Autism
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]
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.[2] These signs often develop gradually, though
some children with autism reach their developmental
milestones at a normal pace and then regress.[3] The
diagnostic criteria require that symptoms become appar-
ent in early childhood, typically before age three.[4]
While autism is highly heritable, researchers suspect both
environmental and genetic factors as causes.[5] In rare
cases, autism is strongly associated with agents that cause
birth defects.[6] Controversies surround other proposed
environmental causes;[7] for example, the vaccine hy-
potheses have been disproven. Autism affects informa-
tion processing in the brain by altering how nerve cells
and their synapses connect and organize; how this occurs
is not well understood.[8] It is one of three recognized dis-
orders in the autism spectrum (ASDs), the other two be-
ing Asperger syndrome, which lacks delays in cognitive
development and language, and pervasive developmental
disorder, not otherwise specified (commonly abbreviated
as PDD-NOS), which is diagnosed when the full set of 1.1
criteria for autism or Asperger syndrome are not met.[9]
Early speech or behavioral interventions can help chil-
dren with autism gain self-care, social, and communica-
tion skills.[2] Although there is no known cure,[2] 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 individu-
als 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 peo-
ple as of 2013.[13] As of 2010, the number of peo-
ple affected is estimated at about 1–2 per 1,000 world-
wide. 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, 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
1
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
Autism is a highly variable neurodevelopmental disor-
der[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 re-
spects 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: im-
pairments in social interaction; impairments in commu-
nication; 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 patho-
logically 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 so-
cial 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 an-
thropologist 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 abil-
ity 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 understand-
ing, approach others spontaneously, imitate and respond
to emotions, communicate nonverbally, and take turns
2 1 CHARACTERISTICS

with others. However, they do form attachments to their overestimate what their audience comprehends.[38]
primary caregivers.[28] Most children with autism display
moderately less attachment security than neurotypical
children, although this difference disappears in children 1.3 Repetitive behavior
with higher mental development or less severe ASD.[29]
Older children and adults with ASD perform worse on Autistic individuals display many forms of repetitive or
tests of face and emotion recognition[30] although this restricted behavior, which the Repetitive Behavior Scale-
may be partly due to a lower ability to define a person’s Revised (RBS-R)[39] categorizes as follows.
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 num-
ber of friends, predicts how lonely they feel. Functional
friendships, such as those resulting in invitations to par-
ties, 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 in-
tellectual disability, autism is associated with aggression,
destruction of property, and tantrums.[33] A young boy with autism who has arranged his toys in a row

• Stereotypy is repetitive movement, such as hand

1.2 Communication flapping, head rolling, or body rocking.
• Compulsive behavior is intended and appears to
About a third to a half of individuals with autism do not
follow rules, such as arranging objects in stacks or
develop enough natural speech to meet their daily com-
[34] lines.
munication needs. Differences in communication may
be present from the first year of life, and may include de- • Sameness is resistance to change; for example, in-
layed onset of babbling, unusual gestures, diminished re- sisting that the furniture not be moved or refusing to
sponsiveness, and vocal patterns that are not synchronized be interrupted.
with the caregiver. In the second and third years, chil-
dren with autism have less frequent and less diverse bab- • Ritualistic behavior involves an unvarying pattern
bling, consonants, words, and word combinations; their of daily activities, such as an unchanging menu or a
gestures are less often integrated with words. Children dressing ritual. This is closely associated with same-
with autism are less likely to make requests or share ex- ness and an independent validation has suggested
periences, and are more likely to simply repeat others’ combining the two factors.[39]
words (echolalia)[35][36] or reverse pronouns.[37] Joint at- • Restricted behavior is limited in focus, interest, or
tention seems to be necessary for functional speech, and activity, such as preoccupation with a single televi-
deficits in joint attention seem to distinguish infants with sion program, toy or game.
ASD:[9] for example, they may look at a pointing hand in-
stead of the pointed-at object,[27][36] and they consistently • Self-injury includes movements that injure or can
fail to point at objects in order to comment on or share an injure the person, such as eye-poking, skin-picking,
[9]
experience. Children with autism may have difficulty hand-biting and head-banging.[9]
with imaginative play and with developing symbols into
language.[35][36] No single repetitive or self-injurious behavior seems to
be specific to autism, but only autism appears to have
In a pair of studies, high-functioning children with autism an elevated pattern of occurrence and severity of these
aged 8–15 performed equally well as, and adults bet- behaviors.[40]
ter than, individually matched controls at basic language
tasks involving vocabulary and spelling. Both autistic
groups performed worse than controls at complex lan- 1.4 Other symptoms
guage tasks such as figurative language, comprehension
and inference. As people are often sized up initially Autistic individuals may have symptoms that are inde-
from their basic language skills, these studies suggest that pendent of the diagnosis, but that can affect the indi-
people speaking to autistic individuals are more likely to vidual 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 fea-
tures 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, rhyth-
mic movements).[45] An estimated 60%–80% of autistic
people have motor signs that include poor muscle tone, Deletion (1), duplication (2) and inversion (3) are all
chromosome abnormalities that have been implicated in
poor motor planning, and toe walking;[43] deficits in mo-
autism.[53]
tor 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 for-
merly a diagnostic indicator. Selectivity is the most
common problem, although eating rituals and food re-
fusal 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 pub-
lished rigorous data to support the theory that children
with autism have more or different gastrointestinal symp-
toms 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]
2 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.[51] However, there is
increasing suspicion that autism is instead a complex dis-
order whose core aspects have distinct causes that often
co-occur.[51][52]
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 Exposure to air pollution during pregnancy, especially
3
1 2 3
variants.[54][55] Complexity arises due to interactions
among multiple genes, the environment, and epigenetic
factors which do not change DNA but are heritable and
influence gene expression.[23] Many genes have been as-
sociated 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 mu-
tations that increase autism risk have not been identi-
fied. Typically, autism cannot be traced to a Mendelian
(single-gene) mutation or to a single chromosome ab-
normality, 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] The
large number of autistic individuals with unaffected fam-
ily members may result from copy number variations—
spontaneous deletions or duplications in genetic mate-
rial during meiosis.[57] Hence, a substantial fraction of
autism cases may be traceable to genetic causes that are
highly heritable but not inherited: that is, the muta-
tion 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.[8] Some rare mutations may lead
to autism by disrupting some synaptic pathways, such as
those involved with cell adhesion.[58] Gene replacement
studies in mice suggest that autistic symptoms are closely
related to later developmental steps that depend on ac-
tivity in synapses and on activity-dependent changes.[59]
All known teratogens (agents that cause birth defects) re-
lated 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 af-
fected later, there is strong evidence that autism arises
very early in development.[6]
4 3 MECHANISM

