User:WBTtheFROG/sandbox/t32q4/Autism

Source: Wikipedia, the free encyclopedia.
This article is about the classic autistic disorder; some writers use the word autism when referring to the range of disorders on the
autism spectrum or to the various pervasive developmental disorders.[1]
WBTtheFROG/sandbox/t32q4/Autism

Autism is a

Pervasive Developmental Disorder-Not Otherwise Specified (commonly abbreviated as PDD-NOS), which is diagnosed when the full set of criteria for autism or Asperger syndrome are not met.[4]

Autism has a strong genetic basis, although the

heavy metals, pesticides or childhood vaccines;[7] the vaccine hypotheses are biologically implausible and lack convincing scientific evidence.[8] The prevalence of autism is about 1–2 per 1,000 people worldwide; however, the Centers for Disease Control and Prevention (CDC) reports approximately 9 per 1,000 children in the United States are diagnosed with ASD.[9][10] The number of people diagnosed with autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.[11]

Parents usually notice signs in the first two years of their child's life.

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.[16]

Characteristics

Autism is a highly variable neurodevelopmental disorder[17] that first appears during infancy or childhood, and generally follows a steady course without remission.[18] Overt symptoms gradually begin after the age of six months, become established by age two or three years,[19] and tend to continue through adulthood, although often in more muted form.[20] 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.[21] 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.[22]

Social development

Social deficits distinguish autism and the related

neural development, as leaving her feeling "like an anthropologist on Mars".[23]

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

attachments to their primary caregivers.[25] Most autistic children display moderately less attachment security than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD.[26] Older children and adults with ASD perform worse on tests of face and emotion recognition.[27]

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.[28]

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 mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in non-autistic children with language impairments.[29] A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.[30]

Communication

About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.[31] 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, autistic children 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 are more likely to simply repeat others' words (echolalia)[32][33] or reverse pronouns.[34] Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:[4] for example, they may look at a pointing hand instead of the pointed-at object,[24][33] and they consistently fail to point at objects in order to comment on or share an experience.[4] Autistic children may have difficulty with imaginative play and with developing symbols into language.[32][33]

In a pair of studies, high-functioning autistic children 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.[35]

Repetitive behavior

Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R)[36] categorizes as follows.

Young boy asleep on a bed, facing the camera, with only the head visible and the body off-camera. On the bed behind the boy's head is a dozen or so toys carefully arranged in a line, ordered by size.
A young boy with autism, and the precise line of toys he made
  • Stereotypy is repetitive movement, such as hand flapping, making sounds, head rolling, or body rocking.
  • Compulsive behavior is intended and appears to follow rules, such as arranging objects in stacks or lines.
  • Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
  • Ritualistic behavior involves an 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.[36]
  • Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.
  • skin picking, hand biting, and head banging.[4] A 2007 study reported that self-injury at some point affected about 30% of children with ASD.[29]

No single repetitive or self-injurious behavior seems to be specific to autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.[37]

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.[21] 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.[38] Many individuals with ASD show superior skills in perception and attention, relative to the general population.[39]

Sensory abnormalities are found in over 90% of those with autism, and are considered core features by some,[40] although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.[41] 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).[42]
An estimated 60%–80% of autistic people have motor signs that include
poor muscle tone, poor motor planning, and toe walking;[40] deficits in motor coordination are pervasive across ASD and are greater in autism proper.[43]

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;

gastrointestinal (GI) symptoms, there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual;[44] studies report conflicting results, and the relationship between GI problems and ASD is unclear.[45]

Parents of children with ASD have higher levels of stress.[46] Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children or those with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.[47]

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.[18] These symptoms do not imply sickness, fragility, or emotional disturbance.[20]

Of the five PDD forms,

traits, such as avoiding eye contact.[50]


The manifestations of autism cover a wide

overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.[54]

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,[13][24][32][55] or that there is a continuum of behaviors between autism with and without regression.[56]



