMID 18425890.
^ Volta U, Caio G, De Giorgio R, Henriksen C, Skodje G, Lundin KE (Jun 2015). "Non-celiac gluten sensitivity: a work-in-progress entity in the spectrum of wheat-related disorders". Best Pract Res Clin Gastroenterol. 29 (3): 477–91. 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.
^ San Mauro I, Garicano E, Collado L, Ciudad MJ (Dec 2014). "[Is gluten the great etiopathogenic agent of disease in the XXI century?] [Article in Spanish]". Nutr Hosp. 30 (6): 1203–10. doi:10.3305/nh.2014.30.6.7866. PMID 25433099.
^ Catassi C, Bai JC, Bonaz B, Bouma G, Calabrò A, Carroccio A, Castillejo G, Ciacci C, Cristofori F, Dolinsek J, Francavilla R, Elli L, Green P, Holtmeier W, Koehler P, Koletzko S, Meinhold C, Sanders D, Schumann M, Schuppan D, Ullrich R, Vécsei A, Volta U, Zevallos V, Sapone A, Fasano A (Sep 2013). "Non-Celiac Gluten sensitivity: the new frontier of gluten related disorders". Nutrients. 5 (10): 3839–53. doi:10.3390/nu5103839. PMC 3820047. PMID 24077239. The above data suggest that removing gluten from the diet may positively affect the clinical outcome in some children diagnosed with ASD, indicating that autism may be part of the spectrum of NCGS, at least in some cases. However, a word of caution is necessary to stress the fact that only a small, selected sub-group of children affected by ASD may benefit from an elimination diet. Additional investigations are required in order to identify phenotypes based on best- and non-response to dietary modifications and assess any biological correlates including anthropometry before considering a dietary intervention.
^ Federal Reserve Bank of Minneapolis Community Development Project. "Consumer Price Index (estimate) 1800–". Federal Reserve Bank of Minneapolis. Retrieved January 2, 2017.
^ Ganz ML (2007). "The lifetime distribution of the incremental societal costs of autism". Arch Pediatr Adolesc Med. 161 (4): 343–9. doi:10.1001/archpedi.161.4.343. PMID 17404130. Archived from the original on 12 December 2009. Lay summary – Harvard School of Public Health (25 April 2006).
^ Sharpe DL, Baker DL (2007). "Financial issues associated with having a child with autism". J Fam Econ Iss. 28 (2): 247–64. doi:10.1007/s10834-007-9059-6.
^ Montes G, Halterman JS (2008). "Association of childhood autism spectrum disorders and loss of family income". Pediatrics. 121 (4): e821–6. doi:10.1542/peds.2007-1594. PMID 18381511. Archived from the original on 4 March 2010.
^ Montes G, Halterman JS (2008). "Child care problems and employment among families with preschool-aged children with autism in the United States". Pediatrics. 122 (1): e202–8. doi:10.1542/peds.2007-3037. PMID 18595965. Archived from the original on 6 December 2009.
^ Reinke T (2008). "States increasingly mandate special autism services". Manag Care. 17 (8): 35–6, 39. PMID 18777788. Archived from the original on 24 March 2014.
^ Aman MG (2005). "Treatment planning for patients with autism spectrum disorders". J Clin Psychiatry. 66 (Suppl 10): 38–45. PMID 16401149.
^ Trivedi, Bijal. "Autistic and proud of it". New Scientist. Retrieved 2015-11-10.
^ Shapiro, Joseph (2006-06-26). "Autism Movement Seeks Acceptance, Not Cures". NPR.org. Retrieved 2015-11-10.
^ "World Autism Awareness Day, 2 April". United Nations. Retrieved 2015-11-17.
^ "What is LIUB". Autism Speaks. Retrieved 2015-11-17.
^ Bascom, Julia (2015-06-18). "Autistic Pride Day 2015: A Message to the Autistic Community". Retrieved 2015-11-18.
^ "Autism Sunday – Home". Autism Sunday. 2010. Retrieved 2015-11-17.
^ "About Autreat". Autreat.com. 2013. Retrieved 2015-11-17.
^ "Other Autism Organizations". Autism Speaks. 2012-07-25. Retrieved 2015-11-17.
^ Silverman, Chloe (2008). "Fieldwork on Another Planet: Social Science Perspectives on the Autism Spectrum". BioSocieties. 3 (3): 325–341. doi:10.1017/S1745855208006236. ISSN 1745-8552.