heavy metals and particulates, may increase the risk

of autism.[60] Although no links have been found, and
some have been completely disproven, environmental
factors that have been claimed to contribute to or exac-
erbate autism, include certain foods, infectious diseases,
solvents, diesel exhaust, PCBs, phthalates and phenols
used in plastic products, pesticides, brominated flame re-
tardants, alcohol, smoking, illicit drugs, vaccines,[18] and
prenatal stress.[61]
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 “over-
load”, a vaccine preservative, or the MMR vaccine for
causing autism.[62] The latter theory was supported by
a litigation-funded study that has since been shown to
have been “an elaborate fraud”.[63] Although these the-
ories lack convincing scientific evidence and are biolog-
ically implausible,[62] parental concern about a poten-
tial vaccine link with autism has led to lower rates of
childhood immunizations, outbreaks of previously con-
trolled childhood diseases in some countries, and the pre-
ventable deaths of several children.[64][65]

3 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.[66] The behaviors appear to have multiple
pathophysiologies.[25]
Autism affects the amygdala, cerebellum, and many other parts
of the brain.[67]
with autism. It seems to be most prominent in brain
areas underlying the development of higher cognitive
specialization.[43] Hypotheses for the cellular and molec-
ular bases of pathological early overgrowth include the
following:

• An excess of neurons that causes local overconnec-

3.1 Pathophysiology tivity in key brain regions.[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,[68] and to disturb the timing of brain devel-
opment more than the final product.[67] Neuroanatomical
studies and the associations with teratogens strongly sug-
gest that autism’s mechanism includes alteration of brain
development soon after conception.[6] This anomaly ap-
pears to start a cascade of pathological events in the
brain that are significantly influenced by environmental
factors.[69] Just after birth, the brains of children with
autism tend to grow faster than usual, followed by nor-
mal or relatively slower growth in childhood. It is not
known whether early overgrowth occurs in all children
• Disturbed neuronal migration during early
gestation.[71][72]
• Unbalanced excitatory–inhibitory networks.[72]
• Abnormal formation of synapses and dendritic
spines,[72] for example, by modulation of the
neurexin–neuroligin cell-adhesion system,[73]
or by poorly regulated synthesis of synaptic
proteins.[74][75] Disrupted synaptic development
may also contribute to epilepsy, which may explain
why the two conditions are associated.[76]
The immune system is thought to play an important role
in autism. Children with autism have been found by re-
searchers to have inflammation of both the peripheral and
central immune systems as indicated by increased lev-
els of pro-inflammatory cytokines and significant activa-
tion of microglia.[77][78][79] Biomarkers of abnormal im-
mune function have also been associated with increased
3.1 Pathophysiology 5