Research into causes has been hampered by the inability to identify biologically meaningful subpopulations

neurogenetic studies of autism;[58] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.[3] It has been proposed to classify autism using genetics as well as behavior.[59]


Classification (unmodified)

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.[18] These symptoms do not imply sickness, fragility, or emotional disturbance.[20]

Of the five PDD forms,

traits, such as avoiding eye contact.[62]


The manifestations of autism cover a wide

overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.[66]

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,[13][24][32][55] or that there is a continuum of behaviors between autism with and without regression.[67]



Research into causes has been hampered by the inability to identify biologically meaningful subpopulations

neurogenetic studies of autism;[70] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.[3] It has been proposed to classify autism using genetics as well as behavior.[71]


Causes

Main article: Causes of autism

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.[72] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.[72][73]

chromosome abnormalities that have been implicated in autism.[74]

Autism has a strong genetic basis, although the

Mendelian (single-gene) mutation or to a single chromosome abnormality like fragile X syndrome, and none of the genetic syndromes associated with ASDs have been shown to selectively cause ASD.[5] Numerous candidate genes have been located, with only small effects attributable to any particular gene.[5] The large number of autistic individuals with unaffected family members may result from copy number variations—spontaneous deletions or duplications in genetic material during meiosis.[76] 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.[74]

Several lines of evidence point to

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, it is strong evidence that autism arises very early in development.[6]

Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,

illicit drugs, vaccines,[11] and prenatal stress,[80]
although no links have been found, and some have been completely dis-proven.

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

outbreaks of previously-controlled childhood diseases in some countries, and the preventable deaths of several children.[10][82]

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

neuropsychological linkages between brain structures and behaviors.[83] The behaviors appear to have multiple pathophysiologies.[22]

Pathophysiology

Unlike many other brain disorders such as

teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.[6] This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.[86]


Just after birth, the brains of autistic children 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 autistic children. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization.[40]


Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:

Interactions between the

autoantibodies are found in conditions other than ASD, and are not always present in ASD,[96] the relationship between immune disturbances and autism remains unclear and controversial.[88]


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.[3]



Others have pointed to a role for group I

Fragile X.[97] Some data suggest an increase in several growth hormones; other data argue for diminished growth factors.[98] Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.[99]

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.[100] 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.[101] However, individuals with autism also have abnormal brain activation in many circuits outside the MNS[102] and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.[103]

A human brain viewed from above. About 10% is highlighted in yellow and 10% in blue. There is only a tiny (perhaps 0.5%) green region where they overlap.
Autistic individuals tend to use different areas of the brain (yellow) for a movement task compared to a control group (blue).[104]

ASD-related patterns of low function and aberrant activation in the brain differ depending on whether the brain is doing social or nonsocial tasks.[105] In autism there is evidence for reduced functional connectivity of the

self-referential thought.[106] A 2008 brain-imaging study found a specific pattern of signals in the cingulate cortex which differs in individuals with ASD.[107]

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.

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.[109] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.[110]

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, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli.[111] For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.[112]

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.[113]

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

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;[114] this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.[115]

These theories are somewhat related to the 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 autistic children's atypical responses to the Sally–Anne test for reasoning about others' motivations,[114] and the mirror neuron system theory of autism described in Pathophysiology maps well to the hypothesis.[101] 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.[116]

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in working memory, planning, inhibition, and other forms of executive function.[117] Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.[118] A strength of the theory is predicting stereotyped behavior and narrow interests;[119] two weaknesses are that executive function is hard to measure[117] and that executive function deficits have not been found in young autistic children.[27]

perceptual operations in autistic individuals.[121]
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.[73] A combined theory based on multiple deficits may prove to be more useful.[122]

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.[55] According to an article in the Journal of Autism and Developmental Disorders, 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."[21]

  • No babbling by 12 months.
  • No gesturing (pointing, waving bye-bye, etc.) by 12 months.
  • No single words by 16 months.
  • No 2-word spontaneous (not just echolalic) phrases by 24 months.
  • Any loss of any language or social skills, at any age.

