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, or by rare combinations of common genetic variants.[5] In rare cases, autism is strongly associated with agents that cause birth defects.[6] Controversies surround other proposed environmental causes, such as heavy metals, pesticides or childhood vaccines;[7] the vaccine hypotheses are biologically implausible and lack convincing scientific evidence.[8] The prevalence of autism is about 1–2 per 1,000 people worldwide; however, the Centers for Disease Control and Prevention (CDC) reports approximately 9 per 1,000 children in the United States are diagnosed with ASD.[9][10] The number of people diagnosed with autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.[11]
Parents usually notice signs in the first two years of their child's life.[12] The signs usually develop gradually, but some autistic children first develop more normally and then regress.[13] Early behavioral or cognitive intervention can help autistic children gain self-care, social, and communication skills.[12] Although there is no known cure,[12] there have been reported cases of children who recovered.[14] Not many children with autism live independently after reaching adulthood, though some become successful.[15] An autistic culture has developed, with some individuals seeking a cure and others believing autism should be accepted as a difference and not treated as a disorder.[16]
Characteristics
Autism is a highly variable neurodevelopmental disorder[17] that first appears during infancy or childhood, and generally follows a steady course without remission.[18] Overt symptoms gradually begin after the age of six months, become established by age two or three years,[19] and tend to continue through adulthood, although often in more muted form.[20] It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.[21] Autism's individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathologically severe from common traits.[22]
Social development
Social deficits distinguish autism and the related autism spectrum disorders (ASD; see Classification) from other developmental disorders.[20] People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals, or people with normal neural development, as leaving her feeling "like an anthropologist on Mars".[23]Unusual social development becomes apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers differ more strikingly from social norms; for example, they have less eye contact and turn taking, and do not have the ability to use simple movements to express oneself, such as the deficiency to point at things.[24] 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.[25] Most autistic children display moderately less attachment security than non-autistic children, although this difference disappears in children with higher mental development or less severe ASD.[26] Older children and adults with ASD perform worse on tests of face and emotion recognition.[27]
Children with high-functioning autism suffer from more intense and frequent loneliness compared to non-autistic peers, despite the common belief that children with autism prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel. Functional friendships, such as those resulting in invitations to parties, may affect the quality of life more deeply.[28]
There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in non-autistic children with language impairments.[29] A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.[30]
Communication
About a third to a half of individuals with autism do not develop enough natural speech to meet their daily communication needs.[31] Differences in communication may be present from the first year of life, and may include delayed onset of babbling, unusual gestures, diminished responsiveness, and vocal patterns that are not synchronized with the caregiver. In the second and third years, autistic children have less frequent and less diverse babbling, consonants, words, and word combinations; their gestures are less often integrated with words. Autistic children are less likely to make requests or share experiences, and are more likely to simply repeat others' words (echolalia)[32][33] or reverse pronouns.[34] Joint attention seems to be necessary for functional speech, and deficits in joint attention seem to distinguish infants with ASD:[4] for example, they may look at a pointing hand instead of the pointed-at object,[24][33] and they consistently fail to point at objects in order to comment on or share an experience.[4] Autistic children may have difficulty with imaginative play and with developing symbols into language.[32][33]In a pair of studies, high-functioning autistic children aged 8–15 performed equally well as, and adults better than, individually matched controls at basic language tasks involving vocabulary and spelling. Both autistic groups performed worse than controls at complex language tasks such as figurative language, comprehension and inference. As people are often sized up initially from their basic language skills, these studies suggest that people speaking to autistic individuals are more likely to overestimate what their audience comprehends.[35]
Repetitive behavior
Autistic individuals display many forms of repetitive or restricted behavior, which the Repetitive Behavior Scale-Revised (RBS-R)[36] categorizes as follows.
- Stereotypy is repetitive movement, such as hand flapping, making sounds, head rolling, or body rocking.
- Compulsive behavior is intended and appears to follow rules, such as arranging objects in stacks or lines.
- Sameness is resistance to change; for example, insisting that the furniture not be moved or refusing to be interrupted.
- Ritualistic behavior involves an unvarying pattern of daily activities, such as an unchanging menu or a dressing ritual. This is closely associated with sameness and an independent validation has suggested combining the two factors.[36]
- Restricted behavior is limited in focus, interest, or activity, such as preoccupation with a single television program, toy, or game.