impairments in behaviors that are characteristic of the

core features of autism such as deficits in social inter-
actions and communication.[78] Interactions between the
immune system and the nervous system begin early dur-
ing the embryonic stage of life, and successful neurode-
velopment depends on a balanced immune response. It is
thought that activation of a pregnant mother’s immune
system such as from environmental toxicants or infec-
tion can contribute to causing autism through causing a
disruption of brain development.[80][81][82] This is sup-
ported by recent studies that have found that infection
during pregnancy is associated with an increased risk of
autism.[83][84]
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 differ-
ences in its transport.[8] 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 impli-
cations for future autism research into this pathway.[85]
Some data suggests neuronal overgrowth potentially re-
lated to an increase in several growth hormones[86] or Autistic individuals tend to use different areas of the brain (yel-
to impaired regulation of growth factor receptors. Also, low) for a movement task compared to a control group (blue).[92]
some inborn errors of metabolism are associated with
autism, but probably account for less than 5% of cases.[87]
The mirror neuron system (MNS) theory of autism hy- The underconnectivity theory of autism hypothesizes that
pothesizes that distortion in the development of the MNS autism is marked by underfunctioning high-level neu-
interferes with imitation and leads to autism’s core fea- ral connections and synchronization, along with an ex-
tures of social impairment and communication difficul- cess of low-level processes.[95] Evidence for this theory
ties. The MNS operates when an animal performs an ac- has been found in functional neuroimaging studies on
tion or observes another animal perform the same action. autistic individuals[38] and by a brainwave study that sug-
The MNS may contribute to an individual’s understand- gested that adults with ASD have local overconnectivity
ing of other people by enabling the modeling of their be- in the cortex and weak functional connections between
havior via embodied simulation of their actions, inten- the frontal lobe and the rest of the cortex.[96] Other ev-
tions, and emotions.[88] Several studies have tested this idence suggests the underconnectivity is mainly within
hypothesis by demonstrating structural abnormalities in each hemisphere of the cortex and that autism is a dis-
MNS regions of individuals with ASD, delay in the ac- order of the association cortex.[97]
tivation in the core circuit for imitation in individuals From studies based on event-related potentials, transient
with Asperger syndrome, and a correlation between re- changes to the brain’s electrical activity in response to
duced MNS activity and severity of the syndrome in chil- stimuli, there is considerable evidence for differences
dren with ASD.[89] However, individuals with autism also in autistic individuals with respect to attention, orien-
have abnormal brain activation in many circuits outside tation to auditory and visual stimuli, novelty detection,
the MNS[90] and the MNS theory does not explain the language and face processing, and information storage;
normal performance of children with autism on imitation several studies have found a preference for nonsocial
tasks that involve a goal or object.[91] stimuli.[98] For example, magnetoencephalography stud-
ASD-related patterns of low function and aberrant acti- ies have found evidence in children with autism of de-
vation in the brain differ depending on whether the brain layed responses in the brain’s processing of auditory
[99]
is doing social or nonsocial tasks.[93] In autism there is ev- signals.
idence for reduced functional connectivity of the default In the genetic area, relations have been found between
network, a large-scale brain network involved in social autism and schizophrenia based on duplications and dele-
and emotional processing, with intact connectivity of the tions of chromosomes; research showed that schizophre-
task-positive network, used in sustained attention and nia and autism are significantly more common in com-
goal-directed thinking. In people with autism the two net- bination with 1q21.1 deletion syndrome. Research
works are not negatively correlated in time, suggesting an on autism/schizophrenia relations for chromosome 15
imbalance in toggling between the two networks, possibly (15q13.3), chromosome 16 (16p13.1) and chromosome
reflecting a disturbance of self-referential thought.[94] 17 (17p12) are inconclusive.[100]
6 4 DIAGNOSIS