US and Japanese practice is to

genetic screening for autism is generally still impractical, it can be considered in some cases, such as children with neurological symptoms and dysmorphic features.[125]

Diagnosis

DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder.[2] ICD-10 uses essentially the same definition.[18]

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) 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.[24]

A

hearing impairment, and a specific language impairment[127] such as Landau–Kleffner syndrome.[129] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.[130]

Metabolic and neuroimaging tests are sometimes helpful, but are not routine.[1]

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.[55] 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.[127] A 2009 US study found the average age of formal ASD diagnosis was 5.7 years, far above recommendations, and that 27% of children remained undiagnosed at age 8 years.[134] 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.[135]

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.

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.[137]

Management

Main article: Autism therapies
A young child points, in front of a woman who smiles and points in the same direction.
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.[104]

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. No single treatment is best and treatment is typically tailored to the child's needs.

speech and language therapy, social skills therapy, and occupational therapy.[12]

Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children[142] and is well-established for improving intellectual performance of young children.[140] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.[128] It is not known whether treatment programs for children lead to significant improvements after the children grow up,[140] and the limited research on the effectiveness of adult residential programs shows mixed results.[143] 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.[144]

Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.

adverse effects,[12] and no known medication relieves autism's core symptoms of social and communication impairments.[149] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function,[78][97] suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.[77][150]

Although many alternative therapies and interventions are available, few are supported by scientific studies.[27][151] 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.[28] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[152] 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;[153] in 2005, botched chelation therapy killed a five-year-old child with autism.[154]

Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of $5.23 million (

medical care, 30% extra education and other care, and 60% lost economic productivity.[156] 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;[157] one 2008 US study found a 14% average loss of annual income in families of children with ASD,[158] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.[159] US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.[160] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.[161]

Prognosis

No cure is known.

IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism.[164] A 2004 British study of 68 adults who were diagnosed before 1980 as autistic children with IQ above 50 found that 12% achieved a high level of independence as adults, 10% had some friends and were generally in work but required some support, 19% had some independence but were generally living at home and needed considerable support and supervision in daily living, 46% needed specialist residential provision from facilities specializing in ASD with a high level of support and very limited autonomy, and 12% needed high-level hospital care.[15] A 2005 Swedish study of 78 adults that did not exclude low IQ found worse prognosis; for example, only 4% achieved independence.[165] A 2008 Canadian study of 48 young adults diagnosed with ASD as preschoolers found outcomes ranging through poor (46%), fair (32%), good (17%), and very good (4%); 56% of these young adults had been employed at some point during their lives, mostly in volunteer, sheltered or part-time work.[166] Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.[11]

Epidemiology

Main article: Epidemiology of autism
Bar chart versus time. The graph rises steadily from 1996 to 2007, from about 0.7 to about 5.3. The trend curves slightly upward.
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 autism's prevalence.

Most recent

PDD-NOS's prevalence 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.[167] 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,[167][168] though unidentified environmental risk factors cannot be ruled out.[7] The available evidence does not rule out the possibility that autism's true prevalence has increased;[167] a real increase would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.[79]

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 mental retardation and more than 5.5:1 without.[11] 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.[169] 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.[40] Most professionals believe that race, ethnicity, and socioeconomic background do not affect the occurrence of autism.[170]

Several other conditions are common in children with autism.[3] They include:

History

Further information:
Sociological and cultural aspects of autism
Head and shoulders of a man in his early 60s in coat and tie, facing slightly to his right. He is balding and has a serious but slightly smiling expression.
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

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.[183]

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".[184]

The word autism first took its modern sense in 1938 when

child psychology.[185] 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.[183] 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.[34] 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.[73] It is not known whether Kanner derived the term independently of Asperger.[186]