- Self-injury includes movements that injure or can injure the person, such as eye poking, skin picking, hand biting, and head banging.[4] A 2007 study reported that self-injury at some point affected about 30% of children with ASD.[29]
Other symptoms
Autistic individuals may have symptoms that are independent of the diagnosis, but that can affect the individual or the family.[21] An estimated 0.5% to 10% of individuals with ASD show unusual abilities, ranging from splinter skills such as the memorization of trivia to the extraordinarily rare talents of prodigious autistic savants.[38] Many individuals with ASD show superior skills in perception and attention, relative to the general population.[39] Sensory abnormalities are found in over 90% of those with autism, and are considered core features by some,[40] although there is no good evidence that sensory symptoms differentiate autism from other developmental disorders.[41] Differences are greater for under-responsivity (for example, walking into things) than for over-responsivity (for example, distress from loud noises) or for sensation seeking (for example, rhythmic movements).[42] An estimated 60%–80% of autistic people have motor signs that include poor muscle tone, poor motor planning, and toe walking;[40] deficits in motor coordination are pervasive across ASD and are greater in autism proper.[43]Unusual eating behavior occurs in about three-quarters of children with ASD, to the extent that it was formerly a diagnostic indicator. Selectivity is the most common problem, although eating rituals and food refusal also occur;[29] this does not appear to result in malnutrition. Although some children with autism also have gastrointestinal (GI) symptoms, there is a lack of published rigorous data to support the theory that autistic children have more or different GI symptoms than usual;[44] studies report conflicting results, and the relationship between GI problems and ASD is unclear.[45]
Parents of children with ASD have higher levels of stress.[46] Siblings of children with ASD report greater admiration of and less conflict with the affected sibling than siblings of unaffected children or those with Down syndrome; siblings of individuals with ASD have greater risk of negative well-being and poorer sibling relationships as adults.[47]
Classification
Autism is one of the five pervasive developmental disorders (PDD), which are characterized by widespread abnormalities of social interactions and communication, and severely restricted interests and highly repetitive behavior.[18] These symptoms do not imply sickness, fragility, or emotional disturbance.[20]Of the five PDD forms, Asperger syndrome is closest to autism in signs and likely causes; Rett syndrome and childhood disintegrative disorder share several signs with autism, but may have unrelated causes; PDD not otherwise specified (PDD-NOS; also called atypical autism) is diagnosed when the criteria are not met for a more specific disorder.[48] Unlike with autism, people with Asperger syndrome have no substantial delay in language development.[2] The terminology of autism can be bewildering, with autism, Asperger syndrome and PDD-NOS often called the autism spectrum disorders (ASD)[12] or sometimes the autistic disorders,[49] whereas autism itself is often called autistic disorder, childhood autism, or infantile autism. In this article, autism refers to the classic autistic disorder; in clinical practice, though, autism, ASD, and PDD are often used interchangeably.[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.[50]
The manifestations of autism cover a wide spectrum, ranging from individuals with severe impairments—who may be silent, mentally disabled, and locked into hand flapping and rocking—to high functioning individuals who may have active but distinctly odd social approaches, narrowly focused interests, and verbose, pedantic communication.[51] Because the behavior spectrum is continuous, boundaries between diagnostic categories are necessarily somewhat arbitrary.[40] Sometimes the syndrome is divided into low-, medium- or high-functioning autism (LFA, MFA, and HFA), based on IQ thresholds,[52] or on how much support the individual requires in daily life; these subdivisions are not standardized and are controversial. Autism can also be divided into syndromal and non-syndromal autism; the syndromal autism is associated with severe or profound mental retardation or a congenital syndrome with physical symptoms, such as tuberous sclerosis.[53] Although individuals with Asperger syndrome tend to perform better cognitively than those with autism, the extent of the overlap between Asperger syndrome, HFA, and non-syndromal autism is unclear.[54]
Some studies have reported diagnoses of autism in children due to a loss of language or social skills, as opposed to a failure to make progress, typically from 15 to 30 months of age. The validity of this distinction remains controversial; it is possible that regressive autism is a specific subtype,[13][24][32][55] or that there is a continuum of behaviors between autism with and without regression.[56]
Research into causes has been hampered by the inability to identify biologically meaningful subpopulations[57] and by the traditional boundaries between the disciplines of psychiatry, psychology, neurology and pediatrics.[58] Newer technologies such as fMRI and diffusion tensor imaging can help identify biologically relevant phenotypes (observable traits) that can be viewed on brain scans, to help further neurogenetic studies of autism;[59] one example is lowered activity in the fusiform face area of the brain, which is associated with impaired perception of people versus objects.[3] It has been proposed to classify autism using genetics as well as behavior.[60]
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.[61] However, there is increasing suspicion that autism is instead a complex disorder whose core aspects have distinct causes that often co-occur.[61][62]
Several lines of evidence point to synaptic dysfunction as a cause of autism.[3] Some rare mutations may lead to autism by disrupting some synaptic pathways, such as those involved with cell adhesion.[66] Gene replacement studies in mice suggest that autistic symptoms are closely related to later developmental steps that depend on activity in synapses and on activity-dependent changes.[67] All known teratogens (agents that cause birth defects) related to the risk of autism appear to act during the first eight weeks from conception, and though this does not exclude the possibility that autism can be initiated or affected later, it is strong evidence that autism arises very early in development.[6]
Although evidence for other environmental causes is anecdotal and has not been confirmed by reliable studies,[7] extensive searches are underway.[68] Environmental factors that have been claimed to contribute to or exacerbate autism, or may be important in future research, include certain foods, infectious disease, heavy metals, solvents, diesel exhaust, PCBs, phthalates and phenols used in plastic products, pesticides, brominated flame retardants, alcohol, smoking, illicit drugs, vaccines,[11] and prenatal stress,[69] although no links have been found, and some have been completely dis-proven.