Functional connectivity studies have found both hypo- of locally oriented and perceptual operations in autistic
and hyper-connectivity in brains of people with autism. individuals.[108] These theories map well from the under-
Hypo-connectivity seems to dominate, especially connectivity theory of autism.
for interhemispheric and cortico-cortical functional Neither category is satisfactory on its own; social cog-
connectivity.[101] nition theories poorly address autism’s rigid and repet-
itive behaviors, while the nonsocial theories have dif-
ficulty explaining social impairment and communica-
3.2 Neuropsychology tion difficulties.[52] A combined theory based on multiple
deficits may prove to be more useful.[109]
Two major categories of cognitive theories have been
proposed about the links between autistic brains and be-
havior.
4 Diagnosis
The first category focuses on deficits in social cognition.
Simon Baron-Cohen's empathizing–systemizing theory
postulates that autistic individuals can systemize—that Diagnosis is based on behavior, not cause or
mechanism.[25][110] Under the DSM-5, autism is
is, they can develop internal rules of operation to han-
dle events inside the brain—but are less effective at em- characterized by persistent deficits in social communi-
cation and interaction across multiple contexts, as well
pathizing by handling events generated by other agents.
An extension, the extreme male brain theory, hypothe- as restricted, repetitive patterns of behavior, interests, or
activities. These deficits are present in early childhood,
sizes that autism is an extreme case of the male brain,
defined psychometrically as individuals in whom sys- typically before age three, and lead to clinically signifi-
cant functional impairment. Sample symptoms include
temizing is better than empathizing.[102] These theories
are somewhat related to Baron-Cohen’s earlier theory lack of social or emotional reciprocity, stereotyped and
of mind approach, which hypothesizes that autistic be- repetitive use of language or idiosyncratic language,
havior arises from an inability to ascribe mental states and persistent preoccupation with unusual objects. The
to oneself and others. The theory of mind hypothesis disturbance must not be better accounted for by Rett
is supported by the atypical responses of children with syndrome, intellectual disability or global developmental
autism to the Sally–Anne test for reasoning about oth- delay.[4] ICD-10 uses essentially the same definition.[20]
ers’ motivations,[102] and the mirror neuron system the- Several diagnostic instruments are available. Two are
ory of autism described in Pathophysiology maps well to commonly used in autism research: the Autism Diagnos-
the hypothesis.[89] However, most studies have found no tic Interview-Revised (ADI-R) is a semistructured parent
evidence of impairment in autistic individuals’ ability to interview, and the Autism Diagnostic Observation Sched-
understand other people’s basic intentions or goals; in- ule (ADOS)[111] uses observation and interaction with the
stead, data suggests that impairments are found in under- child. The Childhood Autism Rating Scale (CARS) is
standing more complex social emotions or in considering used widely in clinical environments to assess severity of
others’ viewpoints.[103] autism based on observation of children.[27]
The second category focuses on nonsocial or general pro-A pediatrician commonly performs a preliminary in-
cessing: the executive functions such as working memory,vestigation by taking developmental history and physi-
planning, inhibition. In his review, Kenworthy states that
cally examining the child. If warranted, diagnosis and
“the claim of executive dysfunction as a causal factor in
evaluations are conducted with help from ASD spe-
cialists, observing and assessing cognitive, communica-
autism is controversial”, however, “it is clear that exec-
tion, family, and other factors using standardized tools,
utive dysfunction plays a role in the social and cognitive
deficits observed in individuals with autism”.[104] Tests of
and taking into account any associated medical condi-
core executive processes such as eye movement tasks in- tions.[112] A pediatric neuropsychologist is often asked to
dicate improvement from late childhood to adolescence, assess behavior and cognitive skills, both to aid diagno-
but performance never reaches typical adult levels.[105] A
sis and to help recommend educational interventions.[113]
A differential diagnosis for ASD at this stage might
strength of the theory is predicting stereotyped behavior
and narrow interests;[106] two weaknesses are that exec-also consider intellectual disability, hearing impairment,
utive function is hard to measure[104] and that executive
and a specific language impairment[112] such as Landau–
function deficits have not been found in young children Kleffner syndrome.[114] The presence of autism can make
with autism.[30] it harder to diagnose coexisting psychiatric disorders such
[115]
Weak central coherence theory hypothesizes that a lim- as depression.
ited ability to see the big picture underlies the cen- Clinical genetics evaluations are often done once ASD
tral disturbance in autism. One strength of this theory is diagnosed, particularly when other symptoms already
is predicting special talents and peaks in performance suggest a genetic cause.[1] Although genetic technology
in autistic people.[107] A related theory—enhanced per- allows clinical geneticists to link an estimated 40% of
ceptual functioning—focuses more on the superiority cases to genetic causes,[116] consensus guidelines in the
4.1 Classification
US and UK are limited to high-resolution chromosome
and fragile X testing.[1] A genotype-first model of diag-
nosis has been proposed, which would routinely assess
the genome’s copy number variations.[117] As new genetic
tests are developed several ethical, legal, and social issues
will emerge. Commercial availability of tests may pre-
cede adequate understanding of how to use test results,
given the complexity of autism’s genetics.[118] 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.[119]
In the UK the National Autism Plan for Children recom-
mends at most 30 weeks from first concern to completed
diagnosis and assessment, though few cases are handled
that quickly in practice.[112] Although the symptoms of
autism and ASD begin early in childhood, they are some-
times missed; years later, adults may seek diagnoses to
help them or their friends and family understand them-