^ "Rain Man (1988) - IMDb". IMDb. Retrieved 2015-11-17.
^ "American RadioWorks: Fast Food and Animal Rights – Kill Them With Kindness, Page 1". American Public Media. Retrieved 2015-11-17.
^ Page, Tim (2007-08-20). "Parallel Play". New Yorker. Retrieved 2015-11-17.
^ "Famous People With Autism Spectrum Disorder: Autistic Celebrities (List)". Mental Health Daily. Retrieved 2015-11-18.
^ Pickett E, Pullara O, O'Grady J, Gordon B (2009). "Speech acquisition in older nonverbal individuals with autism: a review of features, methods, and prognosis". Cogn Behav Neurol. 22 (1): 1–21. doi:10.1097/WNN.0b013e318190d185. PMID 19372766.
^ Seltzer MM, Shattuck P, Abbeduto L, Greenberg JS (2004). "Trajectory of development in adolescents and adults with autism". Ment Retard Dev Disabil Res Rev. 10 (4): 234–47. doi:10.1002/mrdd.20038. PMID 15666341.
^ Tidmarsh L, Volkmar FR (2003). "Diagnosis and epidemiology of autism spectrum disorders". Can J Psychiatry. 48 (8): 517–25. PMID 14574827.
^ Hendricks DR, Wehman P (24 March 2009). "Transition From School to Adulthood for Youth With Autism Spectrum Disorders: Review and Recommendations". Focus on Autism and Other Developmental Disabilities. 24 (2): 77–88. doi:10.1177/1088357608329827.
^ ^a ^b ^c Fombonne E (2009). "Epidemiology of pervasive developmental disorders". Pediatr Res. 65 (6): 591–8. doi:10.1203/PDR.0b013e31819e7203. PMID 19218885.
^ CDC | Home | Autism Spectrum Disorder (ASD) | NCBDDD
^ Wing L, Potter D (2002). "The epidemiology of autistic spectrum disorders: is the prevalence rising?". Ment Retard Dev Disabil Res Rev. 8 (3): 151–61. doi:10.1002/mrdd.10029. PMID 12216059.
^ Szpir M (2006). "Tracing the origins of autism: a spectrum of new studies". Environ Health Perspect. 114 (7): A412–8. doi:10.1289/ehp.114-a412. PMC 1513312. PMID 16835042.
^ Schaafsma SM, Pfaf DW (August 2014). "Etiologies underlying sex differences in Autism Spectrum Disorders". Frontiers in neuroendocrinology. 35 (3): 255–71. doi:10.1016/j.yfrne.2014.03.006. PMID 24705124.
^ Gardener H, Spiegelman D, Buka SL (2009). "Prenatal risk factors for autism: comprehensive meta-analysis". Br J Psychiatry. 195 (1): 7–14. doi:10.1192/bjp.bp.108.051672. PMC 3712619. PMID 19567888.
^ Bertoglio K, Hendren RL (2009). "New developments in autism". Psychiatr Clin North Am. 32 (1): 1–14. doi:10.1016/j.psc.2008.10.004. PMID 19248913.
^ Folstein SE, Rosen-Sheidley B (2001). "Genetics of autism: complex aetiology for a heterogeneous disorder". Nature Reviews Genetics. 2 (12): 943–55. doi:10.1038/35103559. PMID 11733747.
^ Zafeiriou DI, Ververi A, Vargiami E (2007). "Childhood autism and associated comorbidities". Brain Dev. 29 (5): 257–72. doi:10.1016/j.braindev.2006.09.003. PMID 17084999.
^ Learning in autism. In: Byrne JH (ed.-in-chief), Roediger HL III (vol. ed.). Learning and Memory: A Comprehensive Reference. Vol. 2. Academic Press; 2008 [Retrieved 26 July 2008]. doi:10.1016/B978-012370509-9.00152-2. ISBN 978-0-12-370504-4. p. 759–72.
^ Chakrabarti S, Fombonne E (2001). "Pervasive developmental disorders in preschool children". JAMA. 285 (24): 3093–9. doi:10.1001/jama.285.24.3093. PMID 11427137. Archived from the original on 28 August 2010.
^ DSM-IV-TR Diagnostical and Statistical Manual of Mental Disorders Fourth edition text revision. American Psychiatric Association, Washington DC; 2000. p. 80.
^ White SW, Oswald D, Ollendick T, Scahill L (2009). "Anxiety in children and adolescents with autism spectrum disorders". Clin Psychol Rev. 29 (3): 216–29. doi:10.1016/j.cpr.2009.01.003. PMC 2692135. PMID 19223098.
^ Spence SJ, Schneider MT (2009). "The role of epilepsy and epileptiform EEGs in autism spectrum disorders". Pediatr Res. 65 (6): 599–606. doi:10.1203/PDR.0b013e31819e7168. PMC 2692092. PMID 19454962.
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External links

