Autism spectrum: Difference between revisions

Autism spectrum
Autism spectrum
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Autism is a brain development disorder that shows symptoms before a child is three years old and has a steady course with no remission. Its characteristic signs are impairments in social interaction and communication, as well as restricted and repetitive behavior.^[1] These characteristics distinguish autism from milder pervasive developmental disorders (PDD) or autism spectrum disorders (ASD),^[2] and reflect Leo Kanner's first descriptions of autism, which emphasized "autistic aloneness" and "insistence on sameness".^[3]

Heritability contributes about 90% of the risk of a child developing autism, but the genetics of autism are complex and typically it is unclear which genes are responsible.^[4] In rare cases, autism is strongly associated with agents that cause birth defects.^[5] Many other causes have been proposed, such as exposure of children to vaccines; these proposals are controversial and the vaccine hypotheses have no convincing scientific evidence.^[6]

Autism affects many parts of the brain, but how this occurs is poorly understood.^[7] Parents usually notice warning signs in the first year or two of their child's life. Rapid evaluation by a specialist is important^[8] as, although there is no cure, early intervention may aid attempts to help children gain self-care and social skills. However, only a very few of these interventions are supported by scientific studies.^[9] With severe autism independent living is unlikely, but with milder autism there are some success stories as adults,^[10] and an autistic culture has developed, with some seeking a cure and others believing that autism is simply another way of being.^[11]

Most recent reviews estimate a prevalence of 1–2 per 1,000 people for autism and close to 6 per 1,000 for ASD, with ASD averaging a 4.3:1 male-to-female ratio. The number of people known to have autism has increased dramatically since the 1980s. Some of this increase is undoubtedly due to changes in diagnostic practice; it is unknown whether prevalence has increased as well.^[12]

Classification

File:Asperger kl2.jpg

Hans Asperger described a form of ASD in the 1940s that later became known as Asperger syndrome.

Autism is a developmental disorder of the human brain that first shows signs during infancy or childhood and follows a steady course without remissions or relapses. Its impairments result from maturation-related changes in various systems of the brain. Autism is one of the five pervasive developmental disorders (PDD) or autism spectrum disorders (ASD), which are characterized by widespread abnormalities of social interactions and communication, as well as severely restricted interests and highly repetitive behavior.^[2]

Of the other four ASD forms, Asperger syndrome is closest to autism; Rett syndrome and childhood disintegrative disorder share several symptoms with autism but may have unrelated causes; finally, pervasive developmental disorder not otherwise specified (PDD-NOS) is diagnosed when the criteria are not met for a more-specific disorder.^[13] The main difference between autism and Asperger syndrome is that in Asperger's there is no significant delay in language development.^[14] The terminology of autism can be bewildering, with autism, Asperger's, and PDD-NOS sometimes called the autistic disorders,^[4] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. This article uses autism to refer to the classic autistic disorder, while other sources sometimes use autism to refer to autistic disorders or even ASD. ASD in turn is a subset of the broader autism phenotype (BAP), which describes individuals who may not have ASD but do have some autistic-like traits, such as avoiding eye contact.^[15]

Autism covers a wide range, from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to less impaired individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication.^[16] Sometimes the syndrome is informally and controversially divided into low-, medium- and high-functioning autism (LFA, MFA, and HFA) based on IQ thresholds,^[17] or on how much support the individual requires in daily life. Autism can also be divided into syndromal and non-syndromal autism, where the former is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis.^[18] Although individuals with Asperger's tend to perform better cognitively than those with autism, it is unclear how much overlap occurs among Asperger's, HFA, and non-syndromal autism.^[19]

Some studies have reported diagnoses of autism in some children due to a loss of language or social skills, as opposed to a failure to make progress. Several terms are used for this phenomenon, including regressive autism, setback autism, and developmental stagnation. The validity of this distinction remains controversial; it is possible regressive autism is a specific subtype.^[20]^[21]

Characteristics

Autism is distinguished by a pattern of symptoms rather than one single symptom. The main characteristics are impairments in social interaction, impairments in communication, restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.

Social development

Autistic people have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals as leaving her feeling "like an anthropologist on Mars".^[22]

Social impairments become 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 have more striking social deviance: for example, they have less eye contact and anticipatory postures and they are less able to use other people's bodies as tools.^[21] Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers.^[23] They display moderately less attachment security than usual, though this difference disappears in groups containing children with higher mental development or with less severe ASD.^[24]

Contrary to common belief, autistic children do not 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 are.^[25]

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. Dominick et al. 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 children with a history of language impairment.^[26]

Communication

About a third to a half of autistic individuals do not develop enough natural speech to meet daily communication needs.^[27] Communications differences may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and desynchronization of vocal patterns 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 more likely to simply repeat others' words (echolalia)^[20] or reverse pronouns.^[3] Autistic children may have difficulty with imaginative play and with developing symbols into language.^[20] They are more likely to have problems understanding pointing; for example, they may look at a pointing hand instead of the pointed-at object.^[21]

In a pair of studies, high-functioning autistic children aged 8–15 performed equally well, and adults better, than individually matched controls at basic language tasks like vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks like figurative language, comprehension, and making inferences. 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.^[28]

Repetitive behavior

A young boy with autism, and the precise line of toys he made

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

Stereotypy is apparently purposeless movement, such as hand flapping, head rolling, body rocking, or spinning a plate.
Compulsive behavior is intended and appears to follow rules, such as arranging objects in a certain way.
Sameness is resistance to change, for example, insisting that the furniture not be moved, or refusing to be interrupted.
Ritualistic behavior performs daily activities the same way each time, such as an unvarying menu or dressing ritual.
Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program.
Self-injury includes movements that injure or can injure the person, such as biting oneself. Dominick et al. reported that self-injury at some point affected about 30% of children with ASD.^[26]

No single repetitive behavior is identified with autism, but only autism appears to have an elevated pattern of occurrence and severity of these behaviors.^[29]

Other symptoms

Autistic individuals may have symptoms that are independent of the diagnosis but can affect the individual or the family.^[8] As many as 10% of individuals with ASD show unusual abilities ranging from splinter skills like trivia memorization to the extraordinarily rare talents of prodigious autistic savants.^[30]

Unusual responses to sensory stimuli are more common and prominent in autistic children, though there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.^[31] The responses may be more common in children: a pair of studies found that autistic children had impaired tactile perception while autistic adults did not. The same two studies also found that autistic individuals had more problems with complex memory and reasoning tasks such as Twenty Questions; these problems were somewhat more marked among adults.^[28] Several studies have reported associated motor problems that include poor muscle tone, poor motor planning, and toe walking; ASD is not associated with severe motor disturbances.^[32]

Atypical eating occurs in about three fourths of children with ASD, so frequently that it used to be a diagnostic indicator. Selectivity is the most common problem, though eating rituals and food refusal also occur;^[26] this does not appear to result in malnutrition. Some children with autism also have gastrointestinal (GI) symptoms, but there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual.^[33]