Parents may first become aware of autistic symptoms in their child around the time of a routine vaccination. This has led to theories blaming vaccine "overload", a vaccine preservative or the MMR vaccine for causing autism.[8] The latter theory was supported by litigation-funded study that has since been shown to have been "an elaborate fraud".[70] Although these theories lack convincing scientific evidence and are biologically implausible,[8] parental concern about a potential vaccine link with autism has led to lower rates of childhood immunizations, outbreaks of previously-controlled childhood diseases in some countries, and the preventable deaths of several children.[10][71]
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.[72] The behaviors appear to have multiple pathophysiologies.[22]Pathophysiology
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.[17] Autism appears to result from developmental factors that affect many or all functional brain systems,[74] and to disturb the timing of brain development more than the final product.[73] Neuroanatomical studies and the associations with teratogens strongly suggest that autism's mechanism includes alteration of brain development soon after conception.[6] This anomaly appears to start a cascade of pathological events in the brain that are significantly influenced by environmental factors.[75] Just after birth, the brains of autistic children tend to grow faster than usual, followed by normal or relatively slower growth in childhood. It is not known whether early overgrowth occurs in all autistic children. It seems to be most prominent in brain areas underlying the development of higher cognitive specialization.[40] Hypotheses for the cellular and molecular bases of pathological early overgrowth include the following:
- An excess of neurons that causes local overconnectivity in key brain regions.[76]
- Disturbed neuronal migration during early gestation.[77][78]
- Unbalanced excitatory–inhibitory networks.[78]
- Abnormal formation of synapses and dendritic spines,[78] for example, by modulation of the neurexin–neuroligin cell-adhesion system,[79] or by poorly regulated synthesis of synaptic protein.[80][81] Disrupted synaptic development may also contribute to epilepsy, which may explain why the two conditions are associated.[82]
The relationship of neurochemicals to autism is not well understood; several have been investigated, with the most evidence for the role of serotonin and of genetic differences in its transport.[3] Others have pointed to a role for group I metabotropic glutamate receptors (mGluR) in the pathogenesis of one type of autism, Fragile X.[86] Some data suggest an increase in several growth hormones; other data argue for diminished growth factors.[87] Also, some inborn errors of metabolism are associated with autism but probably account for less than 5% of cases.[88]
The mirror neuron system (MNS) theory of autism hypothesizes that distortion in the development of the MNS interferes with imitation and leads to autism's core features of social impairment and communication difficulties. The MNS operates when an animal performs an action or observes another animal perform the same action. The MNS may contribute to an individual's understanding of other people by enabling the modeling of their behavior via embodied simulation of their actions, intentions, and emotions.[89] Several studies have tested this hypothesis by demonstrating structural abnormalities in MNS regions of individuals with ASD, delay in the activation in the core circuit for imitation in individuals with Asperger syndrome, and a correlation between reduced MNS activity and severity of the syndrome in children with ASD.[90] However, individuals with autism also have abnormal brain activation in many circuits outside the MNS[91] and the MNS theory does not explain the normal performance of autistic children on imitation tasks that involve a goal or object.[92]
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.[97] Evidence for this theory has been found in functional neuroimaging studies on autistic individuals[35] and by a brainwave study that suggested that adults with ASD have local overconnectivity in the cortex and weak functional connections between the frontal lobe and the rest of the cortex.[98] Other evidence suggests the underconnectivity is mainly within each hemisphere of the cortex and that autism is a disorder of the association cortex.[99]
From studies based on event-related potentials, transient changes to the brain's electrical activity in response to stimuli, there is considerable evidence for differences in autistic individuals with respect to attention, orientiation to auditory and visual stimuli, novelty detection, language and face processing, and information storage; several studies have found a preference for non-social stimuli.[100] For example, magnetoencephalography studies have found evidence in autistic children of delayed responses in the brain's processing of auditory signals.[101]
In the genetic area, relations have been found between autism and schizophrenia based on duplications and deletions of chromosomes; research showed that schizophrenia and autism are significantly more common in combination with 1q21.1 deletion syndrome. Research on autism/schizophrenia relations for chromosome 15 (15q13.3), chromosome 16 (16p13.1) and chromosome 17 (17p12) are inconclusive.[102]