Autism at DMOZ

UpToDate Contents

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1. 小児や青年の自閉症スペクトラム障害：マネージメントの概要 autism spectrum disorder in children and adolescents overview of management
2. 自閉症スペクトラム障害：臨床的特徴 autism spectrum disorder clinical features
3. 自閉症スペクトラム障害：診断 autism spectrum disorder diagnosis
4. 自閉症スペクトラム障害：用語、疫学および病因 autism spectrum disorder terminology epidemiology and pathogenesis
5. 自閉症スペクトラム障害：プライマリケアにおけるサーベイランスおよびスクリーニング autism spectrum disorder surveillance and screening in primary care

English Journal

WearSense: Detecting Autism Stereotypic Behaviors through Smartwatches.

Amiri AM1,2, Peltier N3, Goldberg C4, Sun Y5, Nathan A6, Hiremath SV7, Mankodiya K8.
Healthcare (Basel, Switzerland).Healthcare (Basel).2017 Feb 28;5(1). pii: E11. doi: 10.3390/healthcare5010011.
PMID 28264474

Assessment of plasma amino acid profile in autism using cation-exchange chromatography with postcolumn derivatization by ninhydrin.

Zaki MM1, Abdel-Al H1, Al-Sawi M2.
Turkish journal of medical sciences.Turk J Med Sci.2017 Feb 27;47(1):260-267. doi: 10.3906/sag-1506-105.
PMID 28263499

Distinct Defects in Spine Formation or Pruning in Two Gene Duplication Mouse Models of Autism.

Wang M1,2, Li H3, Takumi T4, Qiu Z1, Xu X5, Yu X6,7,8, Bian WJ9,10.
Neuroscience bulletin.Neurosci Bull.2017 Apr;33(2):143-152. doi: 10.1007/s12264-017-0111-8. Epub 2017 Mar 3.
PMID 28258509

Japanese Journal

精神疾患における腸内細菌叢の意義

長嶺敬彦
精神医学 57(4), 305-308, 2015-04
NAID 40020428334

コミュニケーション力の発達促進を目的とする「遊び」の活用 / 音楽療法における「演奏すること」と「遊び」の関連性を考える

高橋真喜子
鈴鹿短期大学紀要 35, 49-61, 2015-03-10
幼児にとって「遊ぶこと」は内的世界と外的現実を関連付ける作業であり、社会との関わりを持つための入口となる。この遊びの領域があることにより、幼児は幻想の世界に閉じこもることも外的現実に取り込まれて自己を見失うこともなく、外的対象と関わりながら現実を受け入れられるようになるのである。遊びの領域に他者の領域が重なり合うとき、情緒的な繋がりが生まれ、相互にコミュニケーションが可能となる。従って、遊びの領域 …
NAID 110009884782

自閉症スペクトラム児に対する社会的遊びの指導 : 遊びの条件がスキルの獲得と般化に及ぼす影響の検討

藤原あや,園山繁樹
自閉症スペクトラム研究 12(2), 33-43, 2015-03
NAID 40020441209

「自閉症スペクトラム障害」

	Library resources about; Autism
	Resources in your library; Resources in other libraries;

Autism
	Repetitively stacking or lining up objects is associated with autism.
Classification and external resources
Specialty	Psychiatry
ICD-10	F84.0
ICD-9-CM	299.00
OMIM	209850
DiseasesDB	1142
MedlinePlus	001526
eMedicine	med/3202 ped/180
Patient UK	Autism
MeSH	D001321
GeneReviews	Autism overview;
	[edit on Wikidata]

　　[★]

英: autistic spectrum disorder, autism spectrum disorders, ASD
同: 自閉症圏障害、自閉症スペクトラム、自閉症障害、自閉性障害 autistic disorder
関: カナー症候群

[show details]

自閉症圏障害 : 約 8,530 件
自閉症スペクトラム障害 : 約 45,900 件

自閉症とは異なるが類似した臨床像を示す疾患

「カナー症候群」

　　[★]

英: Kanner's syndrome, Kanner syndrome
同: 早期幼児自閉症 early infantile autism, 自閉性障害 autistic disorder
関: 自閉症、広汎発達障害

「自閉症性障害」

　　[★]

英: autistic disorder
関: 自閉症

「disorder」

　　[★]

障害：個人的苦痛や機能の障害があるので「疾病」とは言えるものの、その背景にある臓器障害がもう一つはっきりしない場合に用いられる。(PSY.9)

n.

an untidy state; a lack of order or organization (⇔order)
violent behaviour of large groups of people
an illness that cause a part of the body to stop functioning correctly

注意

disease <> illness <> disorder

vt.