selves, 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 symp-
toms. Conversely, the cost of screening and diagnosis and
the challenge of obtaining payment can inhibit or delay
diagnosis.[120] 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 blind-
ness syndromes or blindisms.[121]
4.1 Classification
Autism is one of the five pervasive developmental dis-
orders (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 other-
wise specified (PDD-NOS; also called atypical autism) is
diagnosed when the criteria are not met for a more spe-
cific disorder.[122] Unlike with autism, people with As-
perger syndrome have no substantial delay in language de-
7
velopment.[123] The terminology of autism can be bewil-
dering, with autism, Asperger syndrome and PDD-NOS
often called the autism spectrum disorders (ASD)[2] or
sometimes the autistic disorders,[124] whereas autism it-
self is often called autistic disorder, childhood autism, or
infantile autism. In this article, autism refers to the clas-
sic autistic disorder; in clinical practice, though, autism,
ASD, and PDD are often used interchangeably.[1] 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.[125]
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 in-
dividuals who may have active but distinctly odd so-
cial approaches, narrowly focused interests, and verbose,
pedantic communication.[126] Because the behavior spec-
trum is continuous, boundaries between diagnostic cate-
gories 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,[127] or on how much support the individual re-
quires in daily life; these subdivisions are not standard-
ized 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 symp-
toms, such as tuberous sclerosis.[128] Although individu-
als with Asperger syndrome tend to perform better cog-
nitively than those with autism, the extent of the overlap
between Asperger syndrome, HFA, and non-syndromal
autism is unclear.[129]
Some studies have reported diagnoses of autism in chil-
dren due to a loss of language or social skills, as op-
posed to a failure to make progress, typically from 15
to 30 months of age. The validity of this distinction re-
mains controversial; it is possible that regressive autism
is a specific subtype,[3][35][119][130] or that there is a con-
tinuum of behaviors between autism with and without
regression.[131]
Research into causes has been hampered by the inabil-
ity to identify biologically meaningful subgroups within
the autistic population[132] and by the traditional bound-
aries between the disciplines of psychiatry, psychology,
neurology and pediatrics.[133] Newer technologies such as
fMRI and diffusion tensor imaging can help identify bio-
logically relevant phenotypes (observable traits) that can
be viewed on brain scans, to help further neurogenetic
studies of autism;[134] one example is lowered activity in
the fusiform face area of the brain, which is associated
with impaired perception of people versus objects.[8] It
has been proposed to classify autism using genetics as
well as behavior.[135]
8 7
5 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.[119] According to an
article in the Journal of Autism and Developmental Disor-
ders, 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 diagno-
sis 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. A three-year-old with autism points to fish in an aquarium, as
• Any loss of any language or social skills, at any age.
US and 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.[8] Screening tools include the Modified Check-
list for Autism in Toddlers (M-CHAT), the Early Screen-
ing 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 chil-
dren 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).[119]
It may be more accurate to precede these tests with a
broadband screener that does not distinguish ASD from
other developmental disorders.[136] Screening tools de-
signed for one culture’s norms for behaviors like eye con-
tact may be inappropriate for a different culture.[137] Al-
though genetic screening for autism is generally still im-
practical, it can be considered in some cases, such as chil-
dren with neurological symptoms and dysmorphic fea-
tures.[138]
6 Prevention
Infection with rubella during pregnancy causes fewer than
1% of cases of autism;[139] vaccination against rubella can
prevent many of those cases.[140]
7 Management
Main article: Autism therapies
The main goals when treating children with autism
are to lessen associated deficits and family distress,
MANAGEMENT
part of an experiment on the effect of intensive shared-attention
training on language development.[92]
and to increase quality of life and functional inde-
pendence. In general, higher IQs are correlated with
greater responsiveness to treatment and improved treat-
ment outcomes.[141][142] No single treatment is best and
treatment is typically tailored to the child’s needs.[2] Fam-
ilies and the educational system are the main resources for
treatment.[8] Studies of interventions have methodolog-
ical problems that prevent definitive conclusions about
efficacy,[143] however the development of evidence-based
interventions has advanced in recent years.[141] Although
many psychosocial interventions have some positive evi-
dence, suggesting that some form of treatment is prefer-
able 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 treat-
ment options.[144] Intensive, sustained special education
programs and behavior therapy early in life can help chil-
dren acquire self-care, social, and job skills,[2] and often
improve functioning and decrease symptom severity and
maladaptive behaviors;[145] claims that intervention by
around age three years is crucial are not substantiated.[146]
Available approaches include applied behavior analy-
sis (ABA), developmental models, structured teaching,
speech and language therapy, social skills therapy, and
occupational therapy.[2] Among these approaches, inter-
ventions either treat autistic features comprehensively, or
focalize treatment on a specific area of deficit.[141] There
is some evidence that early intensive behavioral interven-
tion (EIBI), an early intervention model based on ABA
for 20 to 40 hours a week for multiple years, is an ef-
fective treatment for some children with ASD.[147] Two
theoretical frameworks outlined for early childhood in-
tervention include applied behavioral analysis (ABA) and
developmental social pragmatic models (DSP).[141] One
interventional strategy utilizes a parent training model,
7.3 Alternative medicine 9