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 "

medical specialists still express some beliefs consistent with outdated autism research.[190]

The

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.[16][192]

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  53. PMID 15796126
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  54. ^ Validity of ASD subtypes:
  55. ^
    PMID 18253102
    .
  56. PMID 19360687
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  57. PMID 18519493
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  58. PMID 19482063
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  59. PMID 18179879
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  60. PMID 19220594
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  61. PMID 17033636
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  65. PMID 15796126
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  66. ^ Validity of ASD subtypes:
  67. PMID 19360687
    .
  68. PMID 18519493
    .
  69. PMID 19220592
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  70. PMID 19482063
    .
  71. PMID 18179879
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  72. ^
    PMID 18956240
    .
  73. ^
    PMID 17001340
    .
  74. ^
    PMID 17479094
    .
  75. PMID 19432386
    .
  76. PMID 18923514
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  77. ^
    PMID 19541375
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  78. ^
    PMID 18984148
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  79. ^
    PMC 1513312
    .
  80. PMID 18598714
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  82. PMID 12867830
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  83. PMID 16484102
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  84. PMID 17326118
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  85. PMID 18258309
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  86. PMID 17919128
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  87. PMID 17964254
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  88. ^
    PMID 17971078
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  89. ^
    PMID 16808981
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  90. PMID 18923512
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  91. PMID 18984149
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  92. PMID 17940551
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  93. PMID 19006654
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  94. PMID 16698940
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  96. PMID 17804535
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  97. ^
    PMID 18093519.{{cite journal}}: CS1 maint: multiple names: authors list (link
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  98. PMID 18627794
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  99. ^
    PMID 18079313
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  100. ^ MNS and autism:
  101. ^
    PMID 17115076
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  102. PMC 1693139
    .
  103. PMID 18038342
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  104. ^
    PMC 509312
    .
  105. PMID 18996505
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  106. PMID 18824195
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  107. PMID 18255038
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  108. PMID 16772313
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  109. PMID 17336944
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  110. PMID 17620483
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  111. PMID 18850262
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  112. PMID 18336941
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  113. PMID 19955444.{{cite journal}}: CS1 maint: date and year (link) CS1 maint: multiple names: authors list (link
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  114. ^
    PMID 19338503
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  115. PMID 16366817
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  116. PMID 19508497
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  117. ^
    PMID 18956239
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  118. PMID 18838033
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  119. PMID 14697400
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  120. PMID 16450045
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  121. PMID 16453071
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  122. doi:10.1016/j.dr.2007.02.001
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  123. PMID 18805944
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  124. PMID 18373717
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  125. PMC 2603481
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  126. PMC 188387
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  127. ^
    PMID 17515625
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    PMID 18855144
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  137. doi:10.1177/1362361398022002
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  138. PMC 2582449
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  139. PMID 19191842
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  140. ^
    PMID 18444052
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  141. PMID 19143460
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  142. PMID 18385012
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  146. PMID 17630868
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  147. PMC 2171144
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  148. ^ Lack of research on drug treatments:
  149. PMID 14521196
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  150. PMID 20303363.{{cite journal}}: CS1 maint: multiple names: authors list (link
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  151. ^ Lack of support for interventions:
  152. PMID 16467905
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  153. PMID 17879151
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  154. PMID 16882789
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  156. PMID 17404130
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  157. doi:10.1007/s10834-007-9059-6
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  158. PMID 18381511
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  159. PMID 18595965
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  160. PMID 18777788
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  161. PMID 16401149
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  162. PMID 19372766
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  163. PMID 15666341
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  164. PMID 14574827
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  165. PMID 16119476
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  166. PMID 17764027
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  167. ^
    PMID 19218885
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  168. PMID 12216059
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  169. PMID 19567888
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  170. PMID 19248913
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  171. PMID 11733747
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  172. PMID 17084999
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  174. PMID 11427137
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  175. PMID 19223098
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  176. PMC 2692092
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