乱す、乱雑にする。(人)の(心身の)調子を狂わせる。

vi.

「autistic」

　　[★]

n.

自閉症の人、自閉症性の人

adj.

自閉症の、自閉症性の

関: autism

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[DSM5-3] Autism Spectrum Disorder, 299.00 (F84.0). In: American Psychiatric Association. Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition. American Psychiatric Publishing; 2013.

[4] Chaste P, Leboyer M (2012). "Autism risk factors: genes, environment, and gene-environment interactions". Dialogues in Clinical Neuroscience. 14: 281–92. PMC 3513682. PMID 23226953.

[5] Ornoy A, Weinstein-Fudim L, Ergaz Z (2015), "Prenatal factors associated with autism spectrum disorder (ASD)", Reproductive Toxicology, 56: 155–169, doi:10.1016/j.reprotox.2015.05.007, PMID 26021712

[Rutter-6] Rutter M (2005). "Incidence of autism spectrum disorders: changes over time and their meaning". Acta Paediatr. 94 (1): 2–15. doi:10.1111/j.1651-2227.2005.tb01779.x. PMID 15858952.

[Levy-7] ^ ^a ^b ^c ^d ^e ^f ^g ^h Levy SE, Mandell DS, Schultz RT (2009). "Autism". Lancet. 374 (9701): 1627–38. doi:10.1016/S0140-6736(09)61376-3. PMC 2863325. PMID 19819542.

[Johnson-8] Johnson CP, Myers SM (2007). "Identification and evaluation of children with autism spectrum disorders". Pediatrics. 120 (5): 1183–215. doi:10.1542/peds.2007-2361. PMID 17967920. Archived from the original on 8 February 2009.

[CCD-9] ^ ^a ^b ^c ^d ^e ^f ^g Myers SM, Johnson CP (2007). "Management of children with autism spectrum disorders". Pediatrics. 120 (5): 1162–82. doi:10.1542/peds.2007-2362. PMID 17967921.

[Helt-10] Helt M, Kelley E, Kinsbourne M, Pandey J, Boorstein H, Herbert M, Fein D (2008). "Can children with autism recover? if so, how?". Neuropsychol Rev. 18 (4): 339–66. doi:10.1007/s11065-008-9075-9. PMID 19009353.

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v t e Pervasive developmental disorders and autism spectrum (F84, 299)

Main	Causes Comorbid conditions Epidemiology Heritability Sociological 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) Einstein syndrome 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 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 Autism-related films

Documentary	Autism Every Day Autism Is a World Autism: The Musical Best Kept Secret Children of the Stars Dad's in Heaven with Nixon The Horse Boy How to Dance in Ohio Life Animated Normal People Scare Me Recovered: Journeys Through the Autism Spectrum and Back Refrigerator Mothers Too Sane for This World The Wall or psychoanalysis put to the test for autism

Docudrama and Biopic	After Thomas Cries from the Heart Marathon Son-Rise: A Miracle of Love Temple Grandin Wretches & Jabberers

Educational	The Transporters

Fictional	Adam Backstreet Dreams Barfi! Ben X The Black Balloon Bless the Child The Boy Who Could Fly Breaking and Entering Burning Bright Carne Change of Habit A Child Is Waiting Chocolate Cube Dark Floors David's Mother Dear John Dr. Pomerantz Elling Eeshwar Extremely Loud and Incredibly Close Family Pictures Fly Away Forrest Gump God's Ears Haridas Henry & Verlin House of Cards I Am Sam Imagination Joyful Noise Killer Diller Koi... Mil Gaya Mabul Mario Mary and Max Mercury Rising Midwinter Night's Dream Miracle Run Molly Mozart and the Whale My Name Is Khan Nell Nightworld: Lost Souls Ocean Heaven The Other Sister Quantum Apocalypse Raam Rain Man Relative Fear Run Wild, Run Free Salmon Fishing in the Yemen Season of Miracles Swati Mutyam Swathi Muthu Silent Fall Simple Simon Snow Cake The Story of Luke Touch Under the Piano When the Bough Breaks White Frog Zig Zag

リンク元	「自閉症スペクトラム障害」「カナー症候群」「自閉症性障害」
関連記事	「disorder」「autistic」

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案内

autistic disorder