which teaches parents how to implement various ABA 7.3 Alternative medicine
and DSP techniques, allowing for parents to dissem-
inate interventions themselves.[141] Various DSP pro- Although many alternative therapies and interventions are
grams have been developed to explicitly deliver inter- available, few are supported by scientific studies.[30][157]
vention systems through at-home parent implementation. Treatment approaches have little empirical support in
Despite the recent development of parent training mod- quality-of-life contexts, and many programs focus on suc-
els, these interventions have demonstrated effectiveness cess measures that lack predictive validity and real-world
in numerous studies, being evaluated as a probable effi- relevance.[32] Scientific evidence appears to matter less to
cacious mode of treatment.[141] service providers than program marketing, training avail-
ability, and parent requests.[158] Some alternative treat-
ments may place the child at risk. A 2008 study found
7.1 Education that compared to their peers, autistic boys have signifi-
cantly thinner bones if on casein-free diets;[159] in 2005,
Educational interventions can be effective to vary- botched chelation therapy killed a five-year-old child with
ing degrees in most children: intensive ABA treat- autism.[160] There has been early research looking at
ment has demonstrated effectiveness in enhancing global hyperbaric treatments in children with autism.[161]
functioning in preschool children[148] and is well-
established for improving intellectual performance of Although popularly used as an alternative treatment for
young children.[145] Similarly, teacher-implemented in- people with autism, there is no good evidence that a
[162][163][164]
tervention that utilizes an ABA combined with a de- gluten-free diet is of benefit. In the subset of
velopmental social pragmatic approach has been found people who have gluten sensitivity there is limited evi-
to be a well-established treatment in improving social- dence that suggests that a gluten free diet may improve
[162][165][166][167]
communication skills in young children, although there some autistic behaviours.
is less evidence in its treatment of global symptoms.[141]
Neuropsychological reports are often poorly communi-
cated to educators, resulting in a gap between what a re- 7.4 Cost
port recommends and what education is provided.[113] It
is not known whether treatment programs for children Treatment is expensive; indirect costs are more so. For
lead to significant improvements after the children grow someone born in 2000, a US study estimated an aver-
up,[145] and the limited research on the effectiveness of age lifetime cost of $4.07 million (net present value in
[168]
adult residential programs shows mixed results.[149] The 2016 dollars, inflation-adjusted from 2003 estimate),
appropriateness of including children with varying sever- with about 10% medical care, 30% extra education and
[169]
ity of autism spectrum disorders in the general education other care, and 60% lost economic productivity. Pub-
population is a subject of current debate among educators licly supported programs are often inadequate or inappro-
and researchers.[150] priate for a given child, and unreimbursed out-of-pocket
medical or therapy expenses are associated with likeli-
hood of family financial problems;[170] one 2008 US study
7.2 Medication found a 14% average loss of annual income in families
of children with ASD,[171] and a related study found that
Many medications are used to treat ASD symptoms ASD is associated with higher probability that child care
that interfere with integrating a child into home or problems will greatly affect parental employment.[172]
school when behavioral treatment fails.[23][151] More US states increasingly require private health insurance
than half of US children diagnosed with ASD are to cover autism services, shifting costs from publicly
prescribed psychoactive drugs or anticonvulsants, with funded education programs to privately funded health
the most common drug classes being antidepressants, insurance.[173] After childhood, key treatment issues in-
stimulants, and antipsychotics.[152] Antipsychotics, such clude residential care, job training and placement, sexu-
as risperidone and aripiprazole, have been found to be ality, social skills, and estate planning.[174]
useful for treating irritability, repetitive behavior, and
sleeplessness that often occurs with autism.[153] There is
scant reliable research about the effectiveness or safety of
drug treatments for adolescents and adults with ASD.[154] 8 Society and culture
A person with ASD may respond atypically to medica-
tions, the medications can have adverse effects,[2] and no Main article: Sociological and cultural aspects of autism
known medication relieves autism’s core symptoms of so- The emergence of the autism rights movement has served
cial and communication impairments.[155] Experiments as an attempt to encourage people to be more tolerant
in mice have reversed or reduced some symptoms related of those with autism.[175] Through this movement, peo-
to autism by replacing or modulating gene function,[59][85] ple hope to cause others to think of autism as a differ-
suggesting the possibility of targeting therapies to specific ence instead of a disease. Proponents of this movement
rare mutations known to cause autism.[58][156] wish to seek “acceptance, not cures.”[176] There have also
10 10 EPIDEMIOLOGY

autism after midlife.[189] 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.[190] Most people with autism face sig-
nificant obstacles in transitioning to adulthood.[191]

10 Epidemiology
Main article: Epidemiology of autism
Most recent reviews tend to estimate a prevalence of 1–2

The rainbow-colored infinity is often used as a symbol for the

diversity of the autism spectrum as well as neurodiversity in gen-
eral.

been many worldwide events promoting autism aware-

ness such as World Autism Awareness Day, Light It Up
Blue, Autism Sunday, Autistic Pride Day, Autreat, and
others.[177][178][179][180][181] 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 Na-
tional Committee, Autism Society of America, and many Reports of autism cases per 1,000 children grew dramatically in
others.[182] Social-science scholars have had an increased the US from 1996 to 2007. It is unknown how much, if any,
growth came from changes in rates of autism.
focused on studying those with autism in hopes to learn
more about “autism as a culture, transcultural compar-
isons… and research on social movements.”[183] Media per 1,000 for autism and close to 6 per 1,000 for ASD,[18]
has had an influence on how the public perceives those and 11 per 1,000 children in the United States for ASD
with autism. Rain Man, a film that won 4 Oscars, de- as of 2008;[15][139] because of inadequate data, these
picts a character with autism who has incredible talents numbers may underestimate ASD’s true rate.[1] Glob-
and abilities.[184] While many autistics don't have these ally, autism affects an estimated 21.7 million people as
special abilities, there are some autistic individuals who of 2013, while Asperger syndrome affects a further 31.1
have been successful in their fields.[185][186][187] 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
9 Prognosis 0.6 per 1,000, and childhood disintegrative disorder at
0.02 per 1,000.[192] CDC’s most recent estimate is that 1
There is no known cure.[2][8] Children recover occasion- out of every[193] 68 children, or 14.7 per 1,000, has an ASD
[10] as of 2010.
ally, so that they lose their diagnosis of ASD; this oc-
curs sometimes after intensive treatment and sometimes The number of reported cases of autism increased dra-
not. It is not known how often recovery happens;[145] matically in the 1990s and early 2000s. This increase
reported rates in unselected samples of children with is largely attributable to changes in diagnostic practices,
ASD have ranged from 3% to 25%.[10] Most children referral patterns, availability of services, age at diag-
with autism acquire language by age five or younger, nosis, and public awareness,[192][194] though unidentified
though a few have developed communication skills in environmental risk factors cannot be ruled out.[7] The
later years.[188] Most children with autism lack social sup- available evidence does not rule out the possibility that
port, meaningful relationships, future employment op- autism’s true prevalence has increased;[192] a real increase
portunities or self-determination.[32] Although core dif- would suggest directing more attention and funding to-
ficulties tend to persist, symptoms often become less se- ward changing environmental factors instead of continu-
vere with age.[23] ing to focus on genetics.[195]
Few high-quality studies address long-term prognosis. Boys are at higher risk for ASD than girls. The sex ratio
Some adults show modest improvement in communica- averages 4.3:1 and is greatly modified by cognitive im-
tion skills, but a few decline; no study has focused on pairment: it may be close to 2:1 with intellectual disabil-
 11

ity and more than 5.5:1 without.[18] Several theories about • Sleep problems affect about two-thirds of individ-
the higher prevalence in males have been investigated, but uals with ASD at some point in childhood. These
the cause of the difference is unconfirmed;[81] one theory most commonly include symptoms of insomnia such
is that females are underdiagnosed.[196] as difficulty in falling asleep, frequent nocturnal
Although the evidence does not implicate any single awakenings, and early morning awakenings. Sleep
pregnancy-related risk factor as a cause of autism, the problems are associated with difficult behaviors and
risk of autism is associated with advanced age in either family stress, and are often a focus of clinical atten-
parent, and with diabetes, bleeding, and use of psychi- tion over and above the primary ASD diagnosis.[208]
atric drugs in the mother during pregnancy.[81][197] The
risk is greater with older fathers than with older mothers;
two potential explanations are the known increase in mu- 11 History
tation burden in older sperm, and the hypothesis that men
marry later if they carry genetic liability and show some Further information: History of Asperger syndrome
signs of autism.[43] Most professionals believe that race, A few examples of autistic symptoms and treatments
ethnicity, and socioeconomic background do not affect
the occurrence of autism.[198]
Several other conditions are common in children with
autism.[8] They include:

• Genetic disorders. About 10–15% of autism cases

have an identifiable Mendelian (single-gene) con-
dition, chromosome abnormality, or other genetic
syndrome,[199] and ASD is associated with several
genetic disorders.[200]

• Intellectual disability. The percentage of autis-

tic individuals who also meet criteria for intellec-
tual disability has been reported as anywhere from
25% to 70%, a wide variation illustrating the diffi-
culty of assessing autistic intelligence.[201] In com-
parison, for PDD-NOS the association with intel-
lectual disability is much weaker,[202] and by defini-
tion, the diagnosis of Asperger’s excludes intellec-
tual disability.[203]