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. The empathizing–systemizing theory postulates that autistic individuals can systemize—that is, they can develop internal rules of operation to handle events inside the brain—but are less effective at empathizing by handling events generated by other agents. An extension, the extreme male brain theory, hypothesizes that autism is an extreme case of the male brain, defined psychometrically as individuals in whom systemizing is better than empathizing;[103] this extension is controversial, as many studies contradict the idea that baby boys and girls respond differently to people and objects.[104]
These theories are somewhat related to the earlier theory of mind approach, which hypothesizes that autistic behavior arises from an inability to ascribe mental states to oneself and others. The theory of mind hypothesis is supported by autistic children's atypical responses to the Sally–Anne test for reasoning about others' motivations,[103] and the mirror neuron system theory of autism described in Pathophysiology maps well to the hypothesis.[90] However, most studies have found no evidence of impairment in autistic individuals' ability to understand other people's basic intentions or goals; instead, data suggests that impairments are found in understanding more complex social emotions or in considering others' viewpoints.[105]
The second category focuses on nonsocial or general processing. Executive dysfunction hypothesizes that autistic behavior results in part from deficits in working memory, planning, inhibition, and other forms of executive function.[106] Tests of core executive processes such as eye movement tasks indicate improvement from late childhood to adolescence, but performance never reaches typical adult levels.[107] A strength of the theory is predicting stereotyped behavior and narrow interests;[108] two weaknesses are that executive function is hard to measure[106] and that executive function deficits have not been found in young autistic children.[27]
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.[109] A related theory—enhanced perceptual functioning—focuses more on the superiority of locally oriented and perceptual operations in autistic individuals.[110] These theories map well from the underconnectivity theory of autism.
Neither category is satisfactory on its own; social cognition theories poorly address autism's rigid and repetitive behaviors, while the nonsocial theories have difficulty explaining social impairment and communication difficulties.[62] A combined theory based on multiple deficits may prove to be more useful.[111]
Screening
About half of parents of children with ASD notice their child's unusual behaviors by age 18 months, and about four-fifths notice by age 24 months.[55] According to an article in the Journal of Autism and Developmental Disorders, failure to meet any of the following milestones "is an absolute indication to proceed with further evaluations. Delay in referral for such testing may delay early diagnosis and treatment and affect the long-term outcome."[21]- No babbling by 12 months.
- No gesturing (pointing, waving bye-bye, etc.) by 12 months.
- No single words by 16 months.
- No 2-word spontaneous (not just echolalic) phrases by 24 months.
- Any loss of any language or social skills, at any age.
Diagnosis
Diagnosis is based on behavior, not cause or mechanism.[22][115] Autism is defined in the DSM-IV-TR as exhibiting at least six symptoms total, including at least two symptoms of qualitative impairment in social interaction, at least one symptom of qualitative impairment in communication, and at least one symptom of restricted and repetitive behavior. Sample symptoms include lack of social or emotional reciprocity, stereotyped and repetitive use of language or idiosyncratic language, and persistent preoccupation with parts of objects. Onset must be prior to age three years, with delays or abnormal functioning in either social interaction, language as used in social communication, or symbolic or imaginative play. The disturbance must not be better accounted for by Rett syndrome or childhood disintegrative disorder.[2] ICD-10 uses essentially the same definition.[18]Several diagnostic instruments are available. Two are commonly used in autism research: the Autism Diagnostic Interview-Revised (ADI-R) is a semistructured parent interview, and the Autism Diagnostic Observation Schedule (ADOS) uses observation and interaction with the child. The Childhood Autism Rating Scale (CARS) is used widely in clinical environments to assess severity of autism based on observation of children.[24]
A pediatrician commonly performs a preliminary investigation by taking developmental history and physically examining the child. If warranted, diagnosis and evaluations are conducted with help from ASD specialists, observing and assessing cognitive, communication, family, and other factors using standardized tools, and taking into account any associated medical conditions.[116] A pediatric neuropsychologist is often asked to assess behavior and cognitive skills, both to aid diagnosis and to help recommend educational interventions.[117] A differential diagnosis for ASD at this stage might also consider mental retardation, hearing impairment, and a specific language impairment[116] such as Landau–Kleffner syndrome.[118] The presence of autism can make it harder to diagnose coexisting psychiatric disorders such as depression.[119]