Sleep problems are known to be more common in children with developmental disabilities, and there is some evidence that autistic children are more likely to have even more sleep problems than children with other developmental disabilities, with problems that include difficulty falling asleep, frequent nighttime awakenings, and early morning awakenings. Dominick et al. found that about two thirds of children with ASD had a history of sleep problems.^[26]

Causes

Although many genetic and environmental causes have been proposed for autism, its theory of causation is still incomplete.^[34] Tracking down the causes is often hard, and some researchers argue this is because autism is not a single disorder, but rather a triad of core aspects (social impairment, communication difficulties, and repetitive behaviors) that have distinct causes but often co-occur.^[35]

Genetic factors are the most significant cause for autism spectrum disorders. Early studies of twins estimated heritability to be over 90%, in other words, that genetics explains over 90% of whether a child will develop autism.^[4] Many of the non-autistic co-twins had learning or social disabilities. For adult siblings the risk for having one or more features of the broader autism phenotype might be as high as 30%.^[36]

The genetics of autism is complex.^[4] First, for each autistic individual, mutations in more than one gene may be implicated. Second, mutations in different sets of genes may be involved in different autistic individuals. Third, there may be significant interactions among mutations in several genes or between the environment and mutated genes. By identifying genetic markers inherited with autism in family studies, numerous candidate genes have been located, most of which encode proteins involved in neural development and function.^[37] However, for most of the candidate genes, the actual mutations that increase the risk for autism have not been identified. Typically autism cannot be traced to a single-gene mutation or a single chromosome abnormality such as fragile X syndrome or 22q13 deletion syndrome.^[18]^[38]

The large number of autistic individuals with unaffected family members may result from copy number variations (CNVs)—spontaneous alterations in the genetic material during meiosis that delete or duplicate genetic material. Sporadic (non-inherited) cases have been examined to identify candidate genetic loci involved in autism. Using array comparative genomic hybridization (array CGH), a technique for detecting CNVs, one study found them in 10% of families with one affected child.^[40] Some of the altered loci were identified in previous studies of inherited autism; many were unique to the sporadic cases examined in this study. Hence a substantial fraction of autism may be highly heritable but not inherited: that is, the mutation that causes the autism is new in the child and is not in the parent. The fraction of autism traceable to a genetic cause may grow to 30–40% as the resolution of array CGH improves.^[39] The Autism Genome Project database contains genetic linkage and CNV data that connect autism to genetic loci and suggest that the genetic influence may extend to every human chromosome.^[41]

Teratogens (agents that cause birth defects) related to autism risk include exposure of the embryo to thalidomide, valproic acid, or misoprostol, or to rubella infection in the mother. These cases are rare.^[42] All known teratogens 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.^[5] Other possible contributors to autism include gastrointestinal or immune system abnormalities, allergies, and exposure of children to drugs, vaccines, infection, certain foods,^[43] or heavy metals; the evidence for these risk factors is anecdotal and has not been confirmed by reliable studies,^[6] and extensive further searches are underway.^[42] Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. The overwhelming majority of scientific evidence shows no causal connection between the measles-mumps-rubella vaccine and autism, or between the vaccine preservative thiomersal and autism, but parental concern has led to decreasing uptake of childhood immunizations and increasing likelihood of measles outbreaks.^[44]

Mechanism

Despite extensive investigation, 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.^[7]

Pathophysiology

Autism appears to result from developmental factors that affect many or all functional brain systems, as opposed to localized physical damage.^[38] Many major structures of the human brain have been implicated. Consistent neuroanatomical abnormalities have been found in the development of the cerebral cortex; and in the cerebellum and related inferior olive, which have a significant decrease in the number of Purkinje cells. Brain weight and volume and head circumference tend to be greater in autistic children; the effects of these are unknown.^[45] It may be due to poorly regulated growth of neurons.^[7]

Interactions between the immune system and the nervous system begin early during embryogenesis, and successful neurodevelopment depends on a balanced immune response. Several symptoms consistent with a poorly regulated immune response have been reported in autistic children. It is possible that aberrant immune activity during critical periods of neurodevelopment is part of the mechanism of some forms of ASD.^[46] Given the lack of data in this area, it is still hard to draw conclusions about the role of immune factors in autism.^[47]

Several neurotransmitter abnormalities have been detected in autism, notably increased blood levels of serotonin. Whether these lead to structural or behavioral abnormalities is unclear.^[7]

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 of the same species 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.^[48] 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's, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.^[49]

Functional magnetic resonance imaging provides some evidence for the underconnectivity theory of autism.

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.^[50] Evidence for this theory has been found in functional neuroimaging studies on autistic individuals^[28] and by a brain wave 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.^[51] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.^[52]

Neuropsychology

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

The first category focuses on deficits in social cognition. Hyper-systemizing hypothesizes that autistic individuals can systematize—that is, they can develop internal rules of operation to handle internal events—but are less effective at empathizing by handling events generated by other agents.^[17] It extends the extreme male brain theory, which hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing.^[53] This in turn is related to the earlier theory of mind, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind is supported by autistic children's atypical responses to the Sally-Anne test for reasoning about others' motivations,^[54] and is mapped well from the mirror neuron system theory of autism.^[49]

The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in flexible planning, working memory, and impulse control. One strength of the theory is predicting stereotyped behavior and narrow interests.^[55] Weak central coherence theory hypothesizes that a limited ability to see the big picture underlies the central disturbance in autism. One strength of this theory is predicting special talents and peaks in performance in autistic people.^[56] A related theory—enhanced perceptual functioning—focuses more on the superiority of low-level perceptual operations in autistic individuals.^[57] The latter two 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.^[35]

Screening

Parents are usually the first to notice unusual behaviors in their child: for example, a baby might seem unresponsive to people or might focus intently on one item for long periods of time. Children who seem to have been developing normally might also show signs of autism, for example by becoming silent or indifferent to social overtures.^[58] As delay in evaluation may postpone treatment and affect long-term outcome, any of the following warning signs is reason to have a child evaluated by a specialist immediately:

No babbling by 12 months.
No gesturing (pointing, waving goodbye, etc.) by 12 months.
No single words by 16 months.
No two-word spontaneous phrases (not including echolalia) by 24 months.
Any loss of any language or social skills, at any age.^[8]

The American Academy of Pediatrics recommends that all children be screened for ASD at the 18-month and the 24- or 30-month well-child doctor visits, using autism-specific developmental screening tools.^[59] In contrast, the UK National Screening Committee recommends against screening for ASD in the general population, because screening tools have not been fully validated and interventions lack sufficient evidence for effectiveness.^[60]

Genetic screening for autism is generally still impractical. As genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics.^[61]

Diagnosis

Autism is defined in section 299.00 of 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.^[1] ICD-10 section F84.0 uses essentially the same definition.^[2]

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.^[21]

A pediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions. A differential diagnosis at this stage might also consider ADHD, anxiety, depression, hearing impairment, mental retardation, obsessive-compulsive disorder, and specific speech disorders. Since early diagnosis is important, 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.^[62] ASD can sometimes be diagnosed by age 14 months,^[63] but a 2006 US study found the average age of first evaluation by a qualified professional was 48 months and of formal ASD diagnosis was 61 months, reflecting an average 13-month delay, all far above recommendations.^[64]

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.^[65] It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.^[66]

The symptoms of autism and ASD begin early in childhood but are occasionally missed. Adults may seek retrospective 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.^[67]

Treatment

Early intervention is important. No single treatment is best and treatment is typically tailored to the child's needs. Intensive, sustained special education programs and behavior therapy can help children acquire self-care, social, and job skills. Among the available approaches, applied behavior analysis (ABA) has demonstrated therapeutic effect in clinical trials that is at least as good as other treatments in promoting social and language development and in reducing behaviors that interfere with functioning and learning; ABA focuses on teaching tasks one-on-one using the behaviorist principles of stimulus, response and reward. Cognitive therapies based on comprehensive center-based programs are a common alternative: for example, TEACCH focuses more on structuring the physical environment and using visual supports to ease language development tasks.^[68] A 2005 California study found that early intensive behavior analytic treatment, a form of ABA, was substantially more effective for preschool children with autism than the mixture of methods provided in many programs.^[69] The limited research on the effectiveness of adult residential programs shows mixed results.^[70]

Medications are often used to treat problems associated with ASD. More than half of U.S. children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.^[71] The FDA has approved the antipsychotic risperidone for treating symptomatic irritability in autistic children and adolescents.^[72] Other drugs are prescribed off-label, which means they have not been approved for treating ASD. For example, serotonin reuptake inhibitors and dopamine blockers can sometimes reduce some symptoms.^[7] However, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.^[73] Someone with ASD may respond atypically to medications, the medications can have adverse side effects, and no known medication relieves autism's core symptoms of social and communication impairments.^[58]

Many other therapies and interventions are available. Few are supported by scientific studies.^[9]^[74]^[75] Treatment approaches lack empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.^[25] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.^[76] Even if they do not help, conservative treatments such as changes in diet are probably harmless aside from their bother and cost.^[43] Dubious invasive treatments are a much more serious matter: for example, in 2005, botched chelation therapy killed a 5-year-old autistic boy.^[44]

Treatment is expensive; indirect costs are more so. A U.S. study estimated the average additional lifetime cost due exclusively to autism to be $3.2 million in 2003 US dollars for an autistic individual born in 2000, with about 10% medical care, 30% nonmedical care such as child care and education, and 60% the lost economic productivity of individuals and their parents.^[77] A British study estimated an average lifetime cost of ₤2.4 million in 1997–1998 British pounds.^[78] Legal rights to treatment are complex, vary with location and age, and require advocacy by caregivers.^[75] 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.^[79] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.^[75]

Prognosis

No cure is known for autism. Most children with autism lack social support, meaningful relationships, future employment opportunities or self-determination.^[25] Although core difficulties remain, the severity of symptoms often becomes less marked in later childhood.^[80] Few high-quality studies address long-term prognosis. Some adults show modest improvement in some symptoms, but some decline; no study has focused on autism after midlife.^[81] Acquiring language before age 6, having IQ above 50, and having a marketable skill all predict better outcomes; independent living is unlikely with severe autism.^[82] 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.^[10] Changes in diagnostic practice and increased availability of effective early intervention make it unclear whether these findings can be generalized to recently diagnosed children.^[12]

Epidemiology

Estimates of the prevalence of autism vary widely depending on diagnostic criteria, age of children screened, and geographical location.^[83] One review estimated a prevalence of at least 1.3 per 1,000 for autism and 6.0–6.5 per 1,000 for ASD; PDD-NOS was the vast majority of ASD, Asperger's was about 0.3 per 1,000 and the atypical forms childhood disintegrative disorder and Rett syndrome were much rarer.^[84] Most recent reviews tend to estimate a prevalence of 1–2 per 1,000 for autism and close to 6 per 1,000 for ASD.^[12] A 2006 study of nearly 57,000 British nine- and ten-year-olds reported a prevalence of 3.89 per 1,000 for autism and 11.61 per 1,000 for ASD; these higher figures could be associated with broadening diagnostic criteria.^[85]

The risk of autism is associated with several prenatal and perinatal risk factors. A 2007 review of risk factors found associated parental characteristics that included advanced maternal age, advanced paternal age, and maternal place of birth outside Europe or North America, and also found associated obstetric conditions that included low birth weight and gestation duration, and hypoxia during childbirth.^[86]

About 10–15% of autism cases are caused by a known medical condition such as Prader-Willi syndrome or tuberous sclerosis^[4] and ASD is associated with several other genetic disorders.^[87] Autism is associated with mental retardation: a 2001 British study of 26 autistic children found about 30% with intelligence in the normal range (IQ above 70), 50% with mild to moderate retardation, and about 20% with severe to profound retardation (IQ below 35). For ASD other than autism the association is much weaker: the same study reported about 94% of 65 children with PDD-NOS or Asperger's had normal intelligence.^[88] ASD is also associated with epilepsy, with variations in risk of epilepsy due to age, cognitive level, and type of language disorder.^[89] Boys are at higher risk for autism than girls. The ASD 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. Recent studies have found no association with socioeconomic status, and have reported inconsistent results about associations with race or ethnicity.^[12] Phobias, depression and other psychopathological disorders have often been described along with ASD but this has not been assessed systematically.^[90]

Autism's incidence, despite its advantages for assessing risk, is less useful in autism epidemiology, as the disorder starts long before it is diagnosed, and the gap between initiation and diagnosis is influenced by many factors unrelated to risk. Attention is focused mostly on whether prevalence is increasing with time. Earlier prevalence estimates were lower, centering at about 0.5 per 1,000 for autism during the 1960s and 1970s and about 1 per 1,000 in the 1980s, as opposed to today's 1–2 per 1,000.^[12]

Reports of autism cases grew dramatically in the U.S. in 1996–2005. It is unknown how much, if any, growth came from real changes in autism's prevalence.

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,^[91] though as-yet-unidentified contributing environmental risk factors cannot be ruled out.^[6] A widely cited 2002 pilot study concluded that some of the observed increase in autism in California was real,^[92] but a 2006 analysis found that special education data poorly measured prevalence because so many cases were undiagnosed, and that the 1994–2003 U.S. increase was associated with declines in other diagnostic categories, indicating that diagnostic substitution had occurred.^[93]

It is unknown whether autism's prevalence increased during the same period. An increase in prevalence would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.^[42] Chris Johnson, co-chair of the American Academy of Pediatrics Autism Expert Panel, summed up the 2005 state of the issue by saying, "There is a chance we're seeing a true rise, but right now I don't think anybody can answer that question for sure."^[94]

History

A few examples of autism and its treatment can be found from long before it was named. The Table Talk of Martin Luther contains a story of a 12-year-old boy who may have been severely autistic.^[95] According to Luther's notetaker Mathesius, Luther thought the boy was a soulless mass of flesh possessed by the devil, and suggested that he be suffocated.^[96] Victor 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.^[97]

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 autos (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."^[98]

File:Kanner kl2.jpg

Leo Kanner introduced the label early infantile autism in 1943.

The word autism took its modern sense in 1943 when Leo Kanner of the Johns Hopkins Hospital reported 11 children with striking behavioral similarities and introduced the label early infantile autism.^[3] He suggested autism to describe the children's lack of interest in other people. Almost every characteristic described in Kanner's first paper on the subject is still regarded as typical of the autistic spectrum of disorders.^[35] About the same time, the Viennese pediatrician Hans Asperger described a similar form of ASD now known as Asperger syndrome, though for various reasons it was not widely recognized as a separate syndrome until 1981.^[97]

Kanner's reuse of autism led to decades of confused terminology like "infantile schizophrenia", and child psychiatry's focus on maternal deprivation during the mid-1900s led to misconceptions of autism as an infant's response to "refrigerator mothers". Starting in the late 1960s autism was established as a separate syndrome by demonstrating that it is lifelong, distinguishing it from mental retardation and schizophrenia and from other developmental disorders, and demonstrating the benefits of involving parents in active programs of therapy.^[99] Since then, the rise of parent organizations and the destigmatization of childhood ASD have deeply affected how we view ASD, its boundaries, and its treatments.^[97] The Internet has helped autistic individuals bypass nonverbal cues and emotional sharing that they find so hard to deal with, and has given them a way to form online communities and work remotely.^[100] An autistic culture has developed: some in the community seek a cure, while others believe that autism is simply another way of being.^[11]

Notes

^ ^a ^b American Psychiatric Association (2000). "Diagnostic criteria for 299.00 Autistic Disorder". Diagnostic and Statistical Manual of Mental Disorders (4th ed., text revision (DSM-IV-TR) ed.). ISBN 0890420254. {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
^ ^a ^b ^c World Health Organization (2006). "F84. Pervasive developmental disorders". International Statistical Classification of Diseases and Related Health Problems (10th ed. (ICD-10) ed.). {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)
^ ^a ^b ^c Kanner L (1943). "Autistic disturbances of affective contact". Nerv Child. 2: 217–50.
^ ^a ^b ^c ^d ^e Freitag CM (2007). "The genetics of autistic disorders and its clinical relevance: a review of the literature". Mol Psychiatry. 12 (1): 2–22. doi:10.1038/sj.mp.4001896. PMID 17033636.
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^ ^a ^b ^c Rutter M (2005). "Incidence of autism spectrum disorders: changes over time and their meaning". Acta Paediatr. 94 (1): 2–15. PMID 15858952.
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^ ^a ^b ^c ^d Dominick KC, Davis NO, Lainhart J, Tager-Flusberg H, Folstein S (2007). "Atypical behaviors in children with autism and children with a history of language impairment". Res Dev Disabil. 28 (2): 145–62. doi:10.1016/j.ridd.2006.02.003. PMID 16581226.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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MNS and autism:
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^ Just MA, Cherkassky VL, Keller TA, Minshew NJ (2004). "Cortical activation and synchronization during sentence comprehension in high-functioning autism: evidence of underconnectivity". Brain. 127 (8): 1811–21. doi:10.1093/brain/awh199. PMID 15215213.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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^ Minshew NJ, Williams DL (2007). "The new neurobiology of autism: cortex, connectivity, and neuronal organization". Arch Neurol. 64 (7): 945–950. PMID 17620483.
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^ Hill EL (2004). "Executive dysfunction in autism". Trends Cogn Sci. 8 (1): 26–32. doi:10.1016/j.dr.2004.01.001. PMID 14697400.
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^ Shattuck PT, Grosse SD (2007). "Issues related to the diagnosis and treatment of autism spectrum disorders". Ment Retard Dev Disabil Res Rev. 13 (2): 129–35. doi:10.1002/mrdd.20143. PMID 17563895.
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^ Van Bourgondien ME, Reichle NC, Schopler E (2003). "Effects of a model treatment approach on adults with autism". J Autism Dev Disord. 33 (2): 131–40. doi:10.1023/A:1022931224934. PMID 12757352.{{cite journal}}: CS1 maint: multiple names: authors list (link)
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^
Lack of support for interventions:
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^ ^a ^b ^c Aman MG (2005). "Treatment planning for patients with autism spectrum disorders". J Clin Psychiatry. 66 (Suppl 10): 38–45. PMID 16401149.
^ Stahmer AC, Collings NM, Palinkas LA (2005). "Early intervention practices for children with autism: descriptions from community providers". Focus Autism Other Dev Disabl. 20 (2): 66–79. PMID 16467905. Retrieved 2007-07-12.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Ganz ML (2007). "The lifetime distribution of the incremental societal costs of autism". Arch Pediatr Adolesc Med. 161 (4): 343–9. PMID 17404130.
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^ Tidmarsh L, Volkmar FR (2003). "Diagnosis and epidemiology of autism spectrum disorders". Can J Psychiatry. 48 (8): 517–25. PMID 14574827.
^ Williams JG, Higgins JPT, Brayne CEG (2006). "Systematic review of prevalence studies of autism spectrum disorders". Arch Dis Child. 91 (1): 8–15. doi:10.1136/adc.2004.062083. PMID 15863467.{{cite journal}}: CS1 maint: multiple names: authors list (link)
^ Fombonne E (2005). "Epidemiology of autistic disorder and other pervasive developmental disorders". J Clin Psychiatry. 66 (Suppl 10): 3–8. PMID 16401144.
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^ Kolevzon A, Gross R, Reichenberg A (2007). "Prenatal and perinatal risk factors for autism". Arch Pediatr Adolesc Med. 161 (4): 326–33. PMID 17404128. {{cite journal}}: Check date values in: |date= (help)CS1 maint: multiple names: authors list (link)
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Changes in diagnostic practices:
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^ Byrd RS, Sage AC, Keyzer J; et al. (2002). "Report to the legislature on the principal findings of the epidemiology of autism in California: a comprehensive pilot study" (PDF). M.I.N.D. Institute. Retrieved 2006-09-18. {{cite journal}}: Cite journal requires |journal= (help); Explicit use of et al. in: |author= (help)CS1 maint: multiple names: authors list (link)
^ Shattuck PT (2006). "The contribution of diagnostic substitution to the growing administrative prevalence of autism in US special education". Pediatrics. 117 (4): 1028–37. doi:10.1542/peds.2005-1516. PMID 16585296.
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^ Biever C (2007-06-27). "Web removes social barriers for those with autism". New Scientist. No. 2610. Retrieved 2007-06-28. {{cite news}}: Check date values in: |date= (help)

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Autism spectrum at Curlie
Autism-help.org
National Dissemination Center for Children with Disabilities (NICHCY), autism resources

[DSM-IV-TR-299.00-1] American Psychiatric Association (2000). "Diagnostic criteria for 299.00 Autistic Disorder". Diagnostic and Statistical Manual of Mental Disorders (4th ed., text revision (DSM-IV-TR) ed.). ISBN 0890420254. {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)

[ICD-10-F84.0-2] World Health Organization (2006). "F84. Pervasive developmental disorders". International Statistical Classification of Diseases and Related Health Problems (10th ed. (ICD-10) ed.). {{cite book}}: |access-date= requires |url= (help); External link in |chapterurl= (help); Unknown parameter |chapterurl= ignored (|chapter-url= suggested) (help)

[Kanner1943-3] Kanner L (1943). "Autistic disturbances of affective contact". Nerv Child. 2: 217–50.

[Freitag-4] Freitag CM (2007). "The genetics of autistic disorders and its clinical relevance: a review of the literature". Mol Psychiatry. 12 (1): 2–22. doi:10.1038/sj.mp.4001896. PMID 17033636.

[Arndt-5] Arndt TL, Stodgell CJ, Rodier PM (2005). "The teratology of autism". Int J Dev Neurosci. 23 (2–3): 189–99. doi:10.1016/j.ijdevneu.2004.11.001. PMID 15749245.{{cite journal}}: CS1 maint: multiple names: authors list (link)

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

[Penn-7] Penn HE (2006). "Neurobiological correlates of autism: a review of recent research". Child Neuropsychol. 12 (1): 57–79. doi:10.1080/09297040500253546. PMID 16484102.

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 Of the other four ASD forms, [[Asperger syndrome]] is closest to autism; [[Rett syndrome]] and [[childhood disintegrative disorder]] share several symptoms with autism but may have unrelated causes; finally, [[PDD-NOS|pervasive developmental disorder not otherwise specified (PDD-NOS)]] is diagnosed when the criteria are not met for a more-specific disorder.<ref>{{cite journal|author=Lord C, Cook EH, Leventhal BL, [[David Amaral|Amaral DG]]|title=Autism spectrum disorders|journal=Neuron|volume=28|issue=2|date=2000|pages=355–63|doi=10.1016/S0896-6273(00)00115-X|pmid=11144346|url=http://download.neuron.org/pdfs/0896-6273/PIIS089662730000115X.pdf|format=PDF}}</ref> The main difference between autism and Asperger syndrome is that in Asperger's there is no significant delay in [[language development]].<ref>{{cite book|title=Diagnostic and Statistical Manual of Mental Disorders|edition=4th ed., text revision ([[DSM-IV-TR]])|author=[[American Psychiatric Association]]|date=2000|isbn=0890420254|chapter=Diagnostic criteria for 299.80 Asperger's Disorder (AD)|chapterurl=http://www.behavenet.com/capsules/disorders/asperger.htm|accessdate=2007-06-28}}</ref> The terminology of autism can be bewildering, with autism, Asperger's, and PDD-NOS sometimes called the ''autistic disorders'',<ref name=Freitag>{{cite journal|author=Freitag CM|title=The genetics of autistic disorders and its clinical relevance: a review of the literature|journal=Mol Psychiatry|volume=12|issue=1|pages=2–22|date=2007|doi=10.1038/sj.mp.4001896|pmid=17033636|url=http://www.nature.com/mp/journal/v12/n1/full/4001896a.html}}</ref> whereas autism itself is often called ''autistic disorder'', ''childhood autism'', or ''infantile autism''. This article uses ''autism'' to refer to the classic autistic disorder, while other sources sometimes use ''autism'' to refer to autistic disorders or even ASD. ASD in turn is a subset of the broader autism [[phenotype]] (BAP), which describes individuals who may not have ASD but do have some autistic-like [[Trait (biology)|traits]], such as avoiding eye contact.<ref>{{cite journal|author=Piven J, Palmer P, Jacobi D, Childress D, Arndt S|title=Broader autism phenotype: evidence from a family history study of multiple-incidence autism families|journal=Am J Psychiatry|date=1997|volume=154|issue=2|pages=185–90|pmid=9016266|url=http://ajp.psychiatryonline.org/cgi/reprint/154/2/185.pdf|format=PDF}}</ref>
-Autism covers a wide range, from individuals with severe impairments—who may be silent, [[Developmental Disability|mentally disabled]], and locked into hand flapping and rocking—to less impaired individuals who may have active but distinctly odd social approaches, narrowly-focused interests, and verbose, pedantic communication.<ref>{{cite journal|author=Happé F|title=Understanding assets and deficits in autism: why success is more interesting than failure |journal=Psychologist |volume=12 |issue=11 |pages=540–547 |date=1999|url=http://www.bps.org.uk/publications/thepsychologist/search-the-psychologist-online.cfm?fuseaction=inc_getFile&ID=133&Publication_ID=1|format=PDF}}</ref> Sometimes the syndrome is informally and [[Controversies about functioning labels in the autism spectrum|controversially]] divided into low-, medium- and [[high-functioning autism]] (LFA, MFA, and HFA) based on [[IQ]] thresholds,<ref name=hypersystem/> or on how much support the individual requires in daily life. Autism can also be divided into [[syndrome|syndromal]] and non-syndromal autism, where the former is associated with severe or profound [[mental retardation]] or a congenital syndrome with physical symptoms, such as [[tuberous sclerosis]].<ref name=Cohen>{{cite journal|journal=J Autism Dev Disord|date=2005|volume=35|issue=1|pages=103–16|title=Specific genetic disorders and autism: clinical contribution towards their identification|author=Cohen D, Pichard N, Tordjman S ''et al.''|doi=10.1007/s10803-004-1038-2|pmid=15796126}}</ref> Although individuals with Asperger's tend to perform better cognitively than those with autism, it is unclear how much overlap occurs among Asperger's, HFA, and non-syndromal autism.<ref>{{cite book|author=[[Eric Schopler|Schopler E]], Mesibov GB, Kunce LJ (eds)|title=Asperger syndrome or high-functioning autism?|date=1998|publisher=Springer|isbn=0306457466}}</ref>
+Autism covers a wide range, from individuals with severe impairments—who may be silent, [[Developmental Disability|mentally disabled]], and locked into hand flapping and rocking—to less impaired individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication.<ref>{{cite journal|author=Happé F|title=Understanding assets and deficits in autism: why success is more interesting than failure |journal=Psychologist |volume=12 |issue=11 |pages=540–547 |date=1999|url=http://www.bps.org.uk/publications/thepsychologist/search-the-psychologist-online.cfm?fuseaction=inc_getFile&ID=133&Publication_ID=1|format=PDF}}</ref> Sometimes the syndrome is informally and [[Controversies about functioning labels in the autism spectrum|controversially]] divided into low-, medium- and [[high-functioning autism]] (LFA, MFA, and HFA) based on [[IQ]] thresholds,<ref name=hypersystem/> or on how much support the individual requires in daily life. Autism can also be divided into [[syndrome|syndromal]] and non-syndromal autism, where the former is associated with severe or profound [[mental retardation]] or a congenital syndrome with physical symptoms, such as [[tuberous sclerosis]].<ref name=Cohen>{{cite journal|journal=J Autism Dev Disord|date=2005|volume=35|issue=1|pages=103–16|title=Specific genetic disorders and autism: clinical contribution towards their identification|author=Cohen D, Pichard N, Tordjman S ''et al.''|doi=10.1007/s10803-004-1038-2|pmid=15796126}}</ref> Although individuals with Asperger's tend to perform better cognitively than those with autism, it is unclear how much overlap occurs among Asperger's, HFA, and non-syndromal autism.<ref>{{cite book|author=[[Eric Schopler|Schopler E]], Mesibov GB, Kunce LJ (eds)|title=Asperger syndrome or high-functioning autism?|date=1998|publisher=Springer|isbn=0306457466}}</ref>
 Some studies have reported diagnoses of autism in some children due to a loss of language or social skills, as opposed to a failure to make progress. Several terms are used for this phenomenon, including [[regressive autism]], setback autism, and developmental stagnation. The validity of this distinction remains controversial; it is possible regressive autism is a specific subtype.<ref name=Landa/><ref name=Volkmar>{{cite journal|author=Volkmar F, Chawarska K, Klin A|title=Autism in infancy and early childhood|journal=Annu Rev Psychol|date=2005|volume=56|pages=315–36|doi=10.1146/annurev.psych.56.091103.070159|pmid=15709938}}</ref>
@@ Line 131: / Line 131: @@
 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.<ref name=Volkmar/>
-A [[pediatrician]] commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions. A [[differential diagnosis]] at this stage might consider several other possibilities, including [[ADHD]], [[Anxiety disorder|anxiety]], [[Clinical depression|depression]], [[hearing impairment]], [[mental retardation]], [[obsessive-compulsive disorder]], and specific [[speech disorder]]s. Since early diagnosis is important, 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.<ref>{{cite journal|journal=Arch Dis Child|date=2007|volume=92|issue=6|pages=540–5|title=How to diagnose autism|author=Dover CJ, Le Couteur A|doi=10.1136/adc.2005.086280|pmid=17515625}}</ref> ASD can sometimes be diagnosed by age 14 months,<ref>{{cite journal|journal=Arch Gen Psychiatry|date=2007|volume=64|issue=7|pages=853–64|title=Social and communication development in toddlers with early and later diagnosis of autism spectrum disorders|author=Landa RJ, Holman KC, Garrett-Mayer E|pmid=17606819}}</ref> but a 2006 US study found the average age of first evaluation by a qualified professional was 48 months and of formal ASD diagnosis was 61 months, reflecting an average 13-month delay, all far above recommendations.<ref>{{cite journal|journal=J Dev Behav Pediatr|date=2006|volume=27|issue=2 Suppl|pages=S79–87|title=Examination of the time between first evaluation and first autism spectrum diagnosis in a population-based sample|author=Wiggins LD, Baio J, Rice C|pmid=16685189}}</ref>
+A [[pediatrician]] commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions. A [[differential diagnosis]] at this stage might also consider [[ADHD]], [[Anxiety disorder|anxiety]], [[Clinical depression|depression]], [[hearing impairment]], [[mental retardation]], [[obsessive-compulsive disorder]], and specific [[speech disorder]]s. Since early diagnosis is important, 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.<ref>{{cite journal|journal=Arch Dis Child|date=2007|volume=92|issue=6|pages=540–5|title=How to diagnose autism|author=Dover CJ, Le Couteur A|doi=10.1136/adc.2005.086280|pmid=17515625}}</ref> ASD can sometimes be diagnosed by age 14 months,<ref>{{cite journal|journal=Arch Gen Psychiatry|date=2007|volume=64|issue=7|pages=853–64|title=Social and communication development in toddlers with early and later diagnosis of autism spectrum disorders|author=Landa RJ, Holman KC, Garrett-Mayer E|pmid=17606819}}</ref> but a 2006 US study found the average age of first evaluation by a qualified professional was 48 months and of formal ASD diagnosis was 61 months, reflecting an average 13-month delay, all far above recommendations.<ref>{{cite journal|journal=J Dev Behav Pediatr|date=2006|volume=27|issue=2 Suppl|pages=S79–87|title=Examination of the time between first evaluation and first autism spectrum diagnosis in a population-based sample|author=Wiggins LD, Baio J, Rice C|pmid=16685189}}</ref>
 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.<ref>{{cite journal|author=Shattuck PT, Grosse SD|title=Issues related to the diagnosis and treatment of autism spectrum disorders|journal=Ment Retard Dev Disabil Res Rev|date=2007|volume=13|issue=2|pages=129–35|doi=10.1002/mrdd.20143|pmid=17563895}}</ref> It is particularly hard to diagnose autism among the [[visually impaired]], partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes.<ref>{{cite journal|title=Visual impairment and autism: current questions and future research|author=Cass H|journal=Autism|date=1998|volume=2|issue=2|pages=117–38|doi=10.1177/1362361398022002}}</ref>
@@ Line 141: / Line 141: @@
 Early intervention is important. No single treatment is best and treatment is typically tailored to the child's needs. Intensive, sustained special education programs and behavior therapy can help children acquire self-care, social, and job skills. Among the available approaches, [[applied behavior analysis]] (ABA) has demonstrated [[Efficacy|therapeutic effect in clinical trials that is at least as good as other treatments]] in promoting social and language development and in reducing behaviors that interfere with functioning and learning; ABA focuses on teaching tasks one-on-one using the [[behaviorist]] principles of stimulus, response and reward. Cognitive therapies based on comprehensive center-based programs are a common alternative: for example, [[TEACCH]] focuses more on structuring the physical environment and using visual supports to ease language development tasks.<ref>{{cite book|title=Mental Health: A Report of the Surgeon General|author=U.S. Dept. of Health and Human Services|location=Rockville, MD|publisher=U.S. Department of Health and Human Services, Substance Abuse and Mental Health Services Administration, Center for Mental Health Services, National Institutes of Health, National Institute of Mental Health|date=1999|chapter=Autism|chapterurl=http://www.surgeongeneral.gov/library/mentalhealth/chapter3/sec6.html#autism}} Retrieved on [[2007-07-11]].</ref> A 2005 California study found that early intensive behavior analytic treatment, a form of ABA, was substantially more effective for preschool children with autism than the mixture of methods provided in many programs.<ref>{{cite journal |author=Howard JS, Sparkman CR, Cohen HG, Green G, Stanislaw H |title=A comparison of intensive behavior analytic and eclectic treatments for young children with autism |journal=Res Dev Disabil |volume=26 |issue=4 |pages=359–83 |year=2005 |pmid=15766629 |doi=10.1016/j.ridd.2004.09.005}}</ref> The limited research on the effectiveness of adult residential programs shows mixed results.<ref>{{cite journal|journal=J Autism Dev Disord|date=2003|volume=33|issue=2|pages=131–40|title=Effects of a model treatment approach on adults with autism|author=Van Bourgondien ME, Reichle NC, Schopler E|doi=10.1023/A:1022931224934|pmid=12757352}}</ref>
-Medications are often used to treat problems associated with ASD. More than half of U.S. children diagnosed with ASD are prescribed [[psychoactive drug]]s or [[anticonvulsant]]s, with the most common drug classes being [[antidepressant]]s, [[stimulant]]s, and [[antipsychotic]]s.<ref>{{cite journal|journal=J Child Adolesc Psychopharmacol|date=2007|volume=17|issue=3|pages=348–55|title=Medication use among children with autism spectrum disorders|author=Oswald DP, Sonenklar NA|doi=10.1089/cap.2006.17303|pmid=17630868}}</ref> The FDA has approved the antipsychotic [[risperidone]] for treating symptomatic irritability in autistic children and adolescents.<ref>{{cite press release|publisher=FDA|date=[[2006-10-06]]|url=http://www.fda.gov/bbs/topics/NEWS/2006/NEW01485.html|accessdate=2006-10-02|title=FDA approves the first drug to treat irritability associated with autism, Risperdal}}</ref> Several other drugs are prescribed [[off-label]], which means they have not been approved for treating ASD. For example, [[serotonin reuptake inhibitors]] and [[dopamine]] blockers can sometimes reduce some symptoms.<ref name=Penn/> However, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.<ref>{{cite journal|journal=Autism|date=2007|volume=11|issue=4|pages=335–48|title=Systematic review of the effectiveness of pharmacological treatments for adolescents and adults with autism spectrum disorder|author=Broadstock M, Doughty C, Eggleston M|doi=10.1177/1362361307078132|pmid=17656398}}</ref> Someone with ASD may respond atypically to medications, the medications can have adverse side effects, and no known medication relieves autism's core symptoms of social and communication impairments.<ref name=Strock/>
+Medications are often used to treat problems associated with ASD. More than half of U.S. children diagnosed with ASD are prescribed [[psychoactive drug]]s or [[anticonvulsant]]s, with the most common drug classes being [[antidepressant]]s, [[stimulant]]s, and [[antipsychotic]]s.<ref>{{cite journal|journal=J Child Adolesc Psychopharmacol|date=2007|volume=17|issue=3|pages=348–55|title=Medication use among children with autism spectrum disorders|author=Oswald DP, Sonenklar NA|doi=10.1089/cap.2006.17303|pmid=17630868}}</ref> The FDA has approved the antipsychotic [[risperidone]] for treating symptomatic irritability in autistic children and adolescents.<ref>{{cite press release|publisher=FDA|date=[[2006-10-06]]|url=http://www.fda.gov/bbs/topics/NEWS/2006/NEW01485.html|accessdate=2006-10-02|title=FDA approves the first drug to treat irritability associated with autism, Risperdal}}</ref> Other drugs are prescribed [[off-label]], which means they have not been approved for treating ASD. For example, [[serotonin reuptake inhibitors]] and [[dopamine]] blockers can sometimes reduce some symptoms.<ref name=Penn/> However, there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.<ref>{{cite journal|journal=Autism|date=2007|volume=11|issue=4|pages=335–48|title=Systematic review of the effectiveness of pharmacological treatments for adolescents and adults with autism spectrum disorder|author=Broadstock M, Doughty C, Eggleston M|doi=10.1177/1362361307078132|pmid=17656398}}</ref> Someone with ASD may respond atypically to medications, the medications can have adverse side effects, and no known medication relieves autism's core symptoms of social and communication impairments.<ref name=Strock/>
 Many other therapies and interventions are available. Few are supported by scientific studies.<ref name=Francis>{{cite journal|journal=Dev Med Child Neurol|date=2005|volume=47|issue=7|pages=493–9|title=Autism interventions: a critical update|author=Francis K|pmid=15991872|url=http://journals.cambridge.org/production/action/cjoGetFulltext?fulltextid=313204|format=PDF}}</ref><ref>Lack of support for interventions:
@@ Line 148: / Line 148: @@
 *{{cite journal|journal=J Autism Dev Disord|date=2007|title=Social skills interventions for children with Asperger's syndrome or high-functioning autism: a review and recommendations|author=Rao PA, Beidel DC, Murray MJ|doi=10.1007/s10803-007-0402-4|pmid=17641962}}</ref><ref name=Aman/> Treatment approaches lack empirical support in [[quality of life|quality-of-life]] contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.<ref name=Burgess/> Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.<ref>{{cite journal|url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?pubmedid=16467905|accessdate=2007-07-12|journal=Focus Autism Other Dev Disabl|date=2005|volume=20|issue=2|pages=66–79|title=Early intervention practices for children with autism: descriptions from community providers|author=Stahmer AC, Collings NM, Palinkas LA|pmid=16467905}}</ref> Even if they do not help, conservative treatments such as changes in diet are probably harmless aside from their bother and cost.<ref name=Christison>{{cite journal|journal=J Dev Behav Pediatr|date=2006|volume=27|issue=2 Suppl 2|pages=S162–71|title=Elimination diets in autism spectrum disorders: any wheat amidst the chaff?|author=Christison GW, Ivany K|pmid=16685183}}</ref> Dubious invasive treatments are a much more serious matter: for example, in 2005, botched [[chelation therapy]] killed a 5-year-old autistic boy.<ref name=Doja/>
-Treatment is expensive; indirect costs are more so. A U.S. study estimated the average additional lifetime cost due exclusively to autism to be $3.2 million in 2003 US dollars for an autistic individual born in 2000, with about 10% medical care, 30% nonmedical care such as child care and education, and 60% the lost economic productivity of individuals and their parents.<ref>{{cite journal|journal=Arch Pediatr Adolesc Med|date=2007|volume=161|issue=4|pages=343–9|title=The lifetime distribution of the incremental societal costs of autism|author=Ganz ML|pmid=17404130|url=http://archpedi.ama-assn.org/cgi/content/full/161/4/343}}</ref> A British study estimated an average lifetime cost of ₤2.4 million in 1997–1998 British pounds.<ref>{{cite journal|journal=Autism|date=2001|volume=5|issue=1|pages=7–22|title=The economic impact of autism in Britain|author=Järbrink K, Knapp M|doi=10.1177/1362361301005001002|pmid=11708392}}</ref> Legal rights to treatment are complex, vary with location and age, and require advocacy by caregivers.<ref name=Aman>{{cite journal|journal=J Clin Psychiatry|date=2005|volume=66|issue=Suppl 10|pages=38–45|title=Treatment planning for patients with autism spectrum disorders|author=Aman MG|pmid=16401149}}</ref> 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.<ref>{{cite journal|journal=J Fam Econ Iss|date=2007|volume=28|issue=2|pages=247–64|doi=10.1007/s10834-007-9059-6|title=Financial issues associated with having a child with autism|author=Sharpe DL, Baker DL}}</ref> After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.<ref name=Aman/>
+Treatment is expensive; indirect costs are more so. A U.S. study estimated the average additional lifetime cost due exclusively to autism to be $3.2 million in 2003 US dollars for an autistic individual born in 2000, with about 10% medical care, 30% nonmedical care such as child care and education, and 60% the lost economic productivity of individuals and their parents.<ref>{{cite journal|journal=Arch Pediatr Adolesc Med|date=2007|volume=161|issue=4|pages=343–9|title=The lifetime distribution of the incremental societal costs of autism|author=Ganz ML|pmid=17404130|url=http://archpedi.ama-assn.org/cgi/content/full/161/4/343}}</ref> A British study estimated an average lifetime cost of ₤2.4 million in 1997–1998 British pounds.<ref>{{cite journal|journal=Autism|date=2001|volume=5|issue=1|pages=7–22|title=The economic impact of autism in Britain|author=Järbrink K, Knapp M|doi=10.1177/1362361301005001002|pmid=11708392}}</ref> Legal rights to treatment are complex, vary with location and age, and require advocacy by caregivers.<ref name=Aman>{{cite journal|journal=J Clin Psychiatry|date=2005|volume=66|issue=Suppl 10|pages=38–45|title=Treatment planning for patients with autism spectrum disorders|author=Aman MG|pmid=16401149}}</ref> 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.<ref>{{cite journal|journal=J Fam Econ Iss|date=2007|volume=28|issue=2|pages=247–64|doi=10.1007/s10834-007-9059-6|title=Financial issues associated with having a child with autism|author=Sharpe DL, Baker DL}}</ref> After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.<ref name=Aman/>
 ==Prognosis==
@@ Line 166: / Line 166: @@
 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,<ref>Changes in diagnostic practices:
 *{{cite journal|author=Fombonne E|title=The prevalence of autism|journal=JAMA|date=2003|volume=289|issue=1|pages=87–9|pmid=12503982}}
-*{{cite journal|author=Wing L, Potter D|title=The epidemiology of autistic spectrum disorders: is the prevalence rising?|journal=Ment Retard Dev Disabil Res Rev|volume=8|issue=3|year=2002|pages=151–61|pmid=12216059|doi=10.1002/mrdd.10029}}</ref> though as-yet-unidentified contributing environmental risk factors cannot be ruled out.<ref name=Rutter>{{cite journal|author=[[Michael Rutter|Rutter M]]|title=Incidence of autism spectrum disorders: changes over time and their meaning|journal=Acta Paediatr|volume=94|issue=1|date=2005|pages=2–15|pmid=15858952}}</ref> A widely-cited 2002 pilot study concluded that some of the observed increase in autism in California was real,<ref>{{cite paper|author=Byrd RS, Sage AC, Keyzer J ''et al.''|publisher=[[M.I.N.D. Institute]]|title=Report to the legislature on the principal findings of the epidemiology of autism in California: a comprehensive pilot study|date=2002|url=http://www.ucdmc.ucdavis.edu/mindinstitute/newsroom/study_final.pdf|accessdate=2006-09-18|format=PDF}}</ref> but a 2006 analysis found that special education data poorly measured prevalence because so many cases were undiagnosed, and that the 1994–2003 U.S. increase was associated with declines in other diagnostic categories, indicating that diagnostic substitution had occurred.<ref>{{cite journal|journal=Pediatrics|date=2006|volume=117|issue=4|pages=1028–37|title=The contribution of diagnostic substitution to the growing administrative prevalence of autism in US special education|author=Shattuck PT|doi=10.1542/peds.2005-1516|pmid=16585296|url=http://pediatrics.aappublications.org/cgi/content/full/117/4/1028}}</ref>
+*{{cite journal|author=Wing L, Potter D|title=The epidemiology of autistic spectrum disorders: is the prevalence rising?|journal=Ment Retard Dev Disabil Res Rev|volume=8|issue=3|year=2002|pages=151–61|pmid=12216059|doi=10.1002/mrdd.10029}}</ref> though as-yet-unidentified contributing environmental risk factors cannot be ruled out.<ref name=Rutter>{{cite journal|author=[[Michael Rutter|Rutter M]]|title=Incidence of autism spectrum disorders: changes over time and their meaning|journal=Acta Paediatr|volume=94|issue=1|date=2005|pages=2–15|pmid=15858952}}</ref> A widely cited 2002 pilot study concluded that some of the observed increase in autism in California was real,<ref>{{cite paper|author=Byrd RS, Sage AC, Keyzer J ''et al.''|publisher=[[M.I.N.D. Institute]]|title=Report to the legislature on the principal findings of the epidemiology of autism in California: a comprehensive pilot study|date=2002|url=http://www.ucdmc.ucdavis.edu/mindinstitute/newsroom/study_final.pdf|accessdate=2006-09-18|format=PDF}}</ref> but a 2006 analysis found that special education data poorly measured prevalence because so many cases were undiagnosed, and that the 1994–2003 U.S. increase was associated with declines in other diagnostic categories, indicating that diagnostic substitution had occurred.<ref>{{cite journal|journal=Pediatrics|date=2006|volume=117|issue=4|pages=1028–37|title=The contribution of diagnostic substitution to the growing administrative prevalence of autism in US special education|author=Shattuck PT|doi=10.1542/peds.2005-1516|pmid=16585296|url=http://pediatrics.aappublications.org/cgi/content/full/117/4/1028}}</ref>
 It is unknown whether autism's prevalence increased during the same period. An increase in prevalence would suggest directing more attention and funding toward changing environmental factors instead of continuing to focus on genetics.<ref name=Szpir/> Chris Johnson, co-chair of the [[American Academy of Pediatrics]] Autism Expert Panel, summed up the 2005 state of the issue by saying, "There is a chance we're seeing a true rise, but right now I don't think anybody can answer that question for sure."<ref>{{cite news|author=Stenson J|title=As autism cases soar, a search for clues|date=[[2005-02-24]]|work=MSNBC|url=http://www.msnbc.msn.com/id/6947652/|accessdate=2007-06-26}}</ref>

v t e Autism
Main	Causes Diagnosis Epidemiology Epigenetics Heritability History Memory Pathophysiology Sex and gender Societal and cultural aspects Therapies
Diagnoses	Pervasive developmental disorder Classic autism Asperger syndrome Pervasive developmental disorder not otherwise specified Childhood disintegrative disorder High-functioning autism
Associated conditions and phenomena	Alexithymia Autism and LGBT identities Autistic burnout Autistic catatonia Autistic masking Autistic meltdown Hyperlexia Late talker Monotropism Nonverbal autism Pathological demand avoidance Savant syndrome Special interests Infodumping Stimming
Comorbid conditions	Avoidant/restrictive food intake disorder Attention deficit hyperactivity disorder Anxiety disorder obsessive–compulsive disorder Developmental coordination disorder Epilepsy Intellectual disability Sensory processing disorder Global developmental delay Verbal Dyspraxia
Associated syndromes	22q11.2 deletion syndrome 22q13 deletion syndrome Angelman syndrome CHARGE syndrome Cohen syndrome Cornelia de Lange syndrome Down syndrome Fetal valproate spectrum disorder Fragile X syndrome MECP2 duplication syndrome Neurofibromatosis type I Noonan syndrome PTEN hamartoma tumor syndrome Rett syndrome Smith–Lemli–Opitz syndrome Timothy syndrome Tuberous sclerosis complex Williams syndrome
Related issues	Autism rights movement Critical autism studies Double empathy problem Multiple complex developmental disorder Neurodiversity TEACCH program Violence and autism
Controversies	Facilitated communication Lancet MMR autism fraud MMR vaccine Rapid prompting method Thiomersal Chelation
Diagnostic scales	Autism Diagnostic Interview Autism Diagnostic Observation Schedule Childhood Autism Rating Scale Gilliam Asperger's disorder scale
Screening scales	Autism-spectrum quotient Childhood Autism Spectrum Test Ritvo Autism and Asperger Diagnostic Scale
Lists	Autism-related topics Fictional characters Schools
Accommodations	Autism-friendly Sensory friendly