• 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 bet-
ter explained by ASD itself, or are hard to distin-
guish from ASD’s symptoms.[204]
Leo Kanner introduced the label early infantile autism in 1943.
• Epilepsy, with variations in risk of epilepsy due
to age, cognitive level, and type of language disor- were described long before autism was named. The Table
der.[205] Talk of Martin Luther, compiled by his notetaker, Math-
esius, contains the story of a 12-year-old boy who may
• Several metabolic defects, such as phenylketonuria,
have been severely autistic.[209] Luther reportedly thought
are associated with autistic symptoms.[87]
the boy was a soulless mass of flesh possessed by the devil,
• Minor physical anomalies are significantly in- and suggested that he be suffocated, although a later critic
creased in the autistic population.[206] has cast doubt on the veracity of this report.[210] The ear-
liest well-documented case of autism is that of Hugh Blair
• Preempted diagnoses. Although the DSM-IV of Borgue, as detailed in a 1747 court case in which his
rules out concurrent diagnosis of many other condi- brother successfully petitioned to annul Blair’s marriage
tions along with autism, the full criteria for Attention to gain Blair’s inheritance.[211] The Wild Boy of Avey-
deficit hyperactivity disorder (ADHD), Tourette ron, a feral child caught in 1798, showed several signs of
syndrome, and other of these conditions are often autism; the medical student Jean Itard treated him with
present and these comorbid diagnoses are increas- a behavioral program designed to help him form social
ingly accepted.[207] attachments and to induce speech via imitation.[212]
12
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 pa-
tient to his fantasies, against which any influence from
outside becomes an intolerable disturbance”.[213]
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.[214] Asperger was in-
vestigating an ASD now known as Asperger syndrome,
though for various reasons it was not widely recognized
as a separate diagnosis until 1981.[212] Leo Kanner of the
Johns Hopkins Hospital first used autism in its modern
sense in English when he introduced the label early in-
fantile autism in a 1943 report of 11 children with strik-
ing behavioral similarities.[37] Almost all the characteris-
tics described in Kanner’s first paper on the subject, no-
tably “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.[215]
Kanner’s reuse of autism led to decades of confused ter-
minology like infantile schizophrenia, and child psychi-
atry’s focus on maternal deprivation led to misconcep- [7] Rutter M (2005). “Incidence of autism spectrum disor-
tions of autism as an infant’s response to "refrigerator
mothers". Starting in the late 1960s autism was estab-
lished as a separate syndrome by demonstrating that it is
lifelong, distinguishing it from intellectual disability and [8] Levy SE, Mandell DS, Schultz RT (2009). “Autism”.
schizophrenia and from other developmental disorders,
and demonstrating the benefits of involving parents in ac-
tive programs of therapy.[216] As late as the mid-1970s
there was little evidence of a genetic role in autism; now [9] Johnson CP, Myers SM (2007). “Identification and eval-
it is thought to be one of the most heritable of all psy-
[217]
chiatric conditions. Although the rise of parent or-
ganizations and the destigmatization of childhood ASD
have deeply affected how we view ASD,[212] parents con-
tinue to feel social stigma in situations where their child’s [10] Helt M, Kelley E, Kinsbourne M, Pandey J, Boorstein H,
autistic behavior is perceived negatively by others,[218]
and many primary care physicians and medical specialists
still express some beliefs consistent with outdated autism
[219]
research.
The Internet has helped autistic individuals bypass non-
verbal cues and emotional sharing that they find so hard to
deal with, and has given them a way to form online com-
[220]
munities and work remotely. Sociological and cul- [12] Silverman C (2008). “Fieldwork on another planet: social
tural aspects of autism have developed: some in the com-
munity seek a cure, while others believe that autism is
simply another way of being.[12][221]
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Using Wikipedia for research
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13 Further reading
• Sicile-Kira, C. Autism spectrum disorder: the com-
plete guide to understanding autism. Revised Perigee
trade paperback ed. New York, New York: Perigee;
2014. ISBN 978-0-399-16663-1.
• Waltz, M. Autism: A Social and Medical History.
1st ed. Palgrave Macmillan; 22 March 2013. ISBN
978-0-230-52750-8.

• Silberman, S. NeuroTribes: The Legacy of Autism

and How to Think Smarter About People Who Think
Differently. 1st ed. Crows Nest, New South Wales:
Allen & Unwin; 2015. ISBN 978-1-760-11363-6.

14 External links
• Autism at DMOZ
 23

15 Text and image sources, contributors, and licenses

15.1 Text
• Autism Source: https://en.wikipedia.org/wiki/Autism?oldid=706633067 Contributors: Damian Yerrick, AxelBoldt, Mav, Bryan Derk-
sen, The Anome, Tarquin, -- April, RK, Alex.tan, Novalis, Matusz, Space Cadet, DavidLevinson, Bomfog, Ichelhof, Ryguasu, Olivier,
Stevertigo, Edward, Infrogmation, Michael Hardy, Tim Starling, Soegoe, David Martland, Mahjongg, Ixfd64, Bcrowell, Gaurav, Cyde,
Axlrosen, Karada, Delirium, Skysmith, Candicejvs, Iluvcapra, Ellywa, Ahoerstemeier, Mac, Snoyes, Marumari, LittleDan, Julesd, Kimiko,
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edit.jpg License: CC-BY-SA-3.0 Contributors: Transferred from en.wikipedia; transferred to Commons by User:Christian Giersing using
CommonsHelper.
Original artist: Original uploader was Andwhatsnext at en.wikipedia Original uploader was TimVickers at en.wikipedia
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spectrum_infinity_awareness_symbol.svg License: Public domain Contributors: http://fyeahautismspectrum.tumblr.com/post/
5852385279 Original artist: Eric (last name unknown)
• File:Autismbrain.jpg Source: https://upload.wikimedia.org/wikipedia/commons/8/83/Autismbrain.jpg License: Public domain Contrib-
utors: Originally this was taken from Major Brain Structures Implicated in Autism, but that resource no longer exists. An inferior copy of it,
in GIF form, is in Major Brain Structures Implicated in Autism, an image that appears in: Strock, M (2007). "Autism spectrum disorders
(pervasive developmental disorders)". National Institute of Mental Health. Retrieved on 2007-10-05. Original artist: National Institutes of
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• File:Autistic-sweetiepie-boy-with-ducksinarow.jpg Source: https://upload.wikimedia.org/wikipedia/commons/0/0d/
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Original artist: The original uploader was Andwhatsnext at English Wikipedia
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