Clinical genetics evaluations are often done once ASD is diagnosed, particularly when other symptoms already suggest a genetic cause.[1] Although genetic technology allows clinical geneticists to link an estimated 40% of cases to genetic causes,[120] consensus guidelines in the US and UK are limited to high-resolution chromosome and fragile X testing.[1] A genotype-first model of diagnosis has been proposed, which would routinely assess the genome's copy number variations.[121] As new genetic tests are developed several ethical, legal, and social issues will emerge. Commercial availability of tests may precede adequate understanding of how to use test results, given the complexity of autism's genetics.[122] Metabolic and neuroimaging tests are sometimes helpful, but are not routine.[1]
ASD can sometimes be diagnosed by age 14 months, although diagnosis becomes increasingly stable over the first three years of life: for example, a one-year-old who meets diagnostic criteria for ASD is less likely than a three-year-old to continue to do so a few years later.[55] In the UK the National Autism Plan for Children recommends at most 30 weeks from first concern to completed diagnosis and assessment, though few cases are handled that quickly in practice.[116] A 2009 US study found the average age of formal ASD diagnosis was 5.7 years, far above recommendations, and that 27% of children remained undiagnosed at age 8 years.[123] Although the symptoms of autism and ASD begin early in childhood, they are sometimes missed; years later, adults may seek diagnoses to help them or their friends and family understand themselves, to help their employers make adjustments, or in some locations to claim disability living allowances or other benefits.[124]
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.[125] It is particularly hard to diagnose autism among the visually impaired, partly because some of its diagnostic criteria depend on vision, and partly because autistic symptoms overlap with those of common blindness syndromes or blindisms.[126]
Management
Main article: Autism therapies
Educational interventions can be effective to varying degrees in most children: intensive ABA treatment has demonstrated effectiveness in enhancing global functioning in preschool children[131] and is well-established for improving intellectual performance of young children.[129] Neuropsychological reports are often poorly communicated to educators, resulting in a gap between what a report recommends and what education is provided.[117] It is not known whether treatment programs for children lead to significant improvements after the children grow up,[129] and the limited research on the effectiveness of adult residential programs shows mixed results.[132] The appropriateness of including children with varying severity of autism spectrum disorders in the general education population is a subject of current debate among educators and researchers.[133]
Many medications are used to treat ASD symptoms that interfere with integrating a child into home or school when behavioral treatment fails.[20][134] More than half of US children diagnosed with ASD are prescribed psychoactive drugs or anticonvulsants, with the most common drug classes being antidepressants, stimulants, and antipsychotics.[135] Aside from antipsychotics,[136] there is scant reliable research about the effectiveness or safety of drug treatments for adolescents and adults with ASD.[137] A person with ASD may respond atypically to medications, the medications can have adverse effects,[12] and no known medication relieves autism's core symptoms of social and communication impairments.[138] Experiments in mice have reversed or reduced some symptoms related to autism by replacing or modulating gene function,[67][86] suggesting the possibility of targeting therapies to specific rare mutations known to cause autism.[139][66]
Although many alternative therapies and interventions are available, few are supported by scientific studies.[27][140] Treatment approaches have little empirical support in quality-of-life contexts, and many programs focus on success measures that lack predictive validity and real-world relevance.[28] Scientific evidence appears to matter less to service providers than program marketing, training availability, and parent requests.[141] Some alternative treatments may place the child at risk. A 2008 study found that compared to their peers, autistic boys have significantly thinner bones if on casein-free diets;[142] in 2005, botched chelation therapy killed a five-year-old child with autism.[143]
Treatment is expensive; indirect costs are more so. For someone born in 2000, a US study estimated an average lifetime cost of $3.77 million (net present value in 2011 dollars, inflation-adjusted from 2003 estimate),[144] with about 10% medical care, 30% extra education and other care, and 60% lost economic productivity.[145] 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;[146] one 2008 US study found a 14% average loss of annual income in families of children with ASD,[147] and a related study found that ASD is associated with higher probability that child care problems will greatly affect parental employment.[148] US states increasingly require private health insurance to cover autism services, shifting costs from publicly funded education programs to privately funded health insurance.[149] After childhood, key treatment issues include residential care, job training and placement, sexuality, social skills, and estate planning.[